Very low-carbohydrate diets work for men and upper body fat

Scientists say that low carbohydrate diets, like the Atkins and South Beach Diets, may actually be the best option for men who want to slim. New research, published this week in the Open Access journal, Nutrition & Metabolism, shows that over 70% of men lost more weight and fat on a low carbohydrate diet, despite eating more calories.

Jeff Volek and colleagues, from the University of Connecticut, also show for the first time that a low carbohydrate diet is much more effective in losing fat from the stomach and chest. Upper body fat carries "a greater health risk than fat stored in other regions of the body," say the authors. They found that fat loss in men was three-times greater in the trunk area, when they were on a low-carbohydrate regime compared to the low-fat diet. Nearly all participants in the study (12 of 15 men and 12 of 13 women) lost more fat on their upper body on the low- carbohydrate diet.

Fifteen overweight or obese men, and thirteen women, were randomly assigned to a very low carbohydrate diet or a low fat diet. After fifty days, they were switched to the other diet. 11 of the 15 men did better on the low carbohydrate diet, six lost greater than 10 lbs more on the low carbohydrate diet, and one subject lost almost 25 pounds more. Similar results were found for women although the results were less dramatic.

Volek and colleagues also looked at whether weight and fat loss were affected by what order the diets were done in. Their data seem to favour undertaking a low carbohydrate first, suggesting that those who have concerns about long term 'low carb' diets could follow a low carb diet first followed by a low fat diet.

There is much debate about the health implications of long-term use of low carbohydrate diets. Volek's lab, whose work is the first-ever to be funded in part by the Robert C. Atkins Foundation, has previously shown that low carbohydrate diets improve cardiovascular risk factors.

For more information about low carbohydrate diets read the review by well-known endocrinologist, Samy McFarlane, in Nutrition & Metabolism. Dr McFarlane reviews the new book, 'Atkins Diabetes Revolution', by Mary C. Vernon, M.D. and Jacqueline A. Eberstein, R.N. McFarlane and co-reviewer Surender Arora, M.D. found the book "sufficiently convincing to make us believe that some form of low carbohydrate intervention is worth investigating and should be considered by practitioners. The highly negative un-scientific response of critics, if anything, encourages us in this direction."

This press release is based on:

Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women Volek JS, Sharman MJ, Gómez AL, Judelson DA, Rubin MR, Watson G, Sokmen B, Silvestre R, French DN, and Kraemer WJ. Nutrition & Metabolism 2004, 1:12 (9 November 2004)

The article is freely available at http://www.nutritionandmetabolism.com/content/1/1/12.

Source: EurekAlert

"A calorie is a calorie" violates the second law of thermodynamics

Richard D Feinman and Eugene J Fine

Nutrition Journal 2004, 3:9 doi:10.1186/1475-2891-3-9

Published 28 July 2004

Abstract (provisional)

The principle of "a calorie is a calorie," that is, that weight change in hypocaloric diets is independent of macronutrient composition, is widely held in the popular and technical literature, and is frequently justified by appeal to the laws of thermodynamics. We review here some aspects of thermodynamics that bear on weight loss and the effect of macronutrient composition. The focus is the so-called metabolic advantage in low-carbohydrate diets - greater weight loss compared to isocaloric diets of different composition. Two laws of thermodynamics are relevant to the systems considered in nutrition and, whereas the first law is a conservation (of energy) law, the second is a dissipation law: something (negative entropy) is lost and therefore balance is not to be expected in diet interventions. Here, we propose that a misunderstanding of the second law accounts for the controversy about the role of macronutrient effect on weight loss and we review some aspects of elementary thermodynamics. We use data in the literature to show that thermogenesis is sufficient to predict metabolic advantage. Whereas homeostasis ensures balance under many conditions, as a general principle, "a calorie is a calorie" violates the second law of thermodynamics.

Provisional pdf

Thermodynamic Edge For Low Carbohydrate Diets

SUNY Downstate Researchers Say All Calories Are NOT Alike

In a paper published in Nutrition Journal (Open Access, available without subscription at http://www.nutritionj.com/home), two researchers from SUNY Downstate Medical Center show that low carbohydrate, high protein diets can be expected to be more effective than low fat diets, going against long standing prejudice of the nutritional community, which has claimed that only calories count.

(PRWEB) July 31, 2004 -- “There are numerous examples of low carbohydrate diets being more effective than low fat diets with the same number of calories. It doesn’t always happen but it can happen,” said Dr. Richard Feinman of the Department of Biochemistry. “The nutritional establishment has been reluctant to accept this, because they say it violates the law of thermodynamics. However, they never seriously look at the thermodynamics, which not only says its possible, but it is to be expected.” he added.

In their paper, Dr. Feinman and Dr. Eugene J. Fine explain that thermodynamics is as much about efficiency as it is about energy conservation. Carbohydrate is an efficient fuel, whereas protein is not. On a low carbohydrate/high protein diet, even though total energy is conserved, more energy is wasted as heat, a process known as thermogenesis. This energy comes from burning fat.

The researchers stress that “the human body is not a storage locker. It is a machine and the efficiency of the machine is controlled by hormones and enzymes. Carbohydrates increase insulin and other hormones that regulate enzymes, leading to storage rather than burning of fat.”

“Of course, people are different” said the authors, “but many people are sensitive to the effects of carbohydrates and for them, a low carb diet is going to work well.”

The practical point is that getting rid of the idea that “a calorie is a calorie” opens the door for serious research into what kind of diets will be most effective and which people will benefit most. “This is important,” they explain “because millions of people
are seriously trying to lose weight on low carbohydrate diets, and instead of being given directions on the best way to do this, they have been largely discouraged by health professionals and self-appointed expert groups. The obesity epidemic is too important to allow this to happen.”

Note to editors/reporters: You can read the entire scientific paper by going to http://www.nutritionj.com/home and clicking on “Provisional PDF” at the bottom of the headline.

Confessions of a no-carb chef

From The Times Online

by Ann Treneman
Impressed with his weight loss on Atkins but appalled by the recipes, a gourmet chef has created his own
Henry Harris is a conundrum. On the one hand he is the chef who has brought a taste of award-winning French cuisine to West London. On the other, he has just written a diet cookbook. And, even worse, it’s not any diet, it’s Atkins. Henry is a gourmet who has gone low- carb. It’s almost the stuff of confessions.

Or so it seems before we meet. I am to interview him about the book but, in the name of research, I go along to his restaurant, Racine, first. It is exactly like a proper French restaurant should be, all dark banquettes, seamless service and fresh food dressed in delicate sauces. At first it seems the opposite of low-carb living. But as I salivate over my asparagus and lamb, I realise this is low carb, it is just low carb with glamour.

by Ann Treneman
Impressed with his weight loss on Atkins but appalled by the recipes, a gourmet chef has created his own
Henry Harris is a conundrum. On the one hand he is the chef who has brought a taste of award-winning French cuisine to West London. On the other, he has just written a diet cookbook. And, even worse, it’s not any diet, it’s Atkins. Henry is a gourmet who has gone low- carb. It’s almost the stuff of confessions.

Or so it seems before we meet. I am to interview him about the book but, in the name of research, I go along to his restaurant, Racine, first. It is exactly like a proper French restaurant should be, all dark banquettes, seamless service and fresh food dressed in delicate sauces. At first it seems the opposite of low-carb living. But as I salivate over my asparagus and lamb, I realise this is low carb, it is just low carb with glamour.

This is quite a revelation. The Atkins diet, as outlined in the famous orange book, may work but it has its drawbacks. I have been on it for a year and although none of the horror stories is true — after the first few weeks you can eat quite a lot of carbs — the food is as drab as a faded housedress. I am tired of hamburger patties and cottage cheese, not to mention “snack” avocados.

What I had not realised, until I met Harris, was that there is an alternative. He too went on the diet a year ago. He lost 2½st (16kg) and has kept it off. But he was not content to survive on my kind of dull fare. Nor was he willing to sacrifice his sense of taste in terms of finding substitutes for carbs or sugar. “The recipes at the back of the Atkins book were terrible,” he said. “I tried the chocolate mousse with artificial sugar and had a taste of it and it tasted like artificial sugar.” He didn’t make it again.

Harris believes in real food and that is what he likes to cook, and eat, for himself and his family. He stresses that Racine is not an Atkins restaurant (the breadbasket on every table backs this up). But, as I had discovered, it is relatively easy to order a low-carb meal in a French restaurant. Harris notes that this is not the case if you are eating Italian (because of pasta) or Indian and Chinese (because of rice).

He had written for various newspapers over the years and, as his weight loss became dramatic, was asked to devise his own low-carb recipes. Though sceptical at first, he found the list kept growing and, more importantly, that he was proud of it. The result is the cookbook A Passion for Protein. The name may not be so delectable (I suspect it was a marketing decision) but the recipes are intriguing, not least because they involve no cottage cheese. I never thought that rabbit with mustard sauce and bacon would be low-carb or, for that matter, baked crab with tomato and tarragon hollandaise. But they are.

For those of us who have come to think that a boiled egg is very tasty indeed, this is exciting. Harris also has devised interesting ways to replace the carb element in foods. Some are obvious, such as using crumbled cooked bacon or pork scratchings instead of croutons, but others include using finely shredded celeriac or courgette in place of pasta, and replacing burger buns with cooked large flat mushrooms.

I suspect that chefs and diets do not go together and, as the interview continues, this becomes a bit of a theme. We talk in the morning at Racine. Harris, who is 40, is wearing his chef whites and it is clear that what he is passionate about is food, not diets. In fact, he is downright suspicious of them. “I think that people on diets, whether it’s something really extreme like the cabbage soup diet or WeightWatchers, are very, very constrained by the rules. They put themselves on a diet, say WeightWatchers, mess up and then they say, oh f*** it and binge. It is like an alcoholic; when they fall off the wagon, they have to descend to new depths.”

The way round this, he believes, lies in the attitude. “I avoid the word diet. I use the word regime.” And, for him, the biggest regime change has been rice. “I used to eat risotto two or three times a week.” This was not the case for pasta and bread. A great pasta dish is a joy, he says, but they are few and far between, and the same goes for bread. The last piece of “epic bakery” he experienced was a crusty bread roll at Merchant House in Ludlow. He describes this in sumptuous detail but adds, with what may be relief, that it is a rarity.

We turn to the vexed subject of puddings. Harris announces that he sees sugar as napalm. Cream on its own is harmless but, when you add sugar, something explosively bad for you happens. He refuses to use sugar substitutes, and so the book has only three puddings: pineapple with rum and crème fraiche, raspberries and Jersey cream, and vodka and lemon tonic jelly. He compensates for this somewhat by including some killer cocktails including a classic Martini.

Harris believes that, if you don’t say that something is low carb, then no one will know. He had a dinner party at the weekend at which he served asparagus and then steak au poivre. Other vegetables included button mushrooms, french beans and a salad of watercress and shallots. He also offered, though did not eat himself, new potatoes cooked with whole garlic. Then there was cheese and, finally, squares of delicious dark bitter chocolate. I’m not sure that anyone could describe that as deprivation.

A Passion for Protein, by Henry Harris, is published by Quadrille, £14.99

*TASTE THIS!*

*JAMBON DE BAYONNE WITH CELERIAC REMOULADE*
Serves 8

I large head of celeriac (or 2 smaller ones)
16 slices of Bayonne ham
3 tbsp capers

For the remoulade sauce:
4 egg yolks
6 canned anchovy fillets, drained
3 tbsp Dijon mustard
Splash of red wine vinegar 350ml vegetable oil
Tiny splash of hot water

First make the remoulade sauce: place the egg yolks, anchovy fillets, mustard and red wine vinegar in a food processor. Blitz to a smooth state and then add the oil, initially drop by drop, building up to a more confident stream as the mayonnaise forms. When all the oil is incorporated, add the hot water. Season to taste, and perhaps add more mustard if needed.

Peel the celeriac and cut into very fine strips. Place the celeriac in a bowl and mix in the mustard mayonnaise. Hands work best here. Cover and refrigerate until needed.

To serve, place a pile of the celeriac in the middle of each plate. Arrange 2 slices of ham around the edge, then sprinkle over a few capers.

From The Times Online

Wanker Alert!

By Anthony Colpo.

May 31, 2004.

TheOmnivore.com's BS detector has been sounding off at ear-shattering levels this week, after being triggered by some particularly idiotic claims appearing in the media!

The first of these comes to us courtesy of those sadly misguided anti-meat, vegan fanatics who call themselves the Physicians Committee for Responsible Medicine. After desperately searching for individuals who have allegedly experienced adverse reactions on the Atkins diet and are prepared to sue (the PCRM have an entire web site devoted to this caper), they finally found someone prepared to step up to the plate in the form of one Jody Gorran.

Read full article at: The Omnivore

Drs. Atkins and Agatston, You Were So Right

From the The Scientist

Their low-carb diets are on target--control appetite, control weight | By Ricki Lewis

On January 20, I joined the ranks of those who've sacrificed themselves for science: I started one of those "low-carb" diets. So far, the sacrifice has been worth it.

I'd always resisted celebrity-sponsored diets, smugly thinking my background in genetics and biochemistry made me more of an authority on matters nutritional than the likes of Whoopi Goldberg and Sarah Ferguson. I've even taught the subject.

But this low-carb diet is different. It prescribes "good carbs and good fats" while blacking out most things white and processed, including rice, bread, pasta, and potatoes. Building on conventional wisdom about the evils of excess starch, this program also considers insulin swings.

A new way of viewing carbohydrates began in 1981, when a University of Toronto team measured the glycemic index (GI) for many foods. The GI is a measure of the speed at which foods hike blood glucose and therefore insulin secretion, averaged in numerous individuals.1 A maximum for comparison purposes is either white bread or straight glucose. The idea is that rapid insulin fluctuation, as it shoves glucose into cells, sparks hunger.

GI numbers can be counterintuitive. For example, instant oatmeal sends insulin secretion skyrocketing, whereas whole oats do not, presumably due to digestion-slowing fiber. Even an unembellished baked potato becomes the enemy.

I had long wondered why following the US Department of Agriculture's food pyramid, which endorses a low-fat diet, plus daily exercise, had not vanquished a nanogram of me. Then my younger sister, a person who once wore size zero jeans, lost 10 pounds in two weeks following a low-carb diet. She left me no choice: I had to do it.

Day 1 was OK, my hypothalamus not yet registering glycogen depletion. By day 2, however, my head pounded, and all government-sanctioned painkillers were useless. Then I suddenly envisioned the glycolytic pathway and surreptitiously took a gulp of Pepsi; I felt instant relief. On day 4, I awoke feeling like aliens had replaced my body with a younger, more energetic model. Carb cravings vanished; pounds, too.

Months later, low-carb has become a way of life, even as my husband and daughter continue eating starchy foods, which I cook. I no longer want them. It's part metabolic, part psychological, a Pavlovian response linking a diet of mostly eggs, meat, cheese and certain vegetables with plummeting pounds, illogical as that may seem.

My husband the chemist and ex-marathoner, acknowledging his girth but unwilling to sacrifice pasta and potatoes, invented the NPCAD ("no potato chips after dinner") plan. His strategy: "I've eaten a lot of junk food all my life; now I don't." Being an XY without hormone issues, of course he's had little trouble shedding weight.

Considering my low-carb experience, I'd like to shed the USDA's food pyramid. I write textbooks, and the one I'm working on now carries this suspect guideline, with its broad bottom advocating those forbidden foods (the same ones the USDA oversees, grains), and the bulk of my present diet relegated to the "use sparingly" pyramid tip. Change is slow in textbook land, and my coauthors overruled my objections, this time around.

For years I, too, accepted the almighty pyramid, introduced in 1992, as dogma. When I taught nutrition, I preached that weight was a simple consequence of calories-in versus calories-out, food type unimportant. Because fats impart nine calories per gram compared to four for proteins and carbohydrates, with all intake being equal, fats were out. The fallacy is that all intake isn't equal. The glucose rush from refined carbohydrates does seem to intensify hunger inappropriately. In contrast, fats promote satiety. That's why mounds of spaghetti get polished off easier than large slabs of beef. So while calories-in must balance calories-out, eat fewer carbs and less will go in. The much-maligned Robert Atkins based his diet on the effects of appetite, and Arthur Agatston, who developed the South Beach Diet, iterated it. For me, evidence of friends shrinking on either diet, anecdotal as it is, convinced me that for some people, the USDA pyramid should be flipped.

Controlled studies are beginning to emerge. Two trials comparing low-carb to low-fat declared the former the winner, for both weight loss and improved lipid profiles, within the first six months. After a year, such differences vanished, but many on the low-fat diet dropped out.2,3 However, these studies, like many previous ones, were too short and were limited to obese people. The prescription: more studies.

But I don't need them as proof. I'm unscientifically convinced with my sample of one. I've never felt better, and since January I've lost 25 pounds.

*Ricki Lewis (ralewis@nycap.rr.com) is a freelance writer in Scotia, NY.*

References
1. D.J.A. Jenkins et al., "Glycemic index of foods--a physiological basis for carbohydrate exchange," Am J Clin Nutr, 34:362-6, 1981.

2. F.F. Samaha et al., "A low-carbohydrate as compared with a low-fat diet in severe obesity," N Engl J Med, 348:2074-81, 2003.

3. G.D. Foster et al., "A randomized trial of a low-carbohydrate diet for obesity," N Engl J Med, 348:2082-90, 2003.

LOW-CARB RIPOFFS

From Second Opinions

The overweight and obese have always provided a very lucrative and ready market for food companies to exploit with expensive, nutrient-poor, highly-processed, slimming 'foods' and diet products. Some of these, the liquid powders you made into a drink, were made largely from skim milk powder, with added chemicals and artificial flavours. The ingredients were very cheap for the manufacturers to buy (skim milk powder is almost given away), but were very expensive for the dieter to buy. Others included inert fillers which contained no food at all.

I had hoped that when the new low-carb way of eating caught on, these rip-off merchants would be unable to sell their products and go into liquidation.

How naïve I was!

The current low-carb 'fad' has allowed the food companies to widen their net to ensnare even more people with even more rip-offs, which are even more expensive. Here are some examples on sale to the 'low-carb diet' market (I have written comments in blue below each one):

Read the full article here: Second Opinions

The Atkins Experiment [Guardian]

Guardian science correspondent Alok Jha is going on the Atkins diet in an attempt to find out what it really does to your body and mind. He'll be monitored by a team of scientists who will look at everything from what's happening to his mood to how the chemicals in his blood are changing.

Read his diary at:

26 Feb 2004
The great Atkins experiment. Diet cynic Alok Jha embarks on the low-carb routine to see what it does to his body - and his mind

25 Mar 2004
In the beginning...

08 Apr 2004
How to leave the bread behind

06 May 2004
Why I'm not a low-carb revolutionary just yet

Related message board:
Guardian Unlimited : The Talk

Hunter-Gatherers, Low-carb Diets, and Adrenalin

Full article by Anthony Colpo: The Omnivore

Is a calorie a calorie?

American Journal of Clinical Nutrition, Vol. 79, No. 5, 899S-906S, May 2004
© 2004 American Society for Clinical Nutrition

Andrea C Buchholz and Dale A Schoeller

From the Department of Nutritional Sciences, University of Wisconsin-Madison

The aim of this review was to evaluate data regarding potential thermodynamic mechanisms for increased rates of weight loss in subjects consuming diets high in protein and/or low in carbohydrate. Studies that compared weight loss and energy expenditure in adults consuming diets high in protein and/or low in carbohydrate with those in adults consuming diets low in fat were reviewed. In addition, studies that measured the metabolizable energy of proteins, fats, and carbohydrates were reviewed. Diets high in protein and/or low in carbohydrate produced an 2.5-kg greater weight loss after 12 wk of treatment. Neither macronutrient-specific differences in the availability of dietary energy nor changes in energy expenditure could explain these differences in weight loss. Thermodynamics dictate that a calorie is a calorie regardless of the macronutrient composition of the diet. Further research on differences in the composition of weight loss and on the influence of satiety on compliance with energy-restricted diets is needed to explain the observed increase in weight loss with diets high in protein and/or low in carbohydrate.

Thumbs Down: The South Beach Diet

by Stephen Byrnes, PhD, RNCP

With the popularity of low-carb diets reaching a high point recently, it was only a matter of time before someone adjusted it into “nutritional correctness.” Enter The South Beach Diet by cardiologist Arthur Agatston, MD, of Miami, Florida, which has sold millions of copies and has remained on the best-seller list for many months.

The South Beach Diet is most certainly a low-carb eating regime with the usual carbohydrate foods such as bread (even whole grain), fruit, fruit juices, and rice, potatoes, and pasta excluded (or kept to a bare minimum). Of course, white sugar is out, as well as the whole gamut of processed carbohydrate snack foods.

So far, so good. But then the book gets the dieter into trouble because the author urges high protein consumption in the form of skim milk, lean meat and other nonfat foods, and prohibits the use of animal fats, a dangerous combination that rapidly depletes vitamin A stores leading to auto-immune diseases and underactive thyroid (which can cause weight gain) and even cancer and heart disease.

Furthermore, by eliminating both saturated fats and carbohydrate foods, the body has no ready source of the saturated fats it needs to build healthy cell membranes. Many studies have indicated that a regimen like the South Beach diet, high in unsaturated oils (even the so-called monounsaturated oils) and low in saturated result in disease, including heart disease. This is what happens when weak science is allied to political correctness...

Read full article here: Weston A. Price

Research Shows Low Fat Diet Makes People Moody!

Low-fat, high-carbohydrate diets worsen mood states in both humans and animals.

By Anthony Colpo, April 18, 2004.

In 1998, U.K. researchers reported the results of an experiment involving twenty healthy male and female volunteers. One group continued was placed on a 41% fat diet, while the other group consumed a 25% fat diet. After 4 weeks had passed, the groups were swapped around so that those originally on the low-fat diet were now consuming the high-fat diet, and vice-versa. Throughout the study, all meals were prepared by the university conducting the study and supplied to the participants. Both diets were specially designed to be as palatable and similar in taste as possible.

At the beginning and end of each diet period, every subject underwent a battery of psychological assessments, including various mood state questionnaires and an interview by a psychiatrist who was blinded to the participant's dietary status.

The study was tightly-controlled and adherence to the diets appears to have been high. HDL cholesterol levels declined during the low-fat period, a typical response on low-fat, high-carb diets, indicating that subjects ate the foods as supplied.

I feel fine, you #$%@!

What the researchers found was that, while ratings of anger-hostility slightly declined during the high-fat diet period, they significantly increased during the low-fat, high-carb diet period!

Tension-anxiety ratings declined during the high-fat period, but did not change during the four weeks of low-fat, high-carb eating.

Ratings of depression declined slightly during the high-fat period, but increased during the low-fat, high-carb period, mainly due to two of the low-fat subjects reporting significantly greater depression-dejection ratings.

As the researchers stated, the participants of this study were "a psychologically robust group who had never previously suffered from depression or anxiety, and who were not going through any 'stressful' events during the study." They further stated that "The alterations in mood observed in the present study may have been greater if subjects were feeling more stressed or were more susceptible to mental illness."

These observations raise some interesting questions. Could the low-fat, high-carbohydrate diets that have been so heavily promoted over the last thirty years be at least partially responsible for increases in anti-social behavior witnessed during the same period?

That the answer could well be in the affirmative is supported by studies with our primate cousins...

Monkey business turns nasty on low-fat diet!

For 22 months, adult male monkeys were fed a "luxury" diet - (43% calories from fat, 0.34 mg cholesterol/Calorie of diet) or a "prudent" diet (30% calories from fat, 0.05 mg cholesterol/Calorie of diet).

Researchers observed that the low-fat diet monkeys were more irritable and initiated more aggression than the "luxury" diet animals. Hey, I'd be pretty damn ticked too if I had to follow a low-fat diet for almost 2-years!

The prudent diet resulted in lower total serum cholesterol levels. While our dopey health authorities automatically assume this is a good thing, the researchers noted: "These results are consistent with studies linking relatively low serum cholesterol concentrations to violent or antisocial behavior in psychiatric and criminal populations and could be relevant to understanding the significant increase in violence-related mortality observed among people assigned to cholesterol-lowering treatment in clinical trials."

If you don't want to end up a nasty old grump, then it might pay to regularly sink your teeth into a nice, fat, juicy steak!

C'mon, you know you want it...

References

Wells AS, et al. Alterations in mood after changing to a low-fat diet. British Journal of Nutrition, Jan, 1998; 79 (1): 23-30.

Kaplan JR, et al. The effects of fat and cholesterol on social behavior in monkeys. Psychosom Med. 1991 Nov-Dec; 53 (6): 634-642.

Source: The Omnivore

So who is this 'Omnivore' guy, anyway?

Why one man abandoned his 'healthy' low-fat diet.

Read full article here: The Omnivore

Interview: Gary Taubes

FRONTLINE DIET WARS
Science journalist Gary Taubes wrote the controversial July 7, 2002 New York Times Magazine article, What If It's All Been a Big Fat Lie? which turned the spotlight onto high-fat, low carbohydrate diets. In this interview, Taubes explains his motivation for writing his piece, the science behind the low-carbohydrate diet, and the contention he faced when he published his findings. "I got crucified in a variety of publications," he says "... It was fascinating. They go after the messenger as much as the message." He is currently writing a book that is a historical and scientific exploration of the hypothesis that weight gain and chronic disease are caused by excess consumption of easily digestible and refined carbohydrates. This interview was conducted Dec. 10, 2003.

What made you go after this topic in the first place?

Two things. I'd been reporting on salt and blood pressure, which is a huge controversy, and some of the people involved in that were involved in the advice to tell Americans to eat low-fat diets, and they were terrible scientists. These were some of the worst scientists I'd ever come across in my 20-odd year career of writing about controversial science.

I literally called up my editor and said, "I just got off the phone with so-and-so, and he's [taken] credit for getting Americans to eat less eggs and less fat. This guy's one of the worst scientists I've ever talked to, and if he was involved in this, then there's a story there." And that was it. I didn't know what the story was. I just knew there was a story.

Was there a personal motivation?

Before I did it, I was up at MIT, interviewing an economist about another story, a guy who runs a laboratory of financial engineering. He told me about being on the Atkins diet, and how effective it was. He was an Asian-American who had lost 40-50 pounds by giving up white rice, in effect.

I thought I would try it as an experiment, since I was going to write about fat and whether it really did cause heart disease and weight loss. I tried it, and it was amazing. You know, it's everything -- the 20 pounds that I'd never been able to lose, in six weeks, and I stopped exercising. It was kind of a surreal experience, and probably, in a sense, informed my opinions from there on in. I mean, after that happens, you say, "I want to know what's happening, and I want to know why."

Why is it so easy for us to believe that fat is a bad dietary ingredient?

The idea is that fat has nine calories per gram, and carbohydrates and protein have four calories per gram, and somehow the theory is that the denser the calories, the more easier it is for us to eat more of them. What happened is in the '50s and '60s, when researchers started fingering fat as a cause of heart disease, the obesity researchers, the obesity community started advocating low-fat diets, which they had never done before. A low-fat diet is by definition a high-carbohydrate diet.

But you had this sort of synchronicity where you had the heart disease people saying, "Give up fat, saturated fat, for heart disease," and the obesity people started saying, "Give up fat because it must be the best diet because fat is the densest calories." They moved from there without ever testing actually either of those hypotheses, so the obesity people start recommending low-fat diets; the heart disease people are recommending low-fat diets. They have actually no idea whether it's going to cure heart disease, and the obesity people have no idea whether these diets even work. But because they believe that it's only the calories that [are] important, obviously if you give up the major source of calories in the diet, you must lose weight...

Read the full interview here: pbs.org

Adventures in Diet - By Vilhjalmur Stefansson (Part 1)

Harper's Monthly Magazine, November 1935

In 1906 I went to the Arctic with the food tastes and beliefs of the average American. By 1918, after eleven years as an Eskimo among Eskimos, I had learned things which caused me to shed most of those beliefs. Ten years later I began to realize that what I had learned was going to influence materially the sciences of medicine and dietetics. However, what finally impressed the scientists and converted many during the last two or three years, was a series of confirmatory experiments upon myself and a colleague performed at Bellevue Hospital, New York City, under the supervision of a committee representing several universities and other organizations.

In 1906 I went to the Arctic with the food tastes and beliefs of the average American. By 1918, after eleven years as an Eskimo among Eskimos, I had learned things which caused me to shed most of those beliefs. Ten years later I began to realize that what I had learned was going to influence materially the sciences of medicine and dietetics. However, what finally impressed the scientists and converted many during the last two or three years, was a series of confirmatory experiments upon myself and a colleague performed at Bellevue Hospital, New York City, under the supervision of a committee representing several universities and other organizations.

Not so long ago the following dietetic beliefs were common: To be healthy you need a varied diet, composed of elements from both the animal and vegetable kingdoms. You got tired of and eventually felt a revulsion against things if you had to eat them often. This latter belief was supported by stories of people who through force of circumstances had been compelled, for instance, to live for two weeks on sardines and crackers and who, according to the stories, had sworn that so long as they lived they never would touch sardines again. The Southerners had it that nobody can eat a quail a day for thirty days.

There were subsidiary dietetic views. It was desirable to eat fruits and vegetables, including nuts and coarse grains. The less meat you ate the better for you. If you ate a good deal of it, you would develop rheumatism, hardening of the arteries, and high blood pressure, with a tendency to breakdown of the kidneys - in short, premature old age. An extreme variant had it that you would live more healthy, happily, and longer if you became a vegetarian.

Specifically it was believed, when our field studies began, that without vegetables in your diet you would develop scurvy. It was a "known fact" that sailors, miners, and explorers frequently died of scurvy "because they did not have vegetables and fruits." This was long before Vitamin C was publicized.

The addition of salt to food was considered either to promote health or to be necessary for health. This is proved by various yarns, such as that African tribes make war on one another to get salt; that minor campaigns of the American Civil War were focused on salt mines; and that all herbivorous animals are ravenous for salt. I do not remember seeing a critical appendix to any of these views, suggesting for instance, that Negro tribes also make war about things which no one ever said were biological essentials of life; that tobacco was a factor in Civil War campaigns without being a dietetic essential; and that members of the deer family in Maine which never have salt or show desire for it, are as healthy as those in Montana which devour quantities of it and are forever seeking more.

A belief I was destined to find crucial in my Arctic work, making the difference between success and failure, life and death, was the view that man cannot live on meat alone. The few doctors and dietitians who thought you could were considered unorthodox if not charlatans. The arguments ranged from metaphysics to chemistry: Man was not intended to be carnivorous - you knew that from examining his teeth, his stomach, and the account of him in the Bible. As mentioned, he would get scurvy if he had no vegetables in meat. The kidneys would be ruined by overwork. There would be protein poisoning and, in general hell to pay.

With these views in my head and, deplorably, a number of others like them, I resigned my position as assistant instructor in anthropology at Harvard to become anthropologist of a polar expedition. Through circumstances and accidents which are not a part of the story, I found myself that autumn the guest of the Mackenzie River Eskimos.

The Hudson's Bay Company, whose most northerly post was at Fort McPherson two hundred miles to the south had had little influence on the Eskimos during more than half a century; for it was only some of them who made annual visits to the trading post; and then they purchased no food but only tea, tobacco, ammunition and things of that sort. But in 1889 the whaling fleet had begun to cultivate these waters and for fifteen years there had been close association with sometimes as many as a dozen ships and four to five hundred men wintering at Herschel Island, just to the west of the delta. During this time a few of the Eskimos had learned some English and perhaps one in ten of them had grown to a certain extent fond of white man's foods.

But now the whaling fleet was gone because the bottom had dropped out of the whalebone market, and the district faced an old-time winter of fish and water. The game, which might have supplemented the fish some years earlier, had been exterminated or driven away by the intensive hunting that supplied meat to the whaling fleet. There was a little tea, but not nearly enough to see the Eskimos through the winter - this was the only element of the white man's dietary of which they were really fond and the lack of which would worry them. So I was facing a winter of fish without tea. For the least I could do, an uninvited guest, was to pretend a dislike for it.

The issue of fish and water against fish and tea was, in any case, to me six against a half dozen. For I had had a prejudice against fish all my life. I had nibbled at it perhaps once or twice a year at course dinners, always deciding that it was as bad as I thought. This was pure psychology of course, but I did not realize it.

I was in a measure adopted into an Eskimo family the head of which knew English. He had grown up as a cabin boy on a whaling ship and was called Roxy, though his name was Memoranna. It was early September, we were living in tents, the days were hot but it had begun to freeze during the nights, which were now dark for six to eight hours.

The community of three or four families, fifteen or twenty individuals, was engaged in fishing. With long poles, three or four nets were shoved out from the beach about one hundred yards apart. When the last net was out the first would be pulled in, with anything from dozens to hundreds of fish, mostly ranging in weight from one to three pounds, and including some beautiful salmon trout. From knowledge of other white men the Eskimos consider these to be most suitable for me and would cook them specially, roasting them against the fire. They themselves ate boiled fish.

Trying to develop an appetite, my habit was to get up soon after daylight, say four o'clock, shoulder my rifle, and go off after breakfasts on a hunt south across the rolling prairie, though I scarcely expected to find any game. About the middle of the afternoon I would return to camp. Children at play usually saw me coming and reported to Roxy's wife, who would then put a fresh salmon trout to roast. When I got home I would nibble at it and write in my diary what a terrible time I was having.

Against my expectation, and almost against my will, I was beginning to like the baked salmon trout when one day of perhaps the second week I arrived home without the children having seen me coming. There was no baked fish ready but the camp was sitting round troughs of boiled fish. I joined them and, to my surprise, liked it better than the baked. There after the special cooking ceased, and I ate boiled fish with the Eskimos.

II

By midwinter I had left my cabin-boy host and, for the purposes of anthropological study, was living with a less sophisticated family at the eastern edge of the Mackenzie delta. Our dwelling was a house of wood and earth, heated and lighted with Eskimo-style lamps. They burned seal or whale oil, mostly white whale from a hunt of the previous spring when the fat had been stored in bags and preserved, although the lean meat had been eaten. Our winter cooking however, was not done over the lamps but on a sheet-iron stove which had been obtained from whalers. There were twenty-three of us living in one room, and there were sometimes as many as ten visitors. The floor was then so completely covered with sleepers that the stove had to be suspended from the ceiling. The temperature at night was round 60*F. The ventilation was excellent through cold air coming up slowly from below by way of a trap door that was never closed and the heated air going out by a ventilator in the roof.

Everyone slept completely naked - no pajama or night shirts. We used cotton or woolen blankets which had been obtained from the whalers and from the Hudson's Bay Company.

In the morning, about seven o'clock, winter-caught fish, frozen so hard that they would break like glass, were brought in to lie on the floor till they began to soften a little. One of the women would pinch them every now and then until, when she found her finger indented them slightly, she would begin preparations for breakfast. First she cut off the head and put them aside to be boiled for the children in the afternoon (Eskimos are fond of children, and heads are considered the best part of the fish). Next best are the tails, which are cut off and saved for the children also. The woman would then slit the skin along the back and also along the belly and getting hold with her teeth, would strip the fish somewhat as we peel a banana, only sideways where we peel bananas, endways.

Thus prepared, the fish were put on dishes and passed around. Each of us took one and gnawed it about as an American does corn on the cob. An American leaves the cob; similarly we ate the flesh from the outside of the fish, not touching the entrails. When we had eaten as much as we chose, we put the rest on a tray for dog feed.

After breakfast all the men and about half the women would go fishing, the rest of the women staying at home to keep house. About eleven o'clock we came back for a second meal of frozen fish just like the breakfast. At about four in the afternoon the working day was over and we came home to a meal of hot boiled fish.

Also we came home to a dwelling so heated by the cooking that the temperature would range from 85* to 100*F. or perhaps even higher - more like our idea of a Turkish bath than a warm room. Streams of perspiration would run down our bodies, and the children were kept busy going back and forth with dippers of cold water of which we naturally drank great quantities.

Just before going to sleep we would have a cold snack of fish that had been left over from dinner. Then we slept seven or eight hours and the routine of the day began once more.

After some three months as a guest of the Eskimos I had acquired most of their food tastes. I had to agree that fish is better boiled than cooked any other way, and that the heads (which we occasionally shared with the children) were the best part of the fish. I no longer desired variety in the cooking, such as occasional baking - I preferred it always boils if it was cooked. I had become as fond of raw fish as if I had been a Japanese. I like fermented (therefore slightly acid) whale oil with my fish as well as ever I liked mixed vinegar and olive oil with a salad. But I still had two reservations against Eskimo practice; I did not eat rotten fish and I longed for salt with my meals.

There were several grades of decayed fish. The August catch had been protected by longs from animals but not from heat and was outright rotten. The September catch was mildly decayed. The October and later catches had been frozen immediately and were fresh. There was less of the August fish than of any other and, for that reason among the rest, it was a delicacy - eaten sometimes as a snack between meals, sometimes as a kind of dessert and always frozen, raw.

In midwinter it occurred to me to philosophize that in our own and foreign lands taste for a mild cheese is somewhat plebeian; it is at least a semi-truth that connoisseurs like their cheeses progressively stronger. The grading applies to meats, as in England where it is common among nobility and gentry to like game and pheasant so high that the average Midwestern American or even Englishman of a lower class, would call them rotten.

I knew of course that, while it is good form to eat decayed milk products and decayed game, it is very bad form to eat decayed fish. I knew also that the view of our populace that there are likely to be "ptomaines" in decaying fish and in the plebeian meats; but it struck me as an improbable extension of the class-consciousness that ptomaines would avoid the gentleman's food and attack that of a commoner.

These thoughts led to a summarizing query; If it is almost a mark of social distinction to be able to eat strong cheeses with a straight face and smelly birds with relish, why is it necessarily a low taste to be fond of decaying fish? On that basis of philosophy, though with several qualms, I tried the rotten fish one day, and if memory servers, like it better than my first taste of Camembert. During the next weeks I became fond of rotten fish.

About the fourth month of my first Eskimo winter I was looking forward to every meal (rotten or fresh), enjoying them, and feeling comfortable when they were over. Still I kept thinking the boiled fish would taste better if only I had salt. From the beginning of my Eskimo residence I had suffered from this lack. On one of the first few days, with the resourcefulness of a Boy Scout, I had decided to make myself some salt, and had boiled sea water till there was left only a scum of brown powder. If I had remembered as vividly my freshman chemistry as I did the books about shipwrecked adventurers, I should have know in advance that the sea contains a great many chemicals besides sodium chloride, among them iodine. The brown scum tasted bitter rather than salty. A better chemist could no doubt have refined the product. I gave it up, partly through the persuasion of my host, the English speaking Roxy.

The Mackenzie Eskimos, Roxy told me, believe that what is good for grown people is good for children and enjoyed by them as soon as they get used to it. Accordingly they teach the use of tobacco when a child is very young. It then grows to maturity with the idea that you can't get along without tobacco. But, said Roxy, the whalers have told that many whites get along without it, and he had himself seen white men who never use it, while the few white women, wives of captains, none used tobacco. (This, remember, was in 1906.)

Now Roxy had heard that white people believe that salt is good for, and even necessary for children, so they begin early to add salt to the child's food. That child then would grow up with the same attitude toward salt as an Eskimo has toward tobacco. However, said Roxy, since we Eskimos were mistaken in thinking tobacco so necessary, may it be that the white men are mistaken about salt? Pursuing the argument, he concluded that the reason why all Eskimos dislike salted food and all white men like it was not racial but due to custom. You could then, break the salt habit as easily as the tobacco habit and you would suffer no ill result beyond the mental discomfort of the first few days or weeks.

Roxy did not know, but I did as an anthropologist, that in pre-Columbian times salt was unknown or the taste of it disliked and the use of it avoided through much of North and South America. It may possibly be true that the carnivorous Eskimos in whose language the word salty, mamaitok, is synonymous with with evil-tasting, disliked salt more intensely than those Indians who were partly herbivorous. Nevertheless, it is clear that the salt habit spread more slowly through the New World from the Europeans than the tobacco habit through Europe from the Indians. Even today there are considerable areas, for instance in the Amazon basin, where the natives still abhor salt. Not believing that the races differ in their basic natures, I felt inclined to agree with Roxy that the practice of slating food is with us a social inheritance and the belief in its merits a part of our folklore.

Through this philosophizing I was somewhat reconciled to going without salt, but I was nevertheless, overjoyed when one day Ovayuak, my new host in the eastern delta, came indoors to say that a dog team was approaching which he believed to be that of Ilavinirk, a man who had worked with whalers and who possessed a can of salt. Sure enough, it was Ilavinirk, and he was delighted to give me the salt, a half-pound baking-powder can about half full, which he said he had been carrying around for two or three years, hoping sometime to meet someone who would like it for a present. He seemed almost as pleased to find that I wanted the salt as I was to get it. I sprinkled some on my boiled fish, enjoyed it tremendously, and wrote in my diary that it was the best meal I had had all winter. Then I put the can under my pillow, in the Eskimo way of keeping small and treasured things. But at the next meal I had almost finished eating before I remembered the salt. Apparently then my longing for it had been what you might call imaginary. I finished without salt, tried it at one or two meals during the next few days and thereafter left it untouched. When we moved camp the salt remained behind.

After the return of the sun I made a journey of several hundred miles to the ship Narwhal which, contrary to our expectations of the late summer, had really come in and wintered at Herschel Island. The captain was George P. Leavitt, of Portland, Maine. For the few days of my visit I enjoyed the excellent New England cooking, but when I left Herschel Island I returned without reluctance to the Eskimo meals of fish and cold water. It seemed to me that, mentally and physically, I had never been in better health in my life.

III

During the first few months of my first year in the Arctic, I acquired, though I did not at the time fully realize it, the munitions of fact and experience which have within my own mind defeated those views of dietetics reviewed at the beginning of this article. I could be healthy on a diet of fish and water. The longer I followed it the better I liked it, which meant, at least inferentially and provisionally, that you never become tired of your food if you have only one thing to eat. I did not get scurvy on the fish diet nor learn that any of my fish-eating friends ever had it. Nor was the freedom from scurvy due to the fish being eaten raw - we proved that later. (What it was due to we shall deal with in the second article of this series.) There were certainly no signs of hardening of the arteries and high blood pressure, of breakdown of the kidneys or of rheumatism.

These months on fish were the beginning of several years during which I lived on an exclusive meat diet. For I count in fish when I speak of living on meat, using "meat" and "meat diet" more as a professor of anthropology than as the editor of a housekeeping magazine. The term in this article and in like scientific discussions refers to a diet from which all things of the vegetable kingdom are absent.

To the best of my estimate then, I have lived in the Arctic for more than five years exclusively on meat and water. (This was not, of course, one five-year stretch, but an aggregate of that much time during ten years.) One member of my expeditions, Storker Storkersen, lived on an exclusive meat diet for about the same length of time while there are several who have lived on it from one to three years. These have been of many nationalities and of three races - ordinary European whites; natives of the Cape Verde Islands, who had a large percentage of Negro blood; and natives of the South Sea Islands. Neither from experience with my own men nor from what I have heard of similar cases do I find any racial difference. There are marked individual differences.

The typical method of breaking a party into a meat diet is that three of five of us leave in midwinter a base camp which has nearly or quite the best type of European mixed diet that money and forethought can provide. The novices have been told that it is possible to live on meat alone. We warn them that it is hard to get used to for the first few weeks, but assure them that eventually they will grow to like it and that any difficulties in changing diets will be due to their imagination.

These assertions the men will believe to a varying degree. I have a feeling that in the course of breaking in something like twenty individuals; two or three young men believed me completely, and that this belief collaborated strongly with their youth and adaptability in making them take readily to the meat.

Usually I think, the men believe that what I tell of myself is true for me personally, but that I am peculiar, a freak - that a normal person will not react similarly, and that they are going to be normal and have an awful time. Their past experience seems to tell them that if you eat one thing every day you are bound to tire of it. In the back of their minds there is also what they have read and heard about the necessity for a varied diet. They have specific fears of developing the ailments which they have heard of as caused by meat or prevented by vegetables.

We secure our food in the Arctic by hunting and in midwinter there is not enough good hunting light. Accordingly we carry with us from the base camp provisions for several weeks, enough to take us into the long days. During this time, as we travel away from shore, we occasionally kill a seal or a polar bear and eat their meat along with our groceries. Our men like these as an element of a mixed diet as well as you do beef or mutton.

We are not on rations. We eat all we want, and we feed the dogs what we think is good for them. When the traveling conditions are right we usually have two big meals a day, morning and evening, but when we are storm bound or delayed by open water we eat several meals to pass the time away. At the end of four, six or eight weeks at sea, we have used up all our food. We do not try to save a few delicacies to eat with the seal and bear, for experience has proved that such things are only tantalizing.

Suddenly, then we are on nothing but seal. For while our food at sea averages ten percent polar bear there may be months in which we don't see a bear. The men go at the seal loyally; they are volunteers and whatever the suffering, they have bargained for it and intend to grin and bear it. For a day or two they eat square meals. Then the appetite begins to flag and they discover as they had more than half expected, that for them personally it is going to be a hard pull or a failure. Some own up that they can't eat, while others pretend to have good appetites, enlisting the surreptitious help of a dog to dispose of their share. In extreme cases, which are usually those of the middle-aged and conservative they go two or three days practically or entirely without eating. We had no weighing apparatus; but I take it that some have lost anything from ten to twenty pounds, what with the hard work on empty stomachs. They become gloomy and grouchy and, as I once wrote, "They begin to say to each other, and sometimes to me, things about their judgment in joining a polar expedition that I cannot quote."

But after a few days even the conservatives begin to nibble at the seal meat, after a few more they are eating a good deal of it, rather under protest and at the end of three or four weeks they are eating square meals, though still talking about their willingness to give a soul or right arm for this or that. Amusingly, or perhaps instructively, they often long for ham and eggs or corned beef when, according to theory, they ought to be longing for vegetables and fruits. Some of them do hanker particularly for things like sauerkraut or orange juice; but more usually it is for hot cakes and syrup or bread and butter.

There are two ways in which to look at an abrupt change of diet - how difficult it is to get used to what you have to eat and how hard it is to be deprived of things you are used to and like. From the second angle, I take it to be physiologically significant that we have found our people, when deprived, to long equally for things which have been considered necessities of health, such as salt; for things where a drug addiction is considered to be involved, such as tobacco; and for items of that class of so-called staple foods, such as bread.

It has happened on several trips, and with an aggregate of perhaps twenty men, that they have had to break at one time their salt, tobacco, and bread habits. I have frequently tried the experiment of asking which they would prefer; salt for their meal, bread with it, or tobacco for an after-dinner smoke. In nearly every case the men have stopped to consider, nor do I recall that they were ever unanimous.

When we are returning to the ship after several months on meat and water, I usually say that the steward will have orders to cook separately for each member of the party all he wants of whatever he wants. Especially during the last two or three days, there is a great deal of talk among the novices in the part about what the choices are to be. One man wants a big dish of mashed potatoes and gravy; another a gallon of coffee and bread and butter; a third perhaps wants a stack of hot cakes with syrup and butter.

On reaching the ship each does get all he wants of what he wants. The food tastes good, although not quite so superlative as they had imagined. They have said they are going to eat a lot and they do. Then they get indigestion, headache, feel miserable, and within a week, in nine cases out of ten of those who have been on meat six months or over, they are willing to go back to meat again. If a man does not want to take part in a second sledge journey it is usually for a reason other than the dislike of meat.

Still, as just implied, the verdict depends on how long you have been on the diet. If at the end of the first ten days our men could have been miraculously rescued from the seal and brought back to their varied foods, most of them would have sworn forever after that they were about to die when rescued, and they would have vowed never to taste seal again - vows which would have been easy to keep for no doubt in such cases the thought of seal, even years later, would have been accompanied by a feeling of revulsion. If a man has been on meat exclusively for only three or four months he may or may not be reluctant to go back to it again. But if the period has been six months or over, I remember no one who was unwilling to go back to meat. Moreover, those who have gone without vegetables for an aggregate of several years usually thereafter eat a larger percentage of meat than your average citizen, if they can afford it.

End of Part 1 | Part 2 | Part 3

Adventures in Diet - By Vilhjalmur Stefansson (Part 2)

Harper's Monthly Magazine, December 1935

Now that the experiments in diet which Karsen Anderson and I undertook at Bellevue Hospital have been accepted by the medical world, it is difficult to realize that there could have been such a storm of excitement about the announcement of the plan, such a violent clash of opinions, such near unanimity to the prediction of dire results.

The feeling that decisive controlled test were needed began to spread after I told one of the scientific heads of the Food Administration in 1918 that I had lived for an aggregate of more than five years with enjoyment on just meat and water. A turning point came in 1920 when I had an hour for explaining a meat regimen to the physicians and staff at the Mayo Clinic. The concluding phase began in 1928 when Mr. Anderson and myself entered Bellevue Hospital to give science the first chance in its history to observe human subjects while they lived through the chill of winter and the heat of summer, for twelve months, on an exclusive meat diet. We were to do it under conditions of ordinary city life.

At the beginning of our northern work in 1906 it was the accepted view among doctors and dietitians that man cannot live on meat alone. They believed specifically that a group of serious diseases were either caused directly by meat or preventable only by vegetables. Those views were still being held when the autumn of 1918, an old friend, Frederic C. Walcott (later Senator from Connecticut), decided that my experiences and the resulting opinions were revolutionary in certain fields, and introduced me to Professor Raymond Pearl of John Hopkins, who was then with the U.S. Food Administration in Washington. Pearl considered several of the things I told him upsetting to views then held; he questioned me before a stenographer, and sent the mimeographed results to a number of dietitians. Their replies varied from concurrence with him (and me) to agreement with David Hume that you are likelier to meet a thousand liars than one miracle.

Pearl was convinced that neither fibs nor miracles were involved and proposed that we write a book on dietetics. I agreed. But cares intervened and things dragged.

In 1920 I had the above-mentioned chance to speak at the Mayo Clinic, Rochester, Minnesota. One of the Mayo brothers suggested that I spend two or three weeks there to have a check-over and see whether they could not find evidences of the supposed bad effects of meat. I wanted to do this but commitments in New York prevented.

Then one day while talking with the gastro-enterologist Dr. Clarence W. Lieb, I told him of my regret that I had not been able to take advantage of the Mayo check-over. Lieb said there were good doctors in New York, too, and volunteered to gather a committee of specialists who would put me through and examination as rigid as anything I could get from the Mayos.

The committee was organized, I went through the mill, and Dr. Lieb reported the findings in the Journal of the American Medical Association for July 3, 1926, "The Effects of an Exclusive Long-Continued Meat Diet." The committee had failed to discover any trace of even one of the supposed harmful effects.

With this publication the Lieb and Pearl events merge. For when the Institute of American Meat Packers wrote asking permission to reprint a large number of copies for distribution to the medical profession and to dietitians, Lieb, Pearl and I went into a huddle. The result was a letter to the Institute saying that we refused permission to reprint, but suggesting that they might get something much better worth publishing, and with right to publish it, if they gave a fund to a research institution for a series of experiments designed to check, under conditions of average city life, the problems which had arisen out of my experiences and views. For it was contended by many that an all-meat diet might work in a cold climate though not in a warm, and under the strenuous conditions of the frontier though not in common American (sedentary) business life.

We gave the meat packers warning that, if anything, the institution chosen would lean backward to make sure that nothing in the results could even be suspected of having been influenced by the source of the money.

After much negotiating, the Institute agreed to furnish the money. The organization selected was the Russell Sage Institute of Pathology. The committee in charge was to consist of leaders in the most important sciences that appeared related to the problem, and represented seven institutions:

American Museum of Natural History: Dr. Clark Wissler.
Cornell University Medical College: Dr. Walter L. Niles.
Harvard University: Drs. Lawrence J. Henderson, Earnest A. Hooton, and Percy Howe.
Institute of American Meat Packers: Dr. C. Robert Moulton.
John Hopkins University: Drs. William G. McCallum and Raymond Pearl.
Russell Sage Institute of Pathology: Drs. Eugene F. DuBois and Graham Lusk.
University of Chicago: Dr. Edwin O. Jordan.
Unattached: Dr. Clarence W. Lieb, private practice, and Vilhjalmur Stefansson.

The Chairman of the committee was Dr. Pearl. The main research work of the experiment was headed by Dr. DuBois, who is now Physician-in-Chief of the New York Hospital and was then as he still is, Medical Director of the Russell Sage Institute of Pathology. Among his collaborators were Dr. Walter S. McClellan, Dr. Henry B. Richardson, Mr. V. R. Rupp, Mr. G. F. Soderstrom, Dr. Henry J. Spencer, Dr. Edward Tolstoi, Dr. John C. Torrey and Mr. Vincent Toscani. The clinical supervision was in charge of Dr. Lieb.

After meetings of the supervising committee, the election of a smaller executive committee and much discussion, it was decided that, while the experiment would be directed at strictly scientific problems, there might be side glances now and then toward common folk beliefs and the propaganda of certain groups. For instance, our definition of a meat diet as "a diet from which all vegetable elements are excluded" would permit us to use milk and eggs, for they are not vegetables. But some vegetarians are illogical enough to allow milk and eggs; we agreed to be correspondingly illogical and exclude them. This forestalled the possible cry that we were saved from the ill effects of a vegetable-less diet by the eggs and the milk.

The aim of the project was not, as the press claimed at the time, to "prove" something or other. We were not trying to prove or disprove anything; we merely wanted to get at the facts. Every aspect of the results would be studied, but special attention would be paid to certain common views, such as that scurvy will result from the absence of vegetable elements, that other deficiency diseases may be produced, that the effect will be bad on the circulatory system and on the kidneys, that certain harmful micro-organisms will flourish in the intestinal tract, and that there will be insufficient calcium. The broad question was, of the supervising doctors and by the testimony of the subjects themselves.

The test was originally planned on me alone, but I might be struck by lightening before conclusions were reached, or I might get run over by a truck, and that would be construed, by mixed-dieters and vegetarians, as showing impairment of mental alertness and bodily vigor through the monotony and poison of meat. It was difficult to find a colleague, for you cannot make this sort of experiment on just anybody that appears if you consider two elementary cases.

Assume the news of a stock market crash that ruins them is conveyed to a number of people after they have eaten a good meal. Digestion may stop almost at the point of the mental shock. Obviously the sickness which follows that meal is not caused by the food, as such.

Or ask some impressionable friend to lunch. Serve them veal, of good quality and well cooked. When dinner is over you inquire about the veal; they will answer with the usual compliments. Then you say that your case has been proved. Rover died and they have eaten him. If your stage setting and acting have been at all adequate, a few at least of your company will make a dive from the room. What sickens them is not the meat of a dog but the idea that they have eaten dog.

The Russell Sage experiment then could not be made upon anybody controlled by any strong dietetic belief, such as that meat is harmful, that abstinence from vegetables brings trouble, that you tire of a food if you have to eat the same thing often. But almost everyone holds these or similar beliefs. So we were practically compelled to secure subjects from members of one of my expeditions; they were the only living Europeans we knew who had used meat long enough to eliminate completely the mental hazards.

One man fortunately was available. He was Karsten Anderson, a young Dane who had been a member of my third expedition. During that time he had lived an aggregate of more than a year on strictly meat and water, suffering no ill result and, in fact being on one occasion cured by meat from scurvy which he had contracted on a mixed diet. Moreover, he knew from experience of a dozen members of the expedition that his healthful enjoyment of the diet was not peculiar to himself but common to all those who had tried it, including members of three races - ordinary whites, Cape Verde Islanders with a strain of Negro blood, and South Sea Islanders.

But there were other things which made Anderson almost incredibility suitable for our test. For several years he had been working on his own in Florida spending most of practically every day outdoors, lightly clad and enjoying the benefits (such as they are) of a sub-tropical sunlight. In that mental and physical environment he had naturally been on a diet heavy in vegetable elements, and had suffered constantly from head colds, his hair was thinning steadily; and he had developed a condition involving intestinal toxemia such as would ordinarily cause a doctor to look serious and pronounce: "You must go light on meat." or "I am afraid you'll have to cut out meat entirely."

We could find no one but Anderson whose mind would leave his body unhandicapped. So, in January 1928, the test began with the two of us. It was under the direct charge of Dr. DuBois and his staff in the dietetic ward of Bellevue Hospital, New York City.

A storm of protests from friends broke upon us when the press announced that we were entering Bellevue. These were based mainly upon the report that we were going to eat our meat raw and the belief that we were using lean meat exclusively. The first was just a false rumor; the trouble under the second head was linguistic.

Eating meat raw, our friends chorused, would make us social outcasts. It is proper to serve oysters raw, and clams, in the United States; herring raw in Norway; several kinds of fish raw in Japan; and beef raw almost anywhere in the world if only you change the name and call it rare. The fashion of giving raw meat to infants was spreading, but we were babes neither in years nor in stature and could not take advantage of that dispensation.

The answer to the raw meat scare was to explain a basic procedure of our experiments - Anderson and I were to select our food by palate (so long as it was meat). It proved that in most of our meals for a year he leaned to medium cooking and I to well done.

The linguistic trouble came from a recent change of American usage. In Elizabethan English meat was any kind of food, as in the expression "meat and drink." In modern England this has narrowed down to what is implied by the rhyme about Jack Sprat eating no fat and his wife no lean, although they both ate meat. In the United States meat, in the last few years has become a synonym for lean. The meaning can become even narrower, as when somebody, usually a woman, tells you that she is strictly forbidden by her physician to touch meat, but that she is permitted all the chicken she wants, with an occasional lamb chop. To that woman meat signifies lean beef.

In the linguistic sense, then we pacified our friends by reference to Mr. and Mrs. Sprat. Our diet would be of meat in the English sense. We were just going to live under modern conditions on the food of our more or less remote ancestors; the food, too, of certain contemporary "primitive hunters."

II

During our first three weeks in Bellevue Hospital we were fed measured quantities of what might be called a standard mixed diet; fruits, cereals, bacon and eggs, that sort of thing for breakfast; meats, vegetables including fruits for lunch and dinner. During this time various specialists examined us from practically every angle that seemed pertinent.

Most tedious, and let us hope correspondingly valuable, were the calorimeter studies. With no food since the evening before, we would go in the late morning to the calorimeter room and sit quite for an hour to get over the physiological effect of having perhaps walked up a single flight of stairs. Then as effortlessly as we could, we slid into calorimeters which were like big coffins with glass sides, and everybody waited about an hour or so until we had got over the disturbance of having slid in. The box was now closed up, and for three hours we lay there as nearly motionless as we could well be while a corps of scientists visible through the glass puttered about and studied our chemical and other physiological processes. We were not permitted to read and cautioned even against thinking about anything particularly pleasant or particularly disagreeable, for thoughts and feelings heat or cool you, speed things up or slow them down, play hob generally with "normal" processes.

(Dr. DuBois told of a calorimeter test ruined by mental disturbance. A nervous Romanian had developed an intense dislike for a fellow-patient named Kelly. During the second hour of an experiment that had been going very well, Max caught a glimpse of the hated Kelly through the window. This raised his metabolism ten percent during that whole hour.)

With the air we breathed and the rest of our intakes and excretions carefully analyzed, with our blood chemistry determined and a check on such things as the billions of living organisms which inhabit the human intestinal tract, we were ready for the meat.

During the three weeks of mixed diet and preliminary check-up, we had been free to come and go. Now we were placed under lock and key. Neither of us was permitted at any time, day or night to be out of sight of a doctor or nurse. This was in part the ordinary rigidity of a controlled scientific experiment, but it was in some part a bow to the skepticism of the mixed diet advocates and to the emotional storms which were sweeping the vegetarian realms.

Not was the skepticism and excitement all newspaper talk. One of the leading European authorities, most orthodox and belonging to no particular school, was touring the United States. He called on us during the preliminary three weeks and assured the presiding physicians most solemnly that we should be unable to go more than four or five days on meat. He had tried it out himself on experimental human subjects who usually broke down in about three days. These breakdowns, I thought, were of psychological antecedents; but our European authority instituted they were strictly psychological - quite independent of emotions.

The experiment started smoothly with Andersen, who was permitted to eat in such quantity as he liked such things as he liked, provided only that they came under our definition of meat - steaks, chops, brains fried in bacon fat, boiled short-ribs, chicken, fish, liver and bacon. In my case there was a hitch, in a way foreseen.

For I had published in 1913, on pages 140-142 of My Life with the Eskimo, an account of how some natives and I became ill when we had to go two or three weeks on lean meat, caribou so skinny that there was no appreciable fat behind the eyes or in the marrow. So when Dr. DuBois suggest that I start the meat period by eating as large quantities as I possibly could of chopped fatless muscle, I predicted trouble. But he countered by citing my own experience where illness had not come until after two or three weeks, and he now proposed lean for only two or three days. So I gave in.

The chief purpose of placing me abruptly on exclusively lean was that there would be a sharp contrast with Andersen who was going to be on a normal meat diet, consisting of such proportions of lean and fat as his own taste determined.

As said, in the Arctic we had become ill during the second or third fatless week. I now became ill on the second fatless day. The time difference between Bellevue and the Arctic was due no doubt mainly to the existence of a little fat, here and there in our northern caribou - we had eaten the tissue from behind the eyes, we had broken the bones for marrow, and in doing everything we could to get fat we had evidently secured more than we realized. At Bellevue the meat, carefully scrutinized, had been as lean as such muscle tissue can be. Then, in the Arctic we had eaten tendons and other indigestible matter, we had chewed the soft ends of bones, getting a deal of bulk that way when we were trying to secure fat. What we ate at Bellevue contained no bulk material, so that my stomach could be compelled to hold a much larger amount of lean.

The symptoms brought on at Bellevue by an incomplete meat diet (lean without fat) were exactly the same as in the Arctic, except that they came on faster - diarrhea and a feeling of general baffling discomfort.

Up north the Eskimos and I had been cured immediately when we got some fat. Dr. DuBois now cured me the same way, by giving me fat sirloin steaks, brains fried in bacon fat, and things of that sort. In two or three days I was all right, but I had lost considerable weight.

III

For the first three weeks I was watched day and night by the Institute staff. My exercise was supposed to be about that of an average business man. I went out for walks, but always under guard. If I telephoned, the attendant stood at the door of the booth; if I went into a shop, he was never more than a few feet away; and he was always vigilant. As Dr. DuBois explained, and as I well knew in advance, this was not because the supervising staff were suspicious of me but rather because they wanted to be able to say that they knew of their own knowledge my complete abstinence from all solids and liquids, except those which I received in Bellevue and which I ate and drank under the watch of attendants.

But my affairs unfortunately demanded that I travel widely through the United States and Canada. This was an added reason why Andersen had been secured for the experiment. When after three weeks, they had to put me on parole, so to speak, they retained him under lock and key for a total of something over 90 days.

Those who believed that a meat diet would lead to death had set at anything from four to fifteen days the point where Dr. Lieb, as clinical supervisor, would have to call a halt in view of danger to the subjects. Those who expected a slower breakdown had placed the appearance of the dread symptoms long before 90 days. In any case, Anderen reported back to the hospital constantly after he left it and I whenever I was in town.

After my three weeks and Andersen's thirteen, and with the constant analyses of excretions and blood when we came back to the hospital for check-ups, the doctors felt certain they would catch us if we broke diet. Moreover, long before the thirteen weeks ended they had satisfied themselves that Andersen had no longing for fruits or other vegetable materials and therefore, no motive for breach of contract.

Toward the end of the covenanted year Andersen and I returned to Bellevue for final intensive studies of some weeks on the meat diet, and then our first three weeks on a mixed diet. At this end of the experiment all went smoothly with me, but not so with Andersen.

My trouble, it will be remembered, had been that at the outset they stuffed me with lean, permitting no fat. His difficulty , or at least annoyance, began on the second day after he completed a year on the meat (January 25, 1929) when they asked him to eat all the fat he could, to the nausea limit, permitting only a tiny bit of lean, about 45 grams per day. There they kept him on the verge of nausea for a week. The second week they added his first taste of vegetables in a year, thrice-cooked cabbage netting about 35 grams of carbohydrate per day. The third week they omitted the cabbage but retained the high proportion of fat to lean.

These three weeks, Andersen says, were the only difficult part of the experiment. Looking back at it now, he thinks if it were possible to separate the nausea from the other unpleasantness there would have been a good deal left over - that he wasn't, properly speaking, well at the end of the third week. However, that is speculation if not imagination.

Returning to facts, we have the ominous one that pneumonia epidemic was sweeping New York. The hospital was crowded with patients; some of the staff got the disease, and with them Andersen. It was Type II pneumonia in his case, and the physicians were gravely worried, for this type was proving deadly in that epidemic, carrying off fifty percent of its Bellevue victims. Andersen, however, reacted quickly to treatment, ran an unusually short course, and convalesced rapidly.

IV

The broad results of the experiment were, so far as Andersen and I could tell, and so far as the supervising physicians could tell, that we were in at least as good average health during the year as we had been during the three mixed-diet weeks at the start. We thought our health had been a little better than average. We enjoyed and prospered as well on the meat in midsummer as in midwinter, and felt no more discomfort from the heat than our fellow New Yorkers did.

In view of beliefs that are strangely current it is worth emphasizing that we liked our meat as fat in July as in January. This ought not to surprise Americans (though it usually does) for they know or have heard that fat pork is a staple and relished food of the Negro in Mississippi. Our Negro literature is rich with the praise of opossum fat, nor did Negroes develop the taste for fats in our Southern States for Carl Akerly relates from tropical Africa such yarns of fat gorging as have not yet been surpassed from the Arctic. A frequent complaint of travelers in Spain is against foods that swim in oil and there are similar complaints when we visit Latin America. We find, when we stop to think that many if not most tropical people love greasy food.

Then there is the parallel belief that the largest meat consumption is in cold countries. True, the hundred-percent centers are way up north, the Eskimos, Samoyeds, Chukchis. But the heaviest meat eaters who speak English are the Australians, tropical and sub-tropical., while the nearest you come to an exclusive meat among people of European stock is in tropical Argentina where the cowboys live on beef and maté. They like their meat fat and (so an Argentinian New Yorker tells me) will threaten to quit work, or at least did twenty years ago, if you attempt to feed them in any considerable part on cereal, greens, and fruits.

It appears that, excepting as tastes are controlled by propaganda and fashion, the longing for fat, summer or winter, depends on what else you eat. If yours is a meat diet then you simply must have fat with your lean; other wise you would sicken and die. But since fats, sugars, and starches are in most practical respects dietetically equivalent, you eat more of any one of them on a mixed diet if you decrease the combined amount of the other two.

Sir Hubert Wilkins, when we were living in the Arctic together, both living exclusively on meats, told me what remains my best single instance of how fats are crowded out by commerce, fashion and expense. The expense is frequently not the least fat, which is only about twice as nourishing as sugar, costs, as I write at my neighborhood grocery 50 cents per pound (bacon) or 35 cents a pound (butter) while sugar is only 5 1/2.

Sir Hubert's father, the first white child born in South Australia, told that when he was young the herdsman, who were the majority of the population, lived practically exclusively on mutton (sometimes on beef) and tea. At all times of year they killed the fattest sheep for their own use and when in the open, which was frequently, they roasted the fattest parts against a fire with a dripping pan underneath, later dipping the meat into the drippings as they ate. But then gradually commerce developed, breads and pastries began to be used, jams and jellies were imported or manufactured, and with the advance of starches and sugars, the use of fat decreased. Now, except that the Australians eat rather more meat per year than people do in the British Isles, the proportion of fat to the rest of the diet is probably about the same in Australia as elsewhere within the Empire.

A conclusion of our experiment which the medical profession seemingly find difficult to assimilate, but which at the same time is one of our clearest results, is that a normal meat diet is not a high protein diet. We averaged about a pound and a third of lean per day and half a pound of fat (this is about like eating a two pound broiled sirloin with the fat such a steak usually has on it). That seems like eating mostly lean; but grow technical and you find, in energy units, that we were really getting three-quarters of our calories from the fat. That is what the scientists meant when they said at the end of our diet had proved to be not so very high in protein.

That meat, as some have contended is a particularly stimulating food I verified during our New York experiment to the extent that it seems to me I was more optimistic and energetic than ordinarily. I looked forward with more anticipation to the next day or the next job and was more likely to expect pleasure or success. This may have a bearing on the common report that the uncivilized Eskimos are the happiest people in the world. There have been many explanations - that a hunter's life is pleasant, and that the poor wretches just don't know how badly off they are. We now add the suggestion that the optimism may be directly caused by what they eat.

Some additional fairly precise things can be said of how we fared during the year on meat. For instance, with Dr. DuBois as a pacemaker, we used every few weeks to run around the reservoir in Central Park and thence to his house, going up the stairs two or three at a time, plumping down on cots and having scientific attendants register our breathing, pulse rate, and other crude reactions. These tests appear to show that our stamina increased with the lengthening of the meat period.

Andersen, who had had one head cold after another when working nearly stripped outdoors in his Florida orange grow, suffered only two or three attacks during the meat year in New York, and those light. He did not regain his hair but he reported that there had been a marked decrease in the shedding. As said, according to the reports of the doctors, Andersen was troubled when he came from Florida with certain toxin-producing intestinal micro-organisms in relation to which physicians at that time ordinarily prescribed elimination of meat from the diet. This condition did not make trouble for him while on the meat.

A phase of our experiment has a relation to slimming, slenderizing, reducing, the treatment of obesity. I was "about ten pounds overweight" at the beginning of the meat diet and lost all of it. This reminds me to say that Eskimos, when still on their native meats, are never corpulent - at least I have seen none. They may be well fleshed. Some especially women, are notably heavier in middle age than when young. But they are not corpulent in our sense.

When you see Eskimos in their native garments you do get the impression of fat round faces on fat round bodies, but the roundness of face is a racial peculiarity and the rest of the effect is produced by loose and puffy garments. See them striped and you do not find the abdominal protuberances and folds which are numerous at Coney Island beaches and so persuasive in arguments against nudism.

There is no racial immunity among Eskimos to corpulence. You prove that by how quickly they get fat and how fat they grow on European diets.

Only one serious fear of the experiments was realized - our diet for the year turned out low in calcium. This was not demonstrated by any tests upon Andersen or me, and certainly you could not have proved it by asking us or looking at us, for we felt better and looked healthier than our average for the years immediately previous. The calcium deficiency appeared solely through the food analysis of the chemists.

Part of our routine was to give the chemists for analysis pieces of meat as nearly as possible identical with those we ate. For instance, lamb would be split down through the middle of the spine and we had the chops from one side cooked for us, while they got the chops from the other side to analyze. When the diet was sirloin steaks, they received ones matching ours. The only way in which the diet was not identical with the food analyzed was that Andersen and I followed the Eskimo custom of eating fish bones and chewing the rib ends; from these sources we no doubt obtained a certain amount of calcium.

Toward the latter part of the test it became startlingly clear, on paper that we were not getting enough calcium for health. But we were healthy. The escape from that dilemma was assume that a calcium deficiency which did not hurt us in our one year might destroy us in ten or twenty.

You study bones when you look for a calcium deficiency. The thing to do then, was to examine the skeletons of people who had died at a reasonably high age after living from infancy upon an exclusive meat diet. Such skeletons are those of Eskimos who are known to have died before the European influences came in. The Institute of American Meat Packers were induced to make a subsidiary appropriation to the Peabody Museum of Harvard University where Dr. Earnest A. Hooton, Professor of Physical Anthropology, under took a through going study with regard to the calcium problem in the relation to the Museum's collection of the skeletons of meat eaters. Dr. Hooton reported no signs of calcium deficiency. On the contrary, there was every indication that the meat eaters had been liberally, or at least adequately, supplied. The had suffered no more in a lifetime from calcium deficiency than we had in our short year (really short, by the way for we enjoyed it).

End of Part 2 of 3 | Part 1 | Part 3

Adventures in Diet - By Vilhjalmur Stefansson (Part 3)

Harper's Monthly Magazine, January 1936

Scurvy has been the great enemy of explorers. When Magellan sailed around the world four hundred years ago many of his crew died from it and most of the others were at times so weakened that they could barely handle the ships. When Scott's party of four went to the South Pole twenty three years ago their strength was sapped by scurvy; they were unable to maintain their travel schedule and died. Nor has scurvy been the nemesis of explorers only. Twenty years ago the British Army in the Near East was seriously handicapped, and last October an American doctor reported a hundred Ethiopian soldiers per day dying of scurvy. The disease worked havoc during the Alaska and Yukon gold rushes following 1896. Scores of miners died and hundred suffered.

Medical profession and laity equally believed for more than a hundred years that they knew exactly how to prevent and cure the disease, yet the method always failed on severe test.

The premise from which the doctors started was that vegetables, particularly fruits, prevent and cure scurvy. Since diet consists of animals and plants, the statement came to take the form that scurvy is cause by meat and cured by vegetables. Finally the doctors standardized on lime juice as the best of preventatives and cures. They name it a sure cure, a specific. Lawmakers followed the doctors. It is on the statute books of many countries that on long voyages the crews are to be supplied with lime juice and induced or compelled to take it.

Obtained from officers of the Royal Canadian Mounted Police, and from sourdoughs, I have in my diaries and notes many a case of suffering and death caused by scurvy in the Alaska and Yukon gold rushes. The miner generally began to sicken toward the end of winter. He had been living on beans and bacon, on biscuits, rice, oatmeal, sugar, dried fruits and dried vegetables. When he recognized his trouble as scurvy he made such efforts as were possible to get the things which he believed would cure him. Apparently the miners had the strongest faith in raw potatoes. These had to be brought from afar, and there are heroic tales of men who struggled through the wilderness to succor a comrade with a few pounds of them. There were similar beliefs in the virtues of onions and some other vegetables. Curiously, there was either no belief in those vegetables which were obtainable, or else there was a belief that they should be treated in a way which. we now understand, destroys their value. For instance a man might have been cured or at least helped with a salad of leaves or even bark of trees. What the miners did with the pine needles and willow drink the tea. If they had fresh meat they boiled it to shreds and drank the broth. Death frequently occurred in two to four months from recognized onset of the disease.

Ignoring the decimation of armies, and the burden of this disease in many walks of civil life through past ages, we turn to the explorers, the class most widely publicized as suffering from and dying of scurvy.

It is unusual to rank James Cook of a hundred and fifty years ago with the foremost explorers of all time. Part of his fame may be attributed to his having discovered how to prevent and cure scurvy. Medical books name him as pioneer in the field, saying that we owe to him the conquest of a dread disease. For he demonstrated that with vegetables (again particularly fruits) scurvy could be prevented on the longest voyages. By statement or inference these books assert that from this developed the knowledge according to which we extract and bottle the juice of the lime, stock ships with it, prevent and cure scurvy.

As show above intimated, however, the good physicians, with their faith in lime juice as a specific, overlooked its constant failure upon severe test.

How stoutly the faith was kept is shown by the British polar expedition of Sir George Nares. When he returned to England in 1876 after a year and a half, he reported much illness from scurvy, some deaths, and a partial failure of his program as a result. In his view fresh meat could have saved his men. But the doctors, as we shall see when we consider how they later advised Scott, soon forgot whatever impression was made by Nares. They seem to have scared themselves with the old doctrines by a series of assumptions: that the lime juice on the Nares expedition might have been deficient in acid content; that some of the victims did not takes as much of it as needed; and that perhaps it was too much to expect of even the marvelous juice to cope with all the things which tended to bring on scurvy - absence of sunlight, bad ventilation, lack of amusement and exercise, insufficient cleanliness.

Particularly because Nares medical court of inquiry had closed on a note of cleanliness and "modern sanitation," you would think the medical world might have felt a severe jolt when they read how Nansen and Johansen had wintered in the Franz Josef Islands, (now Nansen Land) in 1895-96. They had lived in a hut of stones and walrus leather. The ventilation was bad, to conserve fuel; the fire smoked, so that the air was additionally bad; there was not a ray of daylight for months; during this time they practically hibernated, seldom going outdoors at all and taking as little exercise as appears humanly possible. Yet their health was perfect all winter and they came out of their hibernation in as good physical condition as any men ever did out of any kind of Arctic wintering. Their food had been lean and the fat of walrus.

Tens, if not hundreds of thousand of scientists in medicine and the related branches must have seen this account, for Nansen's books were bestsellers in practically every language and newspapers were full of the story. Yet the effect was negligible. The doctors and dietitians still continued to pontificate on meat producing scurvy and on the contributory bad effects of what they called insufficience of ventilation, cleanliness, sunlight and exercise. They still prescribed lime juice and put their whole dependence on it and other vegetable products.

Excuses for lime juice have persisted to our day. It was for instance, demonstrated with triumph recently that the meaning of "lime" had changed during the last hundred years, explaining the claim that it worked better in the eighteenth than in the nineteenth century - then the juice was made from lemons called limes; now it is made from limes called limes.

The antiscorbutic value of lemons may be far greater than that of limes per ounce, but that does not go to the root of the matter. For proof of this consider how Nansen's experience was re-enforced and interpreted by four expeditions during two decades, two of them commanded by Robert Falcon Scott, one by Ernest Henry Shackleton, one by me.

II

Scott, in 1900, sought the most orthodox scientific counsel when outfitting his first expedition. He followed advice by carrying lime juice and by picking up quantities of fruits and vegetable things as he passed New Zealand on his way to the Antarctic. He saw to it that the diet was "wholesome," that the men took exercise, that they bathed and had plenty of fresh air. Yet scurvy broke out and the subsequently famous Shackleton was crippled by it on a journey. They were pulling their own sledges at the time so they must of had enough exercise. There was plenty of light with the sun beating on them, and there was plenty of fresh air. To believers in the catch words and slogans of their day, to believers in the virtues of lime juice, the onset of the scurvy was a baffling mystery.

That is was Shackleton's scurvy which most interfered with the success of the first Scott expedition was particularly unfortunate, if you think of the jealousies it aroused, the enmities it caused. Scurvy, as disease go, is really one of the cleanest and least obnoxious; but in English the name of it is a term of opprobrium - "a scurvy fellow," "a scurvy trick." Shackleton may have smarted as much under that word-association as he did under the charge that his weakness had been Scott's main handicap. The passion to clear his name, in every sense, drove him to the organization of an expedition, which many in Britain considered unethical - a subordinate, with indecent haste and insistence, crowding forward to eclipse his commander.

The crucial element in the first Shackleton expedition, to the students of scurvy, is the fact that Shackelton was an Elizabethan throwback in the time of Edward VII. He was a Hawkins or a Drake, a buccaneer in spirit and method. He talked louder and more than is good form in modern England. He approached near to brag and swagger. He caused frictions, aroused and fanned jealousies, and won the breathless admiration of youngsters who would have followed Dampier and Frobisher with equal enthusiasm in their piracies and in their explorations.

The organization, and the rest of the first Shackleton expedition, went with a hurrah. They were as careless as Scott had been careful; they did not have Scott's type of backing, scientific or financial. They arrived helter skelter on the shores of the Antarctic Continent, pitched camp, and discovered that they did not have enough food for the winter, nor had they taken such painstaking care as Scott to provide themselves with fruits or other antiscorbutics in New Zealand. Compared with Scott's, their routine was slipshod as to cleanliness, exercise, and several of the ordinary hygienic prescriptions.

What signifies is that Scott's men, with unlimited quantities of jams and marmalades, cereals and fruits, grains, curries, and potted meats, had been little inclined to add seals and penguins to their dietary. With Shackleton it was neither wisdom or acceptance of good advise but dire necessity which drove to such use of penguin and seal that Dr. Alister Forbes Mackay, physician from Edinburgh, who was a member of that Shackleton expedition and later physician of my ship the Karluk, told me he estimated half the food during their stay in the Antarctic was fresh meat.

In spite of the lack of care, (indeed, as we now see it, because of their lack), Shackleton had better average health than Scott. There was never a sign of scurvy; every man retained his full strength; and they accomplished that spring what most authorities still consider the greatest physical achievement ever made in the southern polar regions. With men dragging the sledge a considerable part of the way, they got to latitude 88° 23 S., practically within sight of the Pole.

Scott began his second venture as he had begun the first, by asking the medical profession of Britain for protection from scurvy and by receiving from them once more the good old advice about lime juice, fruits, and the rest. In winter quarters he again placed reliance on that advice and on constant medical supervision, on a planned and carefully varied diet, on numerous scientific tests to determine the condition of the men, on exercise, fresh air, sanitation in all its standard forms. The men lived on the foods of the United Kingdom, supplemented by the fruit and garden produce of New Zealand. Because they had so much which they were used to, they ate little of what they had never learned to like, the penguins and seals.

Once more they started their sledge travel after a winter of sanitation. The results had previously be disappointing; now they were tragic. While scurvy did not prevent them from reaching the South Pole, it began to weaken them on the return and progressed so rapidly that the growing weakness prevented them, if only by ten miles, from being able to get back to the final provision depot.

Those who have ignored the scurvy have sometimes claimed that if Scott had reached the depot he would have been able to reach the base camp eventually. This becomes more than doubtful when you realize that the progressive decrease of vigor, both mental and bodily, was not going to be helped by even the largest meals, if those meals were of food lacking antiscorbutic value.

The story of Scott and his companions, especially through the last few weeks, is among the boldest in any language; through it they became national heroes and world heroes. But in the speech of their countrymen (though not in many another European tongue), scurvy sounds unclean. It appeared necessary to Scott's surviving comrades, and to those in Britain who knew the truth, to take care that the tabooed word should not sully a glorious deed.

To suppress the association of a disease with the beauty and heroism of Scott's death may have been worth while at the time; but it can scarcely be deplored by anyone - and must be praised by scientists - that Commander Edward G. R. Evans, now Admiral, Scott's second-in-command, after a time gave out the scurvy information, including the statement that he himself had been ill.

It is irrational, at least now that emotions have calmed, to blame Scott. No one was to blame, for they all acted according to the light of their day. If anybody was to blame it was primarily those who gave medical advice to the expedition before it sailed; secondarily, it was the chief medical officer, rather than the commanding officer, of the expedition.

It seems strange, now, that a comparison of the Scott and Shackleton experiences did not fully enlighten the doctors on the true inwardness of scurvy; but of course part of the explanation is that the Scott medical information was suppressed. Therefore, it remained for my own expedition to demonstrate, so far as polar expeditions are concerned, and for the Russell Sage experiments to call to the attention of the medical profession, the most practical and only simple way of curing scurvy. For no matter how good the juice of limes (or lemons), it is difficult to carry, it deteriorates, and you may lose it, as by a shipwreck. The thing to do is to find you antiscorbutics where you are, pick them up as you go.

On my third expedition it happened as circumstantially related in a book called "The Friendly Arctic", that three men came down with scurvy though disobeying the instructions of the commander and living without his knowledge for two or three months chiefly on European foods when they were supposed to be living chiefly on meat.

It seems to take from one to three months for even a bad diet to produce recognizable scurvy, but there after developments are rapid through the next few weeks. In the case of my men it was about three weeks ( as they later thought) after they noticed the trouble and about ten days after they complained of it to me, when one of them was so weak we had to carry him on a sledge, while the other was barely able to stagger along, holding on behind. By then every joint pained, their gums were as soft as "American" cheese, their teeth so loose that they came out with almost the gentlest of pulls.

We were 60 or 80 miles from land on drifting sea ice when the trouble stared, and we hastened ashore to get a stable camp for the invalids. It would have been no fun, with sick men on your hands, if the site of your camp started disintegrating under pressure and tumbling about.

We reached an island (about 900 miles north of the Arctic Circle) the coast of which was known although the interior had never been explored. We traveled a few miles inland, established a camp, hunted caribou (there were two of us well, out of four) and began the all-meat cure. Fuel was pretty scarce, so we cooked only one meal a day; besides, I thought raw food might work better. We cooked the breakfast in a lot of water. The patients finished the boiled meat while it was hot and kept the broth to drink during the rest of the day. For their other meals they ate slightly frozen raw meat, with normal digestion and good appetite. We divided up the caribou Eskimo style, so the dogs got organs and entrails, hams, shoulders, and tenderloin, while the invalids, and we hunters got heads, briskets, ribs, pelvis and the marrow from the bones.

On this diet all pain disappeared from every joint within four days and the gloom was replaced by optimism. Inside a week both men said that they had no realization of being ill as long as they lay still in bed. In two weeks they were able to begin traveling, at first riding on the sledges and walking alternately. At the end of a month they felt as if they had never been ill. No signs of the scurvy remained except that the gums, which had receded from the teeth, only partly regained their position.

By comparing notes later with Dr. Alfred Hess, the leading New York authority on scurvy, I found that when I was getting these results with a diet from which all vegetable elements were absent, he was getting the same results in the same length of time through a diet where the main reliance was upon grated raw vegetables and fruits and upon fresh fruit juices.

There is no doubt, as the quantitative studies have shown, that the percentage of Vitamin C, the scurvy preventing factor, is higher in certain vegetable elements than in any meats. But it is equally true that the human body needs only such a tiny bit of Vitamin C that if you have some fresh meat in your diet every day, and don't over cook it, there will be enough C from that source alone to prevent scurvy. If you live exclusively on meat you get from it enough vitamins not only to prevent scurvy but as said in a previous article, to prevent all other deficiency diseases.

Closing the subject of vitamins in relation to long expeditions, we had better emphasize that there has recently been such progress in the extraction, concentration and storage of Vitamin C that it is now possible to carry with you enough to last several years and of such quality that it will not deteriorate to the point of uselessness. But why carry coals to Newcastle? if you are in the tropics, pick a fruit, or eat a green; if you are at sea, throw a line outboard and catch a fish; if you are in the Antarctic, use seals and penguins; if in the Arctic, hunt polar bears, and seals, caribou and the rest of the numerous game. True enough, if you make a journey inland into the Antarctic Continent or toward the center of Greenland, where there is no game because the land is permanently snow-covered, you have to carry food with you. In that case you might as well take lemon juice. It is one of the most portable sources and they know now how to make and pack it so that its qualities as well as quantities will last you.

III

A bulletin conspicuous in the subways co-operated some time ago with the New York Commissioner of Health by displaying this notice:

FOR SOUND TEETH
BALANCED DIET with
VEGETABLES : FRUIT : MILK
BRUSH TEETH
VISIT DENTIST REGULARLY

Shirley W. Wynne, M.D.
Commissioner of Health

During the same time the ether was full and the magazine pages were crowded with advertising which told you that mouth chemistry is altered by a paste, a powder, or a gargle so as to prevent decay, that a clean tooth never decays, that a special kind of toothbrush reaches all the crevices, that a particular brand of fruit, milk or bread is rich in elements for tooth health. There were toothbrush drills in the schools. Mothers throughout the land were scolding, coaxing, and bribing to get children to use the preparations, eat the foods, and follow the rules that insured perfect oral hygiene.

Meantime there appeared a statement from Dr. Adelbert Fernald, Curator of the Museum of Dental School, Harvard University, that he had been collecting mouth casts of living Americans, from the most northerly Eskimos south to the Yucatan. The best teeth and the healthiest mouths were found among people who never drank milk since they had ceased to be suckling babes and who never in their lives tasted any of the other things recommended for sound teeth by the New York Commissioner of Health. These people, Eskimos, never use tooth paste, tooth powder, tooth brushes, mouth wash, or gargle. They never take any pains to cleanse their teeth or mouths. They do not visit their dentist twice a year or even once in a lifetime. Their food is exclusively meat. Meat, be it noted, was not mentioned in the advertisement issued by Dr. Wayne.

Teeth superior on the average to those of the presidents of our largest tooth-paste companies are found in the world to-day, and have existed during past ages, among people who violate every precept of current dentifrice advertising. Not all of them have lived exclusively on meat; but so far as an extensive correspondence with authorities has yet been able to show me, a complete absence of tooth decay from entire communities has never existed in the past, and does not exist now, except among people in whose diet meat is either exclusive or heavily predominant.

Our Bellevue experiments threw a light on tooth decay, but the key to the situation lies more in the broad science of anthropology. I now give, by sample and by summary, things personally known to me from anthropological field work.

My first anthropological commission was from the Peabody Museum of Harvard University when they sent John W. Hasting and me to Iceland in 1905. We found in one place a medieval graveyard that was being cut away by the sea. Skulls were rolling about in the water at high tide, at low tide we gathered them and picked up scattered teeth here and there. As wind and water shifted the sands we found more and more teeth until there was a handful. Later we got permission to excavate the cemetery, and eventually we brought with us to Harvard a miscellaneous lot of bone which included 80 skull, and as said, a great many loose teeth.

The collection has been studied by dentists and physical anthropologists without the discovery of a single cavity in even one tooth.

The skulls in the Hastings-Stefansson collection represent persons of ordinary Icelandic blood. There were no aborigines in that island when the Irish discovered it some time before 700 A. D. When the Norsemen got there in 860 they found no people except the Irish. It is now variously estimated that in origin the Icelanders are from 10 percent to 30 percent Irish, 40 percent to 50 percent Norwegian, the remainder, perhaps 10 percent, from Scotland, England, Sweden, and Denmark.

None of the people whose blood went into the Icelandic stock are racially immune to tooth decay, nor are the modern Icelanders. Then why were the Icelanders of the Middle Ages immune?

An analysis of the various factors make it pretty clear that their food protected the teeth of the medieval Icelanders. The chief elements were fish, mutton, milk and milk products. There was a certain amount of beef and there may have been a little horse flesh, particularly in the earliest period of the graveyard. Cereals were little important and might be used for beer rather than porridge. Bread was negligible and so were all other elements from the vegetable kingdom, native or imported.

My mother, who as born on the north coast of Iceland, remembered from the middle of the nineteenth century a period when bread still was as rare as caviar is in New York to-day - she tasted bread only three or four times a year and then only small pieces when she went with her mother visiting. So far as bread existed at her own house, it was used as a treat for visiting children. The diet was still substantially that of the Middle Ages, though the use of porridge was increasing. She did not remember hearing of toothache in her early youth but did remember accounts of it as a painful rarity about the time when she left for America in 1876. Soon after arrival in the United States (Wisconsin, Minnesota, Dakota,) and in Canada (Nova Scotia, Manitoba) the Icelandic colonists became thoroughly familiar with the ravages of caries. They probably had teeth as bad as those of the average American long before 1900.

There is then at least one case of a north-European people whose immunity from caries (to judge from the Hastings-Stefansson collection and common report) approached 100 percent for a thousand years, down to approximately the time of the American Civil War. The diet was mainly from the animal kingdom. Now that it has become, both in America and Iceland approximately the same as the average for the United States or Europe, Icelandic teeth show a high percentage of decay.

I began to learn about another formerly toothacheless people when I joined the Mackenzie River Eskimos in 1906. Some of them had been eating European foods in considerable amount since 1889, and toothache and tooth decay were appearing, but only in the mouths of those who affected the new foods secured from the Yankee whalers. The Mackenzie people agreed that toothache and cavities had been unknown in the childhood of those then approaching middle age while there were many of all ages still untouched, the ones who kept mainly or wholly to the Eskimo diet. Here and in many other places, this is somewhere between 98 and 100 percent from animal sources. There are districts, like parts of Labrador and of western and southwestern Alaska, where even before the coming of Europeans there was considerable use of native vegetable elements nowhere furnished as much as 5 percent of the average yearly caloric intake of the primitive Eskimos, even in south-western Alaska.

Dr. Alex Hirdlicka, Curator of Anthropology in the National Museum, Washington, writes me that he knows of no case of tooth decay among Eskimos of the present or past who were uninfluenced by European habits. Dr. S. G. Ritchie, of Dalhousie University, wrote after studying the skeletal collection gathered by Mr. Diamond Jenness on my third expedition: " In all the teeth examined there is not the slightest trace of caries."

I brought about 100 skulls of Eskimos, who had died before Europeans came in, to the American Museum of Natural History, New York. These have been examined by many students, but no sign of tooth decay has yet been discovered.

Dr. M. A. Pleasure examined at the American Museum of Natural History 283 skulls said to be Eskimo of pre-European date. He found a small cavity in one tooth; but when the records where check it turned out that the collector, Rev. J. W. Chapman of the Episcopal Board of Missions, who now lives in New York City, had sent that skull to the Museum as one of an Athabasca Indian, not of an Eskimo.

The slate is, therefore, clean to date. Not a sign of tooth decay has yet been discovered among that one of all peoples which most completely avoids the foods, the precepts, and the practices favored for dental health by the New York Commissioner of Health, the average dentist, the toothbrush drillmasters of the schools, and the dentifrice publicists.

IV

When addressing conventions and societies of medical men, I usually state the oral hygiene case somewhat as above but in more detail. If there is rebuttal from the floor, it invariably takes the form of contending that the tooth health of primitive people is due to their chewing a lot and eating coarse food. The advantage of that argument to the dentist, whose best efforts have failed to save your teeth is obvious. It gives him an excuse. He can from the doctrine make a case that not all your care, even when support by his skill and science, can preserve teeth in a generation of soft foods, that give no exercise to the teeth and no friction to the gums.

But it is deplorably hard to square anthropology with this comfortable excuse of the dentist. Among the best teeth of a mixed-diet world are those of a few South Sea Islanders who as yet largely keep to their native diets. Similar or better tooth condition is described, for instance, from the Hawaiian Islands by the earliest visitors. But can you think of a case less fortunate for the chewing-and-coarse-food advocates? The animal food of these people was chiefly fish, and fish is soft to the teeth, whether boiled or raw. Among the chief vegetable elements was poi, a kind of soup or paste. Then they used sweet potatoes.

It would be difficult to find a New Yorker or Parisian who does not chew more, and use coarser food, than the South Sea Islanders did on the native diets which gave them in at least some cases 97 percent freedom from caries, a record no block on Park Avenue can approach.

Nor do Eskimos chew much, as compared with us. So far as their meat is raw it can be chewed like a raw oyster - slips down similarly. When perfectly fresh meat is cooked, two main causes determine toughness: the age of the beast and the manner of cooking. The chief food animal of inland Eskimos is the caribou. A young caribou is as fleet as a heifer; an old one is as slow as a cow. Therefore the wolves get the clumsy old which drop behind when the band flees, and the Eskimos seldom have a chance to secure an animal that is more than three or four. Such young caribou are not tough, no matter how cooked.

I do not know a corresponding logical demonstration for seals, but I can testify from helping to eat thousands that their meat is never tough - at least not in comparison with the beefsteaks you sometimes get in New York chophouses.

Then there are Eskimos who live practically exclusively on fish. As said, you can't chew them when they are raw; there is not much chewing when they are eaten boiled. the only condition under which fish become tough, or rather hard, is when they are dried. Some Eskimos use dried fish; others do not.

There is for separated districts a wide difference in the amount of Eskimo chewing, but no one has reported that health of the teeth is better among heavy chewers. How could it be when as yet no caries has been found either among the lightest or heaviest masticators?

It is used as a second line of defense by the mastication advocates that even if Eskimos perhaps don't chew their food so very much they do chew skins a great deal. Their chewing of leather is far less than you might believe from what has been said by a particular kind of writer and pictured in certain movies. In any case, skin chewing is mainly by the women, and it is not easy to bring under the conditions of modern scientific thought the idea that the wife's chewing preserves her husband's teeth.

Once at a talk to a medical group I encountered a further argument. Is it not true that Eskimo men use the teeth a great deal in their crafts? Do they not bite wood, ivory, or metal to hold, pull out, twist, and so one? The best I could think of was to agree that Eskimos pull nails with their teeth because they have good teeth than that they have good teeth because they pull nails.

There are several reasons why the teeth of many Eskimos wear down rapidly. They usually meet edge to edge, where ours frequently overlap, and that tends to cause wear. Some Eskimos wind-dry fish or meat, sand gets in, and to an extent makes them like sandpaper. Both sexes, but especially men, use their teeth for biting on hard materials. Both sexes, but especially the women, use their teeth for softening skins. A wearing toward the pulp may, therefore, take place in early middle-life. What then happens is stated by Dr. Richie (whom we have already quoted) with relation to the Coronation Gulf Eskimos:

"Coincident with this extreme wear of the teeth the dental pulps have taken on their original function with conspicuous success. Sufficient new dentine of fine quality has been formed to obliterate the pulp chambers and in some cases even the root canals of the teeth. This new growth of tissue is found in every case where access to the pulp chambers has been threatened. There has therefore been no destruction of the pulps through infection and consequently alveolar abscesses are apparently unknown."

Total absence of caries from those who live wholly on meat is then definite. Cessation of decay when you transfer from a mixed to a meat diet happens usually, perhaps always. The rest of the picture is not so clear.

Caries has been found in the teeth of mummies in Egypt, Peru, and in our own Southwest. These ancient people were mixed-diet eaters, depending in considerable part on cereals. Their teeth were better than ours, though not so good as the Eskimos. If you want a dental law, you can approximate it by saying that the most primitive people usually have the best teeth. You can add that in some cases a highly vegetarian people while not attaining the 100 percent perfection of meat eaters, do nevertheless, have very good teeth as compared with ours.

It is contended by the Hawaiian Sugar Planters Association Health Research Project that the shift from good to execrable teeth among the mixed diet Polynesians there has been due to years of cereals. I have seen no comment of theirs upon the (I should think) great increase of sugar consumption that has been synchronic with the deterioration of Hawaiian teeth.

On the view that diet is the greatest factor in saving teeth, the anthropologists have been getting support from experiments conducted by institutions and by scattered students. Some dentists are here contributing nobly to a research, and to a campaign of education, that seems bound to deplete their income. My probing has not revealed thus far corresponding unselfishness among the dentifrice manufacturers.

A serious mouth disease, next after caries, is pyorrhea. He who runs cannot read the marks so readily on human skeletons; but it seems at least probable that the medieval Icelanders, the Eskimos, and others who have left teeth free from cavities, were also free from, or at least not severely afflicted by, pyorrhea. Similarly, the modern investigators have found Eskimos who are still living on their native foods to have an unusually good average condition of general oral health, therewith absence of pyorrhea.

One of the things we noticed in the general well-being of our New York year on meat and similar years in the Arctic was the absence of headaches. I used to have them frequently before going north and have them occasionally whenever I am on a mixed diet. The whys and wherefores are not clear and what we say on this point is more tentative than any other part of this statement.

It was noticed in the X-ray pictures during our New York meat year that we had far less gas in the intestinal tract when on meat than when on a mixed diet - practically no gas. The work of Dr. John C. Torrey showed that neither did digestion and elimination produce those offensive smells which are found in vegetarianism and on a mixed diet But whether the freedom from a certain kind of intestinal food decomposition was what led to the freedom from headache is no more than a working hypothesis.

The prevention of headache by abstaining from vegetables has been recorded in books. An outstanding case is that of Francis Parkman, the historian, who suffered with headaches all his life except, as he states, during one period when he was living with an Indian tribe chiefly or exclusively on meat. This testimony, though by an eminent man widely read, and though a fair sample of the testimony of meat eaters, commanded little attention for the physicians. It should be said in their defense, however, that Parkman himself does not proclaim the experience as a triumphant discovery. He rather puts it the other way about, that in spite of being compelled to live on meat, he was free from the headaches that plagued him the rest of his days.

Professor Raymond Pearl, nearly twenty years ago, while he was at the Maine Agricultural Experiment Station, proved that chickens know more than professors about what is good for chickens to eat. Now several experiments appear in a good way to establish that children, if given complete freedom to choose among foods undisguised by sauces and artificial flavors will select better for their own health and strength than the mother or child specialist. One of the things frequently noticed about these children is that they eat large quantities of a single item which they happen to like. Our living for years on a single item which we liked was from the point of view no more than carrying forward a childhood tendency.

V

More than twenty-five years have passed since the completion of my first twelve months on meat and more than six years since the completion in New York of my sixth full meat year. All the rest of my life I have been a heavy meat eater, and I am now fifty-six. That should be long enough to bring out the effects. Dr. Clarence W. Lieb will report in the American Journal of Gastroenterology that I still run well above my age average on those points where meat has been supposed to cause deterioration. The same is the verdict of my own feelings. Rheumatism, for instance, has yet to give me its first twinge.

The broadest conclusion to be drawn from our comfort, enjoyment, and long-range well-being on meat is that the human body is a sounder and more competent job than we give it credit for. Apparently you can eat healthy on meat without vegetables, on vegetables without meat, or on a mixed diet.

Two stories summarize one of the most interesting sides of the case, the dental. In 1903 I heard the Dean of the dental school of the University of Pennsylvania say in a lecture that he thought dentists to that year had done more harm than good, but would thereafter be doing more good than harm. In 1928 when I told this to Dr. Percy Howe, Director of the Forsyth Dental Infirmary for Children, he said he thought the good Dean had been premature by at least twenty years. As I understand Dr. Howe, much good was done in particular cases by dentists long ago, but it is only within the past ten years or so that the average for good has overbalanced the harm by any very heavy proportion.

While meat eaters seem to average well in heath, we must in our conclusion draw a caution from the most complete modern example of them the Eskimos of Coronation Gulf, when he was anthropologist on my third expedition, that the two chief causes of death were accidents and old age. This puts in a different form my saying that these survivors of the stone age were the healthiest people I have ever lived among. I would say the community, from infancy to old age, may have had on the average the health of an equal number of men about twenty, say college students.

The danger is that you may reason from this good health to a great longevity. But meat eaters do not appear to live long. So far as we can tell, the Eskimos, before the white men upset their physiological as well as their economic balance, lived on the average at least ten years less than we. Now their lives average still shorter; but that is partly from communicated diseases.

It has been said in a previous article that I found the exclusive meat diet in New York to be stimulating - I felt energetic and optimistic both winter and summer. Perhaps it may be considered that meat is, overall, a stimulating diet, in the sense that metabolic processes are speeded up. You are then living at a faster rate, which means you would grow up rapidly and get old soon. This is perhaps confirmed by that early maturing of Eskimo women which I have heretofore supposed to be mainly due to their almost complete protection from chill - they live in warm dwellings and dress warmly so that the body is seldom under stress to maintain by physiological processes a temperature balance. It may be that meat as a speeder-up of metabolism explains in part both that Eskimo women are sometimes grandmothers before the age of twenty-three, and that they usually seem as old at sixty as our women do at eighty.

So you could live on meat if you wanted to; but there is no driving reason why you should. Moreover vegetables are fundamentally economical. You can get several times more food value from an acre of corn than from the pigs that ate the corn.

The thing to do then, probably, is to go on as you have been doing, but adding to your mental equipment, if it be a novelty, the idea that several at least of the disadvantages of a meat diet are compensated for by advantages.

End of Part 3 of 3 | Part 1 | Part 2

UK food labelling and fibre count

From the UK Food Labelling & Standards Division - Food Standards Agency:

"There are regulations that stipulate when and how the nutrition information panel must be presented on the food label. In the UK, the term 'carbohydrate' as it appears in the nutrition information panel refers to carbohydrates that are metabolised by man (including sugar alcohols, such as sorbitol, mannitol). Fibre, on UK labels, does not form part of the total 'carbohydrate' value and sometimes it is listed as a completely distinct item. In effect therefore the 'carbohydrate' value does not include the 'fibre' value.

I am aware that nutrition information panels are different in the US. My
understanding is that in the US the 'Total Carbohydrate' value appearing in a nutrition information panel on a US label includes the fibre content of the product, hence the advice to deduct 'Dietary fiber' from 'Total Carbohydrate' in the US."

An Open Letter to Victorian Health Minister Bronwyn Pike

Ms Pike, get off the anti-low-carb bandwagon!

By Anthony Colpo, March 29, 2004.

Dear Ms Pike,

Recently, you announced a new campaign, to be conducted by your government at taxpayer expense, that would endeavor to alert Victorian residents to the alleged "dangers" of low-carbohydrate diets. To the best of my knowledge, this action is unprecedented in Australian political history, for no state government has ever taken it up on themselves to issue warnings against a specific diet, despite the fact that certain dietary regimens have indeed been directly linked to ill-health and death. Such potentially dangerous nutritional regimes include vegan diets, which have claimed the lives of numerous infants around the world, and resulted in legal proceedings against the misguided parents of these youngsters.(1) Along with their potentially fatal effects on infants, vegan diets have also demonstrated the ability to harm children, adolescents, and even adults. So far, while you have had much to say about low-carb nutrition, you have not uttered a word about vegan diets. Before I discuss just why you are so wrong on low-carb diets, lets take a closer look at vegan regimens.

Vegan Diets - Fast Track To Ill-Health

Among their many nutritional shortcomings, vegetarian diets supply sub-optimal amounts of vitamin B12 and essential long-chain omega-3 fatty acids such as DHA and EPA. B12 is essential for optimal cognitive function, while DHA is a major component of brain tissue. Not surprisingly, analyses of blood samples from vegetarians consistently show lower dietary and lower blood levels of long-chain omega-3 fatty acids. (2-7) These fatty acids can be formed in the body from plant-based omega-3 fats, but numerous studies show that the conversion rate is very low.(8,9) Because of their complete abstinence from animal foods, deficiencies of these and other nutrients are much more pronounced in vegans than in lacto-ovo vegetarians. Below are observations, published in peer-reviewed journals, of the harm that can befall those following these truly unbalanced diets:

• In 1986, Dutch researchers observed that vegan infants had markedly lower B12 levels and impaired psychomotor functioning when compared to control infants.(10,11) On the basis of these findings, the researchers made dietary recommendations to the families of the infants, who subsequently began switching their youngsters to lacto-vegetarian, lacto-ovovegetarian, or even omnivorous diets. On average, the children were six years old when the dietary change took place. In 2000, researchers reported on follow-up examinations of these same subjects, who were now aged between 10 to 16. Two-thirds of the formerly vegan adolescents still suffered from B12 deficiency, whereas all of the subjects in a similarly aged omnivorous control group had normal B12 levels. When given a series of cognitive tests, the ex-vegan group achieved poorer results than the lifetime-omnivore group. A significant association was found between low B12 status and poorer performance on tests measuring fluid intelligence, spatial ability, and short-term memory. Because fluid intelligence involves reasoning, the capacity to solve complex problems, abstract thinking ability, and the ability to learn, the authors pointed out that: "Any defect in this area may have far-reaching consequences for individual functioning." (12).
  
  * British researchers found that, compared to omnivores and lacto-ovovegetarians, vegans suffered a higher frequency of abnormal electroencephalogram (EEG) readings, a test designed to detect abnormalities in the electrical activity of the brain (13). In one of their studies, B12 supplementation improved EEG scores in most of those registering abnormalities, but three of the vegans failed to respond to heavy supplementation with either oral or injected B12.
  
  * In 2000, French researchers reported the case of a 33-year-old patient who lost most of his eyesight after following a strict vegan diet since the age of 20. Ironically, the man had adopted the diet for "improved health", and did not use any supplements. Blood samples showed that his levels of vitamin B1, B12, A, C, D, E, zinc, and selenium were all measurably below normal. Vitamin B12, in particular, is vitally important for maintaining the health of the optic nerve that transmits signals from the eye to the brain. Administration of intramuscular and oral multivitamins normalized blood levels of the aforementioned nutrients, but his eyesight did not recover. They concluded that the nutritional deficiencies in the patient's vegan diet - particularly the insufficient amount of vitamin B12 he had been absorbing - were the most likely cause for the optic nerve deterioration that had resulted in irreversible blindness. (14)

In a recent newspaper article, you stated that: "When we know something is bad for people, like smoking, then we let people know what the health risks are". I eagerly await to see if your department issues any warnings against vegan diets, for unlike low-carb diets, these posess a demonstrated poor safety record.

And what about low-carb diets?

In response to criticisms of your sadly misguided campaign against low-carbohydrate diets, you also stated in the aforementioned article: "Some people might come out and say, 'This is a nanny state - now they are telling us what to eat' ... But while I don't think it is the role of the politician to dictate individual preference and behaviour, it is my role to point out when something can actually harm you."

Seeing as you are taking it upon yourself to become a taxpayer-funded dietary commentator, it behooves you to learn as much as possible about the dietary regimens you intend to comment on. The statements you have made so far in regards to low-carbohydrate diets clearly show that you have not done this.

You claim that low-carbohydrate diets raise the risk of cancer, heart disease, osteoporosis, and even depression. From what peer-reviewed literature did you obtain such information?

Heart Disease

The claim that low-carbohydrate diets raise the risk of heart disease strains all boundaries of logic. Low-carbohydrate diets, via a reduction in cereal grain intake and an increase in meat and fruit and vegetable intake, increase the ingestion of many key heart-healthy nutrients. These include vitamin C, bioflavonoids, magnesium, carnitine, long-chain omega-3 fatty acids, vitamins B6, B12, and folic acid.

Bioflavonoids and vitamin C are important for the formation and maintenance of the collagen inside our arteries. Vitamins B6, B12 and folic acid lower blood levels of homocysteine and C-reactive protein (the former is believed to be directly atherogenic, the latter is an accurate measure of inflammatory activity in the body and a far superior predictor of future CHD risk than LDL cholesterol).(15-17) Long-chain omega-3 fatty acids, meanwhile, have demonstrated an ability to reduce CHD and overall mortality in randomized clinical trials, not just in the wishful-thinking minds of health bureaucrats. Magnesium and carnitine are essential for muscular contraction and energy production; both have been shown to lower mortality from CHD and heart failure in overseas trials.(18-20) When researchers compared a low-carbohydrate diet with a high-carb diet, they found that the former increased carnitine absorption, despite the equal carnitine contents of the two diets.(21)

Allegedly "healthy" cereal grains (whole or otherwise) contain no vitamin C, no B12, contain only omega-6 fatty acids but no omega-3 fats, contain phytates that impair the absorption of magnesium, and contain a substance known as pyridoxine glucoside, which has been shown to reduce the availability of vitamin B6 by 75-80%.(22) The only dietary intervention trial to compare the effects of increased whole-grain intake on CHD outcomes was the DART trial; in this study, men assigned to eat more brown bread and wheat fiber actually suffered a slight increase in CHD mortality (in the same study, men who were instructed to eat a low-saturated fat diet experienced no change, while men instructed to consume fish/fish oil reduced their CHD risk by almost a third).(23)

Sorry, but I don't see any reason why cereal grains should even be included in anyone's diet, let alone form the foundation of said diet. No-one "needs" cereal grains; in fact, those with gluten sensitivity and celiac disease should quite literally avoid them like the plague! Maybe you would care to include these facts in your future public awareness efforts...

Meat is by far the richest source of carnitine, vitamin B6, B12 and (in the case of organ meats), folic acid. Animal foods are also the only non-supplemental source of long-chain omega-3 fatty acids (brain tissue is the richest source, followed by fatty fish).

Non-cereal plant foods (fruits, vegetables, and nuts) - the kind encouraged by virtually all of the current crop of low-carb authors - contain magnesium, folic acid, bioflavonoids, and are the richest dietary sources of vitamin C.

Those who are still obsessed with "risk factors" (e.g, much of the medical establishment) should know that low-carb diets typically raise HDL cholesterol, improve the HDL:LDL ratio, and lower elevated triglyceride levels, while low-fat, high-carbohydrate diets often have the opposite effect. In clinical studies, low-carbohydrate diets have repeatedly been shown to produce significant fat loss; overweight and obesity is well-known to be associated with an increased risk of heart disease (and cancer).

Depending on one's food choices, adopting a low-carb diet will result in an increase of saturated fat intake. Despite the hysterical anti-saturated fat rantings of mainstream low-fat proponents, there exists no sound scientific evidence whatsoever to support any causative role for these fats in the pathogenesis of CHD. Consider carefully the following facts, available in the scientific literature for anyone who cares to look:

1) Four decades worth of dietary intervention trials have completely failed to produce any reduction in CHD that can be attributed to cholesterol-lowering or saturated fat restriction.(24)

2) Ironically, the only cholesterol-lowering strategy that has shown any noteworthy benefit in the reduction of CHD - the use of statin drugs - does not even work by cholesterol-lowering. These drugs operate via anti-inflammatory, artery-dilating, and antioxidant mechanisms.(25-41)

Cancer

The confident proclamations of many that meat and animal fats cause cancer are rather remarkable considering the complete lack of reliable clinical evidence to support such a notion. Even the allegedly "strong" epidemiological evidence is highly suspect. For example, if meat and saturated fat caused cancer, then vegetarians should by all rights experience lower rates of cancer. As a pooled analysis of the largest vegetarian studies shows, they don't.(42)

One of the few randomized clinical trials to examine the above topic was the Polyp Prevention Trial. In this study, over two-thousand patients who had one or more confirmed adenomatous colorectal polyps (adenomatous polyps are considered forerunners to colorectal cancer and are used as markers for colorectal cancer risk) removed within the previous 6 months were randomly assigned to follow either their usual diet, or a low fat, high fiber diet. Compared to the controls, subjects assigned to the high-fiber diet significantly increased their intake of whole-grains and legumes, and ate an average of 2.25 more servings of fruits and vegetables each day. The intervention group was also advised to reduce their consumption of red meat, which they did.

Total fat consumption in the control group averaged 34%, while those following the treatment diet reduced their fat intake to only 24%. After 4 years, colorectal cancer was diagnosed in 10 subjects from the high fiber group, and only 4 from the usual diet group eating more red meat. Even after excluding those diagnosed within the first year of the study, the results were similarly unfavorable; 4 cases in the intervention group as compared to 2 in the control group. Polyp recurrence was virtually identical between the two groups.(43)

In animal studies, the one fat that shows consistent tumor-promoting effects is the omega-6 fatty acid linoleic acid (found in so-called "heart-healthy" polyunsaturated vegetable oils).(44) While animal fat consumption in America has remained stable over the last 100 years (in terms of grams consumed per person per day), the consumption of vegetable oils and margarines has risen dramatically.(45,46) During this time, age-adjusted cancer rates have also risen in both males and females. To hold stable animal fat consumption responsible for rising cancer rates requires a complete abandonment of one's rational faculties.

Osteoporosis

Ms. Pike, the well-worn claim that high-protein diets can cause osteoporosis really is a bad joke, considering that it is a well-established fact that protein is an essential component of bones, and that epidemiological studies repeatedly show that it is low-protein intakes, not high protein intakes, that are associated with reduced bone density.(47)

It is typically claimed that high protein intakes will cause an increase in calcium excretion. Researchers recently examined this premise by performing a series of experiments in which intestinal calcium absorption was measured (using dual stable calcium isotopes) in pre- and postmenopausal women who were fed diets of varying protein content. Unlike a number of similar previous experiments, the diets of the women were tightly controlled, and the wide variations between individuals in calcium absorption were countered by using each women as her own control. Under these well-controlled conditions, the researchers found that calcium absorption was significantly lower during periods of low protein consumption (0.8g/kg and below) than during periods of high protein consumption. The researchers concluded, in a rather understated manner, that these studies "call the traditional high protein hypothesis to question". No kidding!(47)

Depression

The claim that low-carb diets cause depression has been doing the media rounds recently after Massachussetts Institute of Technology researcher Judith Wurtman and her team allegedly found an increase in depressive mood symptoms on people eating high protein diets compared to those following low-protein diets. This study has not yet been published, so there is no information on the exact diet the control and intervention groups followed, the methods used to determine mood changes, etc, etc. I contacted the MIT media department shortly after news of the study broke in the media requesting more information, and never received a reply. One should refrain from using this study as evidence until its results are peer-reviewed and published. It should be noted that Judith Wurtman has published several books promoting low-carbohydrate diets. While that in itself is no guarantee of impropriety or bias, she can hardly be considered a totally impartial voice on the subject.

And that's not all...

Ms. Pike, if you intend to be a credible and objective source of information to the Victorian public on low-carb diets, then it is incumbent upon you to point out, in addition to their alleged flaws, any health benefits they may possess. Researchers have indeed uncovered several characteristics of carbohydrate-reduced diets that could prove extremely valuable in the quest for improved public health.

• There have been over a dozen randomized dietary intervention trials published since the mid-eighties, ranging in duration from four weeks to one year, that directly compared the weight-loss efficacy of low- and high-carbohydrate diets. None of these has shown superior weight loss on the latter, apart from a highly suspect study (click here for details) conducted by Richard Fleming, the Nebraska cardiologist who obtained the late Dr. Atkins death report under highly dubious circumstances. In every study except Fleming's, low carbohydrate diets produced either markedly superior weight loss or statistically non-significant differences in weight loss.(48-65) Despite the oft-repeated claim that low-carb diets are hard to stick to, most studies reporting drop out rates have found higher rates of attrition in the low fat, high-carbohydrate diet groups.
  
  * In addition to spiraling obesity rates, we are currently experiencing an epidemic of type 2 diabetes, the prevalence of which began accelerating skywards soon after orthodoxy embraced the low-fat, high-carbohydrate paradigm. Numerous studies have compared the effects of lower- versus higher-carbohydrate diets on blood glucose control and, in virtually every instance, the carbohydrate-restricted regimens produced superior results.(66-84) Given that the United Nations has forecast over 300 million diabetics worldwide by 2025, the potentially beneficial public health implications of carbohydrate-restriction are enormous.
  
  * Low carbohydrate diets are proving themselves to be invaluable in the most surprising of circumstances. High-protein diets have been traditionally regarded as a no-go zone for individuals with kidney impairment, but in a recent issue of Diabetes, Italian researchers reported that a special low-carbohydrate, unrestricted protein diet, based on low-iron foods, produced dramatic benefits in patients with advanced kidney disease. Compared to patients following a traditional low fat, low-protein, high-carbohydrate diet, those on the low-iron, low-carbohydrate diet were 50% less likely to progress to the point where they either died or required kidney replacement.(85) Very low carbohydrate, or ketogenic, diets are also a well-established and effective treatment for childhood epilepsy.
  
  * Low-carbohydrate diets may eventually prove themselves to have life-extending properties. In animal research, the only consistent intervention that produces increases in life span is calorie-restriction. Whether the same applies to humans has not yet been established, but we do know that cutting calorie intake often produces marked improvements in important health parameters, such as blood glucose control. Unfortunately, telling people to voluntarily limit their calorie intake on a long-term basis tends to be a very poorly-received piece of advice. Low carbohydrate diets, however, may render such unpopular admonitions redundant. Dietary intervention studies have revealed a rather unique phenomenon; subjects following low carbohydrate diets, despite being told to limit only carbohydrate intake and to eat unrestricted amounts of protein and fat, often inadvertently reduce their total calorie intake to levels similar to those seen in subjects who have been explicitly instructed to lower their total calorie intake.
  
  * The possible life-extending effects of low carbohydrate diets have not escaped the attention of longevity researchers at Baltimore's National Institute of Aging. In a recent journal article they stated: "The Atkins Diet is ketogenic resulting in reduced appetite and therefore a reduced calorie intake; individuals who can comply with the diet may therefore exhibit some physiological changes observed in rodents and monkeys subjected to caloric restriction including reduced body weight, and decreased insulin and glucose levels."(86)

Do Your Homework.

Ms. Pike, it is unfortunate that you did not sit down and review the evidence before embarking on your misguided crusade to save Victorians from the supposed harm that awaits them if they adopt low-carbohydrate nutrition. Scandalous media reports arising from misleading press releases by vested interests do not constitute reasonable grounds for commencing a campaign that has the potential to affect public health, for better or worse.

Much of the recent media commotion over low-carbohydrate diets can be traced back to an American vegan organization known as the Physicians Committee for Responsible Medicine. If you are not familiar with this group, whose behavior so far has been anything but responsible, then I suggest you click here. This "Committee" in fact serves as a front-group for the People for Ethical Treatment of Animals (PETA), a radical animal rights and vegan activist group that has given documented financial aid to green terrorist groups.

Perhaps your heroic streak was triggered into action after Australia's most popular current affairs show featured footage of a Melbourne nutritionist claiming that "medically-supervised low-carbohydrate diets" had caused sixty deaths. You should know that this individual was referring to deaths that occurrred over twenty years ago among individuals following liquid protein diets, a crucial fact that was conveniently ommitted (click here to see for yourself). These deaths did not occur among people following the current crop of popular low-carbohydrate diets, people eating real food - you know, meats, eggs, dairy, fruits, nuts, and vegetables! Needless to say, several hundred calories per day derived solely from protein-based powder and water does not constitute a healthy diet, regardless of whether it accompanies a low or high carbohydrate intake.

It should also be mentioned that the individual who appeared on A Current Affair issuing these misleading claims also has authored a number of low-fat diet books. You may like to read a detailed critique of this author's work, and his subsequent reply to this critique, at the following links:

Just How Low Will the Anti-Low-Carb Crowd Go?

A Reply to Bilsborough

Ms. Pike, Your Actions Have Consequences - Bad Ones!

Several days ago, I received an e-mail from a business owner in NSW who, a little while back, started an innovative low-carb meal delivery service in response to the growing popularity of low-carb diets. The ready-made meals delivered by her business include lean meats and vegetables, and, to avert the stigma associated with saturated fats (no matter how misguided this sentiment may be), derive their fat content mainly from monounsaturated sources. Until recently, this individual was doing a roaring trade, having established a franchise chain of 15 outlets delivering delicious low-carb meals around the country. This entrepreneurial mother-of-three saw a niche and filled it, via honest and productive effort (something that more of our politicans should try to emulate), and started reaping the rewards that were rightly hers.

That is, until some misguided politician appeared on national TV and in the nation's newspapers announcing her latest novel waste of money - an anti-low-carbohydrate crusade!

"Since the negative PR has appeared in the recent news, my company is really suffering", said our understandably disheartened low-carb entrepreneur. "Here in Sydney it was as if someone has 'turned off the tap', that's how quiet our phones have been. It is a devastating blow to our businesses from which we hope to recover, but there are no guarantees."

Did customers stop ringing because they had subsequently died from heart disease and cancer, or because they were hospitalized with broken osteoporotic bones and/or depression, or because they had fallen prey to some other alleged adverse effect of low-carb diets?

Nope.

Customers stopped ringing because, not being familiar with the scientific literature, they relied on the media to deliver their diet and health information. So when a bunch of radical vegan activists from North America tried to infer that the death of the late Dr. Atkins was a result of his own dietary prescriptions, and the media lapped it up, they became worried. When some axe-grinding nutritionist from Melbourne appeared on A Current Affair and told the nation that low-carb diets had killed sixty people, they got scared. And when a Victorian politician announced that low-carbohydrate diets were such a threat to public health that her government was going to actively warn people away from them, people ran for the doors. Not being familiar with the scientific literature, which actually indicates that low-carb diets possess an array of favorable qualities and are definitely worthy of increasing research attention, these folks evidently believed what they were hearing on TV and in the newspapers.

Despite the volumes I read and hear about how people supposedly distrust politicians and how they distrust what they read in the papers and see on TV, a significant portion of the population in this country appears to have been suckered beautifully by yet another fallacious government and media beat-up!

Forgive me if I'm wrong, but I thought the notion of someone getting off their butt and "having a go" was supposed to be admired here in Australia. I don't know about others, but I think it is extremely unfair for someone who was making an honest, productive living to now be faced with the prospect of going out of business simply because of misleading, sensationalist bullshit.

I also think it is extremely unfair for some politician to take my tax money, and use it to tell me how I should abandon the very diet that has personally brought me nothing but benefits! Puhleez!

Perhaps most unfair of all is that thousands of people are being scared away from diets that have clearly been shown to benefit a number of common conditions - diabetes and obesity, for example - and hold great promise for treating many other ailments.

Conclusion

Ms. Pike, I know you have already travelled a fair way down your proposed path, and it might make you look rather silly if you abandon your sadly-misguided anti-low-carb campaign after creating such a commotion in the media. Nonetheless, I urge you to study the scientific evidence thoroughly, and then carefully reconsider your current stance. There are far better ways to spend taxpayer funds than on discouraging people from trying diets that may just benefit their health, and from sending flourishing businesses down the tube. I know such a change in stance will not impress the flour and baking industry, who are lobbying hard to try and avoid the same fate that is currently befalling their counterparts in the US, where low-carb diets have undergone phenomenal growth, but I think your primary concern should be public health, not the financial well-being of vested industries.

Sincerely,

Anthony Colpo.

To tell Bronwyn Pike that taxpayer funds should be used in a more responsible manner, e-mail: bronwyn.pike@parliament.vic.gov.au

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Anthony Colpo is an independent researcher and certified fitness consultant with 20 years' experience in the physical conditioning arena. To contact: contact@theomnivore.com

Disclaimer: This article is presented for information purposes only and is not intended as medical advice. Persons with medical conditions should institute dietary changes whilst being monitored by a competent medical practitioner.

© Anthony Colpo 2004. Copyright information:

Any articles on this website authored by Anthony Colpo may be reproduced for non-commercial purposes only, providing full credit is given to the author, and that the website name www.theomnivore.com is cited. A hyperlink would also be greatly appreciated. Those wishing to reproduce articles for commercial purposes should e-mail: contact@theomnivore.com

The Not-So-Funny Bloopers of Jane Brody

Celebrating decades of dietary confusion from the New York Times nutrition writer.

By Anthony Colpo.

March 25, 2004.

For decades, Jane Brody has been espousing the virtues of low-fat, high-carbohydrate nutrition from her syndicated column in the New York Times, one of the world's most widely-read newspapers. Reading one of her more recent columns reinforced in my mind just why so much of the population is utterly confused about what constitutes a healthy diet.

I present the following gems of wisdom from Brody's March 23, 2004 column, Sane Weight Loss in a Carb-Obsessed World - High Fiber and Low Fat.

"Name this product", begins Brody. "The ingredients label says it contains the following: "Water, ultrafiltered fat-free milk, calcium caseinate, cream, buttermilk, tricalcium phosphate, salt, disodium phosphate, mono- and di-glycerides, carrageenan, locust bean gum, natural flavor, sucralose (Splenda), acesulfame potassium, vitamin A palmitate and vitamin D3."

No, it's not some weird dessert. It is Hood's Carb Countdown Dairy Beverage, a low-carb substitute for real skim milk that claims to provide "75 percent less carbs and 50 percent more protein than whole milk." A half-gallon of the Hood's beverage sells for $3.99, compared with $1.48 for the same amount of real, unadulterated fat-free milk."

Brody's description of "...real, unadulterated fat-free milk" is an oxymoron if ever I've heard one! Does Brody know that milk comes from cows, and that in nature there's no such thing as a cow that produces fat-free milk? Does she know that when fat is removed from milk, so too are crucially important fat-soluble vitamins such as vitamin A and D? That's why synthetic vitamin A and D - "vitamin A palmitate and vitamin D3" - are added back to low-fat and skim milks!

If Brody is attempting to state, in her own clumsy way, that a healthy diet should be based on whole, minimally-processed fresh foods, regardless of whether it is low- or hi-carb, then I am in full agreement. But alas, that does not appear to be what she is saying at all. Brody proceeds to denigrate the whole low-carb concept, beginning her attack with a misleading interpretation of a recent study that appeared in the January 26 edition of the Archives of Internal Medicine:

"As a recent 12-week study of 34 men and women in their 60's so clearly demonstrated, those who consumed, without caloric restrictions, a diet high in fiber-rich carbohydrates (63 percent of calories, with 26 grams of fiber per 1,000 calories), low in fat (18 percent of calories) and moderate in protein lost more weight and a higher percentage of body fat than did those who ate the same number of calories of a typical American diet, that is, one high in fat (41 percent of calories) and relatively low in carbs (45 percent of calories).

The study showed that a low-fat, high-carbohydrate diet could result in weight loss and reduced body fat while preserving muscle mass, even without any change in caloric intake, as long as the carbs were low in added sugars and refined starches. And the weight is lost without having to avoid delicious, health-promoting fruits and instead eating lots of fiber-free and fat-laden eggs, cheese and meats.

How can this happen? It happens because fiber-rich carbohydrates offer three major benefits to the weight-conscious eater: they hold water in the gut, take longer to digest and some of their calories are eliminated unabsorbed. In other words, they can fill you up before they fill you out."

I have to wonder if Brody even read the full-text of the study, or simply relied on the highly-misleading press-releases sent out by the study's authors; if she did the former, she would have discovered that the study participants in the high-carbohydrate groups actually consumed about 400-600 calories less per day than those in the control group! Over the 12-week period of the study, the high-carbohydrate subjects consumed around 33,000 to 50,000 calories less than the average subject in the control group.(Hays NP) It's no surprise that they lost more weight!

Sure, eating fiber-rich, starchy-carbohydrates can increase satiety, and consequently reduce calorie intake, when compared to the calorie-dense junk that dominates the average American diet; a number of studies have already attested to this. However, in order to increase satiety and reduce one's calorie intake, one does not need to suffer the anti-social consequences of turning one's intestines into a methane-production plant by eating a diet high in whole-grains and legumes! Numerous studies have found that subjects placed on low-carb diets, who are told to restrict carbs but to eat protein and fat without limit, unintentionally reduce their total calorie intake to the same levels seen among dieters explicitly instructed to limit their overall calorie intake!(Brehm B)(Foster GD)(Samaha FF)(Yudkin J)(Westman E)(Westman EC)

The control diet by the way, with a 45% carbohydrate content, was in no way a low-carb diet. Brody skirts around this issue by labelling it as "relatively" low in carbs, but she could have cited the numerous studies that have indeed compared truly low-carb and high-carb diets for fat loss. The overwhelming majority have found either greater weight loss or no statistically significant difference in weight loss between low- and high-carb dieters.(Rabast, et al. 1981)(Baron JA, et al. 1986)(Wadden TA. 1993)(Foreyt et al. 1993)(Alford BB, et al. 1990)(Golay A, et al. 1996, 1996)(Lean et al. 1997)(Torbay et al. 2002)(Sondike et al. 2003)(Volek et al. 2002)(Fleming RM. 2002)(Brehm et al. 2003)(Foster et al. 2003)(Samaha et al. 2003)(Wien et al. 2003) Only one study has ever found greater weight loss on a low-fat, high-carbohydrate diet, and that study just happened to be authored by Richard Fleming, the Nebraska cardiologist and avowed low-carb hater who is currently in doggy-doo over his shonky acquisition of the late Dr. Atkins' death report. I have already explained at length why Fleming's study is a highly questionable piece of literature.

"How many people know, for example, that one pound of uncooked pasta is meant to serve eight — yes, eight, not four or two — people? And how many examined the nutrition facts label on fat-free cakes and realized that a serving was still the same size as the full-fat version, and that the calorie savings per serving was minimal?"

Jane, the blame for the rise in calorie-intake that has occurred over the last thirty years can be placed squarely at the feet of the low-fat movement, whose voluminous anti-fat propaganda led us to believe that, when it came to diet, fat-restriction was the be-all-and-end-all of weight loss. Oh sure, low-fat advocates are now complaining that that was never the intention, that people should have realized that they needed to cut fat intake and total calorie intake in order to lose weight. Maybe the low-fat establishment should have given that a little more thought before enthusiastically embracing and giving "heart-healthy" ticks to high-carbohydrate, fat-free garbage (like the fat-free cake Brody attempts to apologize for); garbage that possesses low satiety value and creates rapid surges in blood sugar, followed by hypoglycemic lows that send dieters running straight back to the pantry for another blood glucose-raising carb-fix.

"A diet high in fat and low in carbs has yet to be tested for long-term safety and effectiveness."

You've got to be joking! High-fat, low-carb diets - comprised of freshly-killed meats, and gathered non-cereal plant foods (nuts, fruits, vegetables) - have been subjected to the longest trial ever known: human evolution. This ongoing trial has so far lasted 2.5 million years, most of which has been spent on what is known as the paleolithic or hunter-gatherer diet. Depending on geographical location, this diet varied from high-carb, low-fat to high-fat, very-low-carb. Low-carb, high-fat diets tended to predominate in colder regions far from the equator, where edible vegetation was far less abundant than in tropical regions. Radioisotope analyses of paleolithic skeletal remains - which tend to be far more robust than those of modern humans - show that meat comprised a significant portion of our ancestors' diets. Depending on the stage of evolution, at least a portion of the earth's inhabitants subsisted on a low-carb, high-fat diet; in colder eras, such as the Ice Age, paleontologists believe that the majority of the population was, by necessity, consuming low-carb diets. Despite the politically-incorrect eating habits that humankind kept throughout much of its evolutionary history, humans have out-survived many other species that have long since been rendered extinct. And we did it all without fat-free cakes, white rice, pasta, or non-fat milk, Jane!

"What do I and my slender friends eat? Mostly — but not exclusively — whole grain breads and cereals; lots of vegetables, salads and fresh and dried fruits; poultry, fish, meat and dried beans and peas and skim milk. But we also eat mostly white rice and pasta, potatoes, winter squash, avocados, regular cheese, eggs, cookies and ice cream and an occasional piece of cake or pie."

Well Jane, I'm glad it works for you. The unfortunate reality is that countless other folks have tried a similar approach, and failed dismally to achieve their health and/or weight loss goals. I'm one of them. Throughout most of the nineties, I followed a low-fat, high-carbohydrate diet, based on so-called "healthy" complex carbohydrates like whole-grain breads, rice, rolled oats, sweet potato, and ate only the leanest meats I could find. As anyone who knew me back then could attest, I followed this diet religiously, so it wasn't my lack of willpower or discipline that failed me - it was the diet. After several years of eating a diet that I now realize humans were never designed to eat, my blood pressure had risen, my blood sugar metabolism had gone to hell, and I developed a rather impressive array of food sensitivities.

If readers are thinking that maybe I was just unlucky and an isolated case, they would do well to read Beyond Pritikin by Louise Ann Gittleman. Gittleman used to be a Director of Nutrition at the Pritikin Longevity Center, and for years she counselled people to follow the low-fat, high-carbohydrate, grain- and legume-based diet espoused by the late Nathan Pritikin. She left after seeing how the diet was continually failing people. She observed significant improvements when people first began the Pritikin program, but noticed during their follow-up visits that many patients were experiencing weight regain, fatigue, ravenous hunger and food sensitivities. What sort of dietary regimen does Gittleman recommend nowadays? A low-carb diet for weight-loss, and a moderate-carbohydrate diet for weight-maintenance!

"The second and equally critical factor in our ability to keep our weight down is regular physical exercise. I mean regular. We walk briskly for an hour each morning and, in addition, I swim three-fourths of a mile nearly every day. My friends and I walk to and from appointments where most other Americans would ride, and I do most of my shopping on foot or bicycle. And, I assure you, none of us view this as a life of deprivation and self-denial."

Ah, now you're talking, Jane! Ladies and gentleman, no matter what diet you follow, physical activity should be a regular part of your schedule. However, while exercise has been shown to at least partially counter some of the hyperglycemic and hyperinsulinemic effects of a high carbohydrate diet, it's no guarantee of protection, as running enthusiasts Jim Fixx and, more recently, Brian Maxwell unfortunately found out. Indeed, intense daily workouts did little to stop the deleterious effects of my own copious complex carbohydrate ingestion.

Upholding The Tradition

I'm hardly the first person to highlight the nutritional nonsense emanating from Brody's NYT column. Back in 1991, Dr. Russell L. Smith pointed out a number of Brody Bloopers in his outstanding tome, The Cholesterol Conspiracy, including the following from her November 15, 1986 column: "It is not advisable to consume large amounts of polyunsaturated fats because, while they lower the damaging LDL and VLDL cholesterol in the blood, they also reduce the protective HDL cholesterol." Less than a month later (December 10, 1986), Brody was reportedly telling readers that "Experts recommend substituting unsaturated liquid vegetable oils (corn, safflower, sunflower, soybean [all rich in polyunsaturates] and olive oils, for example) for saturated fats. Unsaturated fats help to lower cholesterol levels in the blood."(Smith RL)

Smith went on to quote a few more contradictory Brody-Bytes; "A problem results from overconsumption of polyunsaturates, which can interfere broadly with immune responses. Too much total fat, particularly too many polyunsaturates, can also promote the growth of cancers of the breast, colon, and prostate...a wise consumer would stick to a low-fat diet and keep consumption of polyunsaturates to a minimum level." These words were printed in the NYT on March 11, 1987; four days later, Smith reports, Brody authored an article in Family Circle advising readers that: "Polyunsaturated fats help lower cholesterol levels in the blood and, thus, offer protection against heart disease ... you'll want to look for a margarine that lists a higher proportion of polyunsaturates than saturates." Then in the October-November 1988 issue of Modern Maturity, Brody reportedly told readers to: "Try and use as little fat as possible and, when fat is added, primarily use vegetable oils such as olive, corn oil and safflower oil, and margarine."

Brody complained in a 1986 column, "the dozens of letters I have received in response to recent columns on fats and cholesterol in foods indicated that many readers remain uncertain about how to choose a heart-healthy menu." No kidding! If I relied on Brody's columns for dietary advice, I'd be pretty damn perplexed too!

More recently, nutritionist Sally Fallon and biochemist Mary G. Enig, PhD, were driven to write a letter to the editor of NYT (which remains unpublished, but can nonetheless be read here) after reading some rather remarkable claims in Brody's July 15, 2003 column (Cholesterol: When It’s Good, It’s Very, Very Good).

Wrote Fallon and Enig:

"According to Jane E. Brody, your nutrition “expert,” the human anatomy “more closely resembles herbivores like cows and deer, strict vegetarians consuming only plant-based foods”... If this is the best the New York Times can do, the public is in serious trouble. Even school children know that the human digestive tract is completely different from that of ruminants like cows and deer, which have multiple stomachs, do not produce hydrochloric acid and have extremely long intestines compared to humans. The human digestive tract is much more like that of a dog than any herbivorous animal. If Brody is so wrong on this elementary fact, how can we trust anything else she says, including the merits of the plant-based diet she espouses? The Times is just emerging from the scandal of a journalist who made up news reports, but in your health section your most prominent health writer is still passing off falsehoods as fact."

That someone like Brody can have her Keystone Cop-like nutritional bloopers published in a major paper like the New York Times is a sad, sad indictment on the pitifully low standards that most media outlets demand of the nutritional information that graces their pages. As Dr. Smith wrote back in 1991:

"It is unfortunate for the American people that they have been and continue to be influenced by columnists who claim to be authorities but who are, in fact, not experts at all but purveyors of a montage of contradictory and inconsistent nonsense."

Smith's words are even more relevant today than they were back in '91, given the increasingly desperate behavior of low-fat proponents. As recent events have shown, these folks are not above misquoting studies and even telling outright lies in their attempt to suppress the rapidly rising popularity of low-carb nutrition (for recent examples of some rather bizzarre and misleading behavior by so-called low-fat experts, click here, and here).

References

Hays NP, et al. Effects of an Ad Libitum Low-Fat, High-Carbohydrate Diet on Body Weight, Body Composition, and Fat Distribution in Older Men and Women: A Randomized Controlled Trial. Archives of Internal Medicine, 2004; 164: 210-217.

Brehm B, et al. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. Journal of Clinical Endocrinology and Metabolism, 2003; 88 (4): 1617-1623.

Foster GD, et al. A randomized trial of a low-carbohydrate diet for obesity. New England Journal of Medicine, May 22, 2003; 348: 2082-2090.

Samaha FF, et al. A low-carbohydrate diet as compared with a low fat diet in severe obesity. New England Journal of Medicine, May 22, 2003; 348: 2074-2081.

Yudkin J, Carey M. The treatment of obesity by the "high fat" diet: the inevitability of calories. Lancet, Oct 29, 1960; 2; 939-941.

Westman EC, et al. Effect of 6-month adherence to a very low carbohydrate diet program. American Journal of Medicine, Jul, 2002; 113 (1): 30-36.

Rabast U, et al. Loss of weight, sodium and water in obese persons consuming a high or low carbohydrate diet. Annals of Nutrition and Metabolism, 1981; 25: 341-349.

Baron JA, et al. A randomized controlled trial of low carbohydrate and low fat/high fiber diets for weight loss. American Journal of Public Health, 1986; 76 (11): 1293-1296.

Wadden TA. Treatment of obesity by moderate and severe caloric restriction. Annals of Internal Medicine, Oct. 1993; 119 (7, Pt. 2): 688-693.

Foreyt JP, Goodrick GK. Evidence for success of behavior modification in weight loss and control. Annals of Internal Medicine, Oct. 1993; 119 (7, Pt. 2): 698-701.

Alford BB, et al. The effects of variations in carbohydrate, protein, and fat content of the diet upon weight loss, blood values, and nutrient intake of adult obese women. Journal of the American Dietetic Association, 1990; 90: 534-540.

Golay A, et al. Weight-Loss With Low or High Carbohydrate Diet? International Journal of Obesity, 1996; 20 (12): 1067-1072.

Golay A, et al. Similar weight loss with low- or high carbohydrate diets. American Journal of Clinical Nutrition, 1996; 63: 174-178.

Lean ME, et al. Weight loss with high and low carbohydrate 1200 kcal diets in free living women. European Journal of Clinical Nutrition, Apr. 1997; 51 (4): 243-248.

Torbay N, et al. High protein vs high carbohydrate hypoenergetic diet in treatment of obese normoinsulinemic and hyperinsulinemic subjects. Nutrition Research, May 2002; 22 (5): 587-598.

Sondike SB, et al. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factors in overweight adolescents. Journal of Pediatrics, March 2003; 142: 253-258.

Volek JS, et al. Body composition and hormonal responses to a carbohydrate-restricted diet. Metabolism, July 2002; 51 (7): 864-870.

Fleming RM. The Effect of High-, Moderate-, and Low-Fat Diets on Weight Loss and Cardiovascular Disease Risk Factors. Preventive Cardiology, 2002; 5 (3): 110-118.

Brehm, et al. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. Journal of Clinical Endocrinology and Metabolism, 2003; 88 (4): 1617-1623.

Foster GD, et al. A randomized trial of a low-carbohydrate diet for obesity. New England Journal of Medicine, May 22, 2003; 348: 2082-2090.

Samaha FF, et al. A low-carbohydrate diet as compared with a low fat diet in severe obesity. New England Journal of Medicine, May 22, 2003; 348: 2074-2081.

Wien MA, et al. Almonds vs complex carbohydrates in a weight reduction program. International Journal of Obesity and Related Metabolic Disorders, Nov 2003; 27 (11): 1365-1372.

Smith RL. The Cholesterol Conspiracy. Warren H. Green, June 1991.

Source: The Omnivore

Digestive Tract Comparision

From the site: "FUNCTIONAL AND STRUCTURAL COMPARISON OF MAN'S DIGESTIVE TRACT WITH THAT OF A DOG AND SHEEP"

Full table: paleodiet.com

Did the Atkins Diet Really Kill Dr. Atkins?

Science, not scare-mongering, should be dominating the low-carbohydrate versus low-fat diet debate.

By Anthony Colpo.
February 17, 2004.

Dr. Robert Atkins was never a stranger to controversy. His high-fat, low-carbohydrate dietary guidelines contradicted virtually every closely-held tenet of mainstream nutrition, bringing him under constant attack from defenders of the low-fat diet doctrine. Atkins died in April last year from a head injury he sustained after falling on an icy New York footpath, but his demise has done little to stem the controversy surrounding his dietary recommendations. As the recent commotion surrounding the New York diet guru's death report clearly illustrates, his nutritional legacy is still a subject of heated debate.

The current uproar began after a Nebraska-based cardiologist by the name of Richard Fleming wrote to the New York medical examiner's office requesting a copy of Atkins' death report. Despite the confidential nature of such reports, someone at the office readily obliged Fleming, who, after receiving the report, passed a copy along to his acquaintances at the Physicians Committee for Responsible Medicine (PCRM). The PCRM in turn contacted the Wall Street Journal, who broke the story and ignited a world-wide debate in the process.

The ease with which the PCRM has been able to cause such an uproar is a sad indictment of the woefully inadequate investigative methods employed by many journalists reporting on health and nutrition issues. As an independent researcher, one of the first things I do when studying new information is to verify its source. Foremost among my concerns is whether or not the information has come from someone with a vested interest, and whether the information is being issued in order to advance some sort of concealed agenda.

Read full article here: theomnivore.com

On The First Law of Thermodynamics

From the British Medical Journal

Author: Barry Groves, Independent Researcher OX7 6LP

Weight loss on a low-carb diet has two components:

1. Reducing carb (and protein if necessary) intake so that the body no longer has a ready supply of glucose.

2. Increasing fat intake to supply an alternative energy supply.

The aim is to get the body to burn fats -- and crucially for weight loss, this includes body fats. The body will only do this in two circumstances:

1. Starvation (including low-calorie dieting)

2. When glucose is restricted by other means and fats are the only fuel supply available (low-carb, high-fat diets).

But what about the Laws of Thermodynamics?

The laws of thermodynamics, so often quoted by 'experts' (I have another word for them: 'ignorants') in support of the 'calories in = calories out' hypothesis, is a complete red herring as it takes no account of the way the body deals with different nutrients.

One major flaw in their argument is that the body does not use all the food we eat to provide energy. The primary function of dietary proteins, for example, is body cell manufacture and repair: making skin, blood, hair, and finger- and toe-nails, enzymes, etc. The amount of protein needed for this purpose is generally accepted to be about one gram per kilogram of lean body weight. As meats contain approximately 23 grams of protein per 100 grams, a person weighing, say, 70 kg (154 lbs) needs to eat about 300 g (11 oz) of meat, or its equivalent, every day just to supply his basic protein needs. Even eating this volume of lean chicken would provide some 465 kcals. These calories are not used to supply energy, they contribute nothing to the body's calorie needs and so must be deducted if you are counting calories.

Much of the fat we eat is also used to provide materials used by the body in processes other than the production of energy: the manufacture of body cell membranes, bile acids, hormones, the essential fatty acids for the brain and nervous system, and so on. All these must be deducted as well. Thus trying to determine, from food intake and energy expenditure alone, how much excess energy your body will store as fat will give a completely wrong answer. However, these other factors cannot be measured. Calorie counting, which is the foundation of practically every modern slimming diet, is both totally misleading and a complete waste of time.

There are also other anomolies: A figure often used is that one kilogram of body fat represents about 3500 calories. But according to the United States Department Of Health, Education and Welfare:

'On a high-fat diet, 4703 to 8471 excess calories were required for each kilogram of added weight. On a low carbohydrate VLCD [very low calorie diet], replacing fat calories with 8g/day of equivalent carbohydrate calories reduced weight loss by 1.68kg, corresponding to 3300 calories of carbohydrate/kilogram, possibly 2500 calories per kilogram for carbohydrate alone.'(Department of HEW Publication: NIH 75-708, Government Printing Office, 165-86.)

Are they are saying that it takes 4,703 to 8,471 excess calories of fat to add a kilogram of weight, yet it takes only 2,500 to 3,300 calories of carbohydrate to add the same amount? If so 'a calorie is a calorie is a calorie' is not so meaningful after all: a carbohydrate calorie is obviously much more fattening than a fat calorie. So do calories count? Well, perhaps -- but some don't count half as much as others.

Actually, excess fats aren't stored in the body. Any unused fat calories are excreted in urine and faeces. (Endocrinology 1962; 70: 579. Experientia 1963; 19: 319. Metabolism 1964; 13: 87-97. Proc Soc Exp Biol Med 1964; 115:424. Nature 1964; 201: 924)

There is an emerging scientific consensus that weight control is a highly complex topic and the old ideas that overweight people are lazy gluttons are now realised to be as absurd and insulting as the overweight have always thought they were.

By the way, ketones are derived from fats in food which has been bought and paid for. They are a valuable source of energy for cells that usually use glucose. It makes no sense to create in the body a situation where they are flushed down the lavatory.

Source: British Medical Journal

The Carbohydrate Conspiracy

From The Washington Dispatch

Opinion
The Carbohydrate Conspiracy
Exclusive commentary by Greg Lewis

Fred Smerlas, for those of you who don't follow pro football, is a retired five-time All-Pro defensive lineman for the Buffalo Bills. Fred Smerlas is also a Christian and a political conservative, and he's got very definite views on pretty much any issue you'd care to discuss. He's especially articulate when you bring up the subject of the Atkins diet. He's even gone so far as to suggest that there may be some sort of conspiracy associated with the fact that high-carbohydrate diets have been pushed so hard by so many people for so long.

Fred, like me, is an Atkins Diet advocate. He's an Atkins lifer, as are many of us who have been successful with the diet and understand just how important it is, not only to physical health, but to mental well-being as well. Which brings us to the subject of carbohydrates and the possible conspiracy associated with them. Fred's experience, like mine, has been that withdrawing from excessive sugar and refined carbohydrate consumption is just about the same thing as withdrawing from drugs.

In this insight he's right on the money. In fact, so detrimental is the overconsumption of carbohydrates that in End Your Addiction Now, a book I co-authored, high-carbohydrate diets are identified as a risk factor for substance abuse. The more carbos you consume, the more likely you are to also develop a problem with alcohol or drugs.

The Atkins program, as many people now know (and many more are coming to realize), is based on practically eliminating carbohydrates from your diet. On this terrific regimen, you eat lots of protein, lots of green vegetables, lots of fat, and not much else. And you get thinner and healthier. You lose weight until you feel so good you can't believe it, and when your body finds an ideal weight for you, it just directs you to a natural maintenance level, again, with very few carbohydrates. We don't really need carbohydrates, so, after we get off of them, our bodies just don't crave them any more.

This is your brain . . . this is your brain on carbohydrates

Part of the reason we're able to reach a balance without carbohydrates is because of what the excessive consumption of refined carbohydrates does to our brains. First, the consumption of large quantities of sugar and other refined carbohydrates causes the level of a brain chemical called serotonin to increase significantly. Serotonin is a neurotransmitter, one of the chemicals that gets shuttled from one neuron to another as part of the infinitely complex process of communication among brain cells.

Serotonin is one of the important "relaxing" neurotransmitters. When your brain is producing adequate levels of serotonin, you feel calm, relaxed, unflustered. Adequate levels of serotonin also help you sleep soundly. It's one of the important feel-good brain chemicals: when you eat lots of carbohydrates, you feel good. Up to a point, at least. The problem is that when you continue to eat large amounts of carbohydrates, you begin to overtax your brain's ability to produce serotonin.

Let me back up here and explain a little bit about the process. Serotonin is produced from nutrient molecules, particularly amino acids, vitamins, and minerals. (Notice there's no mention of carbohydrates here.) Neurons literally assemble serotonin molecules from these nutrient substances. Then they transmit them across a synapse (or gap) to adjacent neurons in order to send a message that helps you relax. This process takes place billions of times every hour in your brain as hundreds of millions of neurons communicate with each other.

When you stimulate your brain to over-produce serotonin by eating excessive amounts of carbohydrates, you use up your body's supplies of the nutrients necessary to produce serotonin. This often results in a kind of backlash, where your brain will struggle to produce serotonin when it is stimulated, but when it's no longer got the nutrients it needs, serotonin production is actually cut back. Eventually, if you eat lots of carbs, you're going to get fat and you're going to experience symptoms of depression due to reduced serotonin production.

Conspiracy Theory

That's where the carbohydrate conspiracy comes in. For the past 20 years, doctors, politicians, nutritionists, marketing vice presidents, and anyone else who could manage to get a platform have been telling us that we should eat lots of carbohydrates. "Cut down on fats, load up on carbohydrates." That was the message. If you didn't consume massive quantities of carbohydrates, you were doomed to ill health, or worse. The problem is, they were wrong. And not only were they wrong, their advice has caused and is causing millions of Americans to suffer. Obesity levels, incidences of depression and anxiety, and — shudder — cholesterol levels are all up dramatically over the past 20 years, and it's not a stretch to point to excessive carbohydrate consumption as the single most important contributor to all these conditions.

And this is not to mention the fact that if you're not consuming fats in significant quantities, your brain doesn't have another of the most important nutrients it needs. Brain cells (all cells, for that matter) are surrounded by a fatty membrane, and if your body doesn't have adequate amounts of fat, it's not going to be able to patch up the damage its cells incur as part of normal wear and tear. This is especially critical for children on low-fat diets. Kids are often starved for the fatty acids their brains and bodies need for healthy growth, and this hidden malnutrition can play a part in everything from decelerated development to behavioral problems.

And as far as the cholesterol issue is concerned, the notion that if you don't gorge on carbos, your cholesterol levels will go through the roof is simply absurd. The fact is, as we're finally realizing, the exact opposite is true. Levels of bad cholesterol invariably go down and good cholesterol goes up for people on the Atkins diet.

Now, the question becomes, "Who benefits from this?" Obviously, the sicker the American populace, the more drugs you can sell to them, so drug companies benefit enormously from the perpetuation of false information about the need to consume lots of carbohydrates. But politicians also benefit.

As we all know, you can't be a liberal if you don't have an absolutely pessimistic outlook on life. You're simply not going to buy the liberal message — higher taxes, larger and more intrusive federal government, welfare expansion — unless you're convinced that the world is going to hell in a handbasket and there's nothing you can do about it. And it's much easier to get you into that frame of mind if you can be convinced to eat large quantities of carbos.

Bring on the soda, the candy, the baked potatoes, the fruit juices, the doughnuts, the bagels, the pasta . . . you name it, if it's a refined carbohydrate you won't have to look far to find a liberal pushing you to consume it. You have to be depressed to be a true liberal, and eating excessive amounts of carbohydrates is going to help keep you depressed. It's going to burn you out over-producing serotonin and leave you wailing for someone, some doctor or some flak in a socialized medicine scheme, to bail you out with your daily dose of brain destabilizers.

That's one possible reason why the Atkins diet has met with so much resistance until fairly recently. If you go on the Atkins diet for even as short a time as a month or two (depending on your current physical condition), the changes in your frame of mind and your physical well-being will be so dramatic that you'll start to wonder about the motivation of those people who kept pounding home the message that you should eat large quantities of carbohydrates. By the end of your first month, you'll probably have gone through carbohydrate withdrawal, and that carbo brain fog you've been experiencing will have lifted, and you'll start thinking clearly again. Your self-confidence will begin to reassert itself as the low-level depression you've been living with starts to ease up, and you'll begin to understand that you really don't have to be a victim of the liberal mentality. Or the carbohydrate conspiracy.

Liberals hate people who think for themselves, and liberals hate the Atkins diet. OK, maybe conspiracy is a bit too strong a word. But given the other tactics those on the left have tried, don't rule it out completely. If liberals realized that cramming carbohydrates down your throat would soften you up to receive their message, they'd do it in a heartbeat. But don't just take it from me. Take if from Fred Smerlas.

Writer Greg Lewis is the co-author of the Warner Books hardcover "End Your Addiction Now." He can be reached by e-mail by clicking here.

© 2002 The Washington Dispatch. All Rights Reserved.

Why the Atkins diet is healthy

By RFD Columnist Malcolm Kendrick MbChB, MRCGP
(email - malcolm@llp.org.uk )

I was idly watching a programme on the Atkins diet last night which, to my surprise, was reasonably balanced. Yes folks, the Atkins diet has crossed the pond to reach the United Kingdom. Although, in reality, all it is doing is returning. After all we invented it nearly one hundred and fifty years ago.

A man called Banting promoted a diet pretty much indistinguishable from that of Atkins in 1863. In fact, the verb to ‘bant’ is used in Sweden as a term for going on a diet

To find out more about the Banting diet (now known as the Atkins diet) go here.

Anyway, reasonably balanced or not, on this programme there was still an unquestioned view that, even if the Atkins diet did help with weight loss, it was still damaging to health. It would cause kidney disease, and osteoporosis and heart disease. Various professors of nutrition were wheeled out to condemn the Atkins diet as dangerous nonsense.

Ignoring the kidney disease and the osteoporosis for now, the nutritional professors made the usual statements. For example, ‘It is known that saturated fat increases the level of blood cholesterol and causes CHD.’ They didn’t quote any evidence for this. As far as they were concerned it is just a known fact.

Read full article:redflagsdaily.com

Fruit: Are you missing it?

For most Low-carbers, the answer to the above question is “Oh golly gosh yes!” Me, I never was a “fruit fan”, so when I started LCing in 1999, it was one thing I never missed.

However, over 3 1/2 years on, and my taste buds have adapted to my lowered sweetness diet and I now enjoy, in moderation of course, many fruits that I thought were too bland, sour, or tart.

As a general rule, a fruit’s sugar content is governed by when the fruit is naturally produced by the plant. The amount of sun the plant gets controls the sugar content. (See Table 1)

Full article: Low Carb in the UK

Hackers on Atkins

Geeks who go low-carb see it as more than just taking off pounds -- they're reengineering the human organism, overclocking their own bodies.

- - - - - - - - - - - -
By Katharine Mieszkowski
The Salon

For Dave Sifry, 35, attending LinuxWorld in the summer of 2002 meant more than just a chance to luxuriate in the latest insider buzz about Red Hat, Suse and Debian. It also was an unexpected chance to learn about a body-reengineering hack increasingly popular with computer programmers and affiliated geeks.

When Sifry, now the co-founder and CTO of Sputnik, a wireless device company, saw Cory Doctorow, the boingboing blogger and science-fiction author, at the conference at San Francisco's Moscone Center, he almost didn't recognize him.

"I hadn't seen him in a while, and he had lost so much weight with Atkins -- maybe 35 or 40 pounds -- that he just looked like a changed man," says Sifry, who founded the Bay Area Linux Users Group and co-founded Linuxcare, a start-up aimed at providing support services for Linux users. But Doctorow, a self-described "renaissance geek," wasn't the only slimmed-down figure among the usual crew of techie conference-goers. Doc Searls, coauthor of "The Cluetrain Manifesto," was also looking svelter, from his own regime of low-carbing.

"To be perfectly frank, I thought it was nuts," says Sifry. "OK: You can eat as many bacon cheeseburgers as you want, and you still lose weight? Why doesn't this sound healthy? But when I saw two people who I respect do it, it really forced me to take a second look at it."

"We see people when we go to conferences that used to be a lot wider than they are now. Now, they're down to, like, one chin," says Searls, who lost 25 pounds last year in time for the Linux Geek Cruise in October, and has kept it off. "Cory blew my mind when I saw him. He looks like a skinny kid."

Picking up dieting tips at a computer conference could sound like the setup for a real groaner of a bad joke. Fairly or not, computer geeks have become cultural stereotypes for their embodiment of the modern-day version of the classic mind/body split: Many geeks tend to live their "real" lives in the virtual domain, while their bodies become forgotten blobs, crouched behind a monitor in some featureless room. Even the iconic penguin that reigns over all things Linux has a bit of a cuddly paunch.

But while there's nothing particularly bleeding-edge about eating the hamburger but not the bun, now that low-carb dieting has gone mainstream, the diet does appear to hold a special attraction for hackers, programmers and other close-to-the-machine dwellers. For some geeks, the low-carb diet is itself a clever hack, a sneaky algorithm for getting the body to do what you want it to do, a way of reprogramming yourself. Programmers, who are used to making their computers serve their will, are now finding that low-carb diets enable the same kind of control over their bodies.

Advocating eating protein in the form of burgers and eggs, while avoiding bread and pasta, as a way to lose weight is a diet plan that's drawn ridicule and sneers from mainstream nutritionists since the early 1970s, when the now-deceased Dr. Atkins started promoting the idea. But Dr. Atkins and other low-carb adherents argue that without an influx of sugar and carbohydrates for quick energy, the body is forced to burn off its fat. And the zealous advocates of the diet make this controversial claim: that when your body gets into this fat-burning state, dieters can actually eat more calories than they could on a low-fat diet, and still lose weight.

Doctorow, who lost 75 pounds by cutting out carbohydrates, sees a natural affinity between his brethren and the diet: "Read the alt.support.diet.low-carb FAQ, and you'll find people attacking their bodies like they would attack a logic board," he says. "Substitute 'faster bus speed' for 'metabolism,' and you've got something pretty close to an overclocking FAQ, he adds, referring to a practice popular with hardware hackers in which computer processors are tweaked so that they run faster than their out-of-the-box speeds.

"The low-carb thing is essentially a way of forcing control over the metabolism much like coders, geeks and hackers tweak their code and config files to make their machines run smoother," writes Sean Sosik-Hamor, a 27-year-old systems administrator for Pepper Computer, a wi-fi start-up in Lexington, Mass., in an e-mail. Sosik-Hamor says he lost more than 100 pounds through such dietary tweaking, a feat that took him down from 330 to 222 pounds, and which he blogs about here.

As digital-rights attorney Mike Godwin, who lost more than 80 pounds by cutting carbs, says, "It's like you're exploiting a security hole in your own body." He's quoting hacker Ian Goldberg, who should know -- Goldberg is famous in hacker circles for breaking the encryption on Netscape Navigator 1.1.

Since the LinuxWorld conference last year where Sifry caught the low-carb virus, he's lost 70 pounds, his blood pressure has dropped 30 points and his overall cholesterol numbers have gone down. And while he's reluctant to declare victory prematurely -- "I don't know where I'm going to be in a year" -- he's glad he's discovered this "backdoor" into his own body's workings. "All of a sudden," he muses, "[I've] found a new metabolic pathway."

Chat with low-carb dieters about their regimen, and they will soon bring up "ketosis" -- the state where your body is forced to burn off its fat reserves. On dieting message boards, they trade strategies about how to get to ketosis faster, stay in ketosis longer, and get back into it when you get off track, with all the ardor of teenage stoners on a quest to achieve and prolong the perfect high. Ketosis is their version of dieter's nirvana, where the weight is just steadily falling off, when your body is getting its energy from stored fat reserves instead of carbohydrates.

"Atkins makes this connection between reducing the amount of carbs and reducing the amount of fat storage," says Searls. "It works very cleanly at a conceptual level. Technical people like technical prescriptions, and Atkins offers them a pretty good technical prescription."

But look up "ketosis" in the dictionary, instead of on a dieting Web site, and you'll find all sorts of uncomfortable words associated with it, like "pathological" and "starvation." Oddly, the negative connotations of the concept perversely make it more attractive to hackers, who delight in using unexpected means to achieve a solution.

"The true definition of hacking is that of simple problem-solving, and making something do a task that it wasn't designed to do," writes Sosik-Hamor. "Ketosis is not a natural body state so the sheer thought of intentionally utilizing ketosis for weight loss is appealing."

There's also a subversive element. Go low-carb, and you're going against the dietary establishment, against the conventional diet wisdom from the USDA's food pyramid. You're doing something that you're maybe not supposed to do.

Mike Godwin started low-carb dieting back in 1998, when he weighed more than 300 pounds. He says he was "a little bit ahead of the curve" on the low-carb thing, since back then, all the dieters he knew were "still cutting their steak into 3-ounce portions" and avoiding fat like it was the blubbery enemy. He'd tried that, but found that the low-fat regimen of the likes of diet guru Susan Powter "was like eating grass," and it wasn't working for him.

"I'm perfectly willing to believe that what everyone knows is true is wrong, or at least might be wrong for me," says Godwin. "I had known about Atkins' popularity in the '70s. Because it was so counter to what everyone was saying I should do, I thought: I'll try it."

Sure, if you eat fewer calories and exercise more you'll lose weight, but if, like so many dieters, you're unable to follow that advice, who cares if it's an airtight theory? "If that's science, then it's science that has yet to produce a lot of results because American asses grow rounder every day," says Doctorow. "If you ask people to reduce their caloric intake and increase their exercise, you won't get a lot of good results. It's like going around complaining that people have crappy passwords."

"The hacker ethic is not necessarily being a formally trained engineer, not necessarily being someone who understands the science. It's a reverse-engineering perspective: Sometimes you're right and sometimes you're wrong, but it's based on empiricism," says Doctorow. "That's kind of the low-carb approach, which goes against the conventional wisdom about how you do nutrition and weight loss."

Scientific studies sanctioning the approach are just starting to appear, but there's a still a sense that one is tinkering with one's own body to somewhat unknown ends. "Maybe it will make us all grow third arms and go blind in 20 years," quips Doctorow. "It's sort of hard to tell. It represents a kind of hacker's approach, grounded as it is in jack-legged engineering rather than science."

The most controversial aspect of low-carb dieting -- which is only now being studied -- is the claim that you can actually eat more calories on a low-carb regime than you could on a low-fat one, and still lose weight. To borrow some jargon from the world of engineering: There's the possibility that you can actually run your body at a "specification" it wasn't designed for, in order to burn off more fat.

"I firmly believe that the low-carb system used by Atkins is a perfect example of hacking your body," writes Sosik-Hamor. "Massive reduction of carbs and carefully designing a balanced diet allows you to safely push the body into a state of ketosis and excrete fat out of the system faster than the standard burn rate of 1 pound per 3,500 calories. When in full induction mode I can eat 3,000 to 4,000 calories per day and lose up to 4 pounds per week."

But Searls warns against taking the hacking metaphor too far. Overclocking a computer processor has negative aspects that he believes don't have parallels in the low-carb dieting world.

"I think on the downside of what that metaphor suggests is that you are operating your body out of spec," says Searls. "Overclocking says that your body is specced for a certain performance speed, and overclocking it gets you a tradeoff between performance and heat, essentially."

"In a way, you are in fact burning off some of your body fat, and in that respect the metaphor is accurate. It's not accurate in the sense that you may be damaging your body in some way. It raises the suggestion that maybe you're doing something a bit unhealthy. And I don't think that's the case."

Godwin goes even further: "It might be that we're designed actually to operate that way, instead of eating a whole bunch of processed carbs. [With a low-carb diet] it actually may be that we're gearing our diets to how we should be eating. It might be a feature, not a bug."

But it's also useful to remember that no matter how attractive the metaphor, or the algorithm, dieting, like programming, is about doing what works, not the latest hot theory.

"We are not machines," says Searls. "It helps techies sometimes to think of their bodies as a machine, but it really comes down to whatever works for you."

Source: The Salon

ATKINS MUST BE DESTROYED!

"I wanted to make it clear that the attacks on Atkins are not scientific, not rational. Atkins, may he rest in peace, is being attacked because his diet threatens the mainstream. He and his supporters are being subjected to the secular equivalent of the Spanish Inquisition…."
By RFD Columnist, Dr. Malcolm Kendrick

Read full article: redflagsweekly.com

The Myths and Realities of Ketosis

Critics of low-carb eating often cite the metabolic state of ketosis as reason enough to forget about restricting carbohydrates in your diet. They offer an assortment of reasons that ketosis is dangerous and to be avoided - without acknowledging that almost everyone enters a state of ketosis at some point within a 24 hour period of time...when they sleep!

I'd like to use this edition of the Low-Carb Guru to sort the fact from fiction and provide you with information you can use to make your own decision whether to follow a low-carb plan low enough to trigger ketosis, or low enough to lose while remaining in primary glucose metabolism!

Let's start with what ketosis is. It is a metabolic state where your body "switches" from primarily using glucose for energy to primarily using fat for energy. The fat used for energy will come from both dietary fat sources and body fat. Ketosis is the natural result of limiting carbohydrates in your diet to a low enough level - you're NOT eliminating them - that your body can't meet its energy needs primarily from glucose. This is because all carbohydrates are converted to glucose for energy and if you limit your intake, the body will still need energy (calories) and will find another way to get them - ketosis - fat burning is its source of its primary energy.

But wait, you say, the body needs glucose!

Read full article: countcarbs.com

Eat Fat And Grow Slim

by Richard Mackarness, M.B.,B.S. (1958)

From the Foreword by Sir Heneage Ogilvie, KBE, DM, M CH, FRCS
Consultant Surgeon, Guy's Hospital, Editor of 'The Practitioner'
Late: Vice-President of the Royal College of Surgeons

THE STATISTICIAN looks on nutrition as a mater of calories, and on obesity as a question of upset caloric equilibrium. A calorie is a unit of heat, a unit of potential energy, but not a unit of nutrition. Prison governors, school superintendents, dictators whether of a nation or of a small community, talk in calories to prove that they are feeding their charges or their victims adequately. Fellows of the Royal Society, and doctors with political leanings, talk in calories as if the human body were a machine requiring a certain amount of fuel to enable it to do a certain amount of work.

A motor-car needs calories, and we give it calories in the form of petrol. If we give it good petrol it will do good work for quite a long time. But even a Rolls-Royce cannot find its own fuel. It cannot separate motor spirit and lubricating oil from the crude mixture brought by a tanker from the wells of Kuwait. It cannot clean its own pipes, clear its own choked jets, grind its own valves, re-line its own bearings when they are worn, and replace defective parts as they need renewal. The body can do all these things. but the body is not a machine, and to do them it needs food not fuel...

Full access to the book here: Eat Fat And Grow Slim

The Fat Fast (Atkins)

Counterintuitive as it may sound, if you can't budge the scale on Induction, a few days on this regimen may well allow you to break through metabolic resistance.

Certain individuals are so metabolically resistant that only more intense dietary restrictions prove successful. Once medications, thyroid problems and candida are brought under control, almost all overweight people who diligently adhere to the Atkins Nutritional Approach™ will lose and keep off weight. But for the small group of people for whom it does not work, more extreme measures are necessary.

To help these metabolically resistant people, Dr. Atkins has modified what he calls "the most effective weight-loss eating pattern ever described." British researchers Alan Kekwick and Gaston Pawan developed it, and Frederick Benoit and his team confirmed its superiority in burning off fat, compared to an absolute total fast. This extreme diet consists of 1,000 calories daily, comprised of 90 percent fat. No other weight-loss regimen has matched its ability to burn off stored fat. Dr. Atkins modified the Kekwick diet to make it as enjoyable as possible and dubbed it the "Fat Fast." He tried it on scores of patients and found it often worked for those who were unable to lose weight in any other safe, drug-free way.

The Kekwick diet forces the body into lipolysis so it burns its stores of fat. Lipolysis cannot take place if there is a significant source of glucose. Since all carbohydrates and some protein convert to energy by way of glucose, eliminating almost everything but fat from the diet forces even the most resistant body into lipolysis. That explains the 90 percent dietary-fat component. Lowering the caloric intake accelerates the need to burn up body fat—thus the
1,000-calorie limit.

The Fat Fast is one controlled carb program where you do have to count calories. You'll eat 1,000 calories a day, with 75 percent to 90 percent comprised of fat. Frequent feedings prevent hunger better than three meals a day, so you consume five feedings, perhaps one every four hours, comprising 200 calories
each. Because of the high fat content and frequent feedings, very few people
experience much hunger. The stumbling block for some people is the absence of
conventional meals. But most are willing to stick with it for a few days, even
if the food selections are unfulfilling.

Caution: The Fat Fast is actually dangerous for anyone who is not metabolically resistant. For people who lose weight fairly easily, the rate of weight loss is too rapid to be safe. But it carries very little risk for people who can barely lose on any other regimen.

Step One: Eat Mostly Fat
Begin with five 200-calorie feedings per day and follow for four or five days. Each item equals approximately 200 calories:

*[Note:* 1 ounce is about 25g]

• one ounce of macadamia nuts or macadamia nut butter
• two ounces of cream cheese or Brie
• one ounce of tuna or chicken salad with two teaspoons of mayonnaise served in one-quarter of an avocado
• two deviled eggs made with two teaspoons of mayonnaise
• two ounces of sour cream and two tablespoons black or red caviar
• two and a half ounces whipped heavy cream topped with sucralose zero-calorie syrup
• two ounces of pâté (check label for fat content)
• two egg yolks (hard-boiled) with one tablespoon of mayonnaise

Step Two: Modify the Fat Fast
If increasing the fat-to-carbohydrate ratio and cutting calories work, any
dietary change in that direction might get the job done. Next, you can try four
meals a day of roughly 300 calories for a total of 1,200 calories. That should
work, too, and what it allows is definitely more appealing to the taste buds:

• two ounces of beef chuck (do not drain fat) cooked in two tablespoons of
  olive oil
• two scrambled eggs with two strips of nitrate-free bacon
• two tablespoons of full-fat sour cream with a tablespoon of sugar-free syrup
  one-quarter cup chicken or tuna salad made with two tablespoons of mayonnaise
• three ounces of pâté (check label for fat content)
• one-and-a-half ounces of macadamia nuts

Step Three: Return to Induction
Try the 1,200-calorie regimen for a week, then go back to Induction. Or simply follow the concept of increasing the ratio of fat to protein. No one should have to feel that losing weight is hopeless. Sometimes the key to achieving your goal weight permanently is quite difficult to adhere to, but rarely is it simply impossible.

Source: atkins.com

Further reading: CarbSmart

Low-Carb Diets

by Stephen Byrnes Ph.D., RNCP

Richard Allen knew something was very wrong. In the late 1980s, at the age of only 35, the graphic designer and father of two suffered a heart attack. Thankful that he survived, Richard followed his doctor’s instructions to the letter to avoid another heart attack and to avoid making a widow of his wife.

“I did everything they told me. I took my medication religiously. I exercised more. And I followed a low-fat, low- cholesterol diet. I stopped eating eggs (too much cholesterol). I cut back on meat and trimmed all the fat off what little meat I did allow myself. I started eating more fruit, vegetables, and whole grains and avoided butter. It was not exactly the tastiest diet, but I figured I was helping to preserve my health, so it was worth it.”

In 1995, however, something unexpected happened:

“I went in for a routine check-up and some blood was drawn for some tests. I was stunned to find out that my blood sugar levels were extremely high and I was subsequently diagnosed with adult-onset diabetes. I was dumbfounded. I had done everything they told me. I thought I was living and eating healthy and here I was a diabetic who now needed to take a new set of medication for a new disease.”

Full article: positivehealth.com

Taubes' Response

Michael Fumento's article "Big Fat Fake" in the March issue of Reason led Gary Taubes to make the following response. Taubes is the author of the New York Times Magazine story "What if It's All Been a Big Fat Lie?," which Fumento examined in his Reason story. To read Fumento's reply to Taubes, click here.

Michael Fumento’s March article Big Fat Fake is an exercise in vitriol rather than sound journalism

By Gary Taubes

To the editors:

I am ambivalent about writing this response to Michael Fumento's article ("Big Fat Fake"). On the one hand, the article simply doesn't deserve a response. It is a noteworthy exercise in vitriol, and perhaps self-aggrandizement, but it falls far short of legitimate journalism. On the other hand, journalists and historians, not to mention the occasional lay reader, have a tendency to assume that if something makes it into publication it is somehow de facto true or justifiable. This is never necessarily the case. For that reason, which I find slightly more persuasive, a published response might mitigate that tendency toward excessive credulity, at least in this particular circumstance.

Fumento's article attacks my work and my credibility, and then tries to sell it as a commentary on the state of science and medical journalism. His attempt might have been compelling had he managed to get at least a small percentage of his facts right and to avoid journalistic sins of omission and commission worse than any of which he accuses me. To put it simply, even on those rare and splendid occasions when Fumento does get a fact right, he still manages to thoroughly misrepresent my article and mangle the interpretation of the relevant science. While it's effectively impossible, even in the copious space I've taken, to rectify all Fumento's excessive distortions, the following attempts to clarify the key issues and correct some of the more egregious errors.

For starters, in his second paragraph, Fumento characterizes my article as arguing "that the consumption of too little fat [Fumento's emphasis] could explain the explosion in obesity." He does not quote the article, which would have been easy to do had it included such a declaration anywhere in its nearly 8,000 words, but it doesn't. Rather my article challenged the accepted dogma that obesity and excess weight are caused by the excessive consumption of fat calories, and instead suggested that it was caused by the excessive consumption of calories from refined carbohydrates and starches. I referred to this proposition repeatedly as the "alternative hypothesis", using the word "hypothesis" to imply strongly that it is not a fact but a supposition that should be rigorously tested. The article discussed the possibility that refined carbohydrates and starches might have a unique effect on our metabolism that either causes excessive hunger or an unbalanced deposition of calories in fat tissue. If so, it suggested, such a metabolic effect could explain the 150-year-old popularity of low carbohydrate diets for weight loss.

Dr. Robert Atkins and his eponymous diet played a major role in the article because Atkins has been preaching the evils of carbohydrates for at least 30 years. Only recently, however, have mainstream medical researchers concluded that perhaps his very-low-carbohydrate diet is worth testing. These trials, as a result, might shed light on whether the alternative hypothesis is scientifically meaningful.

Among Fumento's primary criticisms are that I only cite individuals who support my thesis and disregard those who don't. He ignores the fact that because the article challenges the accepted dietary dogma, and indeed acknowledges that challenge in the opening paragraph, by definition it implies that considerably more than half of all researchers and administrators believe the accepted dogma. If they didn't, it wouldn't be dogma. The point of writing the article was precisely to note that some equally respectable scientists question this dogma, and then to explain why. I defined the state of the argument as having undergone "a subtle shift in the scientific consensus" over the past five years: "It used to be that even considering the possibility of the alternative hypothesis, let alone researching it, was tantamount to quackery by association. Now a small but growing minority of establishment researchers have come to take seriously what the low-carb diet doctors have said all along." The phrase "small but growing minority" implies a large, albeit perhaps shrinking majority that will disagree with what I say. The obvious point is that this majority has gotten plenty of space to air their views over the decades. They didn't need my help.

Moreover, I interviewed close to 100 researchers for The New York Times Magazine article, to go with 150 or so for its March 2001 predecessor in the journal Science ("The Soft Science of Dietary Fat"). I quoted or attributed information to two dozen of them. Once again, as in any good work of journalism, the opinions of the great majority of those interviewed were left out--up to 90 percent in my case, depending on how you want to do the calculation. One hopes this is true of Fumento's research as well. If he is implying otherwise, then he only interviewed a dozen people for his story, which is woefully insufficient for such a complex and controversial subject.

If Fumento did interview more, then it's conceivable he omitted the comments, for instance, of those who believed that my article had merit. And then he was undeniably selective about which opinions he would publicly embrace in support of his thesis from those researchers he did interview. For instance, he first cites Harvard's Walter Willett chastising me for neglecting his anxieties about red meat and colon and prostate cancer. But then Fumento characterizes me as "clipping the data" for saying "that the percentage [Fumento's emphasis] of fat in the American diet has been decreasing for two decades," when Fumento thinks it would be more relevant to discuss the absolute number of fat calories consumed. Yet Willett is perhaps the most outspoken proponent of the idea that total fat calories are irrelevant to the obesity epidemic, a point he makes in print several times a year. A recent example was an article in the American Journal of Medicine just last December, co-authored with Columbia University researcher Rudy Leibel, in which Willett and Leibel phrase the point almost exactly as I did. "Moreover, within the United States," they wrote, "a substantial decline in the percentage of energy from fat [my emphasis] during the last 2 decades has corresponded with a massive increase in the prevalence of obesity."

As for Willett's red meat/cancer anxieties, which he did indeed reiterate to me numerous times, Willett himself acknowledges that the data are ambiguous. Willett's own Nurses' Health Study revealed an elevated risk of colorectal cancer in women who ate red meat frequently, but the Nurses' Health Study has recently arrived at the wrong answer on several major health issues--most notably, the effects of post-menopausal hormone replacement therapy--and so its credibility is debatable. Moreover, Willett played a major role in preparation of a 1997 report published by the World Cancer Research Fund and the American Institute for Cancer Research. That report noted that of seven studies similar to Willett's, three, including Willett's, saw an association between red meat and colorectal cancer, while the other four did not. As for prostate cancer, the authors of the report could find neither "convincing" nor even "probable" reason to believe that diets high in red meat increase risk. I could have mentioned this but, like Fumento, I was working with limited space and chose to use what seemed most relevant.

Fumento next accuses me of tricking Stanford University researcher John Farquhar into seeming to support the Atkins diet and he quotes an infuriated Gerald Reaven, also of Stanford, calling my article "outrageous" and saying that I set him up.

For starters, Reaven was not quoted in the article, a fact that he and Fumento apparently consider irrelevant. Reaven's name and research were mentioned in the context of two paragraphs on the history of Syndrome X that have precisely zero to say about the Atkins's diet and sit over 3000 words and 24 paragraphs after one discussion of the Atkins diet and 1500 words and 18 paragraphs before the next. When I interviewed Reaven last year, however, he did say the following about Atkins's diet, on tape, on the record, and I trust he won't mind me repeating it: "I think it's a great way to lose weight. That's not the issue." The issue, he said, was whether it was safe for long-term weight maintenance, which he doubted. Reaven believes saturated fat should be avoided, as well as carbohydrates. Atkins only advocates avoiding the latter.

As for Farquhar, if Fumento's reporting is accurate, then he would like an apology for how I used him in the article. Fumento reports it this way:

"I was greatly offended by how Gary Taubes tricked us all into coming across as supporters of the Atkins diet," he wrote in an e-mail he broadcast to reporters and to colleagues who were stunned that Farquhar might actually hold the beliefs Taubes attributed to him. "We are against the Atkins Diet," he wrote, speaking for himself and Reaven. "I told him [Taubes] there is the minor degree of merit" to the idea that "people are getting fatter because too much emphasis is being placed on just cutting fats," Farquhar told me. But "once I gave him that opening -- bingo -- he was off and running, even though I said about six times that this is not the cause of the obesity epidemic."

It is conceivable, however, that Farquhar's memory on this issue is not up to snuff. The relevant interview, in this case, occurred through e-mail and so relying on his memory is unnecessary.

Here's the specific context: Farquhar is quoted only in the last paragraph of my story. It follows directly from a discussion of my own difficulty in accepting the seemingly counter-intuitive possibility that fat might be beneficial to one's health and weight, and carbohydrates detrimental. The story then ends with the Farquhar paragraph:

This is the state of mind I imagine that mainstream nutritionists, researchers and physicians must inevitably take to the fat-versus-carbohydrate controversy. They may come around, but the evidence will have to be exceptionally compelling. Although this kind of conversion may be happening at the moment to John Farquhar, who is a professor of health research and policy at Stanford University and has worked in this field for more than 40 years. When I interviewed Farquhar in April, he explained why low-fat diets might lead to weight gain and low-carbohydrate diets might lead to weight loss, but he made me promise not to say he believed they did. He attributed the cause of the obesity epidemic to the ''force-feeding of a nation.'' Three weeks later, after reading an article on Endocrinology 101 by David Ludwig in the Journal of the American Medical Association, he sent me an e-mail message asking the not-entirely-rhetorical question, ''Can we get the low-fat proponents to apologize?"

I had interviewed Farquhar over the telephone on April 25, 2002. Two and half weeks later, we had the following aforementioned e-mail exchange: Farquhar initiates the exchange with his e-mail using the "apology" line.

From: Dr. John Farquhar

To: taubes@nyc.rr.com

>
Sent: Friday, May 10, 2002 7:55 PM

Subject: article on glycemic index

dear mr taubes

you may find a recent article in jama of interest in a search for

blood sugar, a compensating increase in insulin, and an increase in

"hunger".

the article in question is by ludwig--- jama 2002;287:2414-2423.

you recall that i believed, in contrast to reaven perhaps, that the

blood sugar swings could contribute to post-prandial hunger and,

thus, could be a factor that would contribute to obesity. (see page

2417 of ludwig's article). he adds some fancy biochemistry that you

may find interesting.

can we get the low-fat proponents to apologize?

hope the article is coming along well.

regards, jack farquhar

--

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

I then replied to Farquhar, asking him if he meant what he said, and whether he minded if I used the line in question.

Jack;

Thanks for the note. I'm featuring Ludwig prominently in the article. My idea is to portray the glycemic index and low carb diets docs as promoters of the alternative hypothesis to the low fat dogma. And, of course, one implication of the alternative hypothesis is that those low-fat proponents are at least part of the reason for the obesity epidemic. So were you just having fun with me when you wrote that maybe they should apologize, or do you, at least on occasions, wonder if it's true?

All the best,

Gary

Then Farquhar responded. Readers can judge for themselves whether Farquhar's take on the exchange and how I used it is justified:

From: Dr. John W. Farquhar

To: gary taubes

Sent: Sunday, May 12, 2002 8:17 PM

Subject: Re: article on glycemic index

dear gary--yes, i do think that they should apologize, but i don't expect it--so, that part is kidding. there is a long trail of nay-sayers in the CV medicine area. you might consider doing an article on sodium at some point.

i hope that i did make it clear that i believe the "low fat is good, therefore lower fat is better" crowd is dead wrong on many fronts--including that it is a good way to lose weight.

i know that low fat diets are really very bad for the overall type of lipid pattern that emerges. incidentally, ludwig didn't give that sufficient prominence. i believe that this more harmful lipid pattern accounts for the major disadvantage of low-fat diets (namely, that triglycerides rise, bringing HDL cholesterol down in the process and creating the "small dense" type of LDL that is more harmful than the larger varieties).

regarding the possibility that low fat diets contribute to the obesity epidemic--i am remaining a bit cagey on that point. i think that it might contribute, given the swings of glucose and insulin--and the possibility that an increase in hunger occurs on the tail end (when the insulin overcompensates and the blood sugar falls---or, at least, starts to fall and a compensating drive to snack keeps it from falling, assisted by a bit of catecholamine release). i thought that ludwig gave some support for that notion. in your interview with me i believe i emphasized that the portion size issue was staring us in the face and that the passive response of eating what is in front of us certainly gives the average person more calories than they would choose on their own. all the stuff about soft drink sizes going up, etc, etc.

of potential interest to you is that the famous dean ornish was recently not as dogmatic as i expected. i had to miss the session, held at stanford last saturday, because of my medical school class reunion. the session had reaven and ornish debating (as well as other speakers on other topics). i was told that ornish agreed that low fat diets make triglycerides rise, (a remarkable admission!!!)--he said his purpose of advocating such diets was to assist in weight loss (i need to confirm this point with jerry reaven), and to find an easy way to cut down on saturated fats. jerry and i would challenge the assertion that low fat diets work on weight loss better than any type of lowered calorie diets---this of course begs the question of whether these low fat diets are less successful than others.

regards, jack

Moving on, we get to Fumento's disagreement with my use of percentage of fat as a legitimate variable in the obesity epidemic. He says it's true that the percentage is decreasing, as I reported, but irrelevant: "The amount of fat consumed has been steadily climbing, as has consumption of all calories. Individual caloric consumption jumped from 3,300 calories per day in 1970-79 to 3,900 in 1997, an 18 percent increase. Per-person consumption of fat grams increased from 149 to 156, a 4.5 percent increase."

Fumento's source for these numbers, although he doesn't cite it, is the U.S. Department of Agriculture. The USDA has a variety of mechanisms for estimating macronutrient intake--i.e., protein, carbohydrates and fat--and has published a variety of reports on the subject. For instance, in April 1998, the USDA published an article entitled "Is Total Fat Consumption Really Decreasing?" This article reported that average total fat consumption for men aged 19 to 50, for instance, dropped from 113 grams per day in 1977-78 to 96 in 1989, the period that encompasses the beginning of the obesity epidemic. In 19- to 50-year-old women, the relevant numbers are 73 grams of fat per day in 1977-1978 and 62 grams in 1989.

Fumento prefers to use what are known as food availability data, as do I in most circumstances, although not this one. The USDA calculates how much food is provided by industry, and then adds imports, subtracts exports, and tries to adjust for waste--i.e., how much food is eventually thrown out. Fumento's data could have come from any number of these USDA reports but one that provides the same numbers is "Nutrient Content of the U.S. Food Supply, 1909-1997," by S. Gerrior and L. Bente of the Center for Nutrition Policy and Promotion (Home Economic Research Report No. 54). On page 26, Gerrior and Bente report that fat consumption from red meat, butter, lard and milk products all declined during the 1970s and 1980s. Thus the 7 gram per day, 63 calorie increase in total fat consumption noted by Fumento, was due to "the greatly expanded use of fried foods by the fast-food industry and in food service outlets as well as the increased use of salad oils on salads consumed both at home and away."

While the increase in fried foods might seem like a bad thing, the increase in oils on salad dressing would seem to be a good thing. The point, however, is that this particular data measures the availability of these fats in the food supply and, as Gerrior and Bente then emphasize, this particular category--cooking and salad oils--is almost impossible to estimate accurately:

While food supply estimates reflect trends in the availability of fats and oils for human food, they have never accurately measured the amount of food eaten because the portion of food wasted or discarded is difficult to determine. With the growth of the fast-food industry in the past three decades, it has become even more difficult to estimate the waste portion or discard of deep-frying fats. Since this discard is not available for human consumption, these estimates are limited as indicators of actual intake. A 1993 study estimated that about 50 percent or more of deep-frying fat used in food service operations is discarded after use and is not available for consumption. Reliable estimates of total fats and oils are difficult to determine partly because the actual amount of frying fat discarded by food service operations, particularly fast-food restaurants, varies with the type of the establishment.

As a result, the numbers Fumento uses to bolster this point are the least accurate available. It is the primary reason that I use percentage of fat calories, and may be why Willet does as well. It's safe to say that percentage of fat calories has been decreasing; it's a dubious proposition to make that claim about the total fat consumption.

More interesting, however, is what Fumento skates over in his quickie analysis: those extra 600 calories per day. Using the same report and this time taking Fumento's 1978 to 1997 as the period of interest, the American food supply, minus estimated wastage, offered up 448 more calories of carbohydrates, 48 more calories of protein and 63 more calories of fat. Fumento might want to blame the obesity epidemic on the extra 63 fat calories of fat or even the extra 48 protein calories, but he'll have to ignore the 448 calories from carbohydrates to do it. Under the circumstances, what I said in my article seems like a reasonable assessment: "If these trends are correct, then the obesity epidemic can certainly be explained by Americans' eating more calories than ever -- excess calories, after all, are what causes us to gain weight -- and, specifically, more carbohydrates. The question is why?"

Fumento then goes on to accuse me of shoving aside "decades of published, controlled randomized clinical trials comparing nutrient intake and weight loss." Regrettably, Fumento seems unclear on the concept of a "controlled randomized clinical trial," an unfortunate failing for a wannabe medical journalist. The relevant clue and the salient point is that there were no such trials. There are decades of trials looking at the effects of diet on weight loss, but they are for the most part, neither randomized nor controlled, and there are decades of observational studies trying to compare what people say they eat to how much they weigh. The latter are meaningless in this context and would require more time than I prefer to spend to explain why.

What Fumento does is turn for support to an April 2002 article in the Journal of the American Dietetic Association <(JADA) that was, he says, "`a review of all studies identified' that looked at diet nutrient composition and weight loss. It found over 200." It is this article he cites as one leg of a three-legged "crushing" mass of evidence rejecting the efficacy of Atkins-like low carbohydrate diets. On his own Web site, Fumento refers to this article repeatedly as evidence that he has done his library research, as though he himself personally read all 200 articles.

If Fumento even read this particular review article, however, he does a poor job of demonstrating that fact. For starters, it was not published in April 2002, but in April 2001. Secondly, while the authors of the study refer to the "more than 200 individual studies" that they allegedly included, they reference only 58, thus begging the question of what happened to the other 142+. Thirdly, the study was written by 4 employees and former acting undersecretary of the USDA, an organization that has been, bar none, the foremost advocate of high-carb, low-fat diets in America for 25 years.

This raises the issue of whether the authors might be tempted to bias their review to support the USDA's long-standing public position on the health-benefits of fat-reduced diets. It doesn't suggest they did, but it does beg the question of why Fumento readily intimates that a researcher who received funding for a diet trial from Atkins's Foundation would assuredly slant his results to please Atkins, while Fumento treats these government employees as somehow inherently beyond suspicion of the same kind of bias. Who knows. Maybe they might be motivated to please the bureaucrats who pay their salaries? Maybe their goal, consciously or subconsciously, was to get an article into print that appeared to support the agency's ubiquitous low-fat diet advice? Either way, it seems only fair that Fumento hold government employees up to the same level of malicious insinuation to which he holds private citizens. Why he doesn't escapes me.

Finally, biased or not, the USDA authors do happen to come to conclusions, which Fumento promptly quotes, that are not supported by the data from the studies they reference. In some points they simply err on the side of low-fat diets and against the low-carb diets. For instance, the authors state that of the 22 low carbohydrate diet trials they included, "there is a pattern of weight loss ranging from -2.8 to -12.0 kg." This happens to be incorrect. The range reported in the trials referenced runs from -2.8 to -16.8 kilograms. Compare this, in any case, to the range of weight loss in the low-fat studies referenced: +0.4 kg to -11.8 kilograms.

More to the point, it's possible to compare the efficacy of low fat and low carb diets from the data the USDA authors provide. Although the USDA authors chose not to engage in this exercise, and although the two groups are not strictly comparable, it's still relatively easy with a simple calculator to come up with an average rate of weight loss for the two different types of diet. Even Fumento could have done it. The average weight loss for the 28 low fat trials listed--at an average fat intake 25 percent and energy intake of 1665 calories per day--is a little over four kilograms in nearly 23 weeks, or less than 1/2 pound per week. The 22 low carbohydrate diets referenced led to an average weight loss of 7.4 kg over 48 days, or more than two pounds a week at an average intake of 1300 calories each day. This is over four times the rate of weight loss from the low-fat diets. The number speak for themselves, despite the author's conclusions, repeated faithfully by Fumento, that low carbohydrate diets seemed to offer no advantages over low fat diets.

What's more, the USDA authors say that "the results of several of the [low-carb] studies actually refute the contention that low-carbohydrate diets, in the absence of energy restriction, provide a metabolic advantage for weight loss." They cite four studies supporting this proposition. I happen to have two of the four in my files, and neither support their point.

One was an uncontrolled Atkins's diet trial, published in 1980 by Larosa et al., that reported an average weight loss from the Atkins diet of .9 kg (2 lbs) per week. The researchers report they would have predicted only half that from the apparent reduction in calories. They then say they can account for another quarter of a kilogram by taking into account water weight, but still fall nearly .2 kg short per week. This sounds trivial, but if sustainable, it would amount to some 10 kg or 20+ pounds of weight lost in a year beyond that explicable by the reduction in calories. There may be a simple answer to this discrepancy, but Larosa et al. don't offer any. To say this study refutes the contention that low carbohydrate diets provide a metabolic advantage is patently untrue.

The other study is even more interesting, if for no other reason than the fact that one of the co-authors is the recently infuriated Gerald Reaven. His collaborator and first author was Alain Golay, a Swiss researcher. The study was published in 1996. In this study, Golay and company randomly assigned obese individuals to receive one of two 1000-calorie diets. One was a low carb diet--32 percent protein, 15 percent carbohydrates and 53 percent fat--and the other was a high carb diet--29 percent protein, 45 percent carbohydrate and 26 percent fat. After six weeks, the low carb dieters lost an average of 8.9 kg plus or minus .6 kg, while the high carb dieters lost 7.5 kg plus or minus .5 kg. While the authors concluded that there was "no significant difference in the amount of weight loss in response to the diets," the difference between these two diets is 1.4 kg or 3 pounds in six weeks, and the error bars--the plus or minus--do not overlap, which is an elementary measure of statistical significance. If this 3 pounds in six weeks difference were to be real and sustainable, which Golay's study cannot establish, it would translate to an extra 25 pounds of weight loss over a year, without eating a single calorie less. It may or may not be real, but it is certainly evidence that this study does not refute the aforementioned contention. (It's worth noting that Golay did a second study, without Reaven, that was the identical story. When I asked Golay why he didn't follow-up on this suggestion that low-carb diets do offer a metabolic advantage, he said longer term studies were prohibitively expensive.)

Fumento then moves on to tout the merits of a type of review called a meta-analysis and cites a December 2000 study in the International Journal of Obesity and Related Metabolic Disorders co-authored by one of Fumento's favorite sources, James Hill of Colorado. This is the second leg of Fumento's three-legged "crushing" mass of evidence. It is a quasi-systematic review of the literature that concludes that low-fat diets lead to reduction in calories and weight loss.

Fumento then gets something right. He says the only meta-analysis (of which I am aware) on this issue that was properly conducted was done by the Cochrane Collaboration. Fumento doesn't bother to describe this organization, which is what made this statement relevant, so I will. The Cochrane Collaboration is a world-wide network of researchers dedicated to providing unbiased reviews of the scientific literature. The collaboration was created specifically because the 77 scientists from 11 countries who founded it a decade ago believed that meta-analyses could be so easily biased by researchers' prejudices that their disciplines needed a standardized methodology to minimize the influence of such prejudice and a venue that would allow for the publication of unbiased reviews.

The Cochrane methodology makes it effectively impossible for researchers to pick and choose which studies they would like to include in their analyses on the basis of which studies are likely to give them the result they want, a common practice in this field. Cochrane Collaboration reviews must include all studies that fit a pre-specified set of criteria, and they must exclude all that don't. Indeed, the Cochrane review to which Fumento refers started out with 3,000 citations of potential fat-restricted dietary trials and ended up with only a dozen trials that were performed to the Collaboration's standards for what constitutes good science.

Fumento's statement that the review found "no advantage to low-carbohydrate diets" is true but slightly farcical and more than slightly dishonest. The review was only a review of "fat-restricted diets" and so the authors made zero attempt to review the efficacy of carbohydrate-restricted diets. The Cochrane Collaboration review can be found on-line at www.update-software.com/abstracts/ab003640.htm. Its conclusion is worth noting:

The review suggests that fat-restricted diets are no better than calorie restricted diets in achieving long term weight loss in overweight or obese people. Overall, participants lost slightly more weight on the control diets but this was not significantly different from the weight loss achieved through dietary fat restriction and was so small as to be clinically insignificant." [My emphasis.]

Fumento then goes on to communicate in his idiosyncratic style my explanation of the why these dietary trials fail to live up to reasonable criteria of good science. Regrettably, Fumento doesn't seem to understand the critical point, and perhaps even the less critical points, and so makes us both look like idiots.

The point is this: to establish the effect of a diet on weight (or a pill on some physical or mental disorder), researchers have to do what's called a clinical controlled trial. The key word is "controlled". If they do such a study, they can be relatively certain that the effect they witnessed was due to the diet (or the pill) and not some other mysterious uncontrolled variable. The way to do this is by setting up the trial in advance so as to rule out these other variables--control for them, in the lingo, hence a controlledtrial.

One crucial factor in any controlled trial is to assure that the two groups being compared are legitimately comparable, which means among other factors that they must get equal treatment throughout the trial. In drug trials, for instance, placebos are used (hence the phrase "placebo-controlled" diet) to avoid any distortion that might occur when comparing individuals who are taking a pill every day (and, with it, the belief that their condition might improve) to individuals who are not. Drug trials are also done double-blind, which means neither the subjects nor the clinicians know which pills are the placebo and which are not. This controls for any possible effects that might occur if either patient or clinician knows the truth. Thus the common cliché in medical research is that double-blind, placebo-controlled clinical trials are the "gold-standard" for doing research. If a drug trial is not double-blind and placebo-controlled, it can't be trusted to get the right answer.

Diet trials, however, are problematic. It's effectively impossible to do them with placebos or double-blind. It's hard to fool subjects, for instance, into thinking that there are carbohydrates in their diets when there are not. High fat diets don't look and taste like low fat diets. Diets with pasta, bread, potatoes and sugar do not look and taste like diets without them. As a result, most of the trials used to demonstrate the effect of low-fat diets (or low-carb diets, for that fact) put a group of subjects on the diet and either measure their weight loss and nothing more, or compare the results to individuals who never went on the diet. Such trials, though, are uncontrolled. Often, for instance, the individuals on the low fat diet are given counseling, classes, and extensive follow-up to assure they stick to the low-fat diet. This intervention is not matched among the individuals who are simply told to eat their habitual diet. Thus there is a potential intervention effect, in which those getting the counseling and classes may be more motivated to live up to the researchers expectations than those who aren't. And that motivation, rather than the diet, might explain whatever weight they lose. For this reason, the Cochrane Review rejected all studies that were not randomized and did not compare low-fat diets at least to other weight-reducing diets, with the hopes that this would minimize any intervention effect.

Studies in which the level of intervention is unequal are uncontrolled trials and can't be interpreted. As medical statistician Stuart Pocock explained in his classic textbook Clinical Trials: A Practical Approach (John Wiley & Sons, 1983), "Uncontrolled trials have the potential to provide a very distorted view of therapy especially in the hands of slipshod, over-enthusiastic or unscrupulous investigators." The emphasis is Pocock's.

Fumento should know this and he shouldn't need me to explain it to him, and he should at least get it right when he tries to explain it to his readers. Indeed, Hill and his co-authors of the December 2000 International Journal of Obesity and Related Metabolic Disorders meta-analysis should have known this, too. Yet they included in their analysis studies that compared low-fat diets to medium-fat diets or habitual diets. These are uncontrolled trials. Walt Willett has made precisely the same criticism of this meta-analysis: it is a review of uncontrolled trials and so meaningless.

One last note from Pocock, which I happen to agree with whole-heartedly. Once again, the emphasis is Pocock's: "One basic premise is that it is unethical to conduct research which is badly planned or poorly executed. That is, if a trial is of sufficiently poor quality that it cannot make a meaningful contribution to medical knowledge then it should be declared unethical." To do a meta-analysis of such studies and conclude that from such scientific dreck, gold can be spun is of dubious benefit and ethics as well.

Next Fumento accuses me of having "circumvented this mass of peer-reviewed literature readily open to public scrutiny in libraries and often on-line" and basing my entire thesis on five unpublished studies.

So far, however, the mass of peer-reviewed literature that I have circumvented is one error-ridden, potentially biased USDA study, that it's doubtful Fumento read, and one dubious meta-analysis. As for the five studies, the salient point is that they are randomized, controlled trials in which the investigators actually compared a low-fat, calorie-restricted diet of the kind recommended by the American Heart Association, to a low-carbohydrate diet in which the subjects are allowed to eat as much as they want. They are not ideal, but they are better than most of the studies discussed by Hill et al. and about the best that can be done in diet studies. And if there is any intervention effect, it is likely to be biased in favor of the low-fat, low calorie diets, because those require the greater intervention.

Next along in Fumento's not-so-critical analysis, is a quote from Hill saying in reference to my book deal that I "sold out". At the risk of sounding catty and invoking the kind of standards that Fumento applies to these issues (for academicians, at least), Hill might be expected to know about such conflicts. After all, Hill has been funded by the Sugar Association to write an article for their website exonerating sugar or sugary foods as causes of obesity. It can be read on-line at www.sugar.org/science/carbohydrates.html.

Fumento also quotes Hill saying "I haven't seen any data anywhere saying Atkins is better than these other diets for weight loss." In the very next paragraph, Fumento then quotes Hill's collaborator, Gary Foster of the University of Pennsylvania, saying that the recent diet trial he did with Hill resulted in greater weight loss for those on the Atkins diet. Twice the weight loss to be precise. The statements of Hill and Foster are contradictory, which could be more a figment of Fumento's reporting than the actual data or their opinions. It would be nice, however, if the three got together and worked this one out. Maybe they could get back to us.

Fumento also mentions a University of Cincinnati study in which the Atkins group also lost twice as much weight as the low-fat diet group. This begs the question of what I misrepresented, considering my statement on the weight loss in these diets was that in all five studies those on Atkins "lost twice the weight as the subjects on the low-fat, low-calorie diets."

What's more, Fumento neglects to mention one interesting result from the University of Cincinnati study: the Atkins diet group not only lost twice the weight and twice the body fat of those on the low-fat, calorie-restricted American Heart Association-type diet, but they did it eating the same amount of calories. The researchers estimated that both groups consumed 1200 calories a day. This is mildly inexplicable without evoking some metabolic benefit gained by restricting carbohydrates. Fumento might have mentioned it, but it would have run contrary to his thesis, which is that I was irreprehensible in how I selected only those facts and opinions that agreed with my case.

The point I made in my article--not to be confused with Fumento's parody of my article--was that the existing low-carb dietary trials all suggest that when subjects are told to eat freely on a low carb diet, they voluntarily chose to consume considerably less calories. The pertinent question is why? The fact that such a diet is "a low-calorie diet in disguise" is not an answer. Naively, it seems that if a diet that encourages "pigging out", to use Fumento's words, results in a considerable reduction in calories, along with considerably more weight loss then a diet that actively restricts calories and certainly does not advocate "pigging out", it raises interesting questions that shouldn't be dismissed quite so cavalierly.

Fumento then goes on to describe "the kicker" regarding these five studies as the fact that they were "intervention studies [Fumento's emphasis], conducted using the same methodology that Taubes cites to dismiss the mountain of published material that undercuts his position."

Now Fumento confuses intervention studies with intervention effects, demonstrating a degree of what might be willful ignorance that stretches the boundaries of the imagination. The point is all clinical trials are intervention studies. You intervene in someone's life with a diet or a drug and you see what effect you have. The key to a controlled trial is to make the two interventions as similar as humanly possible so as to minimize the intervention effect. The five Atkins studies compared low-fat, low-calorie diets with low-carb diets and so the type and level of intervention were roughly equivalent.

Moreover, Fumento points out that none of the five low-carb/low-fat trials lasted more than a year, but neglects to mention that only one of the 28 low fat trials reviewed in JADA by those USDA researchers of unimpeachable integrity lasted more than a year. The subjects in that study, if our friends from the USDA can be trusted to get this one right, actually reduced their daily calorie intake to 1300 calories for 18 months and lost on average .4 kg, or less than a single pound. I pity those people.

Fumento then says that University of Cincinnati researchers Randy Seeley and David D'Alessio, were "upset that Taubes made use of their material." He neglects to mention that the reason I knew about the results of the trial was because D'Alessio e-mailed me the abstract of results presented at a 2001 meeting of the North American Association for the Study of Obesity (NAASO), with a note that said in part "I think it is fair to use the material we have already presented at meetings (we also had abstracts at the American Diabetes Association and American Dietetics Association last year, but the NAASO abstract is the most complete) in your research." Fumento also neglects to mention that the only reason he knew about the Cincinnati study was because I forwarded D'Alessio's e-mail to him, along with the abstract and the note. Fumento then moves on to the National Weight Control Registry and its 3000 successful dieters, most of whom claim that they lost weight and kept it off using low-fat, calorie-restricted diets and exercise. First he states that since NWCR dieters lost weight on low fat diets that somehow this implies in the world of Fumento-esque logical deductions that "what doesn't [Fumento's emphasis] work is a high-fat diet." This kind of logical sleight-of-hand is a Fumento specialty. The fact that these people say they lost weight by restricting fat calories means only that these people say they lost weight by restricting fat calories. It implies nothing about whether they would have lost more or less weight by restricting carbohydrate calories. That most of them exercised is an interesting fact but irrelevant to the carbohydrate/fat issue.

Fumento then states that the NWCR is meaningful to the debate because it has been "written-up in peer-reviewed medical publications." Fumento's faith in peer review is charming and considerably greater than mine. Here I will quote Pocock again:

There is a tendency for students, and indeed many clinicians, to treat the medical literature with undue respect. Major journals such as the Lancet and the New England Journal of Medicine are presumed to present new medical facts which are not to be disputed. Such a naïve faith in the "clinical gospels" is perhaps encouraged by the dogmatic style that many authors adopt, so that the uncertainties inherent in any research project often receive inadequate emphasis.

In this case, the inadequate emphasis is communicated by ignoring the fact that the NWCR is completely uncontrolled. Fumento does point this out, but then he decides it's irrelevant. He quotes Suzanne Phelan, a Brown University NWCR co-investigator saying, "you cannot get around the problem" that people who sign up for the NWCR are self-selected. Phelan is right. You can't. As a result, the NWCR is no more than an uncontrolled exercise in data collection. The only reliable statement that can be made from the NWCR data is that some 3000 individuals out of the tens of millions each year who try to lose weight, said they succeeded by reducing the fat and calories in their diet and maybe by exercising, as well. That's a nice factoid, but it adds excruciatingly little to the relevant science.

Fumento then rightfully asks why low-carb dieters do not appear in the NWCR. That's a good question and one worth investigating. This is of particular interest considering, for instance, the May 2002 issue of Consumer Reports. CR queried their readers and came up with 8000 who reported that they lost ten percent of their body weight and kept it off for at least a year --including 4000 "super losers" who lost an average of 37 pounds. According to CR, the number one lesson learned from these successful dieters was the need to "tame your blood sugar" and to do so by eating less carbohydrates and particularly less refined carbohydrates and starches. Now this is no scientific survey, but it is no less scientific, regrettably, than the National Weight Control Registry.

Fumento then raises the question of whether low carb diets might suppress hunger. He invokes as evidence that there is no "empirical support for this" an April 2002 review in the Journal of the American College of Nutrition. This is leg number three of his tripodal "crushing" mass of evidence. The JACN article, reports Fumento, reviewed high and low fat treatments when subjects were allowed to eat as much as they wanted, and found that "energy intake on the low-fat diets ranged from 16 percent to 24 percent less than those on high fat diets."

This time Fumento gets the issue date of the article correct, but he incomprehensibly butchers the quote. The relevant quote actually reads "energy intakes on the low fat diets averaged 71 percent (10 days to 2 months) to 84 percent (1-9 days) of intakes on the control higher fat regimes."

Either way, this is an interesting finding but irrelevant. It says nothing about why individuals on low carbohydrate diets or very low carbohydrate diets like Atkins's, as even Fumento reports to be the case, lose considerable weight, and why they apparently find it relatively easy to restrict their calories to do so. Fumento turns to Penn State nutritionist Barbara Rolls on this subject and describes her as "widely considered the nation's top authority on satiety", which is a lovely compliment but a bit of a stretch. Rolls invokes studies in which she and her colleagues infused pure fat and pure carbs into their subjects and found very little difference in subsequent short-term satiety. These experiments, however, say precious little about whether the macronutrient content of the diet would have an impact on the kind of weight loss or gain that takes place in real life and over periods of months or years, not hours. Both Fumento and Rolls, if her opinions are represented accurately, confuse evidence with proof.

It is worth remarking, which Fumento did not, that the sentence in the JACN review that followed his misquote made this point: "it is interesting to note that the changes in body weight observed in the low fat intervention studies are small in absolute terms (0.7 kg-1.0 kg in short-term and long-term studies on average) and also appear small compared to the changes in energy intake." For those, perhaps like Fumento, who might not be expected to read these articles carefully, this was included as one of five "teaching points" of the JACN review: "low fat dietary intervention studies have resulted in small weight loss--less than 1 kg on average in studies of up to one year's duration."

Fumento's next assault on my reporting is to accuse me of not being able to extract a single useful line from five other "top obesity researchers." One of these, however, Xavier Pi-Sunyer, I did not interview for this story. One of them, Marion Nestle, is a nutritionist and administrator with a background in molecular biology. She is not and never has been an obesity researcher, nor has she ever treated obese patients. One of them, Arne Astrup, co-authored with Hill the December 2000 International Journal of Obesity and Related Metabolic Disorders meta-analysis. My earlier comments about meta-analyses and controlled trials would suggest why I might have shied away from quoting Astrup for the enlightenment of my readers. And one of them, Jules Hirsch of Rockefeller University, I did quote in early drafts of my article, but the relevant paragraphs, regrettably, were among the last to be cut for space reasons. First it quoted Hirsch saying "Of all the damn unsuccessful treatments, the treatment of weight reduction by diet for obese people just doesn't seem to work. " It then continued:

This has led Hirsch, for example, into such a state of frustration that when we spoke last March, he said he could no more explain how obese individuals could lose weight, then he could explain how they gained it to begin with. "I've been working on this since 1960," he said. "That's a hell of a long time. You think I would have gotten a little farther along with it." For the last 20 years, Hirsch has worked with Rudy Leibel on some of the seminal experiments in obesity research. When I interviewed Leibel, who is now at Columbia University, he capped our conversation this way: "if you do feel you understand this," he said, "it will probably indicate that you've lost your mind."

I hated to see it go.

Fumento moves next to the subject of glycemic index, which is a measure of the effect of carbohydrates on blood sugar and insulin secretion. My article suggested that the glycemic index concept might be relevant to the question of why we gain weight so easily and have such trouble losing it. Fumento first mangles his explanation of the concept, and then dispenses with it as thoroughly irrelevant to the scientific discussion at hand.

The gist of the glycemic index idea, is that the more easily digested the carbohydrates, the quicker and more dramatic their effect on blood sugar and the greater the resulting secretion of insulin. These effects, so the hypothesis goes, might then have some long-term effect on hunger and fat deposition and eventually on weight. Carbohydrates--such as sugar, white bread or potatoes--have a high glycemic index and are absorbed into the blood stream quickly. Those with a low glycemic index, such as whole grains, are absorbed more slowly.

As to its relevance, it was this glycemic index concept that Consumer Reports had in mind when it advocated "taming your blood sugar" to lose weight. Curiously enough the same April 2002 Journal of the American College of Nutrition review that Fumento misquoted, also discussed the evidence that the glycemic index of carbohydrates could have relevance to hunger, food intake and weight, although Fumento missed this, as well, or ignored it. This point, too, made it into one of the five teaching points; ""short-term studies suggest that low-glycemic index carbohydrates suppress hunger more effectively than high glycemic index carbohydrates, but there are no long-term intervention studies to examine the effects of lowering the glycemic index on body weight."

Moving toward his finale, Fumento returns back to the Atkins diet and the question of whether it is safe for the long term. He cites the five unpublished trials and says they are evidence that the diet might not be "as harmful as was once generally believed" but then says the natures of the fats involved in the diet are "a distinction Taubes decided to lose." Wrong again. To be precise I discussed the effects of the fats on the various cholesterol and fatty acid particles in the blood, which, short of an actual heart attack, is the end result of interest.

I said "In all five studies, cholesterol levels improved similarly with both diets, but triglyceride levels were considerably lower with the Atkins diet. Though researchers are hesitant to agree with this, it does suggest that heart-disease risk could actually be reduced when fat is added back into the diet and starches and refined carbohydrates are removed." I then went on to describe the studies that were in the works to extend this result and see if it would be sustained over longer time periods, and I discussed my own anxiety eating such a diet that included, in my case, eggs and sausage every morning. "I can look down at my eggs and sausage" I wrote, "and still imagine the imminent onset of heart disease and obesity, the latter assuredly to be caused by some bizarre rebound phenomena the likes of which science has not yet begun to describe. The fact that Atkins himself has had heart trouble recently does not ease my anxiety, despite his assurance that it is not diet-related."

Fumento's finale is his insistence that I misrepresented an American Medical Association critique of the Atkins diet that was released publicly in March 1973 by the AMA and published the following June. Fumento agrees with my characterization of the critique as scathing, but he takes exception to my claim that the AMA's anonymous author "acknowledged that the diet probably worked but expressed little interest why." In his own press release touting his article, Fumento accuses me of having "grossly misrepresented" the AMA's position. Fumento then quotes many of the scathing comments included in the critique, but he neglects to mention, as is his wont, one key sentence: "The fact remains, however, that some patients have lost weight on the low-carbohydrate diet `unrestricted in calories'." This seems to me--and perhaps, once again, I'm being naïve here--to be an admission that the diet probably works.

The next sentence, which Fumento does quote, read, "When obese patients reduce their carbohydrate intake drastically, they are apparently unable to make up the ensuing deficit by means of an appreciable increase in protein and fat." To put it in plain English, they consumed less calories. They ate less. The AMA then left it at that. The article did not try to explain--hence my characterization of the position as expressing "little interest"-- why an obese man, for instance, who would, according to the scientific literature of balanced calorie-restricted diets, be ravenous if he lost ten pounds, suddenly find it difficult to eat enough steak or chicken or eggs or cheese, despite his weight loss, to get, say, 2000 calories a day and maintain his weight. Two half-pound burgers, naked, four boiled eggs and a tin of tuna fish (canned in oil), hold the mayo, will do the job nicely and, for many obese men, would constitute little more than hors d'oeuvres.

Fumento then tries to back up his own rough treatment of my reporting with mention of a "fatlash" in response to my article. The substance of that fatlash, however, constituted a single page in Newsweek, by a writer who was having a book published two months later claiming that fatty foods and indolence were the cause of the obesity epidemic; an article in The Washington Post by a diet writer who has been pushing low-fat diets since the mid-1980s, and which happened to be no more accurate nor in command of the relevant science than Fumento's; and an article in the Nutrition Action Healthletter, a publication of the Center for Science in the Public Interest (CSPI). The CSPI is an advocacy group that has been pushing low-fat diets since the 1970s. In January Reason's science correspondent, Ronald Bailey, described CSPI as "a Naderite spin-off that has not been above a bit of sensationalism in trying to get its nutrition message across either. Famous as the self-styled "food police," CSPI launches highly publicized jihads against foods that it feels are not up to snuff nutritionally. That's their right, of course, but others feel that CSPI exaggerates its claims and is misreporting scientific results." The CSPI philosophy on dietary fat and carbohydrates was summed up nicely by its director Michael Jacobson in a 1979 article in the journal Science as "Eat less sugar. Eat less fat. Bread and potatoes are where it's at." It's understandable that the food police might object to an article suggesting that bread and potatoes are not where it's at.

And this is the point: when an article such as mine suggests that three decades of dietary dogma might be both wrong and hazardous to the health, it will elicit public and perhaps angry responses from purveyors of that dogma. These responses will assuredly be exacerbated if the editors of The New York Times Magazine choose to run the article on the cover, as they did in this case. There seems little way to avoid that fact. If Fumento is dedicated to defending the dogma--and with it, the arguments he made six years ago in his book The Fat of the Land--neither malice, vitriol, nor his consistently remarkable ability to screw up both the facts and the science, will take the place of good, solid journalism.

With that note, I'd like to make two last small corrections. One is that Fumento reports that I am one of two writers to ever win the science-in-society award of the National Association of Science Writers three times, which is the maximum the NASW allows. He is half right. I did win it three times, but the only other three-time winner is a documentary film-maker, not a writer. And finally, Fumento refers to my editor at Knopf as "Scott Segal." His name is Jonathan.

Gary Taubes is the author of Bad Science: The Short Life and Weird Times of Cold Fusion and Nobel Dreams: Power, Deceit and the Ultimate Experiment. His article "What if It's All Been a Big Fat Lie?" appeared in the July, 2002 issue of The New York Times Magazine.

For Michael Fumento's response to Gary Taubes, click here. Fumento's story "Big Fat Fake" appeared in the March issue of Reason.

Source: Reason.com

What if It's All Been a Big Fat Lie?

By Gary Taubes
FrontPageMagazine.com | July 8, 2002

If the members of the American medical establishment were to have a collective find-yourself-standing-naked-in-Times-Square-type nightmare, this might be it. They spend 30 years ridiculing Robert Atkins, author of the phenomenally-best-selling ''Dr. Atkins' Diet Revolution'' and ''Dr. Atkins' New Diet Revolution,'' accusing the Manhattan doctor of quackery and fraud, only to discover that the unrepentant Atkins was right all along. Or maybe it's this: they find that their very own dietary recommendations -- eat less fat and more carbohydrates -- are the cause of the rampaging epidemic of obesity in America. Or, just possibly this: they find out both of the above are true.

When Atkins first published his ''Diet Revolution'' in 1972, Americans were just coming to terms with the proposition that fat -- particularly the saturated fat of meat and dairy products -- was the primary nutritional evil in the American diet. Atkins managed to sell millions of copies of a book promising that we would lose weight eating steak, eggs and butter to our heart's desire, because it was the carbohydrates, the pasta, rice, bagels and sugar, that caused obesity and even heart disease. Fat, he said, was harmless.

Atkins allowed his readers to eat ''truly luxurious foods without limit,'' as he put it, ''lobster with butter sauce, steak with bearnaise sauce . . . bacon cheeseburgers,'' but allowed no starches or refined carbohydrates, which means no sugars or anything made from flour. Atkins banned even fruit juices, and permitted only a modicum of vegetables, although the latter were negotiable as the diet progressed.

Atkins was by no means the first to get rich pushing a high-fat diet that restricted carbohydrates, but he popularized it to an extent that the American Medical Association considered it a potential threat to our health. The A.M.A. attacked Atkins's diet as a ''bizarre regimen'' that advocated ''an unlimited intake of saturated fats and cholesterol-rich foods,'' and Atkins even had to defend his diet in Congressional hearings.

Thirty years later, America has become weirdly polarized on the subject of weight. On the one hand, we've been told with almost religious certainty by everyone from the surgeon general on down, and we have come to believe with almost religious certainty, that obesity is caused by the excessive consumption of fat, and that if we eat less fat we will lose weight and live longer. On the other, we have the ever-resilient message of Atkins and decades' worth of best-selling diet books, including ''The Zone,'' ''Sugar Busters'' and ''Protein Power'' to name a few. All push some variation of what scientists would call the alternative hypothesis: it's not the fat that makes us fat, but the carbohydrates, and if we eat less carbohydrates we will lose weight and live longer.

The perversity of this alternative hypothesis is that it identifies the cause of obesity as precisely those refined carbohydrates at the base of the famous Food Guide Pyramid -- the pasta, rice and bread -- that we are told should be the staple of our healthy low-fat diet, and then on the sugar or corn syrup in the soft drinks, fruit juices and sports drinks that we have taken to consuming in quantity if for no other reason than that they are fat free and so appear intrinsically healthy. While the low-fat-is-good-health dogma represents reality as we have come to know it, and the government has spent hundreds of millions of dollars in research trying to prove its worth, the low-carbohydrate message has been relegated to the realm of unscientific fantasy.

Over the past five years, however, there has been a subtle shift in the scientific consensus. It used to be that even considering the possibility of the alternative hypothesis, let alone researching it, was tantamount to quackery by association. Now a small but growing minority of establishment researchers have come to take seriously what the low-carb-diet doctors have been saying all along. Walter Willett, chairman of the department of nutrition at the Harvard School of Public Health, may be the most visible proponent of testing this heretic hypothesis. Willett is the de facto spokesman of the longest-running, most comprehensive diet and health studies ever performed, which have already cost upward of $100 million and include data on nearly 300,000 individuals. Those data, says Willett, clearly contradict the low-fat-is-good-health message ''and the idea that all fat is bad for you; the exclusive focus on adverse effects of fat may have contributed to the obesity epidemic.''

These researchers point out that there are plenty of reasons to suggest that the low-fat-is-good-health hypothesis has now effectively failed the test of time. In particular, that we are in the midst of an obesity epidemic that started around the early 1980's, and that this was coincident with the rise of the low-fat dogma. (Type 2 diabetes, the most common form of the disease, also rose significantly through this period.) They say that low-fat weight-loss diets have proved in clinical trials and real life to be dismal failures, and that on top of it all, the percentage of fat in the American diet has been decreasing for two decades. Our cholesterol levels have been declining, and we have been smoking less, and yet the incidence of heart disease has not declined as would be expected. ''That is very disconcerting,'' Willett says. ''It suggests that something else bad is happening.''

The science behind the alternative hypothesis can be called Endocrinology 101, which is how it's referred to by David Ludwig, a researcher at Harvard Medical School who runs the pediatric obesity clinic at Children's Hospital Boston, and who prescribes his own version of a carbohydrate-restricted diet to his patients. Endocrinology 101 requires an understanding of how carbohydrates affect insulin and blood sugar and in turn fat metabolism and appetite. This is basic endocrinology, Ludwig says, which is the study of hormones, and it is still considered radical because the low-fat dietary wisdom emerged in the 1960's from researchers almost exclusively concerned with the effect of fat on cholesterol and heart disease. At the time, Endocrinology 101 was still underdeveloped, and so it was ignored. Now that this science is becoming clear, it has to fight a quarter century of anti-fat prejudice.

The alternative hypothesis also comes with an implication that is worth considering for a moment, because it's a whopper, and it may indeed be an obstacle to its acceptance. If the alternative hypothesis is right -- still a big ''if'' -- then it strongly suggests that the ongoing epidemic of obesity in America and elsewhere is not, as we are constantly told, due simply to a collective lack of will power and a failure to exercise. Rather it occurred, as Atkins has been saying (along with Barry Sears, author of ''The Zone''), because the public health authorities told us unwittingly, but with the best of intentions, to eat precisely those foods that would make us fat, and we did. We ate more fat-free carbohydrates, which, in turn, made us hungrier and then heavier. Put simply, if the alternative hypothesis is right, then a low-fat diet is not by definition a healthy diet. In practice, such a diet cannot help being high in carbohydrates, and that can lead to obesity, and perhaps even heart disease. ''For a large percentage of the population, perhaps 30 to 40 percent, low-fat diets are counterproductive,'' says Eleftheria Maratos-Flier, director of obesity research at Harvard's prestigious Joslin Diabetes Center. ''They have the paradoxical effect of making people gain weight.''

Scientists are still arguing about fat, despite a century of research, because the regulation of appetite and weight in the human body happens to be almost inconceivably complex, and the experimental tools we have to study it are still remarkably inadequate. This combination leaves researchers in an awkward position. To study the entire physiological system involves feeding real food to real human subjects for months or years on end, which is prohibitively expensive, ethically questionable (if you're trying to measure the effects of foods that might cause heart disease) and virtually impossible to do in any kind of rigorously controlled scientific manner. But if researchers seek to study something less costly and more controllable, they end up studying experimental situations so oversimplified that their results may have nothing to do with reality. This then leads to a research literature so vast that it's possible to find at least some published research to support virtually any theory. The result is a balkanized community -- ''splintered, very opinionated and in many instances, intransigent,'' says Kurt Isselbacher, a former chairman of the Food and Nutrition Board of the National Academy of Science -- in which researchers seem easily convinced that their preconceived notions are correct and thoroughly uninterested in testing any other hypotheses but their own.

What's more, the number of misconceptions propagated about the most basic research can be staggering. Researchers will be suitably scientific describing the limitations of their own experiments, and then will cite something as gospel truth because they read it in a magazine. The classic example is the statement heard repeatedly that 95 percent of all dieters never lose weight, and 95 percent of those who do will not keep it off. This will be correctly attributed to the University of Pennsylvania psychiatrist Albert Stunkard, but it will go unmentioned that this statement is based on 100 patients who passed through Stunkard's obesity clinic during the Eisenhower administration.

With these caveats, one of the few reasonably reliable facts about the obesity epidemic is that it started around the early 1980's. According to Katherine Flegal, an epidemiologist at the National Center for Health Statistics, the percentage of obese Americans stayed relatively constant through the 1960's and 1970's at 13 percent to 14 percent and then shot up by 8 percentage points in the 1980's. By the end of that decade, nearly one in four Americans was obese. That steep rise, which is consistent through all segments of American society and which continued unabated through the 1990's, is the singular feature of the epidemic. Any theory that tries to explain obesity in America has to account for that. Meanwhile, overweight children nearly tripled in number. And for the first time, physicians began diagnosing Type 2 diabetes in adolescents. Type 2 diabetes often accompanies obesity. It used to be called adult-onset diabetes and now, for the obvious reason, is not.

So how did this happen? The orthodox and ubiquitous explanation is that we live in what Kelly Brownell, a Yale psychologist, has called a ''toxic food environment'' of cheap fatty food, large portions, pervasive food advertising and sedentary lives. By this theory, we are at the Pavlovian mercy of the food industry, which spends nearly $10 billion a year advertising unwholesome junk food and fast food. And because these foods, especially fast food, are so filled with fat, they are both irresistible and uniquely fattening. On top of this, so the theory goes, our modern society has successfully eliminated physical activity from our daily lives. We no longer exercise or walk up stairs, nor do our children bike to school or play outside, because they would prefer to play video games and watch television. And because some of us are obviously predisposed to gain weight while others are not, this explanation also has a genetic component -- the thrifty gene. It suggests that storing extra calories as fat was an evolutionary advantage to our Paleolithic ancestors, who had to survive frequent famine. We then inherited these ''thrifty'' genes, despite their liability in today's toxic environment.

This theory makes perfect sense and plays to our puritanical prejudice that fat, fast food and television are innately damaging to our humanity. But there are two catches. First, to buy this logic is to accept that the copious negative reinforcement that accompanies obesity -- both socially and physically -- is easily overcome by the constant bombardment of food advertising and the lure of a supersize bargain meal. And second, as Flegal points out, little data exist to support any of this. Certainly none of it explains what changed so significantly to start the epidemic. Fast-food consumption, for example, continued to grow steadily through the 70's and 80's, but it did not take a sudden leap, as obesity did.

As far as exercise and physical activity go, there are no reliable data before the mid-80's, according to William Dietz, who runs the division of nutrition and physical activity at the Centers for Disease Control; the 1990's data show obesity rates continuing to climb, while exercise activity remained unchanged. This suggests the two have little in common. Dietz also acknowledged that a culture of physical exercise began in the United States in the 70's -- the ''leisure exercise mania,'' as Robert Levy, director of the National Heart, Lung and Blood Institute, described it in 1981 -- and has continued through the present day.

As for the thrifty gene, it provides the kind of evolutionary rationale for human behavior that scientists find comforting but that simply cannot be tested. In other words, if we were living through an anorexia epidemic, the experts would be discussing the equally untestable ''spendthrift gene'' theory, touting evolutionary advantages of losing weight effortlessly. An overweight homo erectus, they'd say, would have been easy prey for predators.

It is also undeniable, note students of Endocrinology 101, that mankind never evolved to eat a diet high in starches or sugars. ''Grain products and concentrated sugars were essentially absent from human nutrition until the invention of agriculture,'' Ludwig says, ''which was only 10,000 years ago.'' This is discussed frequently in the anthropology texts but is mostly absent from the obesity literature, with the prominent exception of the low-carbohydrate-diet books.

What's forgotten in the current controversy is that the low-fat dogma itself is only about 25 years old. Until the late 70's, the accepted wisdom was that fat and protein protected against overeating by making you sated, and that carbohydrates made you fat. In ''The Physiology of Taste,'' for instance, an 1825 discourse considered among the most famous books ever written about food, the French gastronome Jean Anthelme Brillat-Savarin says that he could easily identify the causes of obesity after 30 years of listening to one ''stout party'' after another proclaiming the joys of bread, rice and (from a ''particularly stout party'') potatoes. Brillat-Savarin described the roots of obesity as a natural predisposition conjuncted with the ''floury and feculent substances which man makes the prime ingredients of his daily nourishment.'' He added that the effects of this fecula -- i.e., ''potatoes, grain or any kind of flour'' -- were seen sooner when sugar was added to the diet.

This is what my mother taught me 40 years ago, backed up by the vague observation that Italians tended toward corpulence because they ate so much pasta. This observation was actually documented by Ancel Keys, a University of Minnesota physician who noted that fats ''have good staying power,'' by which he meant they are slow to be digested and so lead to satiation, and that Italians were among the heaviest populations he had studied. According to Keys, the Neapolitans, for instance, ate only a little lean meat once or twice a week, but ate bread and pasta every day for lunch and dinner. ''There was no evidence of nutritional deficiency,'' he wrote, ''but the working-class women were fat.''

By the 70's, you could still find articles in the journals describing high rates of obesity in Africa and the Caribbean where diets contained almost exclusively carbohydrates. The common thinking, wrote a former director of the Nutrition Division of the United Nations, was that the ideal diet, one that prevented obesity, snacking and excessive sugar consumption, was a diet ''with plenty of eggs, beef, mutton, chicken, butter and well-cooked vegetables.'' This was the identical prescription Brillat-Savarin put forth in 1825.

It was Ancel Keys, paradoxically, who introduced the low-fat-is-good-health dogma in the 50's with his theory that dietary fat raises cholesterol levels and gives you heart disease. Over the next two decades, however, the scientific evidence supporting this theory remained stubbornly ambiguous. The case was eventually settled not by new science but by politics. It began in January 1977, when a Senate committee led by George McGovern published its ''Dietary Goals for the United States,'' advising that Americans significantly curb their fat intake to abate an epidemic of ''killer diseases'' supposedly sweeping the country. It peaked in late 1984, when the National Institutes of Health officially recommended that all Americans over the age of 2 eat less fat. By that time, fat had become ''this greasy killer'' in the memorable words of the Center for Science in the Public Interest, and the model American breakfast of eggs and bacon was well on its way to becoming a bowl of Special K with low-fat milk, a glass of orange juice and toast, hold the butter -- a dubious feast of refined carbohydrates.

In the intervening years, the N.I.H. spent several hundred million dollars trying to demonstrate a connection between eating fat and getting heart disease and, despite what we might think, it failed. Five major studies revealed no such link. A sixth, however, costing well over $100 million alone, concluded that reducing cholesterol by drug therapy could prevent heart disease. The N.I.H. administrators then made a leap of faith. Basil Rifkind, who oversaw the relevant trials for the N.I.H., described their logic this way: they had failed to demonstrate at great expense that eating less fat had any health benefits. But if a cholesterol-lowering drug could prevent heart attacks, then a low-fat, cholesterol-lowering diet should do the same. ''It's an imperfect world,'' Rifkind told me. ''The data that would be definitive is ungettable, so you do your best with what is available.''

Some of the best scientists disagreed with this low-fat logic, suggesting that good science was incompatible with such leaps of faith, but they were effectively ignored. Pete Ahrens, whose Rockefeller University laboratory had done the seminal research on cholesterol metabolism, testified to McGovern's committee that everyone responds differently to low-fat diets. It was not a scientific matter who might benefit and who might be harmed, he said, but ''a betting matter.'' Phil Handler, then president of the National Academy of Sciences, testified in Congress to the same effect in 1980. ''What right,'' Handler asked, ''has the federal government to propose that the American people conduct a vast nutritional experiment, with themselves as subjects, on the strength of so very little evidence that it will do them any good?''

Nonetheless, once the N.I.H. signed off on the low-fat doctrine, societal forces took over. The food industry quickly began producing thousands of reduced-fat food products to meet the new recommendations. Fat was removed from foods like cookies, chips and yogurt. The problem was, it had to be replaced with something as tasty and pleasurable to the palate, which meant some form of sugar, often high-fructose corn syrup. Meanwhile, an entire industry emerged to create fat substitutes, of which Procter & Gamble's olestra was first. And because these reduced-fat meats, cheeses, snacks and cookies had to compete with a few hundred thousand other food products marketed in America, the industry dedicated considerable advertising effort to reinforcing the less-fat-is-good-health message. Helping the cause was what Walter Willett calls the ''huge forces'' of dietitians, health organizations, consumer groups, health reporters and even cookbook writers, all well-intended missionaries of healthful eating.

Few experts now deny that the low-fat message is radically oversimplified. If nothing else, it effectively ignores the fact that unsaturated fats, like olive oil, are relatively good for you: they tend to elevate your good cholesterol, high-density lipoprotein (H.D.L.), and lower your bad cholesterol, low-density lipoprotein (L.D.L.), at least in comparison to the effect of carbohydrates. While higher L.D.L. raises your heart-disease risk, higher H.D.L. reduces it.

What this means is that even saturated fats -- a k a, the bad fats -- are not nearly as deleterious as you would think. True, they will elevate your bad cholesterol, but they will also elevate your good cholesterol. In other words, it's a virtual wash. As Willett explained to me, you will gain little to no health benefit by giving up milk, butter and cheese and eating bagels instead.

But it gets even weirder than that. Foods considered more or less deadly under the low-fat dogma turn out to be comparatively benign if you actually look at their fat content. More than two-thirds of the fat in a porterhouse steak, for instance, will definitively improve your cholesterol profile (at least in comparison with the baked potato next to it); it's true that the remainder will raise your L.D.L., the bad stuff, but it will also boost your H.D.L. The same is true for lard. If you work out the numbers, you come to the surreal conclusion that you can eat lard straight from the can and conceivably reduce your risk of heart disease.

The crucial example of how the low-fat recommendations were oversimplified is shown by the impact -- potentially lethal, in fact -- of low-fat diets on triglycerides, which are the component molecules of fat. By the late 60's, researchers had shown that high triglyceride levels were at least as common in heart-disease patients as high L.D.L. cholesterol, and that eating a low-fat, high-carbohydrate diet would, for many people, raise their triglyceride levels, lower their H.D.L. levels and accentuate what Gerry Reaven, an endocrinologist at Stanford University, called Syndrome X. This is a cluster of conditions that can lead to heart disease and Type 2 diabetes.

It took Reaven a decade to convince his peers that Syndrome X was a legitimate health concern, in part because to accept its reality is to accept that low-fat diets will increase the risk of heart disease in a third of the population. ''Sometimes we wish it would go away because nobody knows how to deal with it,'' said Robert Silverman, an N.I.H. researcher, at a 1987 N.I.H. conference. ''High protein levels can be bad for the kidneys. High fat is bad for your heart. Now Reaven is saying not to eat high carbohydrates. We have to eat something.''

Surely, everyone involved in drafting the various dietary guidelines wanted Americans simply to eat less junk food, however you define it, and eat more the way they do in Berkeley, Calif. But we didn't go along. Instead we ate more starches and refined carbohydrates, because calorie for calorie, these are the cheapest nutrients for the food industry to produce, and they can be sold at the highest profit. It's also what we like to eat. Rare is the person under the age of 50 who doesn't prefer a cookie or heavily sweetened yogurt to a head of broccoli.

''All reformers would do well to be conscious of the law of unintended consequences,'' says Alan Stone, who was staff director for McGovern's Senate committee. Stone told me he had an inkling about how the food industry would respond to the new dietary goals back when the hearings were first held. An economist pulled him aside, he said, and gave him a lesson on market disincentives to healthy eating: ''He said if you create a new market with a brand-new manufactured food, give it a brand-new fancy name, put a big advertising budget behind it, you can have a market all to yourself and force your competitors to catch up. You can't do that with fruits and vegetables. It's harder to differentiate an apple from an apple.''

Nutrition researchers also played a role by trying to feed science into the idea that carbohydrates are the ideal nutrient. It had been known, for almost a century, and considered mostly irrelevant to the etiology of obesity, that fat has nine calories per gram compared with four for carbohydrates and protein. Now it became the fail-safe position of the low-fat recommendations: reduce the densest source of calories in the diet and you will lose weight. Then in 1982, J.P. Flatt, a University of Massachusetts biochemist, published his research demonstrating that, in any normal diet, it is extremely rare for the human body to convert carbohydrates into body fat. This was then misinterpreted by the media and quite a few scientists to mean that eating carbohydrates, even to excess, could not make you fat -- which is not the case, Flatt says. But the misinterpretation developed a vigorous life of its own because it resonated with the notion that fat makes you fat and carbohydrates are harmless.

As a result, the major trends in American diets since the late 70's, according to the U.S.D.A. agricultural economist Judith Putnam, have been a decrease in the percentage of fat calories and a ''greatly increased consumption of carbohydrates.'' To be precise, annual grain consumption has increased almost 60 pounds per person, and caloric sweeteners (primarily high-fructose corn syrup) by 30 pounds. At the same time, we suddenly began consuming more total calories: now up to 400 more each day since the government started recommending low-fat diets.

If these trends are correct, then the obesity epidemic can certainly be explained by Americans' eating more calories than ever -- excess calories, after all, are what causes us to gain weight -- and, specifically, more carbohydrates. The question is why?

The answer provided by Endocrinology 101 is that we are simply hungrier than we were in the 70's, and the reason is physiological more than psychological. In this case, the salient factor -- ignored in the pursuit of fat and its effect on cholesterol -- is how carbohydrates affect blood sugar and insulin. In fact, these were obvious culprits all along, which is why Atkins and the low-carb-diet doctors pounced on them early.

The primary role of insulin is to regulate blood-sugar levels. After you eat carbohydrates, they will be broken down into their component sugar molecules and transported into the bloodstream. Your pancreas then secretes insulin, which shunts the blood sugar into muscles and the liver as fuel for the next few hours. This is why carbohydrates have a significant impact on insulin and fat does not. And because juvenile diabetes is caused by a lack of insulin, physicians believed since the 20's that the only evil with insulin is not having enough.

But insulin also regulates fat metabolism. We cannot store body fat without it. Think of insulin as a switch. When it's on, in the few hours after eating, you burn carbohydrates for energy and store excess calories as fat. When it's off, after the insulin has been depleted, you burn fat as fuel. So when insulin levels are low, you will burn your own fat, but not when they're high.

This is where it gets unavoidably complicated. The fatter you are, the more insulin your pancreas will pump out per meal, and the more likely you'll develop what's called ''insulin resistance,'' which is the underlying cause of Syndrome X. In effect, your cells become insensitive to the action of insulin, and so you need ever greater amounts to keep your blood sugar in check. So as you gain weight, insulin makes it easier to store fat and harder to lose it. But the insulin resistance in turn may make it harder to store fat -- your weight is being kept in check, as it should be. But now the insulin resistance might prompt your pancreas to produce even more insulin, potentially starting a vicious cycle. Which comes first -- the obesity, the elevated insulin, known as hyperinsulinemia, or the insulin resistance -- is a chicken-and-egg problem that hasn't been resolved. One endocrinologist described this to me as ''the Nobel-prize winning question.''

Insulin also profoundly affects hunger, although to what end is another point of controversy. On the one hand, insulin can indirectly cause hunger by lowering your blood sugar, but how low does blood sugar have to drop before hunger kicks in? That's unresolved. Meanwhile, insulin works in the brain to suppress hunger. The theory, as explained to me by Michael Schwartz, an endocrinologist at the University of Washington, is that insulin's ability to inhibit appetite would normally counteract its propensity to generate body fat. In other words, as you gained weight, your body would generate more insulin after every meal, and that in turn would suppress your appetite; you'd eat less and lose the weight.

Schwartz, however, can imagine a simple mechanism that would throw this ''homeostatic'' system off balance: if your brain were to lose its sensitivity to insulin, just as your fat and muscles do when they are flooded with it. Now the higher insulin production that comes with getting fatter would no longer compensate by suppressing your appetite, because your brain would no longer register the rise in insulin. The end result would be a physiologic state in which obesity is almost preordained, and one in which the carbohydrate-insulin connection could play a major role. Schwartz says he believes this could indeed be happening, but research hasn't progressed far enough to prove it. ''It is just a hypothesis,'' he says. ''It still needs to be sorted out.''

David Ludwig, the Harvard endocrinologist, says that it's the direct effect of insulin on blood sugar that does the trick. He notes that when diabetics get too much insulin, their blood sugar drops and they get ravenously hungry. They gain weight because they eat more, and the insulin promotes fat deposition. The same happens with lab animals. This, he says, is effectively what happens when we eat carbohydrates -- in particular sugar and starches like potatoes and rice, or anything made from flour, like a slice of white bread. These are known in the jargon as high-glycemic-index carbohydrates, which means they are absorbed quickly into the blood. As a result, they cause a spike of blood sugar and a surge of insulin within minutes. The resulting rush of insulin stores the blood sugar away and a few hours later, your blood sugar is lower than it was before you ate. As Ludwig explains, your body effectively thinks it has run out of fuel, but the insulin is still high enough to prevent you from burning your own fat. The result is hunger and a craving for more carbohydrates. It's another vicious circle, and another situation ripe for obesity.

The glycemic-index concept and the idea that starches can be absorbed into the blood even faster than sugar emerged in the late 70's, but again had no influence on public health recommendations, because of the attendant controversies. To wit: if you bought the glycemic-index concept, then you had to accept that the starches we were supposed to be eating 6 to 11 times a day were, once swallowed, physiologically indistinguishable from sugars. This made them seem considerably less than wholesome. Rather than accept this possibility, the policy makers simply allowed sugar and corn syrup to elude the vilification that befell dietary fat. After all, they are fat-free.

Sugar and corn syrup from soft drinks, juices and the copious teas and sports drinks now supply more than 10 percent of our total calories; the 80's saw the introduction of Big Gulps and 32-ounce cups of Coca-Cola, blasted through with sugar, but 100 percent fat free. When it comes to insulin and blood sugar, these soft drinks and fruit juices -- what the scientists call ''wet carbohydrates'' -- might indeed be worst of all. (Diet soda accounts for less than a quarter of the soda market.)

The gist of the glycemic-index idea is that the longer it takes the carbohydrates to be digested, the lesser the impact on blood sugar and insulin and the healthier the food. Those foods with the highest rating on the glycemic index are some simple sugars, starches and anything made from flour. Green vegetables, beans and whole grains cause a much slower rise in blood sugar because they have fiber, a nondigestible carbohydrate, which slows down digestion and lowers the glycemic index. Protein and fat serve the same purpose, which implies that eating fat can be beneficial, a notion that is still unacceptable. And the glycemic-index concept implies that a primary cause of Syndrome X, heart disease, Type 2 diabetes and obesity is the long-term damage caused by the repeated surges of insulin that come from eating starches and refined carbohydrates. This suggests a kind of unified field theory for these chronic diseases, but not one that coexists easily with the low-fat doctrine.

At Ludwig's pediatric obesity clinic, he has been prescribing low-glycemic-index diets to children and adolescents for five years now. He does not recommend the Atkins diet because he says he believes such a very low carbohydrate approach is unnecessarily restrictive; instead, he tells his patients to effectively replace refined carbohydrates and starches with vegetables, legumes and fruit. This makes a low-glycemic-index diet consistent with dietary common sense, albeit in a higher-fat kind of way. His clinic now has a nine-month waiting list. Only recently has Ludwig managed to convince the N.I.H. that such diets are worthy of study. His first three grant proposals were summarily rejected, which may explain why much of the relevant research has been done in Canada and in Australia. In April, however, Ludwig received $1.2 million from the N.I.H. to test his low-glycemic-index diet against a traditional low-fat-low-calorie regime. That might help resolve some of the controversy over the role of insulin in obesity, although the redoubtable Robert Atkins might get there first.

The 71-year-old Atkins, a graduate of Cornell medical school, says he first tried a very low carbohydrate diet in 1963 after reading about one in the Journal of the American Medical Association. He lost weight effortlessly, had his epiphany and turned a fledgling Manhattan cardiology practice into a thriving obesity clinic. He then alienated the entire medical community by telling his readers to eat as much fat and protein as they wanted, as long as they ate little to no carbohydrates. They would lose weight, he said, because they would keep their insulin down; they wouldn't be hungry; and they would have less resistance to burning their own fat. Atkins also noted that starches and sugar were harmful in any event because they raised triglyceride levels and that this was a greater risk factor for heart disease than cholesterol.

Atkins's diet is both the ultimate manifestation of the alternative hypothesis as well as the battleground on which the fat-versus-carbohydrates controversy is likely to be fought scientifically over the next few years. After insisting Atkins was a quack for three decades, obesity experts are now finding it difficult to ignore the copious anecdotal evidence that his diet does just what he has claimed. Take Albert Stunkard, for instance. Stunkard has been trying to treat obesity for half a century, but he told me he had his epiphany about Atkins and maybe about obesity as well just recently when he discovered that the chief of radiology in his hospital had lost 60 pounds on Atkins's diet. ''Well, apparently all the young guys in the hospital are doing it,'' he said. ''So we decided to do a study.'' When I asked Stunkard if he or any of his colleagues considered testing Atkins's diet 30 years ago, he said they hadn't because they thought Atkins was ''a jerk'' who was just out to make money: this ''turned people off, and so nobody took him seriously enough to do what we're finally doing.''

In fact, when the American Medical Association released its scathing critique of Atkins's diet in March 1973, it acknowledged that the diet probably worked, but expressed little interest in why. Through the 60's, this had been a subject of considerable research, with the conclusion that Atkins-like diets were low-calorie diets in disguise; that when you cut out pasta, bread and potatoes, you'll have a hard time eating enough meat, vegetables and cheese to replace the calories.

That, however, raised the question of why such a low-calorie regimen would also suppress hunger, which Atkins insisted was the signature characteristic of the diet. One possibility was Endocrinology 101: that fat and protein make you sated and, lacking carbohydrates and the ensuing swings of blood sugar and insulin, you stay sated. The other possibility arose from the fact that Atkins's diet is ''ketogenic.'' This means that insulin falls so low that you enter a state called ketosis, which is what happens during fasting and starvation. Your muscles and tissues burn body fat for energy, as does your brain in the form of fat molecules produced by the liver called ketones. Atkins saw ketosis as the obvious way to kick-start weight loss. He also liked to say that ketosis was so energizing that it was better than sex, which set him up for some ridicule. An inevitable criticism of Atkins's diet has been that ketosis is dangerous and to be avoided at all costs.

When I interviewed ketosis experts, however, they universally sided with Atkins, and suggested that maybe the medical community and the media confuse ketosis with ketoacidosis, a variant of ketosis that occurs in untreated diabetics and can be fatal. ''Doctors are scared of ketosis,'' says Richard Veech, an N.I.H. researcher who studied medicine at Harvard and then got his doctorate at Oxford University with the Nobel Laureate Hans Krebs. ''They're always worried about diabetic ketoacidosis. But ketosis is a normal physiologic state. I would argue it is the normal state of man. It's not normal to have McDonald's and a delicatessen around every corner. It's normal to starve.''

Simply put, ketosis is evolution's answer to the thrifty gene. We may have evolved to efficiently store fat for times of famine, says Veech, but we also evolved ketosis to efficiently live off that fat when necessary. Rather than being poison, which is how the press often refers to ketones, they make the body run more efficiently and provide a backup fuel source for the brain. Veech calls ketones ''magic'' and has shown that both the heart and brain run 25 percent more efficiently on ketones than on blood sugar.

The bottom line is that for the better part of 30 years Atkins insisted his diet worked and was safe, Americans apparently tried it by the tens of millions, while nutritionists, physicians, public- health authorities and anyone concerned with heart disease insisted it could kill them, and expressed little or no desire to find out who was right. During that period, only two groups of U.S. researchers tested the diet, or at least published their results. In the early 70's, J.P. Flatt and Harvard's George Blackburn pioneered the ''protein-sparing modified fast'' to treat postsurgical patients, and they tested it on obese volunteers. Blackburn, who later became president of the American Society of Clinical Nutrition, describes his regime as ''an Atkins diet without excess fat'' and says he had to give it a fancy name or nobody would take him seriously. The diet was ''lean meat, fish and fowl'' supplemented by vitamins and minerals. ''People loved it,'' Blackburn recalls. ''Great weight loss. We couldn't run them off with a baseball bat.'' Blackburn successfully treated hundreds of obese patients over the next decade and published a series of papers that were ignored. When obese New Englanders turned to appetite-control drugs in the mid-80's, he says, he let it drop. He then applied to the N.I.H. for a grant to do a clinical trial of popular diets but was rejected.

The second trial, published in September 1980, was done at the George Washington University Medical Center. Two dozen obese volunteers agreed to follow Atkins's diet for eight weeks and lost an average of 17 pounds each, with no apparent ill effects, although their L.D.L. cholesterol did go up. The researchers, led by John LaRosa, now president of the State University of New York Downstate Medical Center in Brooklyn, concluded that the 17-pound weight loss in eight weeks would likely have happened with any diet under ''the novelty of trying something under experimental conditions'' and never pursued it further.

Now researchers have finally decided that Atkins's diet and other low-carb diets have to be tested, and are doing so against traditional low-calorie-low-fat diets as recommended by the American Heart Association. To explain their motivation, they inevitably tell one of two stories: some, like Stunkard, told me that someone they knew -- a patient, a friend, a fellow physician -- lost considerable weight on Atkins's diet and, despite all their preconceptions to the contrary, kept it off. Others say they were frustrated with their inability to help their obese patients, looked into the low-carb diets and decided that Endocrinology 101 was compelling. ''As a trained physician, I was trained to mock anything like the Atkins diet,'' says Linda Stern, an internist at the Philadelphia Veterans Administration Hospital, ''but I put myself on the diet. I did great. And I thought maybe this is something I can offer my patients.''

None of these studies have been financed by the N.I.H., and none have yet been published. But the results have been reported at conferences -- by researchers at Schneider Children's Hospital on Long Island, Duke University and the University of Cincinnati, and by Stern's group at the Philadelphia V.A. Hospital. And then there's the study Stunkard had mentioned, led by Gary Foster at the University of Pennsylvania, Sam Klein, director of the Center for Human Nutrition at Washington University in St. Louis, and Jim Hill, who runs the University of Colorado Center for Human Nutrition in Denver. The results of all five of these studies are remarkably consistent. Subjects on some form of the Atkins diet -- whether overweight adolescents on the diet for 12 weeks as at Schneider, or obese adults averaging 295 pounds on the diet for six months, as at the Philadelphia V.A. -- lost twice the weight as the subjects on the low-fat, low-calorie diets.

In all five studies, cholesterol levels improved similarly with both diets, but triglyceride levels were considerably lower with the Atkins diet. Though researchers are hesitant to agree with this, it does suggest that heart-disease risk could actually be reduced when fat is added back into the diet and starches and refined carbohydrates are removed. ''I think when this stuff gets to be recognized,'' Stunkard says, ''it's going to really shake up a lot of thinking about obesity and metabolism.''

All of this could be settled sooner rather than later, and with it, perhaps, we might have some long-awaited answers as to why we grow fat and whether it is indeed preordained by societal forces or by our choice of foods. For the first time, the N.I.H. is now actually financing comparative studies of popular diets. Foster, Klein and Hill, for instance, have now received more than $2.5 million from N.I.H. to do a five-year trial of the Atkins diet with 360 obese individuals. At Harvard, Willett, Blackburn and Penelope Greene have money, albeit from Atkins's nonprofit foundation, to do a comparative trial as well.

Should these clinical trials also find for Atkins and his high-fat, low-carbohydrate diet, then the public-health authorities may indeed have a problem on their hands. Once they took their leap of faith and settled on the low-fat dietary dogma 25 years ago, they left little room for contradictory evidence or a change of opinion, should such a change be necessary to keep up with the science. In this light Sam Klein's experience is noteworthy. Klein is president-elect of the North American Association for the Study of Obesity, which suggests that he is a highly respected member of his community. And yet, he described his recent experience discussing the Atkins diet at medical conferences as a learning experience. ''I have been impressed,'' he said, ''with the anger of academicians in the audience. Their response is 'How dare you even present data on the Atkins diet!' ''

This hostility stems primarily from their anxiety that Americans, given a glimmer of hope about their weight, will rush off en masse to try a diet that simply seems intuitively dangerous and on which there is still no long-term data on whether it works and whether it is safe. It's a justifiable fear. In the course of my research, I have spent my mornings at my local diner, staring down at a plate of scrambled eggs and sausage, convinced that somehow, some way, they must be working to clog my arteries and do me in.

After 20 years steeped in a low-fat paradigm, I find it hard to see the nutritional world any other way. I have learned that low-fat diets fail in clinical trials and in real life, and they certainly have failed in my life. I have read the papers suggesting that 20 years of low-fat recommendations have not managed to lower the incidence of heart disease in this country, and may have led instead to the steep increase in obesity and Type 2 diabetes. I have interviewed researchers whose computer models have calculated that cutting back on the saturated fats in my diet to the levels recommended by the American Heart Association would not add more than a few months to my life, if that. I have even lost considerable weight with relative ease by giving up carbohydrates on my test diet, and yet I can look down at my eggs and sausage and still imagine the imminent onset of heart disease and obesity, the latter assuredly to be caused by some bizarre rebound phenomena the likes of which science has not yet begun to describe. The fact that Atkins himself has had heart trouble recently does not ease my anxiety, despite his assurance that it is not diet-related.

This is the state of mind I imagine that mainstream nutritionists, researchers and physicians must inevitably take to the fat-versus-carbohydrate controversy. They may come around, but the evidence will have to be exceptionally compelling. Although this kind of conversion may be happening at the moment to John Farquhar, who is a professor of health research and policy at Stanford University and has worked in this field for more than 40 years. When I interviewed Farquhar in April, he explained why low-fat diets might lead to weight gain and low-carbohydrate diets might lead to weight loss, but he made me promise not to say he believed they did. He attributed the cause of the obesity epidemic to the ''force-feeding of a nation.'' Three weeks later, after reading an article on Endocrinology 101 by David Ludwig in the Journal of the American Medical Association, he sent me an e-mail message asking the not-entirely-rhetorical question, ''Can we get the low-fat proponents to apologize?''

Gary Taubes is a correspondent for the journal Science and author of ''Bad Science: The Short Life and Weird Times of Cold Fusion.''

The Soft Science of Dietary Fat

By Gary Taubes

When the U.S. Surgeon General's Office set off in 1988 to write the definitive report on the dangers of dietary fat, the scientific task appeared straightforward. Four years earlier, the National Institutes of Health (NIH) had begun advising every American old enough to walk to restrict fat intake, and the president of the American Heart Association (AHA) had told Time magazine that if everyone went along, "we will have [atherosclerosis] conquered" by the year 2000. The Surgeon General's Office itself had just published its 700-page landmark "Report on Nutrition and Health," declaring fat the single most unwholesome component of the American diet.

All of this was apparently based on sound science. So the task before the project officer was merely to gather that science together in one volume, have it reviewed by a committee of experts, which had been promptly established, and publish it. The project did not go smoothly, however. Four project officers came and went over the next decade. "It consumed project officers," says Marion Nestle, who helped launch the project and now runs the nutrition and food studies department at New York University (NYU). Members of the oversight committee saw drafts of an early chapter or two, criticized them vigorously, and then saw little else.

Finally, in June 1999, 11 years after the project began, the Surgeon General's Office circulated a letter, authored by the last of the project officers, explaining that the report would be killed. There was no other public announcement and no press release. The letter explained that the relevant administrators "did not anticipate fully the magnitude of the additional external expertise and staff resources that would be needed." In other words, says Nestle, the subject matter "was too complicated." Bill Harlan, a member of the oversight committee and associate director of the Office of Disease Prevention at NIH, says "the report was initiated with a preconceived opinion of the conclusions," but the science behind those opinions was not holding up. "Clearly the thoughts of yesterday were not going to serve us very well."

During the past 30 years, the concept of eating healthy in America has become synonymous with avoiding dietary fat. The creation and marketing of reduced-fat food products has become big business; over 15,000 have appeared on supermarket shelves. Indeed, an entire research industry has arisen to create palatable nonfat fat substitutes, and the food industry now spends billions of dollars yearly selling the less-fat-is-good-health message. The government weighs in as well, with the U.S. Department of Agriculture's (USDA's) booklet on dietary guidelines, published every 5 years, and its ubiquitous Food Guide Pyramid, which recommends that fats and oils be eaten "sparingly." The low-fat gospel spreads farther by a kind of societal osmosis, continuously reinforced by physicians, nutritionists, journalists, health organizations, and consumer advocacy groups such as the Center for Science in the Public Interest, which refers to fat as this "greasy killer." "In America, we no longer fear God or the communists, but we fear fat," says David Kritchevsky of the Wistar Institute in Philadelphia, who in 1958 wrote the first textbook on cholesterol.

As the Surgeon General's Office discovered, however, the science of dietary fat is not nearly as simple as it once appeared. The proposition, now 50 years old, that dietary fat is a bane to health is based chiefly on the fact that fat, specifically the hard, saturated fat found primarily in meat and dairy products, elevates blood cholesterol levels. This in turn raises the likelihood that cholesterol will clog arteries, a condition known as atherosclerosis, which then increases risk of coronary artery disease, heart attack, and untimely death. By the 1970s, each individual step of this chain from fat to cholesterol to heart disease had been demonstrated beyond reasonable doubt, but the veracity of the chain as a whole has never been proven. In other words, despite decades of research, it is still a debatable proposition whether the consumption of saturated fats above recommended levels (step one in the chain) by anyone who's not already at high risk of heart disease will increase the likelihood of untimely death (outcome three). Nor have hundreds of millions of dollars in trials managed to generate compelling evidence that healthy individuals can extend their lives by more than a few weeks, if that, by eating less fat (see sidebar on p. 2538). To put it simply, the data remain ambiguous as to whether low-fat diets will benefit healthy Americans. Worse, the ubiquitous admonishments to reduce total fat intake have encouraged a shift to high-carbohydrate diets, which may be no better--and may even be worse--than high-fat diets.

Since the early 1970s, for instance, Americans' average fat intake has dropped from over 40% of total calories to 34%; average serum cholesterol levels have dropped as well. But no compelling evidence suggests that these decreases have improved health. Although heart disease death rates have dropped--and public health officials insist low-fat diets are partly responsible--the incidence of heart disease does not seem to be declining, as would be expected if lower fat diets made a difference. This was the conclusion, for instance, of a 10-year study of heart disease mortality published in The New England Journal of Medicine in 1998, which suggested that death rates are declining largely because doctors are treating the disease more successfully. AHA statistics agree: Between 1979 and 1996, the number of medical procedures for heart disease increased from 1.2 million to 5.4 million a year. "I don't consider that this disease category has disappeared or anything close to it," says one AHA statistician.

Meanwhile, obesity in America, which remained constant from the early 1960s through 1980, has surged upward since then--from 14% of the population to over 22%. Diabetes has increased apace. Both obesity and diabetes increase heart disease risk, which could explain why heart disease incidence is not decreasing. That this obesity epidemic occurred just as the government began bombarding Americans with the low-fat message suggests the possibility, however distant, that low-fat diets might have unintended consequences--among them, weight gain. "Most of us would have predicted that if we can get the population to change its fat intake, with its dense calories, we would see a reduction in weight," admits Harlan. "Instead, we see the exact opposite."

In the face of this uncertainty, skeptics and apostates have come along repeatedly, only to see their work almost religiously ignored as the mainstream medical community sought consensus on the evils of dietary fat. For 20 years, for instance, the Harvard School of Public Health has run the Nurses' Health Study and its two sequelae--the Health Professionals Follow-Up Study and the Nurses' Health Study II--accumulating over a decade of data on the diet and health of almost 300,000 Americans. The results suggest that total fat consumed has no relation to heart disease risk; that monounsaturated fats like olive oil lower risk; and that saturated fats are little worse, if at all, than the pasta and other carbohydrates that the Food Guide Pyramid suggests be eaten copiously. (The studies also suggest that trans fatty acids are unhealthful. These are the fats in margarine, for instance, and are what many Americans started eating when they were told that the saturated fats in butter might kill them.) Harvard epidemiologist Walter Willett, spokesperson for the Nurses' Health Study, points out that NIH has spent over $100 million on the three studies and yet not one government agency has changed its primary guidelines to fit these particular data. "Scandalous," says Willett. "They say, 'You really need a high level of proof to change the recommendations,' which is ironic, because they never had a high level of proof to set them."

Indeed, the history of the national conviction that dietary fat is deadly, and its evolution from hypothesis to dogma, is one in which politicians, bureaucrats, the media, and the public have played as large a role as the scientists and the science. It's a story of what can happen when the demands of public health policy--and the demands of the public for simple advice--run up against the confusing ambiguity of real science.

Fear of fat
During the first half of the 20th century, nutritionists were more concerned about malnutrition than about the sins of dietary excess. After World War II, however, a coronary heart disease epidemic seemed to sweep the country (see sidebar on p. 2540). "Middle-aged men, seemingly healthy, were dropping dead," wrote biochemist Ancel Keys of the University of Minnesota, Twin Cities, who was among the first to suggest that dietary fats might be the cause. By 1952, Keys was arguing that Americans should reduce their fat intake to less than 30% of total calories, although he simultaneously recognized that "direct evidence on the effect of the diet on human arteriosclerosis is very little and likely to remain so for some time." In the famous and very controversial Seven Countries Study, for instance, Keys and his colleagues reported that the amount of fat consumed seemed to be the salient difference between populations such as those in Japan and Crete that had little heart disease and those, as in Finland, that were plagued by it. In 1961, the Framingham Heart Study linked cholesterol levels to heart disease, Keys made the cover of Time magazine, and the AHA, under his influence, began advocating low-fat diets as a palliative for men with high cholesterol levels. Keys had also become one of the first Americans to consciously adopt a heart-healthy diet: He and his wife, Time reported, "do not eat 'carving meat'--steaks, chops, roasts--more than three times a week."

Nonetheless, by 1969 the state of the science could still be summarized by a single sentence from a report of the Diet-Heart Review Panel of the National Heart Institute (now the National Heart, Lung, and Blood Institute, or NHLBI): "It is not known whether dietary manipulation has any effect whatsoever on coronary heart disease." The chair of the panel was E. H. "Pete" Ahrens, whose laboratory at Rockefeller University in New York City did much of the seminal research on fat and cholesterol metabolism.

Whereas proponents of low-fat diets were concerned primarily about the effects of dietary fat on cholesterol levels and heart disease, Ahrens and his panel--10 experts in clinical medicine, epidemiology, biostatistics, human nutrition, and metabolism--were equally concerned that eating less fat could have profound effects throughout the body, many of which could be harmful. The brain, for instance, is 70% fat, which chiefly serves to insulate neurons. Fat is also the primary component of cell membranes. Changing the proportion of saturated to unsaturated fats in the diet changes the fat composition in these membranes. This could conceivably change the membrane permeability, which controls the transport of everything from glucose, signaling proteins, and hormones to bacteria, viruses, and tumor-causing agents into and out of the cell. The relative saturation of fats in the diet could also influence cellular aging as well as the clotting ability of blood cells.

Whether the potential benefits of low-fat diets would exceed the potential risks could be settled by testing whether low-fat diets actually prolong life, but such a test would have to be enormous. The effect of diet on cholesterol levels is subtle for most individuals--especially those living in the real world rather than the metabolic wards of nutrition researchers--and the effect of cholesterol levels on heart disease is also subtle. As a result, tens of thousands of individuals would have to switch to low-fat diets and their subsequent health compared to that of equal numbers who continued eating fat to alleged excess. And all these people would have to be followed for years until enough deaths accumulated to provide statistically significant results. Ahrens and his colleagues were pessimistic about whether such a massive and expensive trial could ever be done. In 1971, an NIH task force estimated such a trial would cost $1 billion, considerably more than NIH was willing to spend. Instead, NIH administrators opted for a handful of smaller studies, two of which alone would cost $255 million. Perhaps more important, these studies would take a decade. Neither the public, the press, nor the U.S. Congress was willing to wait that long.

Science by committee
Like the flourishing American affinity for alternative medicine, an antifat movement evolved independently of science in the 1960s. It was fed by distrust of the establishment--in this case, both the medical establishment and the food industry--and by counterculture attacks on excessive consumption, whether manifested in gas-guzzling cars or the classic American cuisine of bacon and eggs and marbled steaks. And while the data on fat and health remained ambiguous and the scientific community polarized, the deadlock was broken not by any new science, but by politicians. It was Senator George McGovern's bipartisan, nonlegislative Select Committee on Nutrition and Human Needs--and, to be precise, a handful of McGovern's staff members--that almost single-handedly changed nutritional policy in this country and initiated the process of turning the dietary fat hypothesis into dogma.

McGovern's committee was founded in 1968 with a mandate to eradicate malnutrition in America, and it instituted a series of landmark federal food assistance programs. As the malnutrition work began to peter out in the mid-1970s, however, the committee didn't disband. Rather, its general counsel, Marshall Matz, and staff director, Alan Stone, both young lawyers, decided that the committee would address "overnutrition," the dietary excesses of Americans. It was a "casual endeavor," says Matz. "We really were totally naïve, a bunch of kids, who just thought, 'Hell, we should say something on this subject before we go out of business.' " McGovern and his fellow senators--all middle-aged men worried about their girth and their health--signed on; McGovern and his wife had both gone through diet-guru Nathan Pritikin's very low fat diet and exercise program. McGovern quit the program early, but Pritikin remained a major influence on his thinking.

McGovern's committee listened to 2 days of testimony on diet and disease in July 1976. Then resident wordsmith Nick Mottern, a former labor reporter for The Providence Journal, was assigned the task of researching and writing the first "Dietary Goals for the United States." Mottern, who had no scientific background and no experience writing about science, nutrition, or health, believed his Dietary Goals would launch a "revolution in diet and agriculture in this country." He avoided the scientific and medical controversy by relying almost exclusively on Harvard School of Public Health nutritionist Mark Hegsted for input on dietary fat. Hegsted had studied fat and cholesterol metabolism in the early 1960s, and he believed unconditionally in the benefits of restricting fat intake, although he says he was aware that his was an extreme opinion. With Hegsted as his muse, Mottern saw dietary fat as the nutritional equivalent of cigarettes, and the food industry as akin to the tobacco industry in its willingness to suppress scientific truth in the interests of profits. To Mottern, those scientists who spoke out against fat were those willing to take on the industry. "It took a certain amount of guts," he says, "to speak about this because of the financial interests involved."

Mottern's report suggested that Americans cut their total fat intake to 30% of the calories they consume and saturated fat intake to 10%, in accord with AHA recommendations for men at high risk of heart disease. The report acknowledged the existence of controversy but insisted Americans had nothing to lose by following its advice. "The question to be asked is not why should we change our diet but why not?" wrote Hegsted in the introduction. "There are [no risks] that can be identified and important benefits can be expected." This was an optimistic but still debatable position, and when Dietary Goals was released in January 1977, "all hell broke loose," recalls Hegsted. "Practically nobody was in favor of the McGovern recommendations. Damn few people."

McGovern responded with three follow-up hearings, which aptly foreshadowed the next 7 years of controversy. Among those testifying, for instance, was NHLBI director Robert Levy, who explained that no one knew if eating less fat or lowering blood cholesterol levels would prevent heart attacks, which was why NHLBI was spending $300 million to study the question. Levy's position was awkward, he recalls, because "the good senators came out with the guidelines and then called us in to get advice." He was joined by prominent scientists, including Ahrens, who testified that advising Americans to eat less fat on the strength of such marginal evidence was equivalent to conducting a nutritional experiment with the American public as subjects. Even the American Medical Association protested, suggesting that the diet proposed by the guidelines raised the "potential for harmful effects." But as these scientists testified, so did representatives from the dairy, egg, and cattle industries, who also vigorously opposed the guidelines for obvious reasons. This juxtaposition served to taint the scientific criticisms: Any scientists arguing against the committee's guidelines appeared to be either hopelessly behind the paradigm, which was Hegsted's view, or industry apologists, which was Mottern's, if not both.

Although the committee published a revised edition of the Dietary Goals later in the year, the thrust of the recommendations remained unchanged. It did give in to industry pressure by softening the suggestion that Americans eat less meat. Mottern says he considered even that a "disservice to the public," refused to do the revisions, and quit the committee. (Mottern became a vegetarian while writing the Dietary Goals and now runs a food co-op in Peekskill, New York.)

The guidelines might have then died a quiet death when McGovern's committee came to an end in late 1977 if two federal agencies had not felt it imperative to respond. Although they took contradictory points of view, one message--with media assistance--won out.

The first was the USDA, where consumer-activist Carol Tucker Foreman had recently been appointed an assistant secretary. Foreman believed it was incumbent on USDA to turn McGovern's recommendations into official policy, and, like Mottern, she was not deterred by the existence of scientific controversy. "Tell us what you know and tell us it's not the final answer," she would tell scientists. "I have to eat and feed my children three times a day, and I want you to tell me what your best sense of the data is right now."

Of course, given the controversy, the "best sense of the data" would depend on which scientists were asked. The Food and Nutrition Board of the National Academy of Sciences (NAS), which decides the Recommended Dietary Allowances, would have been a natural choice, but NAS president Philip Handler, an expert on metabolism, had told Foreman that Mottern's Dietary Goals were "nonsense." Foreman then turned to McGovern's staffers for advice and they recommended she hire Hegsted, which she did. Hegsted, in turn, relied on a state-of-the-science report published by an expert but very divergent committee of the American Society for Clinical Nutrition. "They were nowhere near unanimous on anything," says Hegsted, "but the majority supported something like the McGovern committee report."

The resulting document became the first edition of "Using the Dietary Guidelines for Americans." Although it acknowledged the existence of controversy and suggested that a single dietary recommendation might not suit an entire diverse population, the advice to avoid fat and saturated fat was, indeed, virtually identical to McGovern's Dietary Goals.

Three months later, the NAS Food and Nutrition Board released its own guidelines: "Toward Healthful Diets." The board, consisting of a dozen nutrition experts, concluded that the only reliable advice for healthy Americans was to watch their weight; everything else, dietary fat included, would take care of itself. The advice was not taken kindly, however, at least not by the media. The first reports--"rather incredulously," said Handler at the time--criticized the NAS advice for conflicting with the USDA's and McGovern's and thus somehow being irresponsible. Follow-up reports suggested that the board members, in the words of Jane Brody, who covered the story for The New York Times, were "all in the pocket of the industries being hurt." To be precise, the board chair and one of its members consulted for food industries, and funding for the board itself came from industry donations. These industry connections were leaked to the press from the USDA.

Hegsted now defends the NAS board, although he didn't at the time, and calls this kind of conflict of interest "a hell of an issue." "Everybody used to complain that industry didn't do anything on nutrition," he told Science, "yet anybody who got involved was blackballed because their positions were presumably influenced by the industry." (In 1981, Hegsted returned to Harvard, where his research was funded by Frito-Lay.) The press had mixed feelings, claiming that the connections "soiled" the academy's reputation "for tendering careful scientific advice" (The Washington Post), demonstrated that the board's "objectivity and aptitude are in doubt" (The New York Times), or represented in the board's guidelines a "blow against the food faddists who hold the public in thrall" (Science). In any case, the NAS board had been publicly discredited. Hegsted's Dietary Guidelines for Americans became the official U.S. policy on dietary fat: Eat less fat. Live longer.

Creating "consensus"
Once politicians, the press, and the public had decided dietary fat policy, the science was left to catch up. In the early 1970s, when NIH opted to forgo a $1 billion trial that might be definitive and instead fund a half-dozen studies at one-third the cost, everyone hoped these smaller trials would be sufficiently persuasive to conclude that low-fat diets prolong lives. The results were published between 1980 and 1984. Four of these trials --comparing heart disease rates and diet within Honolulu, Puerto Rico, Chicago, and Framingham--showed no evidence that men who ate less fat lived longer or had fewer heart attacks. A fifth trial, the Multiple Risk Factor Intervention Trial (MRFIT), cost $115 million and tried to amplify the subtle influences of diet on health by persuading subjects to avoid fat while simultaneously quitting smoking and taking medication for high blood pressure. That trial suggested, if anything, that eating less fat might shorten life. In each study, however, the investigators concluded that methodological flaws had led to the negative results. They did not, at least publicly, consider their results reason to lessen their belief in the evils of fat.

The sixth study was the $140 million Lipid Research Clinics (LRC) Coronary Primary Prevention Trial, led by NHLBI administrator Basil Rifkind and biochemist Daniel Steinberg of the University of California, San Diego. The LRC trial was a drug trial, not a diet trial, but the NHLBI heralded its outcome as the end of the dietary fat debate. In January 1984, LRC investigators reported that a medication called cholestyramine reduced cholesterol levels in men with abnormally high cholesterol levels and modestly reduced heart disease rates in the process. (The probability of suffering a heart attack during the seven-plus years of the study was reduced from 8.6% in the placebo group to 7.0%; the probability of dying from a heart attack dropped from 2.0% to 1.6%.) The investigators then concluded, without benefit of dietary data, that cholestyramine's benefits could be extended to diet as well. And although the trial tested only middle-aged men with cholesterol levels higher than those of 95% of the population, they concluded that those benefits "could and should be extended to other age groups and women and ... other more modest elevations of cholesterol levels."

Why go so far? Rifkind says their logic was simple: For 20 years, he and his colleagues had argued that lowering cholesterol levels prevented heart attacks. They had spent enormous sums trying to prove it. They felt they could never actually demonstrate that low-fat diets prolonged lives--that would be too expensive, and MRFIT had failed--but now they had established a fundamental link in the causal chain, from lower cholesterol levels to cardiovascular health. With that, they could take the leap of faith from cholesterol-lowering drugs and health to cholesterol-lowering diet and health. And after all their effort, they were eager--not to mention urged by Congress--to render helpful advice. "There comes a point when, if you don't make a decision, the consequences can be great as well," says Rifkind. "If you just allow Americans to keep on consuming 40% of calories from fat, there's an outcome to that as well."

With the LRC results in press, the NHLBI launched what Levy called "a massive public health campaign." The media obligingly went along. Time, for instance, reported the LRC findings under the headline "Sorry, It's True. Cholesterol really is a killer." The article about a drug trial began: "No whole milk. No butter. No fatty meats ..." Time followed up 3 months later with a cover story: "And Cholesterol and Now the Bad News. ..." The cover photo was a frowning face: a breakfast plate with two fried eggs as the eyes and a bacon strip for the mouth. Rifkind was quoted saying that their results "strongly indicate that the more you lower cholesterol and fat in your diet, the more you reduce your risk of heart disease," a statement that still lacked direct scientific support.

The following December, NIH effectively ended the debate with a "Consensus Conference." The idea of such a conference is that an expert panel, ideally unbiased, listens to 2 days of testimony and arrives at a conclusion with which everyone agrees. In this case, Rifkind chaired the planning committee, which chose his LRC co-investigator Steinberg to lead the expert panel. The 20 speakers did include a handful of skeptics --including Ahrens, for instance, and cardiologist Michael Oliver of Imperial College in London--who argued that it was unscientific to equate the effects of a drug with the effects of a diet. Steinberg's panel members, however, as Oliver later complained in The Lancet, "were selected to include only experts who would, predictably, say that all levels of blood cholesterol in the United States are too high and should be lowered. And, of course, this is exactly what was said." Indeed, the conference report, written by Steinberg and his panel, revealed no evidence of discord. There was "no doubt," it concluded, that low-fat diets "will afford significant protection against coronary heart disease" to every American over 2 years old. The Consensus Conference officially gave the appearance of unanimity where none existed. After all, if there had been a true consensus, as Steinberg himself told Science, "you wouldn't have had to have a consensus conference."

The test of time
To the outside observer, the challenge in making sense of any such long-running scientific controversy is to establish whether the skeptics are simply on the wrong side of the new paradigm, or whether their skepticism is well founded. In other words, is the science at issue based on sound scientific thinking and unambiguous data, or is it what Sir Francis Bacon, for instance, would have called "wishful science," based on fancies, opinions, and the exclusion of contrary evidence? Bacon offered one viable suggestion for differentiating the two: the test of time. Good science is rooted in reality, so it grows and develops and the evidence gets increasingly more compelling, whereas wishful science flourishes most under its first authors before "going downhill."

Such is the case, for instance, with the proposition that dietary fat causes cancer, which was an integral part of dietary fat anxiety in the late 1970s. By 1982, the evidence supporting this idea was thought to be so undeniable that a landmark NAS report on nutrition and cancer equated those researchers who remained skeptical with "certain interested parties [who] formerly argued that the association between lung cancer and smoking was not causational." Fifteen years and hundreds of millions of research dollars later, a similarly massive expert report by the World Cancer Research Fund and the American Institute for Cancer Research could find neither "convincing" nor even "probable" reason to believe that dietary fat caused cancer.

The hypothesis that low-fat diets are the requisite route to weight loss has taken a similar downward path. This was the ultimate fallback position in all low-fat recommendations: Fat has nine calories per gram compared to four calories for carbohydrates and protein, and so cutting fat from the diet surely would cut pounds. "This is held almost to be a religious truth," says Harvard's Willett. Considerable data, however, now suggest otherwise. The results of well-controlled clinical trials are consistent: People on low-fat diets initially lose a couple of kilograms, as they would on any diet, and then the weight tends to return. After 1 to 2 years, little has been achieved. Consider, for instance, the 50,000 women enrolled in the ongoing $100 million Women's Health Initiative (WHI). Half of these women have been extensively counseled to consume only 20% of their calories from fat. After 3 years on this near-draconian regime, say WHI sources, the women had lost, on average, a kilogram each.

The link between dietary fat and heart disease is more complicated, because the hypothesis has diverged into two distinct propositions: first, that lowering cholesterol prevents heart disease; second, that eating less fat not only lowers cholesterol and prevents heart disease but prolongs life. Since 1984, the evidence that cholesterol-lowering drugs are beneficial--proposition number one--has indeed blossomed, at least for those at high risk of heart attack. These drugs reduce serum cholesterol levels dramatically, and they prevent heart attacks, perhaps by other means as well. Their market has now reached $4 billion a year in the United States alone, and every new trial seems to confirm their benefits.

The evidence supporting the second proposition, that eating less fat makes for a healthier and longer life, however, has remained stubbornly ambiguous. If anything, it has only become less compelling over time. Indeed, since Ancel Keys started advocating low-fat diets almost 50 years ago, the science of fat and cholesterol has evolved from a simple story into a very complicated one. The catch has been that few involved in this business were prepared to deal with a complicated story. Researchers initially preferred to believe it was simple--that a single unwholesome nutrient, in effect, could be isolated from the diverse richness of human diets; public health administrators required a simple story to give to Congress and the public; and the press needed a simple story--at least on any particular day--to give to editors and readers in 30 column inches. But as contrarian data continued to accumulate, the complications became increasingly more difficult to ignore or exclude, and the press began waffling or adding caveats. The scientists then got the blame for not sticking to the original simple story, which had, regrettably, never existed.

More fats, fewer answers
The original simple story in the 1950s was that high cholesterol levels increase heart disease risk. The seminal Framingham Heart Study, for instance, which revealed the association between cholesterol and heart disease, originally measured only total serum cholesterol. But cholesterol shuttles through the blood in an array of packages. Low-density lipoprotein particles (LDL, the "bad" cholesterol) deliver fat and cholesterol from the liver to tissues that need it, including the arterial cells, where it can lead to atherosclerotic plaques. High-density lipoproteins (HDLs, the "good" cholesterol) return cholesterol to the liver. The higher the HDL, the lower the heart disease risk. Then there are triglycerides, which contain fatty acids, and very low density lipoproteins (VLDLs), which transport triglycerides.

All of these particles have some effect on heart disease risk, while the fats, carbohydrates, and protein in the diet have varying effects on all these particles. The 1950s story was that saturated fats increase total cholesterol, polyunsaturated fats decrease it, and monounsaturated fats are neutral. By the late 1970s--when researchers accepted the benefits of HDL--they realized that monounsaturated fats are not neutral. Rather, they raise HDL, at least compared to carbohydrates, and lower LDL. This makes them an ideal nutrient as far as cholesterol goes. Furthermore, saturated fats cannot be quite so evil because, while they elevate LDL, which is bad, they also elevate HDL, which is good. And some saturated fats--stearic acid, in particular, the fat in chocolate--are at worst neutral. Stearic acid raises HDL levels but does little or nothing to LDL. And then there are trans fatty acids, which raise LDL, just like saturated fat, but also lower HDL. Today, none of this is controversial, although it has yet to be reflected in any Food Guide Pyramid.

To understand where this complexity can lead in a simple example, consider a steak--to be precise, a porterhouse, select cut, with a half-centimeter layer of fat, the nutritional constituents of which can be found in the Nutrient Database for Standard Reference at the USDA Web site. After broiling, this porterhouse reduces to a serving of almost equal parts fat and protein. Fifty-one percent of the fat is monounsaturated, of which virtually all (90%) is oleic acid, the same healthy fat that's in olive oil. Saturated fat constitutes 45% of the total fat, but a third of that is stearic acid, which is, at the very least, harmless. The remaining 4% of the fat is polyunsaturated, which also improves cholesterol levels. In sum, well over half--and perhaps as much as 70%--of the fat content of a porterhouse will improve cholesterol levels compared to what they would be if bread, potatoes, or pasta were consumed instead. The remaining 30% will raise LDL but will also raise HDL. All of this suggests that eating a porterhouse steak rather than carbohydrates might actually improve heart disease risk, although no nutritional authority who hasn't written a high-fat diet book will say this publicly.

As for the scientific studies, in the years since the 1984 consensus conference, the one thing they have not done is pile up evidence in support of the low-fat-for-all approach to the public good. If anything, they have added weight to Ahrens's fears that there may be a downside to populationwide low-fat recommendations. In 1986, for instance, just 1 year after NIH launched the National Cholesterol Education Program, also advising low-fat diets for everyone over 2 years old, epidemiologist David Jacobs of the University of Minnesota, Twin Cities, visited Japan. There he learned that Japanese physicians were advising patients to raise their cholesterol levels, because low cholesterol levels were linked to hemorrhagic stroke. At the time, Japanese men were dying from stroke almost as frequently as American men were succumbing to heart disease. Back in Minnesota, Jacobs looked for this low-cholesterol-stroke relationship in the MRFIT data and found it there, too. And the relationship transcended stroke: Men with very low cholesterol levels seemed prone to premature death; below 160 milligrams per deciliter (mg/dl), the lower the cholesterol level, the shorter the life.

Jacobs reported his results to NHLBI, which in 1990 hosted a conference to discuss the issue, bringing together researchers from 19 studies around the world. The data were consistent: When investigators tracked all deaths, instead of just heart disease deaths, the cholesterol curves were U-shaped for men and flat for women. In other words, men with cholesterol levels above 240 mg/dl tended to die prematurely from heart disease. But below 160 mg/dl, the men tended to die prematurely from cancer, respiratory and digestive diseases, and trauma. As for women, if anything, the higher their cholesterol, the longer they lived (see graph on p. 2540).

These mortality data can be interpreted in two ways. One, preferred by low-fat advocates, is that they cannot be meaningful. Rifkind, for instance, told Science that the excess deaths at low cholesterol levels must be due to preexisting conditions. In other words, chronic illness leads to low cholesterol levels, not vice versa. He pointed to the 1990 conference report as the definitive document on the issue and as support for his argument, although the report states unequivocally that this interpretation is not supported by the data.

The other interpretation is that what a low-fat diet does to serum cholesterol levels, and what that in turn does to arteries, may be only one component of the diet's effect on health. In other words, while low-fat diets might help prevent heart disease, they might also raise susceptibility to other conditions. This is what always worried Ahrens. It's also one reason why the American College of Physicians, for instance, now suggests that cholesterol reduction is certainly worthwhile for those at high, short-term risk of dying of coronary heart disease but of "much smaller or ... uncertain" benefit for everyone else.

This interpretation--that the connection between diet and health far transcends cholesterol--is also supported by the single most dramatic diet-heart trial ever conducted: the Lyon Diet Heart Study, led by Michel de Lorgeril of the French National Institute of Health and Medical Research (INSERM) and published in Circulation in February 1999. The investigators randomized 605 heart attack survivors, all on cholesterol-lowering drugs, into two groups. They counseled one to eat an AHA "prudent diet," very similar to that recommended for all Americans. They counseled the other to eat a Mediterranean-type diet, with more bread, cereals, legumes, beans, vegetables, fruits, and fish and less meat. Total fat and types of fat differed markedly in the two diets, but the HDL, LDL, and total cholesterol levels in the two groups remained virtually identical. Nonetheless, over 4 years of follow-up, the Mediterranean-diet group had only 14 cardiac deaths and nonfatal heart attacks compared to 44 for the "Western-type" diet group. The likely explanation, wrote de Lorgeril and his colleagues, is that the "protective effects [of the Mediterranean diet] were not related to serum concentrations of total, LDL or HDL cholesterol."

Many researchers find the Lyon data so perplexing that they're left questioning the methodology of the trial. Nonetheless, says NIH's Harlan, the data "are very provocative. They do bring up the issue of whether if we look only at cholesterol levels we aren't going to miss something very important." De Lorgeril believes the diet's protective effect comes primarily from omega-3 fatty acids, found in seed oils, meat, cereals, green leafy vegetables, and fish, and from antioxidant compounds, including vitamins, trace elements, and flavonoids. He told Science that most researchers and journalists in the field are prisoners of the "cholesterol paradigm." Although dietary fat and serum cholesterol "are obviously connected," he says, "the connection is not a robust one" when it comes to heart disease.

Dietary trade-offs
One inescapable reality is that death is a trade-off, and so is diet. "You have to eat something," says epidemiologist Hugh Tunstall Pedoe of the University of Dundee, U.K., spokesperson for the 21-nation Monitoring Cardiovascular Disease Project run by the World Health Organization. "If you eat more of one thing, you eat a lot less of something else. So for every theory saying this disease is caused by an excess in x, you can produce an alternative theory saying it's a deficiency in y." It would be simple if, say, saturated fats could be cut from the diet and the calories with it, but that's not the case. Despite all expectations to the contrary, people tend to consume the same number of calories despite whatever diet they try. If they eat less total fat, for instance, they will eat more carbohydrates and probably less protein, because most protein comes in foods like meat that also have considerable amounts of fat.

This plus-minus problem suggests a different interpretation for virtually every diet study ever done, including, for instance, the kind of metabolic-ward studies that originally demonstrated the ability of saturated fats to raise cholesterol. If researchers reduce the amount of saturated fat in the test diet, they have to make up the calories elsewhere. Do they add polyunsaturated fats, for instance, or add carbohydrates? A single carbohydrate or mixed carbohydrates? Do they add green leafy vegetables, or do they add pasta? And so it goes. "The sky's the limit," says nutritionist Alice Lichtenstein of Tufts University in Boston. "There are a million perturbations."

These trade-offs also confound the kind of epidemiological studies that demonized saturated fat from the 1950s onward. In particular, individuals who eat copious amounts of meat and dairy products, and plenty of saturated fats in the process, tend not to eat copious amounts of vegetables and fruits. The same holds for entire populations. The eastern Finns, for instance, whose lofty heart disease rates convinced Ancel Keys and a generation of researchers of the evils of fat, live within 500 kilometers of the Arctic Circle and rarely see fresh produce or a green vegetable. The Scots, infamous for eating perhaps the least wholesome diet in the developed world, are in a similar fix. Basil Rifkind recalls being laughed at once on this point when he lectured to Scottish physicians on healthy diets: "One said, 'You talk about increasing fruits and vegetable consumption, but in the area I work in there's not a single grocery store.' " In both cases, researchers joke that the only green leafy vegetable these populations consume regularly is tobacco. As for the purported benefits of the widely hailed Mediterranean diet, is it the fish, the olive oil, or the fresh vegetables? After all, says Harvard epidemiologist Dimitrios Trichopoulos, a native of Greece, the olive oil is used either to cook vegetables or as dressing over salads. "The quantity of vegetables consumed is almost a pound [half a kilogram] a day," he says, "and you cannot eat it without olive oil. And we eat a lot of legumes, and we cannot eat legumes without olive oil."

Indeed, recent data on heart disease trends in Europe suggest that a likely explanation for the differences between countries and over time is the availability of fresh produce year-round rather than differences in fat intake. While the press often plays up the French paradox--the French have little heart disease despite seemingly high saturated fat consumption--the real paradox is throughout Southern Europe, where heart disease death rates have steadily dropped while animal fat consumption has steadily risen, says University of Cambridge epidemiologist John Powles, who studies national disease trends. The same trend appears in Japan. "We have this idea that it's the Arcadian past, the life in the village, the utopia that we've lost," Powles says; "that the really protective Mediterranean diet is what people ate in the 1950s." But that notion isn't supported by the data: As these Mediterranean nations became more affluent, says Powles, they began to eat proportionally more meat and with it more animal fat. Their heart disease rates, however, continued to improve compared to populations that consumed as much animal fat but had less access to fresh vegetables throughout the year. To Powles, the antifat movement was founded on the Puritan notion that "something bad had to have an evil cause, and you got a heart attack because you did something wrong, which was eating too much of a bad thing, rather than not having enough of a good thing."

The other salient trade-off in the plus-minus problem of human diets is carbohydrates. When the federal government began pushing low-fat diets, the scientists and administrators, and virtually everyone else involved, hoped that Americans would replace fat calories with fruits and vegetables and legumes, but it didn't happen. If nothing else, economics worked against it. The food industry has little incentive to advertise nonproprietary items: broccoli, for instance. Instead, says NYU's Nestle, the great bulk of the $30-billion-plus spent yearly on food advertising goes to selling carbohydrates in the guise of fast food, sodas, snacks, and candy bars. And carbohydrates are all too often what Americans eat.

Carbohydrates are what Harvard's Willett calls the flip side of the calorie trade-off problem. Because it is exceedingly difficult to add pure protein to a diet in any quantity, a low-fat diet is, by definition, a high-carbohydrate diet--just as a low-fat cookie or low-fat yogurt are, by definition, high in carbohydrates. Numerous studies now suggest that high-carbohydrate diets can raise triglyceride levels, create small, dense LDL particles, and reduce HDL--a combination, along with a condition known as "insulin resistance," that Stanford endocrinologist Gerald Reaven has labeled "syndrome X." Thirty percent of adult males and 10% to 15% of postmenopausal women have this particular syndrome X profile, which is associated with a several-fold increase in heart disease risk, says Reaven, even among those patients whose LDL levels appear otherwise normal. Reaven and Ron Krauss, who studies fats and lipids at Lawrence Berkeley National Laboratory in California, have shown that when men eat high-carbohydrate diets their cholesterol profiles may shift from normal to syndrome X. In other words, the more carbohydrates replace saturated fats, the more likely the end result will be syndrome X and an increased heart disease risk. "The problem is so clear right now it's almost a joke," says Reaven. How this balances out is the unknown. "It's a bitch of a question," says Marc Hellerstein, a nutritional biochemist at the University of California, Berkeley, "maybe the great public health nutrition question of our era."

The other worrisome aspect of the carbohydrate trade-off is the possibility that, for some individuals, at least, it might actually be easier to gain weight on low-fat/high-carbohydrate regimens than on higher fat diets. One of the many factors that influence hunger is the glycemic index, which measures how fast carbohydrates are broken down into simple sugars and moved into the bloodstream. Foods with the highest glycemic index are simple sugars and processed grain products like pasta and white rice, which cause a rapid rise in blood sugar after a meal. Fruits, vegetables, legumes, and even unprocessed starches--pasta al dente, for instance--cause a much slower rise in blood sugar. Researchers have hypothesized that eating high-glycemic index foods increases hunger later because insulin overreacts to the spike in blood sugar. "The high insulin levels cause the nutrients from the meal to get absorbed and very avidly stored away, and once they are, the body can't access them," says David Ludwig, director of the obesity clinic at Children's Hospital Boston. "The body appears to run out of fuel." A few hours after eating, hunger returns.

If the theory is correct, calories from the kind of processed carbohydrates that have become the staple of the American diet are not the same as calories from fat, protein, or complex carbohydrates when it comes to controlling weight. "They may cause a hormonal change that stimulates hunger and leads to overeating," says Ludwig, "especially in environments where food is abundant. ..."

In 1979, 2 years after McGovern's committee released its Dietary Goals, Ahrens wrote to The Lancet describing what he had learned over 30 years of studying fat and cholesterol metabolism: "It is absolutely certain that no one can reliably predict whether a change in dietary regimens will have any effect whatsoever on the incidence of new events of [coronary heart disease], nor in whom." Today, many nutrition researchers, acknowledging the complexity of the situation, find themselves siding with Ahrens. Krauss, for instance, who chairs the AHA Dietary Guidelines Committee, now calls it "scientifically naïve" to expect that a single dietary regime can be beneficial for everybody: "The 'goodness' or 'badness' of anything as complex as dietary fat and its subtypes will ultimately depend on the context of the individual."

Given the proven success and low cost of cholesterol-lowering drugs, most physicians now prescribe drug treatment for patients at high risk of heart disease. The drugs reduce LDL cholesterol levels by as much as 30%. Diet rarely drops LDL by more than 10%, which is effectively trivial for healthy individuals, although it may be worth the effort for those at high risk of heart disease whose cholesterol levels respond well to it.

The logic underlying populationwide recommendations such as the latest USDA Dietary Guidelines is that limiting saturated fat intake--even if it does little or nothing to extend the lives of healthy individuals and even if not all saturated fats are equally bad--might still delay tens of thousands of deaths each year throughout the entire country. Limiting total fat consumption is considered reasonable advice because it's simple and easy to understand, and it may limit calorie intake. Whether it's scientifically justifiable may simply not be relevant. "When you don't have any real good answers in this business," says Krauss, "you have to accept a few not so good ones as the next best thing."

SIDEBAR 1 - What If Americans Ate Less Saturated Fat?

Eat less saturated fat, live longer. For 30 years, this has stood as one cornerstone of nutritional advice given to Americans (see main text). But how much longer? Between 1987 and 1992, three independent research groups used computer models to work out the answer. All three analyses agreed, but their conclusions have been buried in the literature, rarely if ever cited.

All three models estimated how much longer people might expect to live, on average, if only 10% of their calories came from saturated fat as recommended. In the process their total fat intake would drop to the recommended 30% of calories. All three models assumed that LDL cholesterol--the "bad cholesterol"--levels would drop accordingly and that this diet would have no adverse effects, although that was optimistic at the time and has become considerably more so since then. All three combined national vital statistics data with cholesterol risk factor data from the Framingham Heart Study.

The first study came out of Harvard Medical School and was published in the Annals of Internal Medicine in April 1987. Led by William Taylor, it concluded that individuals with a high risk of heart disease--smokers, for instance, with high blood pressure--could expect to gain, on average, one extra year by shunning saturated fat. Healthy nonsmokers, however, might add 3 days to 3 months. "Although there are undoubtedly persons who would choose to participate in a lifelong regimen of dietary change to achieve results of this magnitude, we suspect that some might not," wrote Taylor and his colleagues.

The following year, the U.S. Surgeon General's Office funded a study at the University of California, San Francisco, with the expectation that its results would counterbalance those of the Harvard analysis. Led by epidemiologist Warren Browner, this study concluded that cutting fat consumption in America would delay 42,000 deaths each year, but the net increase in life expectancy would average out to only 3 to 4 months. The key word was "delay," for death, like diet, is a trade-off: Everyone has to die of something. "Deaths are not prevented, they are merely delayed," Browner later wrote. "The 'saved' people mainly die of the same things everyone else dies of; they do so a little later in life." To be precise, a woman who might otherwise die at 65 could expect to live two extra weeks after a lifetime of avoiding saturated fat. If she lived to be 90, she could expect 10 additional weeks. The third study, from researchers at McGill University in Montreal, came to virtually identical conclusions.

Browner reported his results to the Surgeon General's Office, then submitted a paper to The Journal of the American Medical Association (JAMA). Meanwhile, the Surgeon General's Office--his source of funding--contacted JAMA and tried to prevent publication, claiming that the analysis was deeply flawed. JAMA reviewers disagreed and published his article, entitled "What If Americans Ate Less Fat?" in June 1991. As for Browner, he was left protecting his work from his own funding agents. "Shooting the messenger," he wrote to the Surgeon General's Office, "or creating a smoke screen--does not change those estimates."

SIDEBAR 2 - The Epidemic That Wasn't?

For half a century, nutritionists have pointed to soaring death rates as the genesis of their research into dietary fat and heart disease and as reason to advise Americans to eat less fat (see main text). "We had an epidemic of heart disease after World War II," obesity expert Jules Hirsch of Rockefeller University in New York City said just 3 months ago in The New York Times. "The rates were growing higher and higher, and people became suddenly aware of that, and that diet was a factor."

To proponents of the antifat message, this heart disease epidemic has always been an indisputable reality. Yet, to the statisticians at the mortality branch of the National Center for Health Statistics (NCHS), the source of all the relevant statistics, the epidemic was illusory. In their view, heart disease deaths have been steadily declining since the late 1940s.

According to Harry Rosenberg, director of the NCHS mortality branch since 1977, the key factor in the apparent epidemic, paradoxically, was a healthier American population. By the 1950s, premature deaths from infectious diseases and nutritional deficiencies had been all but eliminated, which left more Americans living long enough to die of chronic diseases such as heart disease. In other words, the actual risk of dying from a heart attack at any particular age remained unchanged: Rather, the rising number of 50-year-olds dropping dead of heart attacks was primarily due to the rising number of 50-year-olds.

The secondary factor was an increase from 1948 to 1968 in the probability that a death would be classified on a death certificate as arteriosclerotic disease or coronary heart disease. This increase, however, was a figment of new diagnostic technologies--the wider use of electrocardiograms, for instance—and the changing terminology of death certificates. In 1949, the International Classification of Diseases (ICD) added a new category, "arteriosclerotic heart disease," under the more general rubric "diseases of the heart." The result, as a 1958 report to the American Heart Association noted, was dramatic: "In one year, 1948 to 1949, the effect of this revision was to raise coronary disease death rates by about 20% for white males and about 35% for white females." In 1965, the ICD added a category for coronary heart disease, which added yet more deaths and capped off the apparent epidemic.

To Rosenberg and others at NCHS, the most likely explanation for the postwar upsurge in coronary heart disease deaths is that physicians slowly caught on to the new terminology and changed the wording on death certificates. "There is absolutely no evidence that there was an epidemic," says Rosenberg.

NOTE: A .pdf version of The Soft Science of Dietary Fat is also available.
The reproduction of this article is intended for non-commercial, educational purposes only.

Source: NASW

Gary Taubes is a correspondent for the journal Science and author of ''Bad Science: The Short Life and Weird Times of Cold Fusion.''