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

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.
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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.''