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 conclusio