Reason Magazine - Contributors

Big Fat Fake

react@reason.com (Michael Fumento) — Sat, 01 Mar 2003 00:00:00 EST

It was exactly what millions of obese Americans wanted to hear: Diet guru Robert Atkins has been right all along; conversely, the "medical establishment" that has routinely criticized him has been entirely wrong. Unlimited-calorie, high-fat meals are the key to low-fat bodies. So claimed award-winning science writer Gary Taubes in an 8,000-word New York Times Magazine blockbuster that appeared last July, "What If It's All Been a Big Fat Lie?"

The magazine's cover was even juicier than the title: It featured a slab of steak topped with butter and asked, "What If Fat Doesn't Make You Fat?" In fact, Taubes declared in his article, the consumption of too little fat could explain the explosion in obesity.

Atkins quickly wrote an editorial for his Web site claiming the article "validated" his work. Gushingly favorable follow-up stories appeared on NBC's Dateline, CBS' 48 Hours, and ABC's 20/20. Dr. Atkins' New Diet Revolution, with 11 million copies already in print, shot up from No. 5 to the top spot on the New York Times paperback bestseller list for "Advice, How-To, and Miscellaneous" books. It went from No. 178 to No. 5 in Amazon's rankings. Taubes himself landed a book contract from publisher Alfred A. Knopf for a big fat $700,000.

But there were serious problems with this revolutionary argument about one of our nation's most serious health problems. For example, Taubes omitted any reference to hundreds of refereed scientific studies published during the last three decades that contradicted his position. Researchers from whom he could not pull even a single useful quote supportive of his thesis were banished from the piece, while many of those whom Taubes did end up quoting now complain that he twisted their words.

"I was greatly offended by how Gary Taubes tricked us all into coming across as supporters of the Atkins diet," says one such source, Stanford University cardiologist John Farquhar. "I think he's a dangerous man. I'm sorry I ever talked to him."

Upon closer examination, Taubes' "What If It's All Been a Big Fat Lie?" turns into a big fat mess. The misguided hoopla over the New York Times Magazine article and the Atkins Diet is a short study in the sorry state of scientific and medical reporting, not to mention a diet industry that routinely panders to people's worst impulses.

The Fat Shall Set Ye Free?

In Dr. Atkins' New Diet Revolution, Robert Atkins claims that by simply minimizing your carbohydrate intake you can quickly lose massive amounts of weight, even while pigging out daily on fatback, pork rinds, and lard. He also claims his diet will relieve "fatigue, irritability, depression, trouble concentrating, headaches, insomnia, dizziness, joint and muscle aches, heartburn, colitis, premenstrual syndrome, and water retention and bloating."

Claims like those should make anyone suspicious, even those who have barely scraped through high school biology. Gary Taubes has gone well beyond that level. He's a contributing correspondent to America's preeminent scientific journal, Science. He has won the National Association of Science Writers' Science in Society Journalism Award three times -- the maximum allowed. Only one other writer has ever achieved that status.

Nonetheless, at the very outset of his piece (viewable in its entirety at www.atkinsdiet.com) Taubes set forth the proposition that Atkins was crucified by the "American medical establishment," which claimed his diet was ineffective and possibly dangerous and in so doing encouraged the "rampaging epidemic of obesity in America."

There is a nugget of truth in Taubes' criticisms of establishment dietary fat advice. Well-meaning but misguided health officials and health reporters, joined by opportunistic anti-fat diet book gurus, have convinced much of the public that the major culprit -- perhaps the only culprit -- in obesity is dietary fat. Avoid fat, we were told, and you won't get fat. Given license to eat as many calories as we wanted from the other nutrient groups, many of us have done exactly that. This goes far to explain why almost one-third of us are obese and almost two-thirds of us are overweight. But even here Taubes is no pioneer; the damage caused by fat-free fanaticism was pointed out long before. (See, for example, my own 1997 book, The Fat of the Land.)

Moreover, the Atkins-Taubes thesis of "fat won't make you fat" encourages obesity in a similar way: It offers carte blanche for consuming limitless calories, only this time swapping carbohydrates for fat. Taubes made that swap while presenting a far less scientific case than is presented in an Atkins infomercial.

Ask Stanford endocrinologist Gerald Reaven. He's best known for calling attention to "Syndrome X," a cluster of conditions that may indicate a predisposition to diabetes, hypertension, and heart disease. Among Reaven's recommendations for lowering the risk of that syndrome is to reduce consumption of highly refined carbohydrates such as those present in soft drinks and table sugar. But that's where the overlap with Atkins ends.

"I thought [Taubes'] article was outrageous," Reaven says. "I saw my name in it and all that was quoted to me was not wrong. But in the context it looked like I was buying the rest of that crap." He adds, "I tried to be helpful and a good citizen, and I ended up being embarrassed as hell. He sort of set me up." When I first contacted Reaven, he was so angry he wouldn't even let me interview him.

But his position on Atkins was all over the Internet in interviews posted long before Taubes talked to him. Do "low-carb diets like The Zone [by Barry Sears] and Atkins work?" one asked. Answer: "One can lose weight on a low-calorie diet if it is primarily composed of fat calories or carbohydrate calories or protein calories. It makes no difference!"

The very person with whom Taubes chose to end his article, Stanford's John Farquhar, was as livid as Reaven. Taubes said that Farquhar had sent Taubes "an e-mail message asking the not-entirely-rhetorical question, 'Can we get the low-fat proponents to apologize?'" On this powerful note, the article ended.

But it's Taubes whom Farquhar wants to apologize. "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."

Diets and Data

Taubes proved as adept at clipping data as at clipping quotes. Thus he claimed that one of the "reasons to suggest that the low-fat-is-good-health hypothesis has now effectively failed the test of time" is "that the percentage of fat in the American diet has been decreasing for two decades." (Emphasis added.)

That's true, 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. "We're eating just too darned much of everything," says Farquhar.

Taubes also shoved aside decades of published, controlled, randomized clinical trials comparing nutrient intake and weight loss. His apparent justification in the article was that the "research literature [is] so vast that it's possible to find at least some published research to support virtually any theory." But that's sheer nihilism. Good science is cautious and skeptical, not permanently open-ended. That's why terms like weight of the evidence are used. And the evidence against Atkins-like low-carbohydrate diets is crushing.

In April 2002, for example, the Journal of the American Dietetic Association (JADA) published a review of "all studies identified" that looked at diet nutrient composition and weight loss. It found over 200, with "no studies of the health and nutrition effects of popular diets in the published literature" excluded. In some, subjects were put on "ad libitum" diets, meaning they were allowed to eat as much as they wanted as long as they consumed fat, protein, and carbohydrates in the directed proportions. In others, subjects were put on controlled-calorie diets that also had directed nutrient proportions. The conclusion: Those who ate the least fat carried the least fat.

An alternative method of comparing diets is a meta-analysis, which means not looking at the sum of the whole but actually combining the data. One such meta-analysis, covering 16 ad libitum studies and almost 2,000 people, appeared in the International Journal of Obesity and Related Metabolic Disorders in December 2000. The conclusion: Those on low-fat diets had "a greater reduction in energy intake" and a "greater weight loss than control groups."

"Aren't all these studies highly relevant to the issue of whether an Atkins-like diet works, and don't they indicate that it does not?" I ask Dr. Louis Aronne, director of the Comprehensive Weight Control Program at New York's Weill Cornell Medical Center. "I agree completely," he says. "You're absolutely right."

This wasn't the first time Taubes had published a lengthy article on fat while leaving out this vital information. He also did so in one of his award-winning pieces, a precursor to the "Big Fat Lie" article called "The Soft Science of Dietary Fat" that appeared in Science in March 2001. In a subsequent letter to the journal, three obesity research co-authors, including James Hill, director of the University of Colorado Center for Human Nutrition in Denver, noted, "What Taubes does not mention are the meta-analyses of intervention studies comparing ad libitum intakes of higher fat diets with low-fat diets that clearly show reduced caloric intake and weight loss on the low-fat diet." Taubes responded to the letter but again refused to address these studies.

Why? "They're not worth mentioning," he told me in a telephone interview. They weren't done correctly. None of them? None. The one meta-analysis Taubes thinks was properly conducted appeared in 2002 in The Cochrane Library. Yet it, too, found no advantage to low-carbohydrate diets, merely that "fat-restricted diets are no better than calorie restricted" ones.

Where, I ask Taubes, did all these researchers go wrong? The problem is inherent to an intervention study, he says. "When you counsel people you change their behavior." But doesn't that apply to all the groups in a study? Yes, he grants. "But the idea is to make the intervention effect equal for everyone, whichever diet they happen to be on," he says. "If the interventions aren't the same, then you just don't know how to interpret the results." That may be true, but it's also irrelevant. There's no reason to think persons on either low-fat or high-fat diets got more or less intervention in these myriad studies. Indeed, in some of them virtually all the intervention emphasis was on exercise, with little nutrition counseling one way or the other.

Finally, the comprehensive JADA review published last April also looked at persons who weren't in intervention studies at all but rather were part of the U.S. Department of Agriculture's Continuing Survey of Food Intake by Individuals. An updated report on the survey appeared last June in the Journal of the American College of Nutrition. Both survey reports came to the same conclusion as the intervention studies.

Dr. Aronne is quick to point out that this wealth of data supporting lower-fat diets "is not an endorsement for eating unlimited amounts of nonfat muffins and soda simply because they're fat-free." All carbohydrate sources are not equal. For example, fiber appears to play a powerful role in weight control, but there is no more fiber in a soda than there is in a steak. That said, a high-fat diet does carry an inherent metabolic disadvantage in that fat has nine calories per gram, while carbohydrates and protein each have four.

Abstract Weight Loss

Having circumvented this mass of peer-reviewed literature readily open to public scrutiny in libraries and often online, Taubes instead tried to make his case with a mere five studies. All five were (and are) available only in abstract form. That is, they are summaries of about 300 words each that have been presented at various obesity conferences. "The results of all five of these studies are remarkably consistent," Taubes averred. "Subjects on some form of the Atkins diet...lost twice the weight as the subjects on the low-fat, low-calorie diets."

One of the five studies, conducted at the Durham Veterans Administration Medical Center in North Carolina, was funded by the Atkins Center. Those researchers repeatedly have publicized their interpretation of their findings and unsurprisingly have conferred their full blessings on the diet.

They did so most recently in late November, garnering tremendous favorable media attention. (See "Hold the Lard" at www.reason.com/hod/mf120502.shtml.) The authors of the other four studies, however, have been reticent about releasing their data, in part because pre-publicity in the lay press makes it more difficult to get published in medical journals. But when I interviewed researchers for two of the other studies, they all insisted Taubes grossly mischaracterized their findings.

"The Atkins diet produces weight loss, as does the grapefruit diet, the rotation diet, and every other fad diet out there," says one of the researchers, Colorado's James Hill. "I haven't seen any data anywhere saying Atkins is better than these other diets for weight loss. Taubes is trying to fly in the face of the scientific evidence." Referring to the book deal, he says, "Taubes sold out."

Hill's co-researcher, Gary Foster of the University of Pennsylvania, says "the probable explanation for the greater weight loss in the groups on the Atkins regimen" is that it "gives people a framework to eat fewer calories, since most of the choices in this culture are carbohydrate driven....You're left eating a lot of fat, and you get tired of that. Over time people eat fewer calories." That would make the Atkins plan nothing more than a low-calorie diet in disguise.

Another of the abstracts came from the University of Cincinnati. The Atkins-like group "did have twice as much weight loss, and to completely lose that point would be unfair," says one of the co-authors, Randy Seeley of the university's Obesity Research Center. But his explanation is similar to Foster's, if more colorful. "If you're only allowed to shop in two aisles of the grocery store, does it matter which two they are?" he asks.

All the researchers I interviewed also insisted the studies weren't long enough to be conclusive, with none lasting more than a year. And the kicker is that all five were intervention studies, conducted using the same methodology that Taubes cites to dismiss the mountain of published material that undercuts his position.

Seeley and co-researcher David D'Alessio were also upset that Taubes made use of their material at all and not just because it hurt their chances of publication. "One of the things I object to most in the Taubes article is the idea that we're going to carry out this scientific debate in the lay press with data that's unavailable for scientists to review," says Seeley. "I believe in the peer-review process." Indeed, one "danger of trying to conduct this out in the lay press," he says, is that "you have a guy like Taubes going through it and just picking up the pieces that support his opinion."

3,000 MIAs

Taubes also ignored the approximately 3,000 members of a database called the National Weight Control Registry. For 10 years, the registry has tracked people who have lost at least 30 pounds and kept it off for at least a year. The average member has maintained a loss of about 60 pounds for about five years.

Co-administered by Hill in Denver and Rena Wing of the University of Pittsburgh, the registry is aimed at finding out what works and what doesn't. According to its members, what doesn't work is a high-fat diet. On average, they consume only 23 percent of calories from fat. "Almost nobody's on a low-carbohydrate diet," Hill says. Another important lesson that may be drawn from the registry is that the importance of any type of diet in weight control may be overemphasized. Ninety-one percent of the subjects said they regularly exercised.

While relying on self-interpretation of unpublished abstracts is valid methodology to Taubes, he insists the registry is so unscientific as to be worthless. One problem, he told me, is that it represents only a tiny fraction of all those who have succeeded at weight loss. Further, the sample is entirely self-selected rather than randomized. "Its method of recruiting could bias the selection toward those who use low-fat diets," he says.

Yet the registry data have been considered valid and important enough to have been written up in such peer-reviewed medical publications as the American Journal of Clinical Nutrition, the Journal of the American Dietetic Association, the International Journal of Obesity, Health Psychology, and Obesity Research.

"You can't get around" the problem of self-selection, says Suzanne Phelan, a co-investigator of the registry at Brown University Medical School. "But why would non-Atkins people select in and Atkins ones stay out?" Atkins dieters, she notes, "seem to be very dedicated." (Other researchers have described them as having an almost religious fervor.) Originally, recruits were selected "based on a random-digit dialing procedure," she says. But that proved onerous, and "as media such as USA Today and CNN began talking about the registry, we just let them take over" the recruiting process. "There's no reason to think that people who see those media are more likely to have a certain diet," Phelan says.

Oh, and there's another place where joining the registry has been promoted: the Atkins Web site. So we're left wondering why successful low-fat eaters would be especially likely to select into the registry or why the purchasers of over 11 million Atkins diet books consistently opt out.

Feeling Full

For all its 8,000 words, there were few actual data in the Taubes piece. It was rather like reading a treatise explaining how the Chicago Cubs may well be the best team in baseball history without being informed they haven't won a pennant since 1945. Instead readers were regaled with explanations of physiological mechanisms -- the basis for which, Taubes wrote, is "Endocrinology 101" -- that might explain how dieters shed pounds and inches. Endocrinology 101 is a term popularized by Dr. David Ludwig, who runs the pediatric obesity clinic at Children's Hospital Boston.

According to Taubes, Endocrinology 101 "requires an understanding of how carbohydrates affect insulin and blood sugar and in turn fat metabolism and appetite." In brief, it says there are aspects of a high- or low-carbohydrate diet that affect both how much we want to eat (referred to as "satiety") and how efficiently the body converts the various nutrients into body fat. And the theory says an Atkins-like diet is both more satiating and less efficient in converting calories to fat.

Yet the published literature that Taubes ignored says otherwise. The aforementioned review of over 200 studies in the Journal of the American Dietetic Association expressly nixed the idea that any type of food converts less efficiently to body fat. "None of the popular diet research we reviewed suggests a metabolic advantage with respect to weight loss," it declared.

Nor can Taubes fall back on his five studies, according to Seeley.

"Ultimately our data do not support any of the mechanisms" for why a low-carbohydrate diet might be especially effective in inducing weight loss "that Atkins and proponents of the diet have [suggested]," he told me. Indeed, each explanation that Taubes presents for how an Atkins diet might cause weight loss collapses under the weight of the published research he ignores.

Consider the matter of satiety. How, Taubes wondered, could a low-calorie regimen "suppress hunger, which Atkins insisted was the signature characteristic of the diet." One possibility, he said, was, yes, "Endocrinology 101: that fat and protein make you sated and, lacking carbohydrates and the ensuing swings of blood sugar and insulin, you stay sated."

But is there any empirical support for this? No, according to an April 2002 review of studies in the Journal of the American College of Nutrition that summarized "high and low fat treatments when subjects were allowed to eat ad libitum." It found "energy intake on the low-fat diets ranged from 16 percent to 24 percent less than those on high fat diets."

"We've done masses of studies on fat and satiety," says Barbara Rolls, professor of nutrition at Pennsylvania State University, where she has authored four books and written about 60 medical journal articles on human food intake. She's widely considered the nation's top authority on satiety. Some of her experiments involved ingestion; in others, "We directly infused pure fat and pure carbohydrates both directly into [human] veins and directly into stomachs." Says Rolls, "We found very little difference between fats and carbohydrates."

Rolls does say there is some evidence that high-protein diets may be more satiating, but Atkins isn't really high protein; it's just high fat. According to an analysis in the journal Circulation, Atkins starts off at 36 percent protein from calories and declines to 24 percent in the "maintenance" stage.

What really counts when it comes to satisfying hunger, Rolls says, is "foods that give big portions without a lot of calories. We call these low-energy-density foods." She adds, "The Atkins diet would not be a good way to reduce energy density at all, especially with the restrictions on fruits and vegetables that are really the keys to a low-energy diet." Further, because fat contains more than twice the energy per ounce as either carbohydrates or protein, "high-fat foods are so energy-dense that it's really easy to eat excessive portions."

Rolls says she sent a big pile of her material on satiety to Taubes, but he "just brushed it aside." She says he also interviewed her for over six hours, but every last sentence disappeared into a black hole. Likewise for the interviews Taubes conducted with James Hill and at least five other top obesity researchers from whom he apparently couldn't extract even a single useful line: Dr. F. Xavier Pi-Sunyer of St. Luke's-Roosevelt Hospital in New York; Marion Nestle, chairwoman of the Department of Nutrition and Food Studies at New York University; Dr. Arne Astrup of Denmark; and Dr. Jules Hirsch, whom Taubes interviewed in his office at Rockefeller University in New York. "I just kept telling him, it doesn't matter what kind of calories you eat," says Hirsch.

Taubes is "very selective in what he chooses to include because he's trying to sell a specific line," Rolls says. "He is a good writer; that's the thing that scares me. This is such a good example of how you can pick and choose your facts to present the story you want. But that's not how science should be done. You can't interview everybody and simply ignore the people you don't want to hear." She means that rhetorically, of course.

Gorging on Theory

Stacking theory atop theory, Taubes roared on. Something called "hyperinsulinemia" could also favor the Atkins dieter, he insisted. When carbohydrates are ingested they are broken down in the intestine into glucose and other sugars. Glucose then stimulates cells in the pancreas to secrete insulin to remove that glucose and take it into tissues to be used as fuel or stored. Protein and fat consumption don't have nearly the same impact on insulin production because the whole point of insulin is to maintain the stability of the sugar level.

The Atkins hyperinsulinemia theory, ex-plained Taubes, is that carbohydrates can "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." The brain receives a signal that the body needs more food, and the vicious circle repeats itself. Carbohydrates at the top of what's called the "hypoglycemic index" are the most evil of the evil, since they cause blood sugar to rise the fastest. The index ranks potatoes as slightly worse than jelly beans.

For support, Taubes once again fell back on "Endocrinology 101." David Ludwig "notes that when diabetics get too much insulin, their blood sugar drops and they get ravenously hungry," wrote Taubes. "They gain weight because they eat more, and the insulin promotes fat deposition." But according to Seeley, this applies to diabetics injecting massive amounts of insulin into the bloodstream, not to carbohydrate consumers.

"Yes," Seeley says, "if you give people a big wallop of insulin they do eat a lot, but do people under normal circumstances ever get close to that by eating? No. Is it possible that some people are that reactive? Yes. Is it likely that lots of people fall into that category? No."

Taubes presented University of Washington endocrinologist Michael Schwartz, whom he had interviewed, as a proponent of the idea that blood insulin levels as altered by carbohydrates could be a significant contributor to weight gain. But a commentary in the same magazine Taubes writes for, Science, sharply contradicted that position. "Although the concept that insulin triggers weight gain has little scientific merit, it remains a key selling point for advocates of diets that are low in carbohydrate and high in protein and fat," it read. "If hyperinsulinemia has adverse consequences, obesity does not appear to be among them," it concluded. Who wrote that? Michael Schwartz.

Indeed, Schwartz was also the primary author of a study concluding that obese people whose systems secrete insulin at high levels may be protected against further weight gain. "Relatively reduced insulin secretion," he concluded, "is a significant and independent predictor of the tendency to gain weight and adiposity in Pima Indians."

The Pima in Arizona have been the focus of a tremendous amount of research because even by American standards they are incredibly obese and suffer horrific rates of diabetes and heart disease. Comparisons of the Arizona Pima with genetically similar Pima in Mexico find that the Arizonans eat about twice as much fat (although the Mexicans also do far more manual labor) and are almost 60 pounds heavier on average. A National Institutes of Health evaluation of the traditional Pima diet (that is, back when they were thin and healthy) found that it was extremely high in carbohydrates, from 70 percent to 80 percent.

Schwartz says it's not that he believes insulin can't play a role in promoting weight gain, but he rejects "Endocrinology 101" based on what he calls "Scientific Methodology 101." "Before you draw conclusions you need data," he says. "There is no compelling evidence that in normal individuals day-to-day fluctuations of the blood glucose level are an important determinant of how much food is consumed."

The Diet Revolution That Isn't

Two distinct controversies have always swirled around the Atkins diet. First, is it effective for long-term weight loss? Second, could those using it be harming themselves by raising their blood lipids (cholesterol and trigylcerides)? The five unpublished abstracts do seem to indicate that for people who manage to stick to a high-fat Atkins diet, it may not be as harmful as was once generally believed. But this finding is quite preliminary and in any case certainly must depend greatly on which types of fat are consumed.

This is a distinction Taubes decided to lose.

Thus he quoted or invoked the name of the chairman of the Department of Nutrition at the Harvard School of Public Health, Walter Willett, seven times during his piece. Willett protests, however, that "I told Taubes several times that red meat is associated with higher risk of colon and possibly prostate cancer, but he left that out." And don't forget the illustration on the cover of The New York Times Magazine; that wasn't a flounder with heart-healthy flaxseed oil sitting on top of it.

Taubes also told readers that a metabolic process called ketosis, often invoked to show the Atkins diet could be dangerous, was quite harmless, providing reassuring words from National Institutes of Health researcher Richard Veech that "ketosis is a normal physiologic state." Veech told me by e-mail that the quote was correct, but that Taubes "omitted to say that I strongly urged people to not use the Atkins diet without the supervision of a physician because of the likely elevation of blood cholesterol and lipid on a high fat diet." But you don't have an impact if you insist that a fad diet be supervised by a doctor.

There's nothing "revolutionary" about the Atkins diet. A similar diet appeared in an 1863 booklet by a British undertaker named William Banting, who got the idea from a surgeon. It has popped up in various guises ever since, including a 1946 book extolling the virtues of eating whale blubber, and a 1958 book, Eat Fat and Grow Slim, written by a psychiatrist.

Likewise, there has long been convincing evidence that the diet fails to live up to its claims. Taubes wrote that "when the American Medical Association (AMA) released its scathing critique of Atkins' diet in March 1973, it acknowledged that the diet probably worked but expressed little interest in why."

The heavily endnoted document, which appeared in the June 4, 1973, issue of The Journal of the American Medical Association but unfortunately is not available on the Internet even in abstract form, was indeed scathing. But the rest of Taubes' description is false.

"The notion that sedentary persons, without malabsorption or hyperthyroidism, can lose weight on a diet containing 5,000 calories a day is incredible," the article says. Statements such as "No scientific evidence exists to suggest that the low-carbohydrate ketogenic diet has a metabolic advantage over more conventional diets for weight reduction," and "there is no reason to associate a diet rich in carbohydrate with obesity" hardly seem to acknowledge "that the diet probably worked."

Other terms the AMA used to described Atkins' theories included "naïve," "biochemically incorrect," "inaccurate," and "without scientific merit."

It also explained why the diet didn't work, mocking Atkins' basic thesis that fat and protein cannot cause weight gain in the absence of carbohydrate consumption as a "thermodynamic miracle."

Three additional decades of research have merely played "pile on" with the AMA's findings. The explanation for weight loss on Atkins given by Foster and Seeley was right there. "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 diet," said the AMA.

Girth of a Nation

What has changed drastically in the last three decades is the girth of a nation. American obesity is increasing at a terrifying rate.

Since the publication of Taubes' article, numerous doctors, scientists, and health writers have picked apart various pieces of his argument. A fatlash has formed against Taubes, The New York Times Magazine, and Knopf. Originally riding an adulatory wave, Taubes complained bitterly to the weekly New York Observer in November that he was "being attacked by sleazebags."

The New York Times Magazine has printed no clarification or retraction of any kind. Yet not only should the magazine's editors have known there were serious problems with the piece, but Farquhar says he told them so outright, based on what he had gleaned from two fact checkers. He says he told those checkers that if Taubes "tries to make it look like I'm saying that I was supporting the idea that the obesity epidemic was from overloading on carbohydrates that this was so far off the mark that I would have to vomit."

At Knopf, Taubes' acquisitions editor, Scott Segal, has wrapped himself in the flag, telling the Observer, "It's a free country: First Amendment," as if he believes the Constitution requires publishers to hand out $700,000 checks to all authors. Equally bizarre is his effort to distance the book acquisition from the article. They "chose to put a certain picture on the cover and to use a certain approach to the subject in 5,000 [sic] words, but that's not the book," he said. Critics "are reacting to a magazine piece I had nothing to do with." Yet Taubes told me that his article had barely hit the stands when Knopf's offer dropped in his lap, as did an even larger offer from another publisher that he says he rejected because it's the publisher of Atkins' book and it might hurt his credibility.

But obesity and the millions of individual tragedies it has produced are ultimately far more important than this skirmish over a single story. Louis Aronne says, "I think people are getting increasingly confused about what to do. I'm afraid they'll just give up." Randy Seeley says journalism like Taubes' "just makes people confused and frustrated."

Taubes "gave his readers what they wanted to hear," says James Hill. "But what people want to hear is killing them."

Gary Taubes responds to Michael Fumento.

Hold the Lard!

react@reason.com (Michael Fumento) — Thu, 05 Dec 2002 00:00:00 EST

Issue settled. The Atkins Diet—the famous high-fat, low-carb regime that lets dieters load up on pork rinds and Scrapple as long as they avoid potatoes and Wheaties—works. The American Heart Association has been wrong all along, as has essentially the entirely American medical establishment. Not only is gorging on fat the key to becoming thin, it's heart-healthy to boot. So say the headlines:

• "High Fat, Low Carb Diet May Finally Be Getting Its Due" (CNN)
• "Fats Win Latest Round in Diet War" (Chicago Tribune)
• "Low-carb Atkins Diet Beats Low-Fat American Heart Association Plan in Head-To-Head Comparison" (CNBC)
• "High-Fat Diet Shows Promise in Study" (AP)
• "Doctors Eat Crow on Banning Celebrity Diet" (The Australian)

The public responded predictably to the pro-Atkins results of an Atkins-funded study last month. Sales of Dr. Robert Atkins' diet book skyrocketed over 900 percent on Amazon.com the day the news broke. Dr. Atkins' New Diet Revolution has now sold over 10 million copies; according to one Atkins stooge, more than 20 million people have signed on for the diet. Celebrities ranging from callipygian lovelies Jennifer Lopez and Minnie Driver to formerly porky Spice Girl Geri Halliwell to one-man body mass rollercoaster Matthew Perry have reportedly taken the Atkins plan straight to the scales.

And they've all been sold one greasy fat bill of goods.

There are two issues here. One is the effect of the Atkins diet on weight loss. The other is its effect on cholesterol and triglycerides, a group of fatty compounds that circulate in the bloodstream and are stored in the fat tissue.

In the study in question, Dr. Eric Westman of the Duke University Medical Center looked at both. He followed two groups of 60 dieters each, one on a high carbohydrate diet and one on the high-fat, low-carbohydrate Atkins diet. He reported that the Atkins group lost twice as much weight during the six-month study period as did the high-carb group. But this is both unsurprising and meaningless.

Gary Foster of the University of Pennsylvania co-authored a study conducted in virtually the same manner as Westman's. Foster, whose work will soon appear in a major medical journal, provides a simple explanation for the Atkins weight loss. The regimen "gives people a framework to eat fewer calories, since most of the choices in this culture are carbohydrate driven," he says. "Over time people eat fewer calories."

Randy Seeley of the University of Cincinnati co-authored yet another "sister study" with similar results. His explanation is the same as Foster's. Ultimately, Atkins is nothing more than a low-calorie diet in disguise.

In any event, the main issue with any diet—be it Atkins, popcorn, or jelly bean—isn't whether people can lose weight in the short-term but rather whether they can stick to the regimen and keep the pounds off not for just half a year but essentially forever. Yet completely lost in the media mania was that among the 60 Atkins dieters in the Westman group analyzed for blood lipids, the dropout rate was 43 percent.

Thus almost half the Atkins cohort couldn't stay with the steak and bacon routine for even six months. By comparison, only 25 percent of the high-carb eaters dropped out.

Moreover, it's generally accepted that drop-out rates anywhere near this level completely invalidate a study because you don't know how all those drop-outs would have affected the result. Maybe those Atkins dieters were quitting not only because of carbohydrate cravings but also because they weren't losing weight or losing it fast enough to satisfy them.

Why would Westman's interpretation be so different from those of Foster and Seeley? It may help to know not only that this particular study was paid for by the Atkins Center, but that it's part of a long-term funding arrangement.

Analyses such as one published in the New England Journal of Medicine (NEJM) in May 2000 have shown that funding sources do in fact influence study results and the interpretations (or "spin" if you will) of those results. "When the boundaries between industry and academic medicine become as blurred as they are now, the business goals of industry influence the mission of medical schools in multiple ways," declared an accompanying NEJM editorial.

Westman's interpretation, based on his handful of subjects observed over a mere six months, also directly contradicts three decades of randomized controlled studies published in peer-reviewed journals. A review of over 200 of these published last year in a major medical journal concluded bluntly: "The BMIs [a surrogate measure of weight] were significantly lower for men and women on the high carbohydrate diet; the highest BMIs were noted for those on a low carbohydrate diet."

But what about the blood findings? Wasn't it a real shocker that Atkins dieters consuming heavy amounts of fat saw their HDL ("good cholesterol") levels increase by 11 percent while harmful triglycerides fell 49 percent? (LDL or "bad cholesterol" levels remained the same.)

No.

"Often just losing weight alone will cause improvement in triglyceride and cholesterol levels," the president of the American Heart Association Dr. Robert Bonow told me. Since the Atkins dieters did lose more weight than those on the high-carb diet, it only stands to reason that by comparison their blood levels would also improve more.

Says Seeley, Westman's "weight loss data look just like ours and my argument is that the weight loss accounts for the beneficial effects."

Westman told me that he doesn't believe this to be the case, because another study, in the July 2002 Journal of Nutrition, claims to have found a similar improvement on an Atkins-type diet regardless of weight loss. But the same researchers, using the same group of dieters, published another study at the same time reporting that the Atkins dieters lost an average of 7.5 pounds over a six-week period. So again, blood fat levels merely fell with body fat levels.

Ultimately this fat-fest over a single study shows nothing more than the media's amazing ability to pick out and flaunt a will o' the wisp—even to the point that one American network repeatedly used on-the-air interviews from a representative of the Atkins Institute to interpret a study paid for by the Atkins Institute!

Why? Our increasingly obese population is desperate for some magical formula to avoid the physiological law that body fat is determined by calories in and calories out. The media tried to fill the need, but ultimately failed the public. "It just makes people confused and frustrated," an exasperated Seeley said. Yes, and fatter by the day.

Bumps in the Night

react@reason.com (Michael Fumento) — Wed, 23 Jan 2002 00:00:00 EST

In the movie One-Eyed Jacks, Marlon Brando asks Marshall Karl Malden if he'll get a fair trial. "Oh sure, kid, sure," answers Malden, soothingly. "You're gonna get a fair trial. And then I'm gonna hang you! Personally!"

That pretty much sums up how everybody--but the patients themselves--have treated Roche Laboratories' acne drug Accutane.

Recently the capsules were back in the news after a 15-year-old St. Petersburg, Florida boy named Charles Bishop stole a light plane and flew it into the 28th floor of a 42-story Tampa building. A sample of the media coverage:

* CNN Live Today: "Tampa Authorities Say They Found Acne Drug Accutane at Home of Teen Pilot Charles Bishop"

* ABC's Good Morning America: "Charles Bishop May Have Used Accutane before Crash"

* United Press International: "Teen Pilot Had Accutane Prescription"

* Newsday: "Pilot's Acne Drug Linked to Suicides"

* And this one says it all, from London's "The Mirror: Plane Boy Drugs Link "

More bizarre yet: Police found a note on Bishop's body expressing sympathy for Osama bin Laden and support for the September 11 attacks.

Clearly something was troubling this young man, but it wasn't Accutane. As only a handful of media outlets bothered to report a week later, an autopsy showed no trace of the drug in the boy's system.

Nonetheless, the story will add to the undeservedly bad reputation of a drug used by 5 million Americans and 7 million others worldwide since 1982 to combat one of the most disfiguring forms of acne, the "severe recalcitrant nodular" variety. Yet there's no evidence linking the drug to so much as a single suicide (much less support for international terrorism) unless you count non-causal associations, rumor, innuendo, and the efforts of lawyers and politicians.

Three things quickly sent Accutane down the road to infamy, despite clear evidence of its tremendous benefits to users. The first is that it was known from the beginning that Accutane is a powerful teratogen, meaning it causes birth defects. It's been labeled as such since its introduction, and Roche has worked aggressively (albeit not completely successfully) to prevent any woman who might possibly be pregnant or become so soon from getting a prescription.

Medically, teratogenicity has nothing to do with depression or thoughts of suicide. But this gave the drug immediate notoriety. From its launch, doctors were keeping a sharp eye out for any other possible serious side effect and reporting those possible connections to the FDA under its adverse event reporting system (AERS).

"When there's public awareness or publicity about a drug for any reason, there may be an increase in reports because people may not have otherwise thought about associations," points out FDA spokeswoman Kathleen Kolar. Nevertheless, she immediately adds that while "Accutane is safe and effective when used as directed, any drug that has had that many warnings does merit concern."

Hmm . . . In any case, this concern led the FDA to require that Roche warn on the drug's label that it may cause "depression, psychosis, suicidal ideation, suicide, and attempts at suicide." This in turn no doubt has and will lead to more adverse event reports.

Indeed, according to Roche spokeswoman Gail Safian, the Tampa incident is being reported to the FDA as an Accutane-related suicide, notwithstanding that there's no evidence Bishop ever took the drug. All the stories that fingered Accutane in his death will probably lead to more adverse reports.

The second association between Accutane and suicide is that the drug is used primarily by people whose age group is especially prone to suicide. According to the U.S. Centers for Disease Control and Prevention in Atlanta, for persons "15-24 years old, suicide is the third leading cause of death, behind unintentional injury and homicide."

And the problem is getting worse. "From 1952-1995, the incidence of suicide among adolescents and young adults nearly tripled," says the CDC. "From 1980-1997, the rate of suicide among persons aged 15-19 years increased by 11% and among persons aged 10-14 years by 109%." Accutane, introduced in 1982, arrived about 30 years too late to have been the cause of this increase.

The third association between Accutane and suicide is that researchers have found what appears to be a cause-and-effect link between even mild acne and depression. You might expect that Clearasil users have a higher rate of suicide. Nevertheless, while the overall rate of suicide in the general population is about 11.1 per 100,000; that of Accutane users, according to a Roche survey, is 1.8 per 100,000. There have been about 90,000 U.S. suicides since 1982 compared to 167 FDA adverse reports for Accutane-related suicides.

Moreover, nobody has found any kind of biological plausibility for how Accutane might even cause depression. The active ingredient in Accutane (isotretinoin) is a Vitamin A derivative and overdoses of Vitamin A can be toxic. But there is no evidence that hypervitaminosis A can cause psychiatric reactions.

Another important contributor to the hysteria are the sharks in suits. After all, suicide cases are natural heart-tuggers and you never know when you'll get lucky before a judge or jury. If you go to a Web site with an innocuous-sounding name like http://www.accutane_suicide_help.com/ you'll find you've actually come across a lawyer-referral service.

It's indicative of the weak case against Accutane that one of the most powerful indictments came from the allegations of a single man with no medical background and a powerful motive to lay blame. In late 2000, the son of Rep. Bart Stupak (D-Mich.) committed suicide. As do so many grieving parents whose children have taken their own lives, Stupak sought desperately for a reason. What he found was that Bart Jr. had been taking Accutane.

Stupak's accusation, though, didn't just go to the FDA; it was broadcast in his own press conference, in which the lawyer and former state trooper took on the role of both forensic specialist and epidemiologist. This in turn led to House hearings, plenty more media coverage, and no doubt more adverse event reports.

So it has been and always will be for Accutane. Bad publicity leads to more bad publicity which leads to even more bad publicity. It is a vicious cycle from which Accutane and Roche will never escape. There's a valuable lesson in here; but don't expect that anyone will learn it.

Gulf War Syndrome, Round 38

react@reason.com (Michael Fumento) — Mon, 24 Dec 2001 00:00:00 EST

Here we go again.

"VA, DoD find Lou Gehrig Risk in Gulf War Service," boomed the Copley News Service. "U.S. Reports Disease Link to Gulf War," proclaimed the New York Times. It's "A Measure of Vindication for Ailing Gulf Vets," declared the Raleigh News and Observer. All the major TV news broadcasts ran with the story about the new study, providing an identical spin.

This game has continued for eight years now, and as always the pawns are America's vets. Somebody purportedly finds a link between Gulf service and some health problem. But the studies are either unreproducible or outright refuted. This one is different in only one way, but it's a big one.

The Defense Department, exhausted by years of defending itself against charges of cover-ups and callousness, finally -- indeed eagerly -- capitulated. It announced it would immediately start paying benefits to any Gulf War vet with the muscle-wasting and ultimately fatal disease amyotrophic lateral sclerosis (ALS). Such payments are labeled "presumptive," because ALS can strike anyone and no vet will ever be able to prove that, but for his service, he wouldn't have gotten it.

The dam is now cracked and will probably soon begin to crumble. We will begin making presumptive payments for more and more illnesses among Gulf vets. And that's a shame for several reasons.

First, the study (paid for by Defense Department and the VA) is worthless. Second, even if the study were valid, it would not -- indeed could not -- establish the existence of a Gulf War Syndrome, yet that's how it's being used. Seven hundred thousand Gulf vets and their spouses will now live in permanent fear of contracting something that doesn't exist.

Here's what's wrong with both the study and the uncritical response to it.

The secretary of veterans affairs, Anthony Principi, has called the study "preliminary," and with good reason. It is not finished, it has not been published, it has not been reviewed by other scientists, and in the wake of the announcement, it still wasn't available for outside critique.

Conversely, there have been a plethora of previous studies making every possible health comparison between Gulf vets and non-Gulf vets. They looked at specific diseases and complaints, all diseases combined, hospitalizations, deaths, diseases in offspring, and miscarriages. Many were published in peer-reviewed medical journals, such as The New England Journal of Medicine and the American Journal of Epidemiology. None found any links between Gulf service and illness.

Even Principi admitted that two prior studies had specifically looked for an ALS link and found none. A major British study also looked for an ALS link and it found none. Why should an aberrational study become the defining one?

Yet this study actually wasn't aberrational: It too found no link between ALS and Gulf service. Here's what it did find.

Of the nation's 700,000 Gulf vets, 40 were identified with ALS. Among 1.8 million vets who didn't deploy to the Gulf, 67 cases were identified. Adjusting for age and other variables to which we are not privy, that comes out to a risk of contracting ALS of 6.7 per million among Gulf vets, and 3.5 million among non-deployed vets. That's the doubling that Principi spoke of and the media parroted.

But a more accurate way to express the numbers is that the expected rate of cases among Gulf vets, according to the researchers, was 33 and instead there were 40. That's a mere 21% elevation. Suddenly the differences between the groups don't look very different. It looks like chance variation could easily affect the outcome.

This is all the more so when you look at the breakdown between the services.

Curiously, the highest rate of ALS was among Air Force Gulf vets, who had 2.7 times that of their non-deployed counterparts. Army soldiers had twice the risk, and Navy and Marine Corps veterans did not show rates of disease that were statistically higher than those not deployed. Yet Air Force servicemen were least likely to be in forward areas, where all the alleged toxins were. (You might think the Navy had few personnel in forward positions, but sizeable numbers of Navy combat engineers were in the area.)

Are blue uniforms a risk factor for ALS? Doubtful. This merely shows that when you're dealing with a tiny number of cases in a huge overall population, just a few can cause a huge statistical swing. Resample these groups in a couple of years and the apparent increase may well disappear.

That has been the experience of the Air Force researchers who for decades have followed a group of men who sprayed Agent Orange and as a result had extremely high exposures. One year there would be an excess of one disease but three years later it would disappear, only to be replaced by a slight excess of another. The latest slight excess is diabetes, but that too could well disappear by the next examination time.

What's more, it turns out that whether the Gulf vets actually had any excess of ALS depends on the group to whom you compare them.

An exact comparison to the civilian population is impossible because, as noted, the researchers didn't release their data. But the incidence of ALS in the U.S. male population is about two per million per year. So for 1.8 million such persons over ten years we'd expect 36 cases. Consider that the vast majority of vets deployed were men, that men are 50% more likely to get ALS than women, and that there are almost no ALS cases in persons under age 20 and -- voila! -- the rate of ALS among Gulf vets appears to be about the same as among civilians.

It's not that the Gulf vets are sicker than we would expect, but that the non-Gulf vets are healthier.

Arguably vets are the better control group, but this does call into question compensating people who have disease rates no higher than civilians. And again it shows that tiny numbers lead to unreliable outcomes -- or outcomes that can be thrown off by the smallest of errors.

The study also committed a whopper. The researchers told the New York Times that they identified ALS cases among Gulf vets in part by appealing to GWS activist groups. There are no activist groups for the non-deployed vets they used as controls.

This would be like conducting a public opinion poll in which the men surveyed were drawn from liberal groups and the women surveyed were contacted by random dialing, then announcing that the results show men are more likely to be liberals.

In short, every headline about the study should have been a variation of "Yet Again, No Link Found between Gulf Service and Illness." But even if the study had shown a link -- indeed, even if it had shown a cause-and-effect association -- it could not establish the existence of this beast known as Gulf War Syndrome.

The findings applied to a mere 40 vets and one illness. Yet tens of thousands of Gulf vets (150,000 according to the Raleigh paper, using a fabricated number) have complained of over 120 different illnesses that they claim are service-connected. Does establishing that a man robbed one bank prove that he robbed a thousand?

No matter; the activists have spoken and the media have given them a bullhorn. As U.S. News & World Report put it, "The findings were heralded by some veterans groups as a major victory in their 10-year fight to have their symptoms connected to their deployment in the gulf."

A Boston Globe editorial touting the study said, "At a time when US soldiers are again in harm's way, the military must be alert to all possible hazards." Right. That includes the hazard of telling soldiers going into harm's way that while they may survive the war unscathed, they could actually become exposed to some undetectable sort of magical pixie dust that will make them sicken and die years or even decades later. There's never a good time for nonsense like this, but during a war is the worst time of all.

Vietnam Flashback

react@reason.com (Michael Fumento) — Sat, 01 Jul 2000 00:00:00 EDT

U.S. veterans groups have long considered Agent Orange, the controversial herbicide used to defoliate jungles during the Vietnam War, a bigger villain than Ho Chi Minh and Henry Kissinger combined. Agent Orange exposure has been blamed for virtually any disease Vietnam vets and their offspring have ever suffered since the soldiers finished their tours of duty. These include everything from recurring rashes, dizziness, nausea, migraine headaches, stomach aches, and clinical depression to a plethora of cancers and birth defects.

Congress and the Department of Veterans Affairs have responded with two official presumptions. First, that all Vietnam vets had Agent Orange exposure, even though blood testing has shown that only a handful had any exposure. Second, that certain cancers and one type of severe birth defect, spina bifida, are caused by the presumptive exposure.

Never mind that studies in both the United States (by the Centers for Disease Control) and Australia found that the children of Vietnam vets had as few or fewer birth defects than the general population. Another CDC study found that one type of cancer was abnormally prevalent among vets, but only among sailors who served on ships off the coast and hence couldn't have been exposed to the defoliant. Miscarriage studies also have found no significant increase among vets or their spouses. Agent Orange has been cleared by every serious scientific study.

Until, it seems, now. Air Force researchers think they've finally, unquestionably pinned a disease on Agent Orange. Or so major media coverage of the study would indicate. The headlines in late March were unequivocal:

"Study Finds Strong Link Between Vietnam War Herbicide and Diabetes" (Associated Press)
"Air Force Study Finds Strong Link Between Exposure to Agent Orange and Diabetes" (CBS Evening News)
"Agent Orange Harmful" (ABC's World News Tonight)
"Vets Say VA Must Act on Agent Orange-Diabetes Link" (Copley News Service)

As Dr. Joel Michalek, head of the Air Force research team, said at a press conference: "This report includes the strongest evidence...that exposure to Agent Orange is associated with adult-onset diabetes."

But the implications of the headlines, and Michalek's statement, are wrong. And the proof can be readily found in the introduction and conclusion of the 1,700-page report itself, which is available on the Web at www.brooks.af.mil/AFRL/HED/hedb/afhs/97report.shtml. While the report doesn't support claims that Agent Orange causes diabetes, its media treatment is an object lesson in how weak science gets used for political purposes--and how those who should know better needlessly spread fear and anxiety. How the Agent Orange story has been spread is emblematic of other war "syndromes," including Gulf War Syndrome (See "Gulf Lore Syndrome," March 1997), and even something called "Korea Vet Early Death Syndrome," which may be catching on in Canada (but has yet to invade the U.S.).

The Air Force study is based on exhaustive health evaluations performed every five years since 1982 on veterans of Operation Ranch Hand, the Air Force operation that sprayed 90 percent of all the Agent Orange herbicide used in Vietnam. Many Ranch Hand veterans still have elevated levels of dioxin--a contaminant always present in the herbicide--in their bodies as a result of their long-ago exposures. For anyone interested in the possible health effects of Agent Orange and dioxin, it makes sense to examine the men with the highest exposures. If you don't find health problems in them, there's no reason to expect problems in persons with barely detectable or wholly undetectable exposures.

The latest examination results, based on 1997-98 examinations just now emerging from the long pipe of scientific report-writing, found that Ranch Hands had no more adult-onset diabetes than vets who flew the same types of aircraft in Southeast Asia but didn't spray any herbicides, be it Agent Orange or something else. But the 238 Ranch Hands with the highest dioxin levels in their blood (more than 10 parts per trillion) were 47 percent more likely to have diabetes than those 232 Ranch Hands with the lowest dioxin levels.

That's all the evidence for the diabetes-Agent Orange connection--and it's not the kind of evidence any district attorney would want to go to court with. First, as the report itself notes (on page 19-9), the 47 percent increase was not statistically significant. "Statistical significance" is a term epidemiologists use to describe whether an increase or decrease falls outside the bounds of what could be expected by chance. Scientists sometimes find 1,000 percent increases of some risk or other, but if few enough people were included in the study, they can't reliably conclude that such apparently huge risk elevations weren't merely random chance.

Yet even if the 47 percent increase (which epidemiologists refer to as a "relative risk" of 1.47) was statistically significant, it wouldn't mean much. Says who? The authors of the Air Force report (on page 1-10): "Statistically significant relative risks less than 2.0 are generally considered to be less important than larger risks because relative risks less than 2.0 can arise more easily because of unrecognized bias or confounding." Bias and confounding variables are possible contributing factors which epidemiologists might not have been able to keep out of their data that confuse results. Dietary habits are a common one, for example, though in this study the Air Force authors took such matters as the amount of fruits, vegetables, and fats in the vets' diets into account.

But there's a result of dietary habits that may well have influenced the results. That particular confounder was the whole reason the Ranch Hand study could even be done. Dioxin, the marker for Agent Orange exposure decades ago, is stored in body fat and works its way out into the bloodstream so slowly that it can be measured many years later. Fatter people don't release fat-soluble compounds like dioxin nearly as quickly as thinner people, notes Michael Gough, a biologist who was chairman of a federal advisory panel for the Ranch Hand study from 1990 to 1995. Thus, higher dioxin levels are associated with higher obesity levels. And what's one of the main risk factors for adult-onset diabetes? Obesity. "It's far less likely that Agent Orange is the cause of the diabetes than is obesity," says Gough.

Dr. Michalek, the Air Force project leader, himself told New York Times science writer Gina Kolata, "We know diabetes is highly related to body fat, and so is dioxin. That's why these diabetes findings are so difficult to interpret. People are concerned that we haven't done the right body fat adjustment."

Kolata, my Nexis searches indicate, appears to be the only reporter who voiced the least bit of skepticism about the Agent Orange-diabetes "connection." Her very headline did not refer to any diabetes "link" or "connection" but merely said, "Agent Orange and Diabetes: Diving into Murky Depths." Unfortunately, the Times' main article on the study was written not by any of the paper's excellent science writers but by its military reporter. Military reporters specialize in areas more or less exclusive to the military, such as equipment, needs of personnel, tactics, and strategy. They are not expected to, and as a general rule do not have, any background or expertise in medicine, nor even names in a Rolodex to help them out.

None of this is to dispute Michalek's claim that his report is the "strongest evidence" of an Agent Orange link to diabetes. He's absolutely right about that. It is the strongest evidence, which actually speaks volumes about its weakness. For example, notes Gough, "There have been several large studies of chemical plant workers in the U.S. and Europe exposed to huge levels of dioxin and the components of Agent Orange. None of them has found excesses of diabetes."

Veterans Affairs now pays compensation to Vietnam veterans who develop any of several "Agent Orange-related diseases." It's a virtual given that the current clamor from veterans groups and politicians will convince the VA to add diabetes to that list. "Based on the evidence we have seen, the VA should make a decision that diabetes is presumed to be service-connected based on Agent Orange exposure," says John Sommer, executive director of the Washington office of the American Legion.

Sommer may want to think twice about using the report. Beyond diabetes rates, the Air Force study looked at the other "Agent Orange-associated diseases," including nine different cancers, for which groups like the American Legion had lobbied to get compensation. What did it find? "Ranch Hand enlisted ground crew, the occupation with the highest dioxin levels and, presumably, the highest herbicide exposure, exhibited a decreased prevalence" of cancer. The Ranch Hands got cancer about 21 percent less often than the comparison group of Vietnam vets who sprayed no herbicide at all.

Like the 47 percent increase in diabetes, that decrease is statistically insignificant. But if you want to follow the lead of those media types and politicians who tossed statistical significance to the four winds in the case of diabetes, you can conclude that Agent Orange and dioxin exposure reduce cancer risks.

That said, don't expect to find dioxin capsules in the vitamin store next to shark cartilage. Do expect this latest report to become part of the lore surrounding Agent Orange. And while some vets will receive compensation they don't deserve, many more who bravely served in Vietnam will simply live out their lives in fear that they are at elevated risk for diabetes or cancer. That's not the kindest way to thank them for their service.

Good News, Bad News

react@reason.com (Michael Fumento) — Thu, 01 Jun 2000 00:00:00 EDT

Crop Busters

react@reason.com (Michael Fumento) — Sat, 01 Jan 2000 00:00:00 EST

One night last August, a group calling itself Seeds of Resistance used machetes to hack down a half-acre plot of corn at a farm operated by the University of Maine. The crop's offense: It had been genetically engineered to resist herbicides.

This characteristic would reduce the number of herbicide applications needed, saving farmers money and reducing chemical runoff into water supplies. It could also reduce or eliminate tilling and hence control topsoil erosion. To gain these advantages, a specially chosen gene from another plant had been inserted into the corn.

For that, the corn had to die. Seeds of Resistance said it was sending "a message to those who seek to benefit from the risky endeavor of genetically engineering the food supply."

So far this year, anti-biotechnology vandals have struck 13 crop sites in the United States, from Maine to California. The attacks tell us much about biotech opponents, many of whom have increasingly abandoned rational persuasion in favor of "direct action" that shows contempt for the choices of the people they claim to represent.

The U.S. vandals acknowledge a debt to overseas activists, especially in the U.K., where wrecking crops that offend one's sensibilities is commonplace. "Many thanks to our comrades in other countries for the inspiration to join them," declared a September communiqué from Reclaim the Seeds, one of the more active American crop-busting groups. The British attacks are not random and are not exclusively the work of tiny fringe groups. Some have been carried out by the world's most prominent environmentalist group, Greenpeace. Most environmentalist groups that don't participate nonetheless refuse to criticize the sabotage.

According to an August report in the London Guardian, between the U.K. and the Continent, more than 70 sites where biotech plants were being tested, out of an estimated 150 to 200, "have been wholly or partly destroyed, with almost 50 in the past 12 weeks." The British biotech-bashing Genetic Engineering Network, which gleefully claims that "over 80 [European biotech crop] trial sites have been decontaminated over the last two years," sent me a detailed list of 46 sites destroyed between January and mid-August.

On this side of the Atlantic, crop busters started late but are making up for lost time. "There was only one [attack] that I know of in the U.S. in 1998," says Jeffrey Tufenkian, spokesman for the San Diego-based anti-biotech group Genetix Alert, which tracks and applauds crop wrecking. This year there were two attacks in July, three in August, seven in September. Only an end to the growing seasons seems to have kept the numbers from continuing their upward spiral. There was one attack in late October, but it consisted only of vandalizing a building where the corn had already been harvested. "These actions are just starting to expand over here," says Tufenkian. "But I think this is just the start of the trend of resistance to this new technology."

The British terra-terrorists are aided by their government, which insists on giving out the exact locations of the test plots. (Notwithstanding this assistance, non-modified crops are often mistakenly destroyed.) The government is considering changing the disclosure policy, even as it gives out the locations of new test tracts. Though the U.S. government doesn't hand out maps to the homes of the biotech crops, the Bioengineering Action Network of North America (BAN),an anti-biotech group, has a Web site (www.tao.ca/~ban/) that claims to offer helpful hints.

Numerous groups with names that sound like high school sports teams, such as the Lincolnshire Loppers and Cropatistas in Britain and the Bolt Weevils and California Croppers in the U.S., are now joining in the fun. Britain's Genetix Snowball published a book describing the best tactics for stealing into a field at night and destroying it. BAN says a "Night-Time Gardener's Guide," which it describes as "a 'how-to' for would-be crop saboteurs," will soon be available on its site.

More than fields are coming under attack. On the last day of September, two groups wrecked sites growing melons, corn, and sunflowers in Woodland, California. They also disabled an irrigation system and vandalized three greenhouses. Earlier in the month, the Bolt Weevils whacked a biotech corn crop at Pioneer Hi-Bred's Minnesota facility, trampling 50 rows of research corn, damaging company vehicles, and spray-painting slogans ("Free the Seed" and "Stop Agribusiness") on sheds. The last confirmed attack as of this writing was by Seeds of Resistance against Pioneer Hi-Bred in Eau Claire, Wisconsin, on October 27. Genetix Alert's press release called the action "nonviolent," though the vandals themselves used the term smash, which has a rather violent sound to it.

The vandals say they won't stop with fields and surrounding facilities. "Crops, research facilities and corporate offices are all sources of this technological threat and should be targeted," say the Weevils. An anonymous e-mail message recently sent to growers of biotech crops declared: "All of a sudden `venture capitalist' scum realize that biotechnology is not such a great investment and they flee with their bags of cash with them....Our view is that if corporations, governments and universities have any relationship to biotechnology, they are targets."

Even those who merely sell the products are being threatened. One British group calling itself Smash Genetic Engineering is warning of violence against clothing stores that use biotech crops such as pesticide-resistant cotton. Genetix Snowball threatens vandalism this autumn, "once we are certain who [the retailers] are." The famous British chain Marks & Spencer has already buckled under the threats by removing biotech foods from its shelves.

While their crimes are serious, the rationalizations and euphemisms served up by the crop busters are laughable. Consider a recent Greenpeace U.K. press release: "At 5:15 a.m. today in a peaceful direct action, a Greenpeace decontamination unit removed genetically modified pollution from the third farm-scale experiment to be disrupted in the U.K. over the last eight weeks." So trespassing on private land and ripping up crops is "peaceful," while destroying something you don't like is "direct action" or "decontamination." And it was "pollution," not the science of transgenics, that was under attack.

Greenpeace U.K. Executive Director Lord Peter Melchett, who was arrested in July for personally "decontaminating" crops, claims vandalism "is not lawlessness," because "we act within strong moral boundaries." Thus the criminality of an act can be negated by the actor's opinion. If you feel morally justified in "peacefully decontaminating" your spouse via "direct action" with a shotgun, your actions are "not lawlessness."

Though these claims come from a nation that prides itself on civility, this is not civil disobedience. The peaceful American civil rights activists who risked, and sometimes lost, life and limb by seating themselves in "white only" establishments or drinking from segregated water fountains never pretended that they weren't lawbreakers. They acknowledged it and accepted incarceration, often accompanied by beatings. They questioned the morality of the law by making the authorities enforce it. That's civil disobedience. "We accept responsibility for the consequences of our action," Melchett claims. Yet after he was jailed for his "decontamination" outing, he sprung himself by complaining to the press that he would miss his already-paid-for vacation in Tanzania.

American groups have adapted the British euphemisms. Reclaim the Seeds speaks of its "nonviolent direct action," while the BAN Web site refers to "direct actionists." The U.S. groups also make similar claims of heroism. "We are risking jail and injury, as well as sacrificing time, energy and sleep," declare the Reclaimers. It's certainly conceivable that an overenthusiastic Reclaimer brandishing what they call "California Corn Cutters" could slice the Achilles tendon of another Reclaimer. But it hasn't happened yet. As for jail, not a single American crop vandal has been arrested so far.

Biotech crop trials are "backdoor commercialization of GM crops that nobody wants," says Doug Parr, campaigns director for Greenpeace U.K. "Sadly," he says, "when democracy fails, direct action is the only recourse. The authorities are not taking the correct action and unfortunately it has fallen to Greenpeace to protect everyone's interests."

While Greenpeace International's latest annual report, released in August, is titled "In the Name of the People," the eco-warriors insist they are "the people." Melchett calls his group's actions a "direct expression of `people's power.'" One Genetix Snowball representative declared, "The public has made it clear they don't want [genetically modified] crops, and there is no need for these tests." Another insisted, "If the government isn't going to get involved, then it's up to us."

Never mind that the government did get involved when it approved the test plots--you can't grow genetically modified crops without regulatory permission--and stays involved as it continues to grant approvals. Never mind that this government was elected by the people and that the electorate's numbers swamp the combined membership of all the green groups.

This contempt for democracy has crossed the Atlantic. Brock Ohlee of the American crop vandalization group Future Farmers declares, "Direct action against corporate greed is both a political necessity and a moral imperative." Thus "the people have the right and the responsibility to fight back." Yet the Future Farmers give hints that they and the nation are at odds, as when they spell the name of the country as "U$A" or "Amerikkka."

After a corn crushing in Minnesota last September, the Bolt Weevils declared "a WARNING to the entire `life-sciences' industry that opposition to its sinister plan is far more widespread than they think, and growing exponentially." That same month, Reclaim the Seeds ripped up a sugar beet field at the University of California at Davis, proclaiming "these acts as self-defensive measures on behalf of all beings against Monsanto, UC-D and the university system's corporate boot-licking, and the global GE [genetic engineering] takeover!" (Emphasis added). So it's not just "the people" any more. This group claims to speak for every living thing, right down to the lowliest amoeba. After crunching a corn crop at the same university, the group stated, "Modern agri-business and genetic mutilation is a capitalist machine that must be dismantled," adding that vandalism "is a direct action that destroys corporate power and authority."

Sometimes it seems the groups can't decide whether they want to be revolutionaries or professional wrestlers. "Seeing their profits as a slap in the face of the earth and all its occupants, we took the liberty of paying them back," Seeds of Resistance said of its attack on the Eau Claire building. "We, Seeds of Resistance, smashed all the windows on one side of their disgusting building. Wisconsin is now another state that cannot hide from this growing resistance against GE culture."

Not to be outdone rhetorically, the Weevils declared, "We see what the corporations give back to the public." They give back "houses we cannot afford to live in" (notwithstanding that home ownership is at an all-time high) and "jobs our bodies cannot do for long without breaking" (notwithstanding that fewer jobs than ever consist of manual labor and occupational accident rates are at an historic low). "Corporations," warned the Weevils, "give back to the people death."

Bio-engineering of food has become symbolic of every evil any corporation has perpetrated (or, more precisely, everything corporations have done that members of these groups don't like). Attacking biotech is therefore just another way of attacking capitalism and technology. The Luddite analogy is one that critics of environmentalism have overused, but here it fits almost too well.

We can always argue over politics, but whenever the crop busters venture into scientific territory, they trip over their shears. When Reclaim the Seeds "decontaminated approximately 7 acres of a `Frankenfood' corn" in its third attack on the University of California at Davis, they invoked their "profound sense of the sacredness of life." Said the Seeds, "We believe that protecting the result of more than three billion years of evolution is a duty to ourselves, all living beings, and the generations to come."

They might be shocked to hear that probably every ear of corn that's been sold in the United States was created by man, using the forerunner of bio-engineering called "cross-breeding." Instead of isolating a single gene or a few genes from one strain of corn and injecting it into the DNA of another, people crossed whole strains, hoping that the desired traits would be expressed. (It reportedly took Orville Redenbacher 30,000 attempts to make the ideal popcorn.)

This process apparently began over 5,000 years ago, when American Indians essentially created corn by combining two types of wild grasses. Modern hybrids were first commercialized in the 1930s. Humans have been doing such "tampering" with livestock for thousands of years as well. Ever see a wild cow or chicken? There are related creatures, but strictly speaking there's no such animal. Indeed, almost nothing we eat, aside from nonfarm fish and things whose names include the word wild (such as Ewell Gibbons' "wild hickory nuts"), is a product merely of undirected evolution.

The groups that attacked the Woodland, California, sites claimed to be part of "the growing movement to protect the fabric of life." If anything could be labeled "the fabric of life," it's simple DNA. There is no inherent difference between the DNA of "natural" plants and those created through selective gene transfer.

Reclaim the Seeds has also said its actions are necessary to "stop the massive destruction of biodiversity." But crop biodiversity began declining long ago, simply because farmers want the best strains, not the most strains. If anything, biotech may improve diversity by developing strains especially suited to a given area's temperature, rainfall, soil type, and pest threats.

Likewise, Reclaim the Seeds is exactly wrong when it says, "If you care about social justice and don't want to poison farm workers with pesticides and herbicides, you should resist genetic engineering." Actually, if you're worried about farm workers' exposure to pesticides, you should resist such propaganda. Probably the main p.r. problem biotech crops have right now is that almost all those currently grown do nothing but allow less use of pesticides (of which herbicides are a subcategory). There's nothing, therefore, to please consumers. Though the situation will soon change, as biotech foods that stay fresh longer and have more nutrients come to market, currently only farm workers and owners, along with the seed developers, benefit from transgenic crops.

The anti-biotech groups pay lip service to environmentalism, as with the Future Farmers' claim to "stand for environmental sustainability" and "community stewardship of resources." But it is the environmentalists who have been demanding reduced use of pesticides, and are now getting it thanks to biotech crops. They are the ones who (rightly) pushed the nation's farmers toward no-till agriculture to prevent topsoil erosion, a goal that is hardly served by destroying corn designed to reduce erosion, as Seeds of Resistance did in Maine. Likewise, it is hard to see the environmental rationale for destroying a plot of poplar trees developed to reduce the use of chlorine and energy during the pulping process, an act of sabotage carried out by an anonymous British group in July.

Despite the ways in which attacks on biotech crops work against the environment, I was able to identify only three environmentalist groups, two British and one American (the Environmental Defense Fund), that have decried such vandalism, and all the criticism has been mild. Many other groups have kept mum.

As for the mainstream British press, it has "uncritically embraced this phenomenon," says Frank Furedi, a sociology professor at the University of Kent at Canterbury. "The activists [say sympathizers in the media] are the good guys," who, "unlike sleazy politicians," are "untainted by corruption or self-interest" and are "portrayed as altruistic and idealistic souls whose motives are beyond reproach." Indeed, many British columnists have lauded the destruction of modified crops, while reporters routinely refer to the crop killers as "protesters," a mild term, or even an accolade.

In the U.S., by contrast, the news media have shown no support for crop busting. News stories routinely refer to the attacks as "vandalism," and opinion pieces on the topic have been critical. "There's nothing wrong with peaceful protest or with insisting that troubling eco-questions be answered," declared a Boston Globe editorial. "But slashing an experiment and attempting to stop science is the height of ignorance." The Sacramento Bee editorialized, "A technological revolution like this can't be kept on course by masked fools with scythes." The problem is that, aside from a few sentences in The Washington Post and Newsweek and a 150-word item in The New York Times, the national press has acted as if the problem doesn't exist.

Still, there are at least a couple of reasons to believe that the crop busters will be defeated.

First, it may not take much for crop growers to resist cowardly groups like Seeds of Resistance. When a call went out over the Internet for a "Day of Action" on October 27, the would-be Transgenic Tet Offensive resulted in but a single act of vandalism. Apparently a little heightened security was enough to keep the self-styled "guerrilla gardeners" at bay. The American vandals know that, unlike their European counterparts, if they're arrested they'll go to jail, not Tanzania.

Second, to use the groups' own analogy, history shows that terrorism is a desperation tactic of guerrillas who've abandoned hope of winning the "hearts and minds" of the people. As a Portland Press Herald put it, "Seeds of Resistance has unilaterally decided that there is `absolutely no benefit to humanity' from the corn its members destroyed. How do they know? By turning to vandalism, they destroyed the chance to learn."

That's the whole point. The eco-terrorists know that just around the corner is the second wave of biotech foods, from which consumers as well as farmers and the environment will benefit. They know that pressure will build in the Third World for crops to relieve malnutrition problems that lead to crippling, blindness, and early death. They know that when that happens, they will not be able to win the ensuing war of ideas.

More for Less

react@reason.com (Michael Fumento) — Thu, 01 Apr 1999 00:00:00 EST

Test Anxiety

react@reason.com (Michael Fumento) — Tue, 01 Dec 1998 00:00:00 EST

It's the Tuskegee syphilis experiment all over again! No, it's worse than that. It's the sort of research you'd expect from Josef Mengele!

Or so you might think based on a report that the Environmental Working Group (EWG) released at a July 27 press conference in Washington. The report documents the testing of various pesticides on human volunteers in England and Scotland beginning in the 1970s. The EWG, a tiny environmental group that nonetheless throws a long shadow, called for an immediate moratorium on such tests, demanding that the Environmental Protection Agency stop accepting them and stick to research with mice and rats. The Natural Resources Defense Council (NRDC), which also participated in the press conference, concurred.

The EWG's report presented no evidence that any of the volunteers in the pesticide studies had been harmed. Furthermore, anyone who understands the science behind this controversy will recognize that the EWG and the NRDC are not simply concerned about the welfare of human subjects. Environmental activists know animal testing is highly inexact, and they like it that way, the better to advance their agenda of hamstringing evil corporations and farmers at every turn.

Because rodents are quite different from humans, current regulatory policy requires the use of "safety factors" that greatly reduce the amount of pesticide that can be sprayed on crops but may not actually enhance safety. Under rules the EPA implemented from the agency's inception, you first determine the minimum amount of pesticide required to make an animal sick, then reduce that dose slightly. This is called the "no-effect level," or NOEL. To allow for the possibility that humans are more sensitive to the chemical than the test animals are, you divide NOEL by 10. Then you divide by 10 again to allow for especially sensitive humans.

The more you divide, of course, the less pesticide farmers can use to protect their crops. And if a given level is already safe, by definition it's impossible to make it safer by allowing even less. But that didn't stop environmentalists from crying, "Let's divide again!" They got their wish two years ago, when Congress passed the Food Quality Protection Act of 1996. The law authorized the EPA, at its discretion, to use yet another tenfold "safety factor"--dividing NOEL by 1,000 instead of 100--to protect children.

The new standard is so onerous that it will probably force farmers to replace many useful pesticides with products that are more costly and less effective. The rationale for the stricter standard is fuzzy, since children are already covered under the safety factor for "more sensitive" humans. Children also receive some coverage under the first safety factor, because animal testing often is done on infant or fetal rodents.

The environmentalists and the EPA know all this. So do the pesticide companies, which is what makes greater use of human testing so attractive to them: It could prove that the first tenfold safety factor, which assumes humans are much more sensitive than rodents, is needlessly strict. Such research obviously makes good economic sense for pesticide companies, farmers, food processors, and produce sellers. But it also makes good scientific sense, because human studies can tell us much more about safety than animal tests can.

Research with lab animals doesn't necessarily enable us to predict reactions in closely related species, let alone in humans. The furor over dioxin that continues to this day began when it was discovered that the tiniest amount knocked over guinea pigs like tenpins. But it took 5,000 times that dose to kill the same percentage of hamsters. Such experiences suggest that we should be careful about extrapolating from rodents to people.

I raised this issue at the EWG press conference. "Just as animals are better indicators than test tube experiments, aren't humans better indicators for human effects than animals?" I asked the group's vice president for research, Richard Wiles. "Absolutely," he conceded. This is precisely what disturbs the folks at the EWG. They've worked long and hard to get that third tenfold safety factor built into the law. If the pesticide companies manage to show that the first tenfold factor is unjustified, the environmentalists will be back at square one. Unable to attack the human testing on scientific grounds, the EWG tried to do so on ethical grounds. "Allowing human experiments, such as those conducted recently in the United Kingdom, to serve as the basis for registering pesticides, is ethically indefensible," EWG President Ken Cook said in a press release. But when questioned at the press conference, Wiles had to admit there was no evidence of unethical treatment. The testing was unquestionably legal under British and U.S. laws. A spokesman for Britain's Ministry of Agriculture, Fisheries, and Food said the tests "seemed to be along the right lines ethically." Medical ethics committees always review test protocols, and their decisions are reviewed every few years by international panels.

The EWG made it sound as if England and Scotland were chosen for the pesticide research because their citizens are easily exploited, like those poor Indians who sell their kidneys. Last time I checked, though, the United Kingdom did not qualify as a Third World country. A spokesman for one of the pesticide companies, Rhone-Poulenc Agro, said its studies were done in the U.K. because they "were commissioned by our parent company" in Lyon, France. In any event, some pesticide research with human subjects has been conducted in the United States.

Indeed, the EPA conducted its own human test to determine skin absorption rates of the medfly killer malathion in the early 1990s. In 1987, what was then called Ciba-Geigy (now part of Novartis) recruited six managers to swallow the herbicide atrazine. They were no more exploited than they were foreign.

The EWG report nevertheless provided fodder for the sensationalist wing of the British press. "Human Lab Rats in Secret Toxic Tests," cried a headline in The Birmingham Post. It's true that most of the tests weren't publicized, but why would they be? When was the last time a negative rodent study made the news? ("Our lead story tonight: Researchers in the United Kingdom have found that a widely used pesticide is harmless to mice. We take you now to our correspondent in London.") In any case, at least one of the human pesticide studies was publicized.

In 1992, Pesticide & Toxic Chemical News published an article about a study conducted in Scotland by Rhone-Poulenc. I know because I found it in the Nexis database. Not exactly a secret. Volunteers for these studies are recruited and paid by labs set up for such testing, not the chemical companies themselves. They are divided into test subjects, who swallow orange juice or corn syrup containing the pesticide, and control subjects, who swallow the liquid without the chemical. The amounts of pesticide involved are so tiny that any reactions are expected to show up only in blood testing, not in any observable symptoms.

In one Rhone-Poulenc study, the chemical was aldicarb, an insecticide in
the carbamate family. Carbamates work by inhibiting production of the enzyme cholinesterase, which is vital for nervous system functioning in humans as well
as insects. The EPA had proposed cutting the maximum permissible amount of aldicarb residues on food to one-fifth the existing standard, which would cause great hardship for farmers who need more to keep insects at bay. Rhone-Poulenc thought that if it showed no symptoms at levels much greater than any possible real-world exposure, it could get the EPA to reconsider.

So in 1992, a British lab administered aldicarb in orange juice to 36 people at four dose levels, while 22 controls had a pesticide-free drink. According to Rhone- Poulenc spokesman Richard Rountree, the doses were set well below the no-effect level established in animal research. Even when the pesticide could be detected in the subjects' blood, none of them displayed any symptoms of aldicarb poisoning, which include nausea, vomiting, diarrhea, blurred vision, muscular weakness, and difficult breathing. Rhone-Poulenc felt it had proven its point, but the EPA refused to budge on the stricter limit, noting that one of the test subjects had sweaty palms--which is not a symptom of aldicarb poisoning.

Apparently this episode was typical of how the EPA treats data from pesticide studies with human subjects. In response to the EWG's claim that "product registrations for [eight] insecticides rely on human studies," the agency insisted that "no human test data has been used by EPA for any final decision"--a point that an EWG spokeswoman later conceded. Last year, in a memo to its scientific advisory panel, the EPA indicated that human data would receive preference over animal data for some tests and that human testing is allowed under federal legislation.

The EWG's insinuation that subjects were exposed to grave danger was also unfounded. The symptoms reported in these studies--which included muscle weakness, headaches, and lightheadedness as well as sweaty palms--are all signs of nervousness. They are about what you would expect from people who believe they have ingested a poison, even if they are assured that the dose is too small to hurt them. The EPA's own evaluation of a study involving the insecticide dichlorvos noted that some subjects reported minor ailments such as headaches, drowsiness, and abdominal colic, but investigators "did not attribute these symptoms to dichlorvos administration."

Of course, human testing of pharmaceuticals is not only routine but required by law prior to FDA approval. "It's sad that companies are taking so much flak over these human pesticide studies because the whole object of these things is to try to identify a level that's absolutely safe," says Chris Wilkinson, a former EPA adviser and now an industry consultant in Arlington, Virginia. "Whereas with drugs, they try to see how much humans will tolerate. They really zap some people with these drugs."

But the EWG squirms around the drug testing, saying, "Exposure to toxic pollutants like pesticides is not undertaken on the assumption that in the future other people can benefit from exposure to the toxic substance." This is sophistry. People don't benefit from ingesting a pesticide, but they do benefit from its use.

Pesticides make food safer by preventing the growth of toxin-generating molds. They also make produce less expensive and more appealing--no small matter in a country where less than a tenth of the population consumes fruits and vegetables in the recommended amounts. Pesticide limits discourage the consumption of fresh produce by driving up its cost and making it look small, shriveled, and ugly (as "organic" crops generally do). Since more than 200 epidemiological studies have shown an association between low produce consumption and cancer risk, it seems likely that the anti-pesticide crusade is harming people's health rather than protecting it.

Although the EWG's report was nonsense from beginning to end, such documents have the power to intimidate. The day it appeared, the EPA proclaimed itself "deeply concerned that some pesticide manufacturers seem to be engaging in health-effects studies on human subjects as a way to avoid more protective results from animal tests." Why wasn't the EPA "deeply concerned" the day before the press conference? Because the suspicion that the agency takes its marching orders from environmental groups is largely correct. Why are animal tests "more protective" of humans than human tests? They're not; they're just more stringent. To a regulator, the tougher the law, the better.

During the EWG press conference, I kept wondering if I would hear the n-word. Sure enough, just before the event ended Wiles said the pesticide studies were reminiscent of experiments conducted by the Germans during World War II. Dan Guttman, an ethicist on the panel, jumped to his feet and exclaimed, "Nobody's suggesting a comparison to the Nazis." To which the woman next to me quietly replied, "Well, he just did."

Heavy Silence

react@reason.com (Michael Fumento) — Wed, 01 Apr 1998 00:00:00 EST

Every October, this country celebrates Breast Cancer Awareness Month. But what are we supposed to be made aware of? That the disease exists? That's hardly necessary. How about that it's the most prevalent female cancer? Most women know that, too. Perhaps women should be made aware of what is probably the single most important controllable risk factor for breast cancer.

No, it's not power lines or DDT or toxic waste dumps. It's obesity.

Federal government weight specialists define obesity for women as having a body mass index of 27.3 or higher. (Your BMI is your weight in kilograms divided by the square of your height in meters.) Many studies have found obesity increases the risk of breast cancer in older women. The National Cancer Institute's 1996 publication "Cancer Rates and Risk" states flatly, "Among postmenopausal women, breast cancer risk increases with weight and body mass."

Obesity greatly raises a woman's risk of getting breast cancer and, because fat obscures the tumor and delays detection, substantially increases the chance that the cancer will be fatal. As a risk factor for breast cancer, obesity is more significant than other risk factors such as an inherited genetic mutation or early puberty. But the connection between obesity and breast cancer is rarely discussed because feminists and fat acceptance activists, aided by sympathetic, intimidated, or clueless journalists, find it ideologically inconvenient.

The evidence is getting harder to ignore. Results from the Boston-based Nurses Health Study, reported last November in The Journal of the American Medical Association, indicate that postmenopausal women who have gained 44 pounds or more since age 18 are twice as likely to get breast cancer as women who have gained less than five pounds. And Harvard University endocrinologist JoAnn Manson, one of the study's lead researchers, says "There seems to be even a stronger association with greater degrees of obesity." Other studies have yielded similar results. The probable explanation, Manson says, is that after menopause fat becomes the primary source of estrogen in a woman's body, swamping outside sources (such as DDT) that environmentalists have tried to link to breast cancer.

A study by researchers at Yale University, reported last September in the American Journal of Epidemiology, found that obese women are more than three times as likely as thin women to have their breast tumors detected at a later, less treatable stage of the disease. The Yale study is the latest of several to report this association. Other studies suggest that severe obesity decreases breast cancer survival rates independent of when the tumor is detected, perhaps because it makes a woman much less likely to survive major surgery. Partly as a result of these tendencies, black women are considerably more likely than white women to die of breast cancer, even though they are significantly less likely to develop the disease in the first place (apparently for genetic reasons). One cause of this disparity may be that black women tend to see doctors less often, but another important factor is that they are about 50 percent more likely than white women to be obese.

Since over a third of American women are obese, obesity probably causes several thousand breast cancer deaths each year. There are also consistently significant links between obesity and other women's cancers, such as those of the uterus, cervix, and ovaries.

Yet the average American woman almost never hears warnings about obesity and cancer. Consider how the issue has been ignored by People, a magazine with some 3.5 million readers, about 65 percent of them women. Like most magazines with a substantial female readership, People has turned breast cancer into a cause célebrè, mentioning the subject in some 200 articles over the past two decades. None of these articles noted the link between obesity and breast cancer. Neither did a recent cover story ("Who Says Size Counts!") that celebrates female obesity.

This sort of silence has been the rule, not the exception. You just don't talk about the link between obesity and breast cancer in polite company. Activist groups object to the implication that women can do anything to reduce their risk of breast cancer. Francine Kritchek, co-chair of Long Island's influential One in Nine, says women are "are tired of being told" to "watch their diets." The National Alliance of Breast Cancer Organizations goes so far as to call the idea that there's any "known way to prevent breast cancer" a "myth."

Why the great silence? Every aspect of breast cancer, from funding to prevention to treatment, is dominated by feminist ideologues. In feminist parlance, to say that a woman has any control over contracting breast cancer--or even to say that she is genetically predisposed--is called "blaming the victim." This is the line pushed by America's top breast cancer activist, Dr. Susan Love. Citing Love, Toronto Sun reporter Marilyn Linton writes, "Beating ourselves up over what we might have eaten, taken and done or not done is of no help at all." (In pushing this line of thinking, feminists and fat-acceptance activists have been abetted by environmentalists who blame cancer on power lines, radar stations, fertilizers, pesticides, toxic waste dumps, and even air pollution--anything connected to industry. Says Samuel Epstein, a physician and environmental activist, "The cancer establishment remains myopically fixed on blame-the-victim theories," while ignoring "evidence of environmental contaminants.")

Just as the language of breast cancer has been shaped by feminists, so has the language of obesity. The titles of psychologist Suzie Orbach's best-selling books say it all: Fat Is a Feminist Issue and Fat Is a Feminist Issue II. "Fat," writes Orbach, is "rebellion against an imprisoning social role." It is "not about lack of self-control or lack of will power" but rather "a response to the inequality of the sexes." Women become fat because they think, "if I get bigger like a man then maybe I'll get taken [as] seriously as a man."

Orbach's thesis cannot explain why, according to 1994-95 government data, 54 percent of American women are healthily thin, while only 40 percent of American men are. But feminists applauded her books. Backlash author Susan Faludi says the first one, originally published in 1978, should "be read by every American woman." And Orbach has spawned a legion of imitators. Sharlene Hesse-Biber's 1997 book Am I Thin Enough Yet? blames women's eating problems on "capitalism and patriarchy." She explains that keeping women fixated on their weight is part of a conspiracy to divert money, time, and energy from more empowering activities.

Yet nobody spreads more diet disinformation than the women's magazines, with their silly "52 Tips to Lose Weight," "Ten Ways to Melt Off That Flab by Bikini Season," and my favorite, "The Last Diet You'll Ever Need," followed up two months later by another "Last Diet You'll Ever Need." The editors and writers for these magazines are almost all women. The largest diet centers, which produce results so dismal most refuse to release their data, are almost entirely staffed by women. Most of the worthless diet books are written by people with names like Susan Powter, Adele Puhn, and Debra Waterhouse. Today the best-selling nonsense diet book is The Zone--authored by a man, but edited and published by a woman, Judith Regan. If it's true that women are being victimized, they are also the prime victimizers.

The "blaming the victim" charge discourages journalists, scientists, and public health officials not only from discussing obesity and breast cancer but from advising women to lose weight for any reason. Doing so almost inevitably provokes the accusation that such advice promotes eating disorders, even though the most serious eating disorders generally result from underlying psychological problems. The National Association for the Advancement of Fat Acceptance claims eating disorders kill 150,000 women a year in the United States. The actual number, reports the National Institutes of Health, is about 150.

Through such tricks, the feminists and fat-acceptance advocates have convinced many of us that thinness kills, to the point where they finally prevailed upon Mattel to fatten up that longtime object of feminist wrath, the Barbie doll. Meanwhile, the number of American women who die of obesity-related breast cancer is probably more than 30 times the number who die as a result of eating disorders. Last year there were about 29,000 postmenopausal breast cancer deaths in the United States, and Zhiping Huang, who collaborated with JoAnn Manson on the Nurses' Health Study, estimates that 16 percent of them--more than 4,600--were caused by obesity. Overall, reports the Centers for Disease Control and Prevention, about 150,000 American women die prematurely each year from obesity-related causes such as heart disease, stroke, and diabetes.

It's true that we don't know what causes all breast cancers, or even most. But prudence, logic, and compassion dictate that women should be informed about the risk factors that have been identified--especially when, as in the case of excess weight, they can do something about them.