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antioxidants: time for a rethink

The antioxidant myth: a medical fairy tale
05 August 2006
NewScientist.com news service
Lisa Melton

Cranberry capsules. Green tea extract. Effervescent vitamin C. Pomegranate concentrate. Beta carotene. Selenium. Grape seed extract. High-dose vitamin E. Pine bark extract. Bee spit.

You name it, if it's an antioxidant, we'll swallow it by the bucket-load. According to some estimates around half the adults in the US take antioxidant pills daily in the belief they promote good health and stave off disease. We have become antioxidant devotees. But are they doing us any good? Evidence gathered over the past few years shows that at best, antioxidant supplements do little or nothing to benefit our health. At worst, they may even have the opposite effect, promoting the very problems they are supposed to stamp out.

It's little surprise that antioxidants have acquired a reputation as miracle health supplements. As long ago as the 1950s, scientists discovered that many diseases - including heart disease, strokes, cancer, diabetes, cataracts, arthritis and neurodegenerative disorders such as Parkinson's and Alzheimer's - were linked to damage caused by highly destructive chemicals called free radicals.

Free radicals are compounds with unpaired electrons that stabilise themselves by oxidising other molecules - including proteins, carbohydrates, lipids and DNA. In the process they often create more free radicals, sparking off a chain of destruction. Oxidative damage accompanies most, if not all, diseases and has even been proposed as a direct cause of some including lung cancer, atherosclerosis and Alzheimer's.

Free radicals are an unavoidable hazard of being alive. We live in an oxygen-rich atmosphere, and radicals, particularly reactive oxygen species (ROS), are natural by-products of respiration. "One per cent of the oxygen we consume turns into ROS," says biochemist Barry Halliwell from the National University of Singapore. "It doesn't sound like much but humans are big animals and we breathe a lot. Over a year a human body makes 1.7 kilograms of ROS." Exposure to X-rays, ozone, tobacco smoke, air pollutants, microbial infections, industrial chemicals and intensive exercise also trigger free radical production.

In the 1980s, however, a potential weapon against free radical damage appeared on the horizon. Scientists had known for a long time that people whose diets are rich in fruits and vegetables have a lower incidence of heart disease, diabetes, dementia, stroke and certain types of cancer - the very diseases that are associated with free radical damage. Now there was an explanation. Fruits and vegetables are a rich source of antioxidants that can neutralise free radicals by donating electrons to them.

Green plants are full of antioxidants for good reason. They are especially vulnerable to oxidative stress since they produce pure oxygen during photosynthesis. To protect themselves they manufacture an assortment of potent antioxidants.

And so a hypothesis was born: dietary antioxidants are free-radical sponges that can stave off the diseases of old age. It was a great idea. "Putting two and two together, scientists assumed that these antioxidants were protective, and that taking them as supplements or in fortified foods should decrease oxidative damage and diminish disease," says Halliwell, who pioneered research into free radicals and disease. "It was simple: we said free radicals are bad, antioxidants are good."

The concept helped spawn a colossal supplements industry. According to the US National Institutes of Health (NIH), more than half of US adults take some form of vitamin or mineral supplement at a total cost of $23 billion a year. The bewildering range of supplements on the shelves makes it hard to say how much of this expenditure goes on antioxidants, but the NIH says it is probably a "large proportion". And their popularity just keeps on growing. SPINS, a market research firm based in San Francisco, estimates that the antioxidant market has grown by 18 per cent in the past year alone.

The best known antioxidants are vitamin E (also known by its chemical name tocopherol), vitamin C, and two broad classes of plant chemicals called polyphenols (including flavonoids) and carotenoids (including beta carotene and lycopene). Most supplements touted as antioxidants contain at least one of these, often as a pure chemical and sometimes as a concentrated plant extract.

Since the early 1990s scientists have been putting these compounds through their paces, using double-blind randomised controlled trials - the gold standard for medical intervention studies. Time and again, however, the supplements failed to pass the test. True, they knock the wind out of free radicals in a test tube. But once inside the human body, they seem strangely powerless. Not only are they bad at preventing oxidative damage, they can even make things worse. Many scientists are now concluding that, at best, they are a waste of time and money. At worst they could be harmful.

The first antioxidant to produce disappointing results was beta carotene. Once a star among supplements, beta carotene pills were recommended to smokers to protect them against lung cancer. This was largely based on the observation, made in the 1970s, that people who ate a lot of carrots - which contain large quantities of beta carotene - had some protection against cancer.

In 1992 researchers at the US National Cancer Institute set about testing beta carotene. They recruited more than 18,000 people at high risk of developing lung cancer, either because they smoked or had been exposed to asbestos, and gave around half of them beta carotene supplements. The trial was supposed to run for six years, but the researchers pulled the plug two-thirds of the way through after discovering, to their surprise and horror, that those taking supplements were faring worse than the controls. Their lung cancer rate was 28 per cent higher, and the overall death rate was up 17 per cent. "It was a shock. It not only did no good but had the potential to do harm," Halliwell says.

The researchers couldn't be sure that these increases were not caused by chance, and beta carotene capsules are still widely sold as an antioxidant. Further trials, though, have strengthened the evidence that beta carotene supplements not only fail to protect people against cancer but can also increase the risk of lung cancer in smokers. In May of this year an expert panel convened by the NIH concluded that there was no evidence to recommend beta carotene supplements for the general population, and strong evidence to recommend that smokers avoid it.

It's a similar story with the world's most popular antioxidant. Vitamin E shot to fame in the early 1990s, after two large studies involving more than 127,000 people in total found that those with a diet high in vitamin E were significantly less likely to develop cardiovascular disease. The first study followed 87,245 female nurses for eight years; it found that the top 20 per cent with respect to vitamin E consumption had a 41 per cent lower incidence of cardiovascular disease than the bottom 20 per cent (New England Journal of Medicine, vol 328, p 1444). The second study, involving 39,910 male health professionals, found a similar reduction in heart disease risk (New England Journal of Medicine, vol 328, p 1450).

The researchers, based at Harvard Medical School and Harvard School of Public Health, even had a plausible mechanism. Evidence was emerging that one of the causes of heart disease was free radical damage to LDLs, tiny packages of lipid and protein that circulate in the bloodstream, delivering fatty acids to cells. It turned out that adding vitamin E to blood samples in the test tube made LDL more resistant to oxidation. Perhaps this was how vitamin E prevented heart disease. "At the biochemical level, the rationale sounded so good - at that time," says Roland Stocker, a biochemist at the University of New South Wales in Sydney, Australia.

Use of vitamin E supplements soared. In 1990, almost nobody took vitamin E; by the end of the decade an estimated 23 million US citizens were knocking back daily doses.

On the back of these positive results, other researchers set up large studies using vitamin E supplements. The results, however, have been almost universally disappointing. Only one experiment - the Cambridge heart antioxidant study (CHAOS) - found a positive effect, a 77 per cent reduced risk of heart attack. Several others found no protective effect and one even concluded that vitamin E increased the risk of heart failure.

Time for a rethink?

Other trials designed to test whether vitamin E supplements could prevent cancers, such as the ATBC study in Finland, also came in negative. Vitamin E also did not halt the progression to Alzheimer's disease in people with mild cognitive impairment.

What is more, when scientists went looking for evidence that vitamin E protected LDL against oxidation in the body, not just in the test tube, they found none - except in people with vitamin E deficiency (Journal of the American Medical Association, vol 285, p 1178). In fact, despite good evidence that vitamin E is a powerful antioxidant in the test tube, there is now serious doubt that it acts the same way in the body. "Vitamin E is not an antioxidant. In fact it must be protected against oxidation," says Angelo Azzi, a biochemist at Tufts University in Boston, Massachusetts. He points out that vitamin E exists in eight different forms in nature, all of which function as antioxidants in the test tube. Yet the body only uses one form, alpha tocopherol, which is pulled out of the bloodstream by a highly specialised protein in the liver. All the other forms are excreted. Azzi argues that evolution is unlikely to have gone to such great lengths simply to obtain an antioxidant from the diet. "There are millions of antioxidants," he says.

Vitamin E is clearly doing something in the body - it is an essential part of the diet and deficiency leads to neurological problems - but whatever it's doing, it's not an antioxidant.

There is even some evidence that vitamin E supplements can be harmful. Last year, a team led by Edgar Miller of the Johns Hopkins Medical Institutions in Baltimore made headline news when they amalgamated the results of 19 separate trials and concluded that high doses of vitamin E increase overall mortality (Annals of Internal Medicine, vol 142, p 37) - though this conclusion remains controversial. "It's flawed," asserts Azzi. "We re-analysed the data and there is no change in mortality." "Most people agree that there is no good evidence that large doses are harmful," adds Stocker.

Vitamin C is another disappointment. "People are still trying to defend it, but you don't get an effect on free radical damage unless you start with people with a vitamin C deficiency," says Halliwell. "I think it is a lost cause." In fact, results from a vast US trial probing the links between diet and health, called the Women's Health Study, suggest that vitamin C supplements may accelerate atherosclerosis in some people with diabetes.

One class of antioxidants that remains relatively unresearched is polyphenols. What little evidence there is comes from epidemiological studies, some of which suggest that polyphenols prevent disease and others of which do not. While polyphenols act as antioxidants in the test tube, it is not clear that they are absorbed into the bloodstream, and if they are, they are swiftly metabolised. For example, 95 per cent of a flavonoid called resveratrol - the one found in red wine - is destroyed by our digestive system before it enters circulation.

The conclusion is becoming clear: whatever is behind the health benefits of a diet rich in fruits and vegetables, you cannot reproduce it by taking purified extracts or vitamin supplements. "Just because a food with a certain compound in it is beneficial, it does not mean a nutraceutical [with the same compound in] is," said Paul Coates, who works in the Office of Dietary Supplements at NIH.

Yet the fact remains that people eating diets abundant in vitamin C, vitamin E, polyphenols and carotenoids are less likely to suffer heart attacks, vascular disease, diabetes and cancer. One explanation is that these people have a generally healthier lifestyle - they exercise more and smoke less, for example. For now, no one knows for sure.

Tough vegetables

There are some ideas. Halliwell still believes that antioxidants are at least partly responsible. He argues that because the polyphenols, carotenoids and vitamins in fruit and vegetables are bound into tough, fibrous material, they hang around in the stomach and colon, where they can neutralise free radicals. The gastrointestinal tract, especially the stomach with its highly acidic environment, is constantly generating reactive oxygen species from food. Supplements may not replicate this effect because they are digested too quickly.

Andrew Shao from the Council for Responsible Nutrition, a supplement industry trade association based in Washington DC, argues along similar lines. He says that pulling a nutrient out of context and testing it in a clinical trial is not appropriate. "Antioxidants should not be expected to perform as drugs," he insists. "That's simply not how nutrients work. They work in concert with each other."

There's yet another, more intriguing explanation. Among the leading sources of dietary antioxidants are tea and coffee, and there is some evidence that green tea in particular is linked with health benefits including reduced risk of cancer and cardiovascular disease. Oddly, though, Halliwell has discovered that tea and coffee are also bursting with reactive oxygen species in the form of hydrogen peroxide.

"Every time you drink a cup of coffee it's a dilute bowl of hydrogen peroxide," says Halliwell. The hydrogen peroxide is there because of the presence of the antioxidants - "antioxidants" is really just another way of saying reducing agent, which can react with oxygen in the water to produce hydrogen peroxide. Think platinum blond, and you get the picture of what you might be drinking.

But if free radicals are bad for us, how come coffee and tea might be beneficial? One possibility is that they can help nudge our own internal antioxidant systems into action. "There has been a considerable rethink as to what free radicals are doing," says Malcolm Jackson, a biochemist at the University of Liverpool, UK. He believes that in the right quantities radicals can be positively health-enhancing, prompting our cells to fire up their own internal defence machinery: a battery of radical-busting enzymes such as catalase and superoxide dismutase. "Cells are very good at protecting themselves against minor stresses, as long as they are not excessive," says Jackson. "The question is: should we be quenching free radicals at all?"

If it turns out that antioxidants in food work because they generate health-promoting quantities of free radicals, that would be an ironic turnaround. It may also explain why supplements and extracts don't seem to work or may even be dangerous: the doses are too high, and produce too many free radicals.

For now, the advice is simple. "Stick to flavonoid-rich foods, red wine in moderation, tea, fruits and vegetables," says Halliwell. "Don't start taking high-dose supplements or heavily fortified foods, until we know more."

From issue 2563 of New Scientist magazine, 05 August 2006, page 40-43

do your worst :)

December 4, 2007
MIND
Unhappy? Self-Critical? Maybe You're Just a Perfectionist
By BENEDICT CAREY
NY Times

Just about any sports movie, airport paperback or motivational tape delivers a few boilerplate rules for success. Believe in yourself. Don’t take no for an answer. Never quit. Don’t accept second best.

Above all, be true to yourself.

It’s hard to argue with those maxims. They seem self-evident — if not written into the Constitution, then at least part of the cultural water supply that irrigates everything from halftime speeches to corporate lectures to SAT coaching classes.

Yet several recent studies stand as a warning against taking the platitudes of achievement too seriously. The new research focuses on a familiar type, perfectionists, who panic or blow a fuse when things don’t turn out just so. The findings not only confirm that such purists are often at risk for mental distress — as Freud, Alfred Adler and countless exasperated parents have long predicted — but also suggest that perfectionism is a valuable lens through which to understand a variety of seemingly unrelated mental difficulties, from depression to compulsive behavior to addiction.

Some researchers divide perfectionists into three types, based on answers to standardized questionnaires: Self-oriented strivers who struggle to live up to their high standards and appear to be at risk of self-critical depression; outwardly focused zealots who expect perfection from others, often ruining relationships; and those desperate to live up to an ideal they’re convinced others expect of them, a risk factor for suicidal thinking and eating disorders.

“It’s natural for people to want to be perfect in a few things, say in their job — being a good editor or surgeon depends on not making mistakes,” said Gordon L. Flett, a psychology professor at York University and an author of many of the studies. “It’s when it generalizes to other areas of life, home life, appearance, hobbies, that you begin to see real problems.”

Unlike people given psychiatric labels, however, perfectionists neither battle stigma nor consider themselves to be somehow dysfunctional. On the contrary, said Alice Provost, an employee assistance counselor at the University of California, Davis, who recently ran group therapy for staff members struggling with perfectionist impulses. “They’re very proud of it,” she said. “And the culture highly values and reinforces their attitudes.”

Consider a recent study by psychologists at Curtin University of Technology in Australia, who found that the level of “all or nothing” thinking predicted how well perfectionists navigated their lives. The researchers had 252 participants fill out questionnaires rating their level of agreement with 16 statements like “I think of myself as either in control or out of control” and “I either get on very well with people or not at all.”

The more strongly participants in the study thought in this either-or fashion, the more likely they were to display the kind of extreme perfectionism that can lead to mental health problems.

In short, these are people who not only swallow many of the maxims for success but take them as absolutes. At some level they know that it’s possible to succeed after falling short (build on your mistakes: another boilerplate rule). The trouble is that falling short still reeks of mediocrity; for them, to say otherwise is to spin the result.

Never accept second best. Always be true to yourself.

The burden of perfectionist expectations is all too familiar to anyone who has struggled to kick a bad habit. Break down just once — have one smoke, one single drink — and at best it’s a “slip.” At worst it’s a relapse, and more often it’s a fall off the wagon: failure. And if you’ve already fallen, well, may as well pour yourself two or three more.

This is why experts have long debated the wisdom of insisting on abstinence as necessary in treating substance abuse. Most rehab clinics are based on this principle: Either you’re clean or you’re not; there’s no safe level of use. This approach has unquestionably worked for millions of addicts, but if the studies of perfectionists are any guide it has undermined the efforts of many others.

Ms. Provost said those in her program at U.C. Davis often displayed symptoms of obsessive-compulsive disorder — another risk for perfectionists. They couldn’t bear a messy desk. They found it nearly impossible to leave a job half-done, to do the next day. Some put in ludicrously long hours redoing tasks, chasing an ideal only they could see.

As an experiment, Ms. Provost had members of the group slack off on purpose, against their every instinct. “This was mostly in the context of work,” she said, “and they seem like small things, because what some of them considered failure was what most people would consider no big deal.”

Leave work on time. Don’t arrive early. Take all the breaks allowed. Leave the desk a mess. Allow yourself a set number of tries to finish a job; then turn in what you have.

“And then ask: Did you get punished? Did the university continue to function? Are you happier?” Ms. Provost said. “They were surprised that yes, everything continued to function, and the things they were so worried about weren’t that crucial.”

The British have a saying that encourages people to show their skills while mocking the universal fear of failure: Do your worst.

If you can’t tolerate your worst, at least once in a while, how true to yourself can you be?

what if no one's ever proved that saturated fat clogs arteries?

What if bad fat isn’t so bad?
No one's ever proved that saturated fat clogs arteries, causes heart disease
By Nina Teicholz
Mens Health
Dec. 13, 2007

Suppose you were forced to live on a diet of red meat and whole milk. A diet that, all told, was at least 60 percent fat — about half of it saturated. If your first thoughts are of statins and stents, you may want to consider the curious case of the Masai, a nomadic tribe in Kenya and Tanzania.

In the 1960s, a Vanderbilt University scientist named George Mann, M.D., found that Masai men consumed this very diet (supplemented with blood from the cattle they herded). Yet these nomads, who were also very lean, had some of the lowest levels of cholesterol ever measured and were virtually free of heart disease.

Scientists, confused by the finding, argued that the tribe must have certain genetic protections against developing high cholesterol. But when British researchers monitored a group of Masai men who moved to Nairobi and began consuming a more modern diet, they discovered that the men's cholesterol subsequently skyrocketed.

Similar observations were made of the Samburu — another Kenyan tribe — as well as the Fulani of Nigeria. While the findings from these cultures seem to contradict the fact that eating saturated fat leads to heart disease, it may surprise you to know that this "fact" isn't a fact at all. It is, more accurately, a hypothesis from the 1950s that's never been proved.

The first scientific indictment of saturated fat came in 1953. That's the year a physiologist named Ancel Keys, Ph.D., published a highly influential paper titled "Atherosclerosis, a Problem in Newer Public Health." Keys wrote that while the total death rate in the United States was declining, the number of deaths due to heart disease was steadily climbing. And to explain why, he presented a comparison of fat intake and heart disease mortality in six countries: the United States, Canada, Australia, England, Italy, and Japan.

The Americans ate the most fat and had the greatest number of deaths from heart disease; the Japanese ate the least fat and had the fewest deaths from heart disease. The other countries fell neatly in between. The higher the fat intake, according to national diet surveys, the higher the rate of heart disease. And vice versa. Keys called this correlation a "remarkable relationship" and began to publicly hypothesize that consumption of fat causes heart disease. This became known as the diet-heart hypothesis.

At the time, plenty of scientists were skeptical of Keys's assertions. One such critic was Jacob Yerushalmy, Ph.D., founder of the biostatistics graduate program at the University of California at Berkeley. In a 1957 paper, Yerushalmy pointed out that while data from the six countries Keys examined seemed to support the diet-heart hypothesis, statistics were actually available for 22 countries. And when all 22 were analyzed, the apparent link between fat consumption and heart disease disappeared. For example, the death rate from heart disease in Finland was 24 times that of Mexico, even though fat-consumption rates in the two nations were similar.

The other salient criticism of Keys's study was that he had observed only a correlation between two phenomena, not a clear causative link. So this left open the possibility that something else — unmeasured or unimagined — was leading to heart disease. After all, Americans did eat more fat than the Japanese, but perhaps they also consumed more sugar and white bread, and watched more television.

Despite the apparent flaws in Keys's argument, the diet-heart hypothesis was compelling, and it was soon heavily promoted by the American Heart Association (AHA) and the media. It offered the worried public a highly educated guess as to why the country was in the midst of a heart-disease epidemic. "People should know the facts," Keys said in a 1961 interview with Time magazine, for which he appeared on the cover. "Then if they want to eat themselves to death, let them."

The seven-countries study, published in 1970, is considered Ancel Keys's landmark achievement. It seemed to lend further credence to the diet-heart hypothesis. In this study, Keys reported that in the seven countries he selected — the United States, Japan, Italy, Greece, Yugoslavia, Finland, and the Netherlands — animal-fat intake was a strong predictor of heart attacks over a 5-year period. Just as important, he noted an association between total cholesterol and heart-disease mortality. This prompted him to conclude that the saturated fats in animal foods — and not other types of fat — raise cholesterol and ultimately lead to heart disease.

Naturally, proponents of the diet-heart hypothesis hailed the study as proof that eating saturated fat leads to heart attacks. But the data was far from rock solid. That's because in three countries (Finland, Greece, and Yugoslavia), the correlation wasn't seen.

For example, eastern Finland had five times as many heart-attack fatalities and twice as much heart disease as western Finland, despite only small differences between the two regions in animal-fat intake and cholesterol levels. And while Keys provided that raw data in his report, he glossed over it as a finding. Perhaps a larger problem, though, was his assumption that saturated fat has an unhealthy effect on cholesterol levels.

Trio of saturated fats
Although more than a dozen types of saturated fat exist, humans predominantly consume three: stearic acid, palmitic acid, and lauric acid. This trio comprises almost 95 percent of the saturated fat in a hunk of prime rib, a slice of bacon, or a piece of chicken skin, and nearly 70 percent of that in butter and whole milk.

Today, it's well established that stearic acid has no effect on cholesterol levels. In fact, stearic acid — which is found in high amounts in cocoa as well as animal fat — is converted to a monounsaturated fat called oleic acid in your liver. This is the same heart-healthy fat found in olive oil. As a result, scientists generally regard this saturated fatty acid as either benign or potentially beneficial to your health.

Palmitic and lauric acid, however, are known to raise total cholesterol. But here's what's rarely reported: Research shows that although both of these saturated fatty acids increase LDL ("bad") cholesterol, they raise HDL ("good") cholesterol just as much, if not more. And this lowers your risk of heart disease. That's because it's commonly believed that LDL cholesterol lays down plaque on your artery walls, while HDL removes it. So increasing both actually reduces the proportion of bad cholesterol in your blood to the good kind. This may explain why numerous studies have reported that this HDL/LDL ratio is a better predictor of future heart disease than LDL alone.

All of this muddies Keys's claim of a clear connection between saturated-fat intake, cholesterol, and heart disease. If saturated fat doesn't raise cholesterol in such a way that it increases heart-disease risk, then according to the scientific method, the diet-heart hypothesis must be rejected. However, in 1977 it was still a promising idea.

That was the year Congress made it government policy to recommend a low-fat diet, based primarily on the opinions of health experts who supported the diet-heart hypothesis. It was a decision met with much criticism from the scientific community, including the American Medical Association. After all, officially endorsing a low-fat diet could change the eating habits of millions of Americans, and the potential effects of this strategy were widely debated and certainly unproved.

We've spent billions of our tax dollars trying to prove the diet-heart hypothesis. Yet study after study has failed to provide definitive evidence that saturated-fat intake leads to heart disease. The most recent example is the Women's Health Initiative, the government's largest and most expensive ($725 million) diet study yet. The results, published last year, show that a diet low in total fat and saturated fat had no impact in reducing heart-disease and stroke rates in some 20,000 women who had adhered to the regimen for an average of 8 years.

But this paper, like many others, plays down its own findings and instead points to four studies that, many years ago, apparently did find a link between saturated fat and heart disease. Because of this, it's worth taking a closer look at each.

The Los Angeles VA Hospital Study (1969) This UCLA study of 850 men reported that those who replaced saturated fats with polyunsaturated fats were less likely to die of heart disease and stroke over a 5-year period than were men who didn't alter their diets. However, more of those who changed their diets died of cancer, and the average age of death was the same in both groups. What's more, "through an oversight," the study authors neglected to collect crucial data on smoking habits from about 100 men. They also reported that the men successfully adhered to the diet only half the time.

The Oslo Diet-Heart Study (1970) Two hundred men followed a diet low in saturated fat for 5 years while another group ate as they pleased. The dieters had fewer heart attacks, but there was no difference in total deaths between the two groups.

The Finnish Mental Hospital Study (1979) This trial took place from 1959 to 1971 and appeared to document a reduction in heart disease in psychiatric patients following a "cholesterol-lowering" diet. But the experiment was poorly controlled: Almost half of the 700 participants joined or left the study over its 12-year duration.

The St. Thomas' Atherosclerosis Regression Study (1992) Only 74 men completed this 3-year study conducted at St. Thomas' Hospital, in London. It found a reduction in cardiac events among men with heart disease who adopted a low-fat diet. There's a major caveat, though: Their prescribed diets were also low in sugar.

Flawed studies
These four studies, even though they have serious flaws and are tiny compared with the Women's Health Initiative, are often cited as definitive proof that saturated fats cause heart disease. Many other more recent trials cast doubt on the diet-heart hypothesis. These studies should be considered in the context of all the other research.

In 2000, a respected international group of scientists called the Cochrane Collaboration conducted a "meta-analysis" of the scientific literature on cholesterol-lowering diets. After applying rigorous selection criteria (219 trials were excluded), the group examined 27 studies involving more than 18,000 participants. Although the authors concluded that cutting back on dietary fat may help reduce heart disease, their published data actually shows that diets low in saturated fats have no significant effect on mortality, or even on deaths due to heart attacks.

"I was disappointed that we didn't find something more definitive," says Lee Hooper, Ph.D., who led the Cochrane review. If this exhaustive analysis didn't provide evidence of the dangers of saturated fat, says Hooper, it was probably because the studies reviewed didn't last long enough, or perhaps because the participants didn't lower their saturated-fat intake enough. Of course, there is a third possibility, which Hooper doesn't mention: The diet-heart hypothesis is incorrect.

Ronald Krauss, M.D., won't say saturated fats are good for you. "But," he concedes, "we don't have convincing evidence that they're bad, either."

For 30 years, Dr. Krauss — an adjunct professor of nutritional sciences at the University of California at Berkeley — has been studying the effect of diet and blood lipids on cardiovascular disease. He points out that while some studies show that replacing saturated fats with unsaturated fats lowers heart-disease risk, this doesn't mean that saturated fats lead to clogged arteries. "It may simply suggest that unsaturated fats are an even healthier option," he says.

But there's more to this story: In 1980, Dr. Krauss and his colleagues discovered that LDL cholesterol is far from the simple "bad" particle it's commonly thought to be. It actually comes in a series of different sizes, known as subfractions. Some LDL subfractions are large and fluffy. Others are small and dense. This distinction is important.

A decade ago, Canadian researchers reported that men with the highest number of small, dense LDL subfractions had four times the risk of developing clogged arteries than those with the fewest. Yet they found no such association for the large, fluffy particles. These findings were confirmed in subsequent studies.

Link to heart disease
Now here's the saturated-fat connection: Dr. Krauss found that when people replace the carbohydrates in their diet with fat — saturated or unsaturated — the number of small, dense LDL particles decreases. This leads to the highly counterintuitive notion that replacing your breakfast cereal with eggs and bacon could actually reduce your risk of heart disease.

Men, more than women, are predisposed to having small, dense LDL. However, the propensity is highly flexible and, according to Dr. Krauss, can be switched on when people eat high-carb, low-fat diets or switched off when they reduce carbs and eat diets high in fat, including the saturated variety. "There's a subgroup of people at high risk of heart disease who may respond well to diets low in fat," says Dr. Krauss. "But the majority of healthy people seem to derive very little benefit from these low-fat diets, in terms of heart-disease risk factors, unless they also lose weight and exercise. And if a low-fat diet is also loaded with carbs, it can actually result in adverse changes in blood lipids."

While Dr. Krauss is much published and highly respected — he has served twice as chairman of the writing committee of the AHA's dietary guidelines — the far-reaching implications of his work have not been generally acknowledged. "Academic scientists believe saturated fat is bad for you," says Penny Kris-Etherton, Ph.D., a distinguished professor of nutritional studies at Penn State University, citing as evidence the "many studies" she believes show it to be true. But not everyone accepts those studies, and their proponents find it hard to be heard. Kris-Etherton acknowledges that "there's a good deal of reluctance toward accepting evidence suggesting the contrary."

Take, for example, a 2004 Harvard University study of older women with heart disease. Researchers found that the more saturated fat these women consumed, the less likely it was their condition would worsen. Lead study author Dariush Mozaffarian, Ph.D., an assistant professor at Harvard's school of public health, recalls that before the paper was published in the American Journal of Clinical Nutrition, he encountered formidable politics from other journals.

"In the nutrition field, it's very difficult to get something published that goes against established dogma," says Mozaffarian. "The dogma says that saturated fat is harmful, but that is not based, to me, on unequivocal evidence." Mozaffarian says he believes it's critical that scientists remain open minded. "Our finding was surprising to us. And when there's a discovery that goes against what's established, it shouldn't be suppressed but rather disseminated and explored as much as possible."

Biased studies
Perhaps the apparent bias against saturated fat is most evident in studies on low-carbohydrate diets. Many versions of this approach are controversial because they place no limitations on saturated-fat intake. As a result, supporters of the diet-heart hypothesis have argued that low-carb diets will increase the risk of heart disease. But published research doesn't show this to be the case. When people on low-carb diets have been compared head-to-head with those on low-fat diets, the low-carb dieters typically scored significantly better on markers of heart disease, including small, dense LDL cholesterol, HDL/LDL ratio, and triglycerides, which are a measure of the amount of fat circulating in your blood.

For example, in a new 12-week study, University of Connecticut scientists placed overweight men and women on either a low-carb or low-fat diet. Those who followed the low-carb diet consumed 36 grams of saturated fat per day (22 percent of total calories), which represented more than three times the amount in the low-fat diet. Yet despite this considerably greater intake of saturated fat, the low-carb dieters reduced both their number of small, dense LDL cholesterol and their HDL/LDL ratio to a greater degree than those who ate a low-fat diet. In addition, triglycerides decreased by 51 percent in the low-carb group — compared with 19 percent in the low-fat group.

This finding is worth noting, because even though cholesterol is the most commonly cited risk factor for heart disease, triglyceride levels may be equally relevant. In a 40-year study at the University of Hawaii, scientists found that low triglyceride levels at middle age best predicted "exceptional survival" — defined as living until age 85 without suffering from a major disease.

According to lead study author Jeff Volek, Ph.D., R.D., two factors influence the amount of fat coursing through your veins. The first, of course, is the amount of fat you eat. But the more important factor is less obvious. Turns out, your body makes fat from carbohydrates. It works like this: The carbs you eat (particularly starches and sugar) are absorbed into your bloodstream as sugar. As your carb intake rises, so does your blood sugar. This causes your body to release the hormone insulin. Insulin's job is to return your blood sugar to normal, but it also signals your body to store fat. As a result, your liver starts converting excess blood sugar to triglycerides, or fat.

All of which helps explain why the low-carb dieters in Volek's study had a greater loss of fat in their blood. Restricting carbs keeps insulin levels low, which lowers your internal production of fat and allows more of the fat you do eat to be burned for energy.

Yet even with this emerging data and the lack of scientific support for the diet-heart hypothesis, the latest AHA dietary guidelines have reduced the recommended amount of saturated fat from 10 percent of daily calories to 7 percent or less. "The idea was to encourage people to decrease their saturated-fat intake even further, because there's a linear relationship between saturated-fat intake and LDL cholesterol," says Alice H. Lichtenstein, Ph.D., Sc.D., who led the AHA nutrition committee that wrote the recommendation.

What about Krauss's findings that not all LDL is equal? Lichtenstein says that her committee didn't address them, but that it might in the future.

It could be that it's not bad foods that cause heart disease, it's bad habits. After all, in Volek's study, participants who followed the low-fat diet — which was high in carbs — also decreased their triglycerides. "The key factor is that they weren't overeating," says Volek. "This allowed the carbohydrates to be used for energy rather than converted to fat." Perhaps this is the most important point of all. If you consistently consume more calories than you burn, and you gain weight, your risk of heart disease will increase — whether you favor eating saturated fats, carbs, or both.

But if you're living a healthy lifestyle — you aren't overweight, you don't smoke, you exercise regularly — then the composition of your diet may matter much less. And, based on the research of Volek and Dr. Krauss, a weight-loss or -maintenance diet in which some carbohydrates are replaced with fat — even if it's saturated — will reduce markers of heart-disease risk more than if you followed a low-fat, high-carb diet.

"The message isn't that you should gorge on butter, bacon, and cheese," says Volek. "It's that there's no scientific reason that natural foods containing saturated fat can't, or shouldn't, be part of a healthy diet."

low carb diet reduces inflammation

Low-carb Diet Reduces Inflammation And Blood Saturated Fat In Metabolic Syndrome
ScienceDaily
Dec. 4, 2007

Metabolic syndrome is a condition afflicting one quarter to one third of adult men and women and is an established pre-cursor to diabetes, coronary heart disease, and other serious illnesses. Patients have long been advised to eat a low-fat diet even though carbohydrate restriction has been found to be more effective at reducing specific markers, such as high triglycerides, characteristic of the syndrome. Now, a new study indicates that a diet low in carbohydrates is also more effective than a diet low in fat in reducing saturated fatty acids in the blood and reducing markers of inflammation.

While there have been contradictory and confusing messages directed at health conscious consumers about dietary recommendations, most researchers agree on the need to limit inflammatory agents. In a report published in the on-line version of the journal Lipids, researchers at the University of Connecticut with co-authors from SUNY Downstate Medical Center in Brooklyn, the University of Minnesota, and the University of California show much greater improvement in inflammatory markers in patients with metabolic syndrome on a very low carbohydrate approach compared to a low fat diet.

Lead researcher Jeff S. Volek, PhD, RD, associate professor of kinesiology at the University of Connecticut, describes the study as "adding to the evolving picture of improvement in general health beyond simple weight loss in keeping blood glucose and insulin under control." The work is part of a larger study (currently under review) showing numerous improvements in blood lipids. The current work concludes that "lowering total and saturated fat only had a small effect on circulating inflammatory markers whereas reducing carbohydrate led to considerably greater reductions in a number of pro-inflammatory cytokines, chemokines, and adhesion molecules. These data implicate dietary carbohydrate rather than fat as a more significant nutritional factor contributing to inflammatory processes."

Richard Feinman, PhD, professor of biochemistry at SUNY Downstate Medical Center, adds, "The real importance of diets that lower carbohydrate content is that they are grounded in mechanism -- carbohydrates stimulate insulin secretion which biases fat metabolism towards storage rather than oxidation. The inflammation results open a new aspect of the problem. From a practical standpoint, continued demonstrations that carbohydrate restriction is more beneficial than low fat could be good news to those wishing to forestall or manage the diseases associated with metabolic syndrome."

One of the remarkable effects in the data presented that may have contributed to the results is that despite the three-fold greater saturated fat in the diet for the low carb group, saturated fat in the blood turned out to be higher in the low fat group due to the process known as carbohydrate-induced lipogenesis. Dr. Volek points out that "this clearly shows the limitations of the idea that 'you are what you eat.' Metabolism plays a big role. You are what your body does with what you eat."

low-carb diet improves metabolic syndrome?

Low-carb Diet Better Than Low-fat Diet At Improving Metabolic Syndrome
ScienceDaily
Nov. 16, 2005

Is a low-carb diet better than low-fat diet at improving metabolic syndrome and the associated diabetes and cardiovascular diseases. In an article published today in the open access journal Nutrition & Metabolism, Jeff Volek and Richard Feinman review the literature and show that the features of metabolic syndrome are precisely those that are improved by reducing carbohydrates in the diet.

Metabolic syndrome is a cluster of health signs that may occur together and indicate a risk for diabetes, stroke and heart disease. The markers of metabolic syndrome -- high blood pressure, low HDL levels, high triglycerides, obesity, high blood glucose and high insulin levels -- are all improved by a low carbohydrate diet. By contrast, the evidence shows that they are not improved, and can even be worsened by low fat/high carbohydrate diets.

Previous research has never explicitly connected low carbohydrate intake and improvement of metabolic syndrome. The general recommendation to patients has been to focus on reducing fat intake. Volek et al. argue that the cause of metabolic syndrome is linked to insulin imbalance. Carbohydrates are the main stimulus for insulin, and reducing carbohydrate can be effective at restoring insulin responses. So reducing carbohydrate intake, not fat intake, should be the main aspect of treatment for metabolic syndrome, the authors argue. This is supported by data from previous research, which shows that carbohydrate reduction is more effective than fat reduction at improving all the components of metabolic syndrome.

what if it's all been a big lie

NY Times
July 7, 2002
What if It's All Been a Big Fat Lie?
By GARY TAUBES

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Scary facts about industrial oils

remember the florence henderson wesson oil commercials? the fried chicken, hmmm... wholesome goodness, right? well, as it turns out, not so much.

modern industrial oils (ie. canola, soy, corn) are poison to your body. big Ag and the US govt has conducted an incredible experiment on the unsuspecting public. saturated fat villified to make way for new market opportunities. on a business level, this strategy has proved a market success. the hidden costs to the american public, however, are difficult to assess.

this is known:

industrial oils are stripped of nutrional value during processing and already rancid at point of purchase.

anza borrego

in god we trust, all others bring data

this most useful phrase comes from my engineering background.

join me in my quest to question nutritional conventional (ie. modern) wisdom with the goal of aggregating data that will serve as an objective reference point.

think a lowfat/high carb diet is healthy? think again.

The brain is 70% fat, which chiefly serves to insulate neurons. Fat is also the primary component of cell membranes. Changing the proportion of saturated to unsaturated fats in the diet changes the fat composition in these membranes. This could conceivably change the membrane permeability, which controls the transport of everything from glucose, signaling proteins, and hormones to bacteria, viruses, and tumor-causing agents into and out of the cell. The relative saturation of fats in the diet could also influence cellular aging as well as the clotting ability of blood cells.

there is a growing body of data that is questioning the validity of health benefit claims associated with a lowfat, high fiber diet. for example, while there seems to be no question that carrying extra weight negatively impacts cholesterol... treating your cholesterol with a lowfat regime isn't necessarily the most healthful option

foodies on the internets

Culinate
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san diego good eats

The Linkery $$$
Mama Testa Taqueria $$
Influx $

recommended food sources

Organic Pastures
OB People's Coop
San Diego Soy Company

nutritional information resources

Weston Price Foundation
The Ethicurean
The Daily Green
Nutrition Data

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To Market, To Market
Livin' La Vida Local
Alice Q. Foodie