Kind of OT, But Kind of On Topic

August 1, 2002

Hi, I found this very long article in the July 7, 2002, edition of

the New York Times on how scientists are rethinking the low-carb

diet. It's a long article, but I thought it might be useful as it

discusses low-carb, low glycemic diets. It doesn't mention rosacea

though.... Matija

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

Atkins, author of the phenomenally-best-selling ''Dr. Atkins' Diet

Revolution'' and ''Dr. Atkins' New Diet Revolution,'' accusing the

Manhattan doctor of quackery and fraud, only to discover that the

unrepentant Atkins was right all along. Or maybe it's this: they find

that their very own dietary recommendations -- eat less fat and more

carbohydrates -- are the cause of the rampaging epidemic of obesity

in America. Or, just possibly this: they find out both of the above

are true.

When Atkins first published his ''Diet Revolution'' in 1972,

Americans were just coming to terms with the proposition that fat --

particularly the saturated fat of meat and dairy products -- was the

primary nutritional evil in the American diet. Atkins managed to sell

millions of copies of a book promising that we would lose weight

eating steak, eggs and butter to our heart's desire, because it was

the carbohydrates, the pasta, rice, bagels and sugar, that caused

obesity and even heart disease. Fat, he said, was harmless.

Atkins allowed his readers to eat ''truly luxurious foods without

limit,'' as he put it, ''lobster with butter sauce, steak with

bearnaise sauce . . . bacon cheeseburgers,'' but allowed no starches

or refined carbohydrates, which means no sugars or anything made from

flour. Atkins banned even fruit juices, and permitted only a modicum

of vegetables, although the latter were negotiable as the diet

progressed.

Atkins was by no means the first to get rich pushing a high-fat diet

that restricted carbohydrates, but he popularized it to an extent

that the American Medical Association considered it a potential

threat to our health. The A.M.A. attacked Atkins's diet as

a ''bizarre regimen'' that advocated ''an unlimited intake of

saturated fats and cholesterol-rich foods,'' and Atkins even had to

defend his diet in Congressional hearings.

Thirty years later, America has become weirdly polarized on the

subject of weight. On the one hand, we've been told with almost

religious certainty by everyone from the surgeon general on down, and

we have come to believe with almost religious certainty, that obesity

is caused by the excessive consumption of fat, and that if we eat

less fat we will lose weight and live longer. On the other, we have

the ever-resilient message of Atkins and decades' worth of best-

selling diet books, including ''The Zone,'' ''Sugar Busters''

and ''Protein Power'' to name a few. All push some variation of what

scientists would call the alternative hypothesis: it's not the fat

that makes us fat, but the carbohydrates, and if we eat less

carbohydrates we will lose weight and live longer.

The perversity of this alternative hypothesis is that it identifies

the cause of obesity as precisely those refined carbohydrates at the

base of the famous Food Guide Pyramid -- the pasta, rice and bread --

that we are told should be the staple of our healthy low-fat diet,

and then on the sugar or corn syrup in the soft drinks, fruit juices

and sports drinks that we have taken to consuming in quantity if for

no other reason than that they are fat free and so appear

intrinsically healthy. While the low-fat-is-good-health dogma

represents reality as we have come to know it, and the government has

spent hundreds of millions of dollars in research trying to prove its

worth, the low-carbohydrate message has been relegated to the realm

of unscientific fantasy.

Over the past five years, however, there has been a subtle shift in

the scientific consensus. It used to be that even considering the

possibility of the alternative hypothesis, let alone researching it,

was tantamount to quackery by association. Now a small but growing

minority of establishment researchers have come to take seriously

what the low-carb-diet doctors have been saying all along. Walter

Willett, chairman of the department of nutrition at the Harvard

School of Public Health, may be the most visible proponent of testing

this heretic hypothesis. Willett is the de facto spokesman of the

longest-running, most comprehensive diet and health studies ever

performed, which have already cost upward of $100 million and include

data on nearly 300,000 individuals. Those data, says Willett, clearly

contradict the low-fat-is-good-health message ''and the idea that all

fat is bad for you; the exclusive focus on adverse effects of fat may

have contributed to the obesity epidemic.''

These researchers point out that there are plenty of reasons to

suggest that the low-fat-is-good-health hypothesis has now

effectively failed the test of time. In particular, that we are in

the midst of an obesity epidemic that started around the early

1980's, and that this was coincident with the rise of the low-fat

dogma. (Type 2 diabetes, the most common form of the disease, also

rose significantly through this period.) They say that low-fat weight-

loss diets have proved in clinical trials and real life to be dismal

failures, and that on top of it all, the percentage of fat in the

American diet has been decreasing for two decades. Our cholesterol

levels have been declining, and we have been smoking less, and yet

the incidence of heart disease has not declined as would be

expected. ''That is very disconcerting,'' Willett says. ''It suggests

that something else bad is happening.''

The science behind the alternative hypothesis can be called

Endocrinology 101, which is how it's referred to by 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 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 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 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 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 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.

ew 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 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 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.''

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 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 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

Mc'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 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

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 La, 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

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 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. , 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 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

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?''

Taubes is a correspondent for the journal Science and author

of ''Bad Science: The Short Life and Weird Times of Cold Fusion.

August 1, 2002