Fw: [NH] What if It's All Been a Big Fat Lie?

September 2, 2002

i never expected to see it in the Times, but here is a good article on

dietary fats if you haven't seen it.

arnold

[NH] What if It's All Been a Big Fat Lie?

What if It's All Been a Big Fat Lie?

By Taubes (New York Times)

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

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

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 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.

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

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.

" A man's mind stretched to a new idea never goes back to its original

dimensions. "

Oliver Wendell Holmes

" I have sworn upon the altar of God, eternal hostility against every form

of tyranny over the mind of man. "

Jefferson*

" For the rest of my life I want to reflect on what Light is. "

Albert Einstein

September 3, 2002

Arnold thanks, you just made my life a little easier by posting this article

from Times magazine. It has been assigned to me for a presentation. Now I do

not have to buy it. Thanks, Tracey

September 3, 2002