In depth NY Times article on weight management

[Guest guest]

What if the " Eat a low fat diet " advice turns out to be WRONG?

That's what an article from the New York Times Sunday Magazine discusses in

depth. The article is long, but informative -- it appears the author did a

good job researching material for the article. The article provides a good

historical perspective and context. This article has altered my thoughts on

the issue of weight management and will affect my eating habits in the

future. To read it, there is a catch. You have to create a free Internet

account with the NY Times.

 

www.nytimes.com/2002/07/07/magazine/07FAT.html?8hpist

 

Rich Putman

 

<A HREF= " http://earnsave.homestead.com/GroceryLetter.html " >What if your grocery

store sent you this letter?</A>

 

 

 

[Guest guest]

>What if the " Eat a low fat diet " advice turns out to be WRONG?

 

" Eat a low fat diet " has many variables not answered, doesn't it?

But, there are successful " diets " of 'eat low carbohydrates', 'eat low

protien', etc.

For *SOME* people it is wrong, for others it isn't.

 

Most of us realise there are subtle differences from one person to the next,

but the AMA still tries for the one-size-fits-all diet!

 

There is a book, " Eat right 4 your type " which considers the possibility

that maybe we are different.

It's a good start.

But also consider that we are capable of more than just calories in minus

calories out equals fat stored. There is no law requiring that relationship.

Our minds regulate our body shape, not the calories we eat.

Obesity is a function of the mind.

 

Be well,

 

steve

[Guest guest]

This article from NYTimes.com

has been sent to you by enquizical.

 

 

 

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

 

July 7, 2002

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 bearnaise sauce . . . bacon cheeseburgers,'' but

allowed no starches or refined carbohydrates, which means

no sugars or anything made from flour. Atkins banned even

fruit juices, and permitted only a modicum of vegetables,

although the latter were negotiable as the diet progressed.

 

 

Atkins was by no means the first to get rich pushing a

high-fat diet that restricted carbohydrates, but he

popularized it to an extent that the American Medical

Association considered it a potential threat to our health.

The A.M.A. attacked Atkins's diet as a ''bizarre regimen''

that advocated ''an unlimited intake of saturated fats and

cholesterol-rich foods,'' and Atkins even had to defend his

diet in Congressional hearings.

 

Thirty years later, America has become weirdly polarized on

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

with almost religious certainty by everyone from the

surgeon general on down, and we have come to believe with

almost religious certainty, that obesity is caused by the

excessive consumption of fat, and that if we eat less fat

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

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

best-selling diet books, including ''The Zone,'' ''Sugar

Busters'' and ''Protein Power'' to name a few. All push

some variation of what scientists would call the

alternative hypothesis: it's not the fat that makes us fat,

but the carbohydrates, and if we eat less carbohydrates we

will lose weight and live longer.

 

The perversity of this alternative hypothesis is that it

identifies the cause of obesity as precisely those refined

carbohydrates at the base of the famous Food Guide Pyramid

-- the pasta, rice and bread -- that we are told should be

the staple of our healthy low-fat diet, and then on the

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

sports drinks that we have taken to consuming in quantity

if for no other reason than that they are fat free and so

appear intrinsically healthy. While the

low-fat-is-good-health dogma represents reality as we have

come to know it, and the government has spent hundreds of

millions of dollars in research trying to prove its worth,

the low-carbohydrate message has been relegated to the

realm of unscientific fantasy.

 

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

shift in the scientific consensus. It used to be that even

considering the possibility of the alternative hypothesis,

let alone researching it, was tantamount to quackery by

association. Now a small but growing minority of

establishment researchers have come to take seriously what

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

Walter Willett, chairman of the department of nutrition at

the Harvard School of Public Health, may be the most

visible proponent of testing this heretic hypothesis.

Willett is the de facto spokesman of the longest-running,

most comprehensive diet and health studies ever performed,

which have already cost upward of $100 million and include

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

Willett, clearly contradict the low-fat-is-good-health

message ''and the idea that all fat is bad for you; the

exclusive focus on adverse effects of fat may have

contributed to the obesity epidemic.''

 

These researchers point out that there are plenty of

reasons to suggest that the low-fat-is-good-health

hypothesis has now effectively failed the test of time. In

particular, that we are in the midst of an obesity epidemic

that started around the early 1980's, and that this was

coincident with the rise of the low-fat dogma. (Type 2

diabetes, the most common form of the disease, also rose

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

weight-loss diets have proved in clinical trials and real

life to be dismal failures, and that on top of it all, the

percentage of fat in the American diet has been decreasing

for two decades. Our cholesterol levels have been

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

incidence of heart disease has not declined as would be

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

''It suggests that something else bad is happening.''

 

The science behind the alternative hypothesis can be called

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

Ludwig, a researcher at Harvard Medical School who runs the

pediatric obesity clinic at Children's Hospital Boston, and

who prescribes his own version of a carbohydrate-restricted

diet to his patients. Endocrinology 101 requires an

understanding of how carbohydrates affect insulin and blood

sugar and in turn fat metabolism and appetite. This is

basic endocrinology, Ludwig says, which is the study of

hormones, and it is still considered radical because the

low-fat dietary wisdom emerged in the 1960's from

researchers almost exclusively concerned with the effect of

fat on cholesterol and heart disease. At the time,

Endocrinology 101 was still underdeveloped, and so it was

ignored. Now that this science is becoming clear, it has to

fight a quarter century of anti-fat prejudice.

 

The alternative hypothesis also comes with an implication

that is worth considering for a moment, because it's a

whopper, and it may indeed be an obstacle to its

acceptance. If the alternative hypothesis is right -- still

a big ''if'' -- then it strongly suggests that the ongoing

epidemic of obesity in America and elsewhere is not, as we

are constantly told, due simply to a collective lack of

will power and a failure to exercise. Rather it occurred,

as Atkins has been saying (along with Barry Sears, author

of ''The Zone''), because the public health authorities

told us unwittingly, but with the best of intentions, to

eat precisely those foods that would make us fat, and we

did. We ate more fat-free carbohydrates, which, in turn,

made us hungrier and then heavier. Put simply, if the

alternative hypothesis is right, then a low-fat diet is not

by definition a healthy diet. In practice, such a diet

cannot help being high in carbohydrates, and that can lead

to obesity, and perhaps even heart disease. ''For a large

percentage of the population, perhaps 30 to 40 percent,

low-fat diets are counterproductive,'' says Eleftheria

Maratos-Flier, director of obesity research at Harvard's

prestigious Joslin Diabetes Center. ''They have the

paradoxical effect of making people gain weight.''

 

Scientists are still arguing about fat, despite a century

of research, because the regulation of appetite and weight

in the human body happens to be almost inconceivably

complex, and the experimental tools we have to study it are

still remarkably inadequate. This combination leaves

researchers in an awkward position. To study the entire

physiological system involves feeding real food to real

human subjects for months or years on end, which is

prohibitively expensive, ethically questionable (if you're

trying to measure the effects of foods that might cause

heart disease) and virtually impossible to do in any kind

of rigorously controlled scientific manner. But if

researchers seek to study something less costly and more

controllable, they end up studying experimental situations

so oversimplified that their results may have nothing to do

with reality. This then leads to a research literature so

vast that it's possible to find at least some published

research to support virtually any theory. The result is a

balkanized community -- ''splintered, very opinionated and

in many instances, intransigent,'' says Kurt Isselbacher, a

former chairman of the Food and Nutrition Board of the

National Academy of Science -- in which researchers seem

easily convinced that their preconceived notions are

correct and thoroughly uninterested in testing any other

hypotheses but their own.

 

What's more, the number of misconceptions propagated about

the most basic research can be staggering. Researchers will

be suitably scientific describing the limitations of their

own experiments, and then will cite something as gospel

truth because they read it in a magazine. The classic

example is the statement heard repeatedly that 95 percent

of all dieters never lose weight, and 95 percent of those

who do will not keep it off. This will be correctly

attributed to the University of Pennsylvania psychiatrist

Albert Stunkard, but it will go unmentioned that this

statement is based on 100 patients who passed through

Stunkard's obesity clinic during the Eisenhower

administration.

 

With these caveats, one of the few reasonably reliable

facts about the obesity epidemic is that it started around

the early 1980's. According to Katherine Flegal, an

epidemiologist at the National Center for Health

Statistics, the percentage of obese Americans stayed

relatively constant through the 1960's and 1970's at 13

percent to 14 percent and then shot up by 8 percentage

points in the 1980's. By the end of that decade, nearly one

in four Americans was obese. That steep rise, which is

consistent through all segments of American society and

which continued unabated through the 1990's, is the

singular feature of the epidemic. Any theory that tries to

explain obesity in America has to account for that.

Meanwhile, overweight children nearly tripled in number.

And for the first time, physicians began diagnosing Type 2

diabetes in adolescents. Type 2 diabetes often accompanies

obesity. It used to be called adult-onset diabetes and now,

for the obvious reason, is not.

 

So how did this happen? The orthodox and ubiquitous

explanation is that we live in what Kelly Brownell, a Yale

psychologist, has called a ''toxic food environment'' of

cheap fatty food, large portions, pervasive food

advertising and sedentary lives. By this theory, we are at

the Pavlovian mercy of the food industry, which spends

nearly $10 billion a year advertising unwholesome junk food

and fast food. And because these foods, especially fast

food, are so filled with fat, they are both irresistible

and uniquely fattening. On top of this, so the theory goes,

our modern society has successfully eliminated physical

activity from our daily lives. We no longer exercise or

walk up stairs, nor do our children bike to school or play

outside, because they would prefer to play video games and

watch television. And because some of us are obviously

predisposed to gain weight while others are not, this

explanation also has a genetic component -- the thrifty

gene. It suggests that storing extra calories as fat was an

evolutionary advantage to our Paleolithic ancestors, who

had to survive frequent famine. We then inherited these

''thrifty'' genes, despite their liability in today's toxic

environment.

 

This theory makes perfect sense and plays to our

puritanical prejudice that fat, fast food and television

are innately damaging to our humanity. But there are two

catches. First, to buy this logic is to accept that the

copious negative reinforcement that accompanies obesity --

both socially and physically -- is easily overcome by the

constant bombardment of food advertising and the lure of a

supersize bargain meal. And second, as Flegal points out,

little data exist to support any of this. Certainly none of

it explains what changed so significantly to start the

epidemic. Fast-food consumption, for example, continued to

grow steadily through the 70's and 80's, but it did not

take a sudden leap, as obesity did.

 

As far as exercise and physical activity go, there are no

reliable data before the mid-80's, according to William

Dietz, who runs the division of nutrition and physical

activity at the Centers for Disease Control; the 1990's

data show obesity rates continuing to climb, while exercise

activity remained unchanged. This suggests the two have

little in common. Dietz also acknowledged that a culture of

physical exercise began in the United States in the 70's --

the ''leisure exercise mania,'' as Robert Levy, director of

the National Heart, Lung and Blood Institute, described it

in 1981 -- and has continued through the present day.

 

As for the thrifty gene, it provides the kind of

evolutionary rationale for human behavior that scientists

find comforting but that simply cannot be tested. In other

words, if we were living through an anorexia epidemic, the

experts would be discussing the equally untestable

''spendthrift gene'' theory, touting evolutionary

advantages of losing weight effortlessly. An overweight

homo erectus, they'd say, would have been easy prey for

predators.

 

It is also undeniable, note students of Endocrinology 101,

that mankind never evolved to eat a diet high in starches

or sugars. ''Grain products and concentrated sugars were

essentially absent from human nutrition until the invention

of agriculture,'' Ludwig says, ''which was only 10,000

years ago.'' This is discussed frequently in the

anthropology texts but is mostly absent from the obesity

literature, with the prominent exception of the

low-carbohydrate-diet books.

 

What's forgotten in the current controversy is that the

low-fat dogma itself is only about 25 years old. Until the

late 70's, the accepted wisdom was that fat and protein

protected against overeating by making you sated, and that

carbohydrates made you fat. In ''The Physiology of Taste,''

for instance, an 1825 discourse considered among the most

famous books ever written about food, the French gastronome

Jean Anthelme Brillat-Savarin says that he could easily

identify the causes of obesity after 30 years of listening

to one ''stout party'' after another proclaiming the joys

of bread, rice and (from a ''particularly stout party'')

potatoes. Brillat-Savarin described the roots of obesity as

a natural predisposition conjuncted with the ''floury and

feculent substances which man makes the prime ingredients

of his daily nourishment.'' He added that the effects of

this fecula -- i.e., ''potatoes, grain or any kind of

flour'' -- were seen sooner when sugar was added to the

diet.

 

This is what my mother taught me 40 years ago, backed up by

the vague observation that Italians tended toward

corpulence because they ate so much pasta. This observation

was actually documented by Ancel Keys, a University of

Minnesota physician who noted that fats ''have good staying

power,'' by which he meant they are slow to be digested and

so lead to satiation, and that Italians were among the

heaviest populations he had studied. According to Keys, the

Neapolitans, for instance, ate only a little lean meat once

or twice a week, but ate bread and pasta every day for

lunch and dinner. ''There was no evidence of nutritional

deficiency,'' he wrote, ''but the working-class women were

fat.''

 

By the 70's, you could still find articles in the journals

describing high rates of obesity in Africa and the

Caribbean where diets contained almost exclusively

carbohydrates. The common thinking, wrote a former director

of the Nutrition Division of the United Nations, was that

the ideal diet, one that prevented obesity, snacking and

excessive sugar consumption, was a diet ''with plenty of

eggs, beef, mutton, chicken, butter and well-cooked

vegetables.'' This was the identical prescription

Brillat-Savarin put forth in 1825.

 

It was Ancel Keys, paradoxically, who introduced the

low-fat-is-good-health dogma in the 50's with his theory

that dietary fat raises cholesterol levels and gives you

heart disease. Over the next two decades, however, the

scientific evidence supporting this theory remained

stubbornly ambiguous. The case was eventually settled not

by new science but by politics. It began in January 1977,

when a Senate committee led by George McGovern published

its ''Dietary Goals for the United States,'' advising that

Americans significantly curb their fat intake to abate an

epidemic of ''killer diseases'' supposedly sweeping the

country. It peaked in late 1984, when the National

Institutes of Health officially recommended that all

Americans over the age of 2 eat less fat. By that time, fat

had become ''this greasy killer'' in the memorable words of

the Center for Science in the Public Interest, and the

model American breakfast of eggs and bacon was well on its

way to becoming a bowl of Special K with low-fat milk, a

glass of orange juice and toast, hold the butter -- a

dubious feast of refined carbohydrates.

 

In the intervening years, the N.I.H. spent several hundred

million dollars trying to demonstrate a connection between

eating fat and getting heart disease and, despite what we

might think, it failed. Five major studies revealed no such

link. A sixth, however, costing well over $100 million

alone, concluded that reducing cholesterol by drug therapy

could prevent heart disease. The N.I.H. administrators then

made a leap of faith. Basil Rifkind, who oversaw the

relevant trials for the N.I.H., described their logic this

way: they had failed to demonstrate at great expense that

eating less fat had any health benefits. But if a

cholesterol-lowering drug could prevent heart attacks, then

a low-fat, cholesterol-lowering diet should do the same.

''It's an imperfect world,'' Rifkind told me. ''The data

that would be definitive is ungettable, so you do your best

with what is available.''

 

Some of the best scientists disagreed with this low-fat

logic, suggesting that good science was incompatible with

such leaps of faith, but they were effectively ignored.

Pete Ahrens, whose Rockefeller University laboratory had

done the seminal research on cholesterol metabolism,

testified to McGovern's committee that everyone responds

differently to low-fat diets. It was not a scientific

matter who might benefit and who might be harmed, he said,

but ''a betting matter.'' Phil Handler, then president of

the National Academy of Sciences, testified in Congress to

the same effect in 1980. ''What right,'' Handler asked,

''has the federal government to propose that the American

people conduct a vast nutritional experiment, with

themselves as subjects, on the strength of so very little

evidence that it will do them any good?''

 

Nonetheless, once the N.I.H. signed off on the low-fat

doctrine, societal forces took over. The food industry

quickly began producing thousands of reduced-fat food

products to meet the new recommendations. Fat was removed

from foods like cookies, chips and yogurt. The problem was,

it had to be replaced with something as tasty and

pleasurable to the palate, which meant some form of sugar,

often high-fructose corn syrup. Meanwhile, an entire

industry emerged to create fat substitutes, of which

Procter & Gamble's olestra was first. And because these

reduced-fat meats, cheeses, snacks and cookies had to

compete with a few hundred thousand other food products

marketed in America, the industry dedicated considerable

advertising effort to reinforcing the

less-fat-is-good-health message. Helping the cause was what

Walter Willett calls the ''huge forces'' of dietitians,

health organizations, consumer groups, health reporters and

even cookbook writers, all well-intended missionaries of

healthful eating.

 

Few experts now deny that the low-fat message is radically

oversimplified. If nothing else, it effectively ignores the

fact that unsaturated fats, like olive oil, are relatively

good for you: they tend to elevate your good cholesterol,

high-density lipoprotein (H.D.L.), and lower your bad

cholesterol, low-density lipoprotein (L.D.L.), at least in

comparison to the effect of carbohydrates. While higher

L.D.L. raises your heart-disease risk, higher H.D.L.

reduces it.

 

What this means is that even saturated fats -- a k a, the

bad fats -- are not nearly as deleterious as you would

think. True, they will elevate your bad cholesterol, but

they will also elevate your good cholesterol. In other

words, it's a virtual wash. As Willett explained to me, you

will gain little to no health benefit by giving up milk,

butter and cheese and eating bagels instead.

 

But it gets even weirder than that. Foods considered more

or less deadly under the low-fat dogma turn out to be

comparatively benign if you actually look at their fat

content. More than two-thirds of the fat in a porterhouse

steak, for instance, will definitively improve your

cholesterol profile (at least in comparison with the baked

potato next to it); it's true that the remainder will raise

your L.D.L., the bad stuff, but it will also boost your

H.D.L. The same is true for lard. If you work out the

numbers, you come to the surreal conclusion that you can

eat lard straight from the can and conceivably reduce your

risk of heart disease.

 

The crucial example of how the low-fat recommendations were

oversimplified is shown by the impact -- potentially

lethal, in fact -- of low-fat diets on triglycerides, which

are the component molecules of fat. By the late 60's,

researchers had shown that high triglyceride levels were at

least as common in heart-disease patients as high L.D.L.

cholesterol, and that eating a low-fat, high-carbohydrate

diet would, for many people, raise their triglyceride

levels, lower their H.D.L. levels and accentuate what Gerry

Reaven, an endocrinologist at Stanford University, called

Syndrome X. This is a cluster of conditions that can lead

to heart disease and Type 2 diabetes.

 

It took Reaven a decade to convince his peers that Syndrome

X was a legitimate health concern, in part because to

accept its reality is to accept that low-fat diets will

increase the risk of heart disease in a third of the

population. ''Sometimes we wish it would go away because

nobody knows how to deal with it,'' said Robert Silverman,

an N.I.H. researcher, at a 1987 N.I.H. conference. ''High

protein levels can be bad for the kidneys. High fat is bad

for your heart. Now Reaven is saying not to eat high

carbohydrates. We have to eat something.''

 

Surely, everyone involved in drafting the various dietary

guidelines wanted Americans simply to eat less junk food,

however you define it, and eat more the way they do in

Berkeley, Calif. But we didn't go along. Instead we ate

more starches and refined carbohydrates, because calorie

for calorie, these are the cheapest nutrients for the food

industry to produce, and they can be sold at the highest

profit. It's also what we like to eat. Rare is the person

under the age of 50 who doesn't prefer a cookie or heavily

sweetened yogurt to a head of broccoli.

 

''All reformers would do well to be conscious of the law of

unintended consequences,'' says Alan Stone, who was staff

director for McGovern's Senate committee. Stone told me he

had an inkling about how the food industry would respond to

the new dietary goals back when the hearings were first

held. An economist pulled him aside, he said, and gave him

a lesson on market disincentives to healthy eating: ''He

said if you create a new market with a brand-new

manufactured food, give it a brand-new fancy name, put a

big advertising budget behind it, you can have a market all

to yourself and force your competitors to catch up. You

can't do that with fruits and vegetables. It's harder to

differentiate an apple from an apple.''

 

Nutrition researchers also played a role by trying to feed

science into the idea that carbohydrates are the ideal

nutrient. It had been known, for almost a century, and

considered mostly irrelevant to the etiology of obesity,

that fat has nine calories per gram compared with four for

carbohydrates and protein. Now it became the fail-safe

position of the low-fat recommendations: reduce the densest

source of calories in the diet and you will lose weight.

Then in 1982, J.P. Flatt, a University of Massachusetts

biochemist, published his research demonstrating that, in

any normal diet, it is extremely rare for the human body to

convert carbohydrates into body fat. This was then

misinterpreted by the media and quite a few scientists to

mean that eating carbohydrates, even to excess, could not

make you fat -- which is not the case, Flatt says. But the

misinterpretation developed a vigorous life of its own

because it resonated with the notion that fat makes you fat

and carbohydrates are harmless.

 

As a result, the major trends in American diets since the

late 70's, according to the U.S.D.A. agricultural economist

Judith Putnam, have been a decrease in the percentage of

fat calories and a ''greatly increased consumption of

carbohydrates.'' To be precise, annual grain consumption

has increased almost 60 pounds per person, and caloric

sweeteners (primarily high-fructose corn syrup) by 30

pounds. At the same time, we suddenly began consuming more

total calories: now up to 400 more each day since the

government started recommending low-fat diets.

 

If these trends are correct, then the obesity epidemic can

certainly be explained by Americans' eating more calories

than ever -- excess calories, after all, are what causes us

to gain weight -- and, specifically, more carbohydrates.

The question is why?

 

The answer provided by Endocrinology 101 is that we are

simply hungrier than we were in the 70's, and the reason is

physiological more than psychological. In this case, the

salient factor -- ignored in the pursuit of fat and its

effect on cholesterol -- is how carbohydrates affect blood

sugar and insulin. In fact, these were obvious culprits all

along, which is why Atkins and the low-carb-diet doctors

pounced on them early.

 

The primary role of insulin is to regulate blood-sugar

levels. After you eat carbohydrates, they will be broken

down into their component sugar molecules and transported

into the bloodstream. Your pancreas then secretes insulin,

which shunts the blood sugar into muscles and the liver as

fuel for the next few hours. This is why carbohydrates have

a significant impact on insulin and fat does not. And

because juvenile diabetes is caused by a lack of insulin,

physicians believed since the 20's that the only evil with

insulin is not having enough.

 

But insulin also regulates fat metabolism. We cannot store

body fat without it. Think of insulin as a switch. When

it's on, in the few hours after eating, you burn

carbohydrates for energy and store excess calories as fat.

When it's off, after the insulin has been depleted, you

burn fat as fuel. So when insulin levels are low, you will

burn your own fat, but not when they're high.

 

This is where it gets unavoidably complicated. The fatter

you are, the more insulin your pancreas will pump out per

meal, and the more likely you'll develop what's called

''insulin resistance,'' which is the underlying cause of

Syndrome X. In effect, your cells become insensitive to the

action of insulin, and so you need ever greater amounts to

keep your blood sugar in check. So as you gain weight,

insulin makes it easier to store fat and harder to lose it.

But the insulin resistance in turn may make it harder to

store fat -- your weight is being kept in check, as it

should be. But now the insulin resistance might prompt your

pancreas to produce even more insulin, potentially starting

a vicious cycle. Which comes first -- the obesity, the

elevated insulin, known as hyperinsulinemia, or the insulin

resistance -- is a chicken-and-egg problem that hasn't been

resolved. One endocrinologist described this to me as ''the

Nobel-prize winning question.''

 

Insulin also profoundly affects hunger, although to what

end is another point of controversy. On the one hand,

insulin can indirectly cause hunger by lowering your blood

sugar, but how low does blood sugar have to drop before

hunger kicks in? That's unresolved. Meanwhile, insulin

works in the brain to suppress hunger. The theory, as

explained to me by Michael Schwartz, an endocrinologist at

the University of Washington, is that insulin's ability to

inhibit appetite would normally counteract its propensity

to generate body fat. In other words, as you gained weight,

your body would generate more insulin after every meal, and

that in turn would suppress your appetite; you'd eat less

and lose the weight.

 

Schwartz, however, can imagine a simple mechanism that

would throw this ''homeostatic'' system off balance: if

your brain were to lose its sensitivity to insulin, just as

your fat and muscles do when they are flooded with it. Now

the higher insulin production that comes with getting

fatter would no longer compensate by suppressing your

appetite, because your brain would no longer register the

rise in insulin. The end result would be a physiologic

state in which obesity is almost preordained, and one in

which the carbohydrate-insulin connection could play a

major role. Schwartz says he believes this could indeed be

happening, but research hasn't progressed far enough to

prove it. ''It is just a hypothesis,'' he says. ''It still

needs to be sorted out.''

 

David Ludwig, the Harvard endocrinologist, says that it's

the direct effect of insulin on blood sugar that does the

trick. He notes that when diabetics get too much insulin,

their blood sugar drops and they get ravenously hungry.

They gain weight because they eat more, and the insulin

promotes fat deposition. The same happens with lab animals.

This, he says, is effectively what happens when we eat

carbohydrates -- in particular sugar and starches like

potatoes and rice, or anything made from flour, like a

slice of white bread. These are known in the jargon as

high-glycemic-index carbohydrates, which means they are

absorbed quickly into the blood. As a result, they cause a

spike of blood sugar and a surge of insulin within minutes.

The resulting rush of insulin stores the blood sugar away

and a few hours later, your blood sugar is lower than it

was before you ate. As Ludwig explains, your body

effectively thinks it has run out of fuel, but the insulin

is still high enough to prevent you from burning your own

fat. The result is hunger and a craving for more

carbohydrates. It's another vicious circle, and another

situation ripe for obesity.

 

The glycemic-index concept and the idea that starches can

be absorbed into the blood even faster than sugar emerged

in the late 70's, but again had no influence on public

health recommendations, because of the attendant

controversies. To wit: if you bought the glycemic-index

concept, then you had to accept that the starches we were

supposed to be eating 6 to 11 times a day were, once

swallowed, physiologically indistinguishable from sugars.

This made them seem considerably less than wholesome.

Rather than accept this possibility, the policy makers

simply allowed sugar and corn syrup to elude the

vilification that befell dietary fat. After all, they are

fat-free.

 

Sugar and corn syrup from soft drinks, juices and the

copious teas and sports drinks now supply more than 10

percent of our total calories; the 80's saw the

introduction of Big Gulps and 32-ounce cups of Coca-Cola,

blasted through with sugar, but 100 percent fat free. When

it comes to insulin and blood sugar, these soft drinks and

fruit juices -- what the scientists call ''wet

carbohydrates'' -- might indeed be worst of all. (Diet soda

accounts for less than a quarter of the soda market.)

 

The gist of the glycemic-index idea is that the longer it

takes the carbohydrates to be digested, the lesser the

impact on blood sugar and insulin and the healthier the

food. Those foods with the highest rating on the glycemic

index are some simple sugars, starches and anything made

from flour. Green vegetables, beans and whole grains cause

a much slower rise in blood sugar because they have fiber,

a nondigestible carbohydrate, which slows down digestion

and lowers the glycemic index. Protein and fat serve the

same purpose, which implies that eating fat can be

beneficial, a notion that is still unacceptable. And the

glycemic-index concept implies that a primary cause of

Syndrome X, heart disease, Type 2 diabetes and obesity is

the long-term damage caused by the repeated surges of

insulin that come from eating starches and refined

carbohydrates. This suggests a kind of unified field theory

for these chronic diseases, but not one that coexists

easily with the low-fat doctrine.

 

At Ludwig's pediatric obesity clinic, he has been

prescribing low-glycemic-index diets to children and

adolescents for five years now. He does not recommend the

Atkins diet because he says he believes such a very low

carbohydrate approach is unnecessarily restrictive;

instead, he tells his patients to effectively replace

refined carbohydrates and starches with vegetables, legumes

and fruit. This makes a low-glycemic-index diet consistent

with dietary common sense, albeit in a higher-fat kind of

way. His clinic now has a nine-month waiting list. Only

recently has Ludwig managed to convince the N.I.H. that

such diets are worthy of study. His first three grant

proposals were summarily rejected, which may explain why

much of the relevant research has been done in Canada and

in Australia. In April, however, Ludwig received $1.2

million from the N.I.H. to test his low-glycemic-index diet

against a traditional low-fat-low-calorie regime. That

might help resolve some of the controversy over the role of

insulin in obesity, although the redoubtable Robert Atkins

might get there first.

 

The 71-year-old Atkins, a graduate of Cornell medical

school, says he first tried a very low carbohydrate diet in

1963 after reading about one in the Journal of the American

Medical Association. He lost weight effortlessly, had his

epiphany and turned a fledgling Manhattan cardiology

practice into a thriving obesity clinic. He then alienated

the entire medical community by telling his readers to eat

as much fat and protein as they wanted, as long as they ate

little to no carbohydrates. They would lose weight, he

said, because they would keep their insulin down; they

wouldn't be hungry; and they would have less resistance to

burning their own fat. Atkins also noted that starches and

sugar were harmful in any event because they raised

triglyceride levels and that this was a greater risk factor

for heart disease than cholesterol.

 

Atkins's diet is both the ultimate manifestation of the

alternative hypothesis as well as the battleground on which

the fat-versus-carbohydrates controversy is likely to be

fought scientifically over the next few years. After

insisting Atkins was a quack for three decades, obesity

experts are now finding it difficult to ignore the copious

anecdotal evidence that his diet does just what he has

claimed. Take Albert Stunkard, for instance. Stunkard has

been trying to treat obesity for half a century, but he

told me he had his epiphany about Atkins and maybe about

obesity as well just recently when he discovered that the

chief of radiology in his hospital had lost 60 pounds on

Atkins's diet. ''Well, apparently all the young guys in the

hospital are doing it,'' he said. ''So we decided to do a

study.'' When I asked Stunkard if he or any of his

colleagues considered testing Atkins's diet 30 years ago,

he said they hadn't because they thought Atkins was ''a

jerk'' who was just out to make money: this ''turned people

off, and so nobody took him seriously enough to do what

we're finally doing.''

 

In fact, when the American Medical Association released its

scathing critique of Atkins's diet in March 1973, it

acknowledged that the diet probably worked, but expressed

little interest in why. Through the 60's, this had been a

subject of considerable research, with the conclusion that

Atkins-like diets were low-calorie diets in disguise; that

when you cut out pasta, bread and potatoes, you'll have a

hard time eating enough meat, vegetables and cheese to

replace the calories.

 

That, however, raised the question of why such a

low-calorie regimen would also suppress hunger, which

Atkins insisted was the signature characteristic of the

diet. One possibility was Endocrinology 101: that fat and

protein make you sated and, lacking carbohydrates and the

ensuing swings of blood sugar and insulin, you stay sated.

The other possibility arose from the fact that Atkins's

diet is ''ketogenic.'' This means that insulin falls so low

that you enter a state called ketosis, which is what

happens during fasting and starvation. Your muscles and

tissues burn body fat for energy, as does your brain in the

form of fat molecules produced by the liver called ketones.

Atkins saw ketosis as the obvious way to kick-start weight

loss. He also liked to say that ketosis was so energizing

that it was better than sex, which set him up for some

ridicule. An inevitable criticism of Atkins's diet has been

that ketosis is dangerous and to be avoided at all costs.

 

When I interviewed ketosis experts, however, they

universally sided with Atkins, and suggested that maybe the

medical community and the media confuse ketosis with

ketoacidosis, a variant of ketosis that occurs in untreated

diabetics and can be fatal. ''Doctors are scared of

ketosis,'' says Richard Veech, an N.I.H. researcher who

studied medicine at Harvard and then got his doctorate at

Oxford University with the Nobel Laureate Hans Krebs.

''They're always worried about diabetic ketoacidosis. But

ketosis is a normal physiologic state. I would argue it is

the normal state of man. It's not normal to have McDonald's

and a delicatessen around every corner. It's normal to

starve.''

 

Simply put, ketosis is evolution's answer to the thrifty

gene. We may have evolved to efficiently store fat for

times of famine, says Veech, but we also evolved ketosis to

efficiently live off that fat when necessary. Rather than

being poison, which is how the press often refers to

ketones, they make the body run more efficiently and

provide a backup fuel source for the brain. Veech calls

ketones ''magic'' and has shown that both the heart and

brain run 25 percent more efficiently on ketones than on

blood sugar.

 

The bottom line is that for the better part of 30 years

Atkins insisted his diet worked and was safe, Americans

apparently tried it by the tens of millions, while

nutritionists, physicians, public- health authorities and

anyone concerned with heart disease insisted it could kill

them, and expressed little or no desire to find out who was

right. During that period, only two groups of U.S.

researchers tested the diet, or at least published their

results. In the early 70's, J.P. Flatt and Harvard's George

Blackburn pioneered the ''protein-sparing modified fast''

to treat postsurgical patients, and they tested it on obese

volunteers. Blackburn, who later became president of the

American Society of Clinical Nutrition, describes his

regime as ''an Atkins diet without excess fat'' and says he

had to give it a fancy name or nobody would take him

seriously. The diet was ''lean meat, fish and fowl''

supplemented by vitamins and minerals. ''People loved it,''

Blackburn recalls. ''Great weight loss. We couldn't run

them off with a baseball bat.'' Blackburn successfully

treated hundreds of obese patients over the next decade and

published a series of papers that were ignored. When obese

New Englanders turned to appetite-control drugs in the

mid-80's, he says, he let it drop. He then applied to the

N.I.H. for a grant to do a clinical trial of popular diets

but was rejected.

 

The second trial, published in September 1980, was done at

the George Washington University Medical Center. Two dozen

obese volunteers agreed to follow Atkins's diet for eight

weeks and lost an average of 17 pounds each, with no

apparent ill effects, although their L.D.L. cholesterol did

go up. The researchers, led by John LaRosa, now president

of the State University of New York Downstate Medical

Center in Brooklyn, concluded that the 17-pound weight loss

in eight weeks would likely have happened with any diet

under ''the novelty of trying something under experimental

conditions'' and never pursued it further.

 

Now researchers have finally decided that Atkins's diet and

other low-carb diets have to be tested, and are doing so

against traditional low-calorie-low-fat diets as

recommended by the American Heart Association. To explain

their motivation, they inevitably tell one of two stories:

some, like Stunkard, told me that someone they knew -- a

patient, a friend, a fellow physician -- lost considerable

weight on Atkins's diet and, despite all their

preconceptions to the contrary, kept it off. Others say

they were frustrated with their inability to help their

obese patients, looked into the low-carb diets and decided

that Endocrinology 101 was compelling. ''As a trained

physician, I was trained to mock anything like the Atkins

diet,'' says Linda Stern, an internist at the Philadelphia

Veterans Administration Hospital, ''but I put myself on the

diet. I did great. And I thought maybe this is something I

can offer my patients.''

 

None of these studies have been financed by the N.I.H., and

none have yet been published. But the results have been

reported at conferences -- by researchers at Schneider

Children's Hospital on Long Island, Duke University and the

University of Cincinnati, and by Stern's group at the

Philadelphia V.A. Hospital. And then there's the study

Stunkard had mentioned, led by Gary Foster at the

University of Pennsylvania, Sam Klein, director of the

Center for Human Nutrition at Washington University in St.

Louis, and Jim Hill, who runs the University of Colorado

Center for Human Nutrition in Denver. The results of all

five of these studies are remarkably consistent. Subjects

on some form of the Atkins diet -- whether overweight

adolescents on the diet for 12 weeks as at Schneider, or

obese adults averaging 295 pounds on the diet for six

months, as at the Philadelphia V.A. -- lost twice the

weight as the subjects on the low-fat, low-calorie diets.

 

In all five studies, cholesterol levels improved similarly

with both diets, but triglyceride levels were considerably

lower with the Atkins diet. Though researchers are hesitant

to agree with this, it does suggest that heart-disease risk

could actually be reduced when fat is added back into the

diet and starches and refined carbohydrates are removed.

''I think when this stuff gets to be recognized,'' Stunkard

says, ''it's going to really shake up a lot of thinking

about obesity and metabolism.''

 

All of this could be settled sooner rather than later, and

with it, perhaps, we might have some long-awaited answers

as to why we grow fat and whether it is indeed preordained

by societal forces or by our choice of foods. For the first

time, the N.I.H. is now actually financing comparative

studies of popular diets. Foster, Klein and Hill, for

instance, have now received more than $2.5 million from

N.I.H. to do a five-year trial of the Atkins diet with 360

obese individuals. At Harvard, Willett, Blackburn and

Penelope Greene have money, albeit from Atkins's nonprofit

foundation, to do a comparative trial as well.

 

Should these clinical trials also find for Atkins and his

high-fat, low-carbohydrate diet, then the public-health

authorities may indeed have a problem on their hands. Once

they took their leap of faith and settled on the low-fat

dietary dogma 25 years ago, they left little room for

contradictory evidence or a change of opinion, should such

a change be necessary to keep up with the science. In this

light Sam Klein's experience is noteworthy. Klein is

president-elect of the North American Association for the

Study of Obesity, which suggests that he is a highly

respected member of his community. And yet, he described

his recent experience discussing the Atkins diet at medical

conferences as a learning experience. ''I have been

impressed,'' he said, ''with the anger of academicians in

the audience. Their response is 'How dare you even present

data on the Atkins diet!' ''

 

This hostility stems primarily from their anxiety that

Americans, given a glimmer of hope about their weight, will

rush off en masse to try a diet that simply seems

intuitively dangerous and on which there is still no

long-term data on whether it works and whether it is safe.

It's a justifiable fear. In the course of my research, I

have spent my mornings at my local diner, staring down at a

plate of scrambled eggs and sausage, convinced that

somehow, some way, they must be working to clog my arteries

and do me in.

 

After 20 years steeped in a low-fat paradigm, I find it

hard to see the nutritional world any other way. I have

learned that low-fat diets fail in clinical trials and in

real life, and they certainly have failed in my life. I

have read the papers suggesting that 20 years of low-fat

recommendations have not managed to lower the incidence of

heart disease in this country, and may have led instead to

the steep increase in obesity and Type 2 diabetes. I have

interviewed researchers whose computer models have

calculated that cutting back on the saturated fats in my

diet to the levels recommended by the American Heart

Association would not add more than a few months to my

life, if that. I have even lost considerable weight with

relative ease by giving up carbohydrates on my test diet,

and yet I can look down at my eggs and sausage and still

imagine the imminent onset of heart disease and obesity,

the latter assuredly to be caused by some bizarre rebound

phenomena the likes of which science has not yet begun to

describe. The fact that Atkins himself has had heart

trouble recently does not ease my anxiety, despite his

assurance that it is not diet-related.

 

This is the state of mind I imagine that mainstream

nutritionists, researchers and physicians must inevitably

take to the fat-versus-carbohydrate controversy. They may

come around, but the evidence will have to be exceptionally

compelling. Although this kind of conversion may be

happening at the moment to John Farquhar, who is a

professor of health research and policy at Stanford

University and has worked in this field for more than 40

years. When I interviewed Farquhar in April, he explained

why low-fat diets might lead to weight gain and

low-carbohydrate diets might lead to weight loss, but he

made me promise not to say he believed they did. He

attributed the cause of the obesity epidemic to the

''force-feeding of a nation.'' Three weeks later, after

reading an article on Endocrinology 101 by David Ludwig in

the Journal of the American Medical Association, he sent me

an e-mail message asking the not-entirely-rhetorical

question, ''Can we get the low-fat proponents to

apologize?''

 

 

 

 

Gary Taubes is a correspondent for the journal Science and

author of ''Bad Science: The Short Life and Weird Times of

Cold Fusion.''

 

http://www.nytimes.com/2002/07/07/magazine/07FAT.html?

ex=1027005307 & ei=1 & en=b8126ee6c5a01c2a

 

 

 

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help.

 

Here is the whole artical. I was writing to someone the other day because

she has taken out all fat out of her diet and switched frin sugar to

sweet-n-low. I new both these changes are bad for you health to but

hadn't gotten around to getting articals to show why. The main thing

about the mind and body is to always remember balance.

 

Copyright 2002 The New York Times Company

 

----- End forwarded message -----

 

 

 

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