Cancer, Obesity and Diabetes: Diseases of Civilization?

[Guest guest]

Cancer, Obesity and Diabetes: Diseases of Civilization?

JoAnn Guest

Jan 09, 2007 08:31 PST

 

Cancer, Obesity and Diabetes: Diseases of Civilization?

 

http://www.willner.com/article.aspx?artid=22

 

Is an overconsumption of white flour, white sugar, and refined

sweeteners such as corn syrup responsible for the frightening

increase of cancer, diabetes and obesity?

 

Is the key to cancer prevention, reduced diabetes and obesity the

avoidance of the same foods that make your blood sugar run wild?

....with coments by Don Goldberg, R.Ph.

 

[Dr. Ralph Moss, a leading author and consultant on cancer, has put

forward an interesting theory on what is behind the tremendous

increase in cancer in our society. He speculates that other

diseases, such as diabetes and obesity, are related to the same

underlying problem.

 

The following comments are excerpted from Dr. Moss's excellent

newsletter,

The Moss Reports. You can to a free email version of The

Moss Reports simply by visiting his web site,

www.cancerdecisions.com.]

 

Cancer: A Disease of Civilization?

 

Is cancer a disease of civilization? Is it related to other diseases

that seem to increase with industrialization? If so, what are the

implications for readers living in the 21st century?

 

Back in the 19th century, many of the diseases that now plague us

were

rare. Diabetes was twenty-seventh on the list of causes of death in

the

statistics of the Metropolitan Life Insurance Company in 1900. By

1950

it had become the third leading cause of death. The famous surgeon

Alton

Ochsner, MD, once related that, when he was in medical school in the

early 20th century, one of his professors took his class to see the

autopsy of a patient who had died of a heart attack. The disease was

so

rare at that time that his professor feared they might never see

another

such instance! Obesity was the subject of circus displays, not an

everyday occurrence.

 

Similarly, until the mid-1800s, cancer was relatively rare and was

not

considered statistically important. This was particularly true

outside

of the major cities. Then, in the mid-19th century, cancer began its

stratospheric rise. Around the same time, well-trained medical

personnel

began to travel and even to live among indigenous peoples (the so-

called

" natives " ). The news they brought back was startling. These diverse

populations, many of whom lived a hand-to-mouth existence, were

generally much healthier than their Western counterparts. True, they

had

a high infant mortality rate and easily succumbed to epidemics that

originated in the West such as measles, smallpox and tuberculosis.

But

they had far less asthma, allergies, indigestion, and heart disease.

The

same disparity in health was seen between rural and urban

populations in

Europe. The French or English farmer was much less likely to develop

cancer than the cosmopolite of Paris or London. And despite the

stereotypical image of Eskimos and South Sea islanders as roly-poly,

obesity was extremely rare among such people.

 

Most startling of all, cancer seemed nonexistent. In 1843, a French

surgeon, Stanislas Tanchou, MD, formulated this observation into

" Tanchou's Doctrine " : the incidence of cancer increases in direct

proportion to the " civilization " of a nation and its people. This

doctrine was embraced by John Le Conte, MD (1818-1891), first

president

of the University of California, and his enthusiasm led medical

missionaries, ship surgeons, anthropologists and others to undertake

an

avid search for cancer among the Alaskan Eskimo (Inuit), northern

Athapaskans of Canada and the native peoples of Labrador. The result

was

always the same: For 75 years, not a single case of cancer was

documented among the tens of thousands of such people studied by

competent medical examiners. The Harvard-trained anthropologist,

Vilhjalmur Stefannson, for instance, lived for 11 years among the

Eskimo

and never saw a case. In later life, he wrote a book on the topic,

Cancer: A Disease of Civilization?

 

Unfortunately, whatever protection these native populations had

against

cancer was lost when they began to adopt Western ways in the 1920s.

By

the early 1930s, cases of cancer were being documented in Alaska and

Canada. On July 27, 1933, an Eskimo named Jobe died of liver cancer

at

the Farthest North Hospital in Alaska. Similarly, in 1935, Michael

Nochasak, an Eskimo, died of colon cancer in Labrador. After that,

the

rates of cancer among these native peoples underwent a steady rise,

until they began to rival that of the white population.

 

Evidence from Africa and Asia

 

Similar stories are told about the indigenous peoples of Africa and

Asia. Albert Schweitzer, MD, the famous Nobel laureate, testified as

follows:

 

" On my arrival in Gabon, in 1913, I was astonished to encounter no

case

of cancer...I cannot, of course, say positively that there was no

cancer

at all, but, like other frontier doctors, I can only say that if any

cases existed they must have been quite rare. The absence of cancer

seemed to me due to the difference in nutrition of the natives as

compared with the Europeans...

 

" In the course of the years, we have seen cases of cancer in growing

numbers in our region. My observations incline me to attribute this

to

the fact that the natives were living more and more after the manner

of

the whites...I have naturally been interested in any research

tracing

the occurrence of cancer to some defect in our mode of nutrition. "

 

The Hunza people, who live in a remote valley of the Himalayas, in

the

territory of Kashmir, provide further evidence of the rarity of

cancer

among indigenous populations. The Hunza were the subject of study

from

the 1910s onward by a number of diligent observers, including Sir

Robert

McCarrison, Major General in the Indian Health Service (1878-1960).

McCarrison's seven years of careful scrutiny led him to conclude

that

there was little if any cancer among this population.

 

It might be objected that cancer is an " occult " disease, difficult

to

diagnose, and that for this reason it may have eluded early

observers. I

do not believe this to be the case. At least one-quarter of all

cancers

are external in nature. Basal and squamous cell carcinomas, tumors

of

the head and neck region, breast cancer and those of the external

genitals, to name but a few, are all readily apparent and do not

take

great diagnostic skills to detect. Breast cancers in particular were

well known and described even by ancient physicians. Other cancers

also

form noticeable lumps or break to the surface.

 

Besides, we are not talking about medieval medicine. By the late

nineteenth and early twentieth centuries cancer pathology had taken

great strides. Such works as James Ewing's Neoplastic Diseases,

which

was first published in 1920, demonstrate the sophistication of

cancer

science at that time. Frontier doctors were, by and large,

competent,

serious and well-trained. I don't think there is any doubt that if

cancer had been widespread, they would have found it. I can only

conclude that cancer is indeed a disease of industrial society.

 

Even today, we find huge disparities in the incidence of cancer

worldwide, with increased rates seemingly tied to the adoption of a

refined diet and other harmful habits. Hungary, for instance, has a

cancer death rate of 272.2 per 100,000 (men) and 138.4 per 100,000

(women). Contrast this with Mexico, where the death rate among men

is

85.0 and among women 78.9 per 100,000.

 

" Civilization " is not only a chauvinistic term but is such an

all-encompassing concept that it is difficult to pinpoint exactly

what

aspects of it have contributed to the dramatic rise of cancer in the

last century. Certainly tobacco has been a major culprit. Hungary

has

the highest rate of lung cancer in the world. I have visited that

country four times and always came away shocked at the amount of

smoking. On one trip I visited a number of famous medical facilities

and

never did my hosts fail to offer me cigarettes. When I met with one

of

the country's highest ranking scientists, he nonchalantly chain-

smoked

throughout the entire meeting. After the fall of Communism, downtown

Budapest became plastered with ads for American cigarettes. Philip

Morris, makers of Marlboro, sponsored televised rock concerts and

young

women in Marlboro suits dispensed free samples of Marlboro

cigarettes.

Concertgoers who agreed to smoke the cigarettes received a

complimentary

pair of " designer Marlboro sunglasses. " There is no doubt that

smoking

has played a role in the rising rates of cancer.

 

However, an overwhelming body of evidence points to drastic changes

in

diet as the primary explanation for the increase in cancer.

Indigenous

people of regions across the globe seem protected so long as they

eat

the diet that their ancestors ate for millennia. But once they adopt

Western dietary habits, cancer appears and then begins its

inexorable

climb towards the same astronomical heights as are seen in the

societies

they emulate.

 

Some scholars who studied vegetarian cultures have concluded that it

was

the high fruit and vegetable content that kept these native peoples

from

getting cancer. Conversely, some researchers who focused on northern

populations in which meat was prominent have advocated a meat-based

diet

for cancer protection. Others have ascribed the healthfulness,

longevity

and lack of cancer in indigenous populations to the intake of

specific

nutrients (such as the " laetrile " found in such abundance in apricot

kernels, a staple of the Hunza diet).

 

But no single, simplistic answer will fit these tremendously varied

cultures. In my opinion, what these diverse populations ate is much

less

important than what they did not eat (at least until

recently): " white "

foods, specifically white sugar, white flour, and salt. The addition

of

these foods to their diet was disastrous to their health, as it has

been

to ours. White sugar and white flour are especially harmful, because

these " high glycemic " foods are quickly absorbed into the

bloodstream,

where they wreak havoc with the regulation of insulin and blood

sugar

levels. This is a major factor in increasing rates of type 2

diabetes

and obesity.

 

Unfortunately, white sugar, white flour, and refined sweeteners are

ubiquitous in the Western diet. They are found in sodas and other

sweet

drinks, breads and snack foods, beer and ice cream, you name it. But

even " natural " forms of carbohydrates may not be as innocent as once

thought. Whole wheat flour, potatoes, and other seemingly healthy

foods

also have a high glycemic index and may not be safe to consume in

anything except small quantities.

 

Atkins Vindicated

 

Robert Atkins, MD, has been preaching against a high-carbohydrate

diet

for 30 years, much to the chagrin of the medical establishment. A

recent

cover story in the New York Times Magazine (7/7/02) vindicated the

low-carbohydrate, high-protein and high-fat diet advocated by

Atkins,

citing a growing body of research which suggests that a diet of

carbohydrate-rich foods is no guarantee of good health, let alone

weight

loss. In fact, as the American public has increased its consumption

of

carbohydrates and decreased its consumption of fatty meat, obesity

rates

have skyrocketed. In 1998, more than 50 percent of adults in the US

were

overweight. Obesity and type II diabetes among American children

have

also increased. At the same time, levels of physical activity have

declined, further contributing to soaring rates of obesity and

obesity-related illnesses in the US.

 

The list of diseases linked to obesity is a lengthy one. According

to

the American Cancer Society, obesity contributes to hypertension,

lipid

disorders, type 2 diabetes, coronary heart disease, stroke,

gallbladder

disease, osteoarthritis, sleep apnea and respiratory problems. And

as

body mass index goes up, rates of cancer also increase, by as much

as 80

percent in women.

 

[We will explore the relationship to low carbohydrate diets in just

a

moment]

 

The Key to Cancer Prevention

 

It seems clear to me that cancer was not a major medical problem in

recorded history until the last 150 years. And even today,

populations

that eat an indigenous diet rarely, if ever, get cancer.

(Unfortunately,

such populations are exceedingly scarce in this century.) However,

in

reviewing the evidence from these cultures as well as our own, the

key

issue for cancer prevention does not seem to be whether the diet is

vegetarian or meat-eating, or whether it contains high quantities of

fat

and protein. The single most drastic change in the Western diet,

which

has occurred simultaneously with rising rates of cancer among those

who

consume it, has been the cheap availability of white flour, white

sugar,

and refined sweeteners such as corn syrup, as well as their

inclusion in

just about every food in the marketplace. The key to cancer

prevention

may turn out to be avoidance of the same foods that make your blood

sugar run wild and that cause a plethora of other illnesses.

 

—Ralph W. Moss, Ph.D.

 

References:

 

American Cancer Society. Cancer Facts and Figures 2001, p. 25.

 

Atkins RC. Dr. Atkins' New Diet Revolution. NY: Avon, 2002.

 

Taubes G. " What if it's all been a big fat lie? " . New York Times

Magazine, July 7, 2002.

 

Stefannson V. Cancer: Disease of Civilization?. NY: Hill & Wang,

1960.

 

[so if cancer, as Dr. Moss proposes, is related to changes in our

diet,

with an overconsumption of white flour, white sugar, and refined

sweeteners such as corn syrup, what about diabetes and obesity. Dr.

Moss

mentions the connection to the Atkin's diet, and I am intrigued by

the

similarities. Lets look at some excerpts from the excellent New York

Times article he referred to, What If It's All Been A Big Fat Lie,

by

Gary Taubes.]

 

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

 

July 7, 2002, By Gary Taubes, The 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 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.

 

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 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.

 

[More recently, new research has demonstrated that " low calories " is

not

what is responsible for the low-carbohydrate type diets. As reported

in

August:]

 

Two recently published studies show that ketosis, the controversial

metabolic process at the heart of the Atkins Nutritional Approach

,

may not only be harmless but may also be beneficial.

 

One study demonstrated that subjects in ketosis, due to a controlled

carbohydrate diet, experienced statistically significant improvement

in

blood markers that have been shown to predict coronary artery

disease.

 

The second study found that people lost fat (an average of seven

lbs.),

while actually gaining muscle (an average of two lbs.) in only six

weeks. In essence these individuals lost an average of five lbs. not

only preserving their muscle mass, but also increasing it.

 

" The commonly held belief that reducing calories is the only reason

controlled carbohydrate nutrition produces fat loss appears to be

false, " explains the principal investigator, Jeff Volek, Ph.D.,

R.D.,

FACN. " In fact, the metabolic process, ketosis, that results from a

properly conducted controlled carbohydrate weight loss program, may

prove to be as much a factor in fat loss and reduction of

cardiovascular

disease risk factors as calorie reduction.

 

And one of the studies even demonstrated a simultaneous increase in

lean

muscle mass along with the loss in fat. "

 

Both published studies come out of the University of Connecticut's

Human

Performance Laboratory and were conducted on normal-weight men with

normal cholesterol levels.

 

The first study, " A Ketogenic Diet Favorably Affects Serum

Biomarkers

for Cardiovascular Disease in Normal-Weight Men, " published in the

July

2002 issue of the Journal of Nutrition, shows that ketosis is not

only

harmless but may actually improve the blood markers that have been

shown

to predict coronary artery disease.

 

The six-week study examined the effects of a ketogenic diet on the

insulin levels, LDL (bad cholesterol), LDL particle size (smaller

particles are more atherogenic or damaging to the arteries), HDL

(good

cholesterol), triglycerides, and post-meal triglycerides of 20

normal-weight, healthy men.

 

The results showed that fasting triglycerides was decreased by 33%,

post-meal lipids by 29%, LDL particle size increased, and fasting

insulin concentrations by 34% after the low carb diet. LDL and total

cholesterol were unchanged by the diet, HDL (the good cholesterol)

tended to be slightly increased, suggesting a favorable outcome in

this

predictor of improved cardiovascular risk.

 

The second study, " Body Composition and Hormonal Responses to a

Carbohydrate Restricted Diet, " published in the July 2002 issue of

Metabolism, examined how the normal-weight body responds to six

weeks of

a controlled carbohydrate diet (8% carbohydrate, 61% fat, 30%

protein)

compared with a traditional diet (47% carbohydrate, 32% fat, 17%

protein) that involved equal caloric intake.

 

At week six, this study, with 12 subjects, found that people lost

fat

(an average of seven lbs.), while actually gaining muscle (an

average of

two lbs.).

 

The average weight loss of five lbs. was achieved while not only

preserving muscle mass, but also increasing it. Because this

positive

change occurred in conjunction with lowered insulin levels (a

hormone

measured in the blood that is stimulated by carbohydrate intake and

has

been associated with the conversion of excess carbohydrate to body

fat),

it is postulated that the reduction in the hormone insulin was

responsible for this.

 

The studies were supported by a grant from the Dr. Robert C. Atkins

Foundation. Established in 1999, the Foundation is a private, non-

profit

foundation dedicated to improving the way medicine is practiced in

the

United States by scientifically validating the safety and efficacy

of

complementary and alternative medicine approaches.

 

[Tauber, in his article, continues:]

 

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.

 

[i disagree with Blackburn's explanation. The protein-sparing

modified

fast was indeed immensely popular, and it seemed to work. Part of

its

popularity was due to the book by Dr. Linn, The Last Chance Diet. It

was

the major topic of conversation at bariatric medical conventions.

Unfortunately, the product associated with the implementation of

this

program was something called " liquid predigested protein. " This was

a

liquid solution of hydrolyzed (predigested) collagen protein, and

was

used as a an easy way to get a high protein low carbohydrate meal.

It

contained no carbohydrate and no fat. One problem was that the

quality

of the protein was abysmal, being composed of gelatin, an incomplete

protein. It is severely deficient in one of the essential amino

acids,

and will not support life if provided as the only source of protein

in

the diet. This was pointed out to many of the leading bariatricians

at

that time, but they didn't want to hear about it. The other stuff

" works, " and that was sufficient. The other problem is that people

started dying while on the program. Suddenly, you would hear on the

6 pm

news, from FDA spokesmen, that these programs were killing people.

It

did not matter that the cause may have been due more to the

popularity

of " liquid predigested protein " than to the concept of the

" protein-sparing modified fast. . . . Don Goldberg]

 

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.''

 

The above was excerpted from the article, " What if It's All Been a

Big

Fat Lie? " by Gary Taubes, in the July 7, 2002, New York Times.

(www.nytimes.com)

 

The excerpt from Dr. Ralph Moss was originally published in his

email

newslettler, The Moss Reports. We highly recommend your subscribing

to

this service. Go to www.cancerdecisions.com

 

Dr. Moss also has several excellent books, including Cancer Therapy:

The

Independent Consumer Guide, Antioxidants Against Cancer, Herbs

Against

Cancer, The Cancer Industry, and Questioning Chemotherapy.

 

These books are available at Willner Chemists and most bookstores.

 

Additional comments by Don Goldberg, R.Ph.

 

 

 

JoAnn Guest

mrsjo-

www.geocities.com/mrsjoguest/Diets