-
The diet
provided fewer servings of grains, vegetables,
and fruits than recommended by the U.S. Dietary
Guidelines.
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.
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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 (photo on left), 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 scie
nce behind
the alternative hypothesis can be called
Endocrinology 101, which is how it’s referred to by
David Ludwig (photo on left), 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.
[Karl Note: I do not believe for one instant
that these lies were unwitting -- but were
deliberate!]
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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 m
ore, 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,
(a psychiatrist -- picture on
left) but it
will go unmentioned that this statement is based on
100 patients who passed through Stunkard’s obesity
clinic during the Eisenhower administration.
[Karl Note: Psychiatrists are particularly poor
at observing and reporting the truth!]
With these caveats,
one of the few reasonably reliable facts about the
obesity epidemic is that it started aro
und 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 st
arches
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.’’
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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?’’
[Karl Note: The whole set of lies behind the
cholesterol myths has been thoroughly exposed by me
--
click here.]
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.’’
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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, (photo on right) 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, (one of the
authors of the publication on the left) 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,
(photo on right) 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.’’
Return To Top
David Ludwig,
(photo on left) 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.
 |
Ingredients:
2 cups of confectioner's sugar
1 egg white
1 tablespoon of corn syrup
½ teaspoon of vanilla
1/3 cup of corn flour
edible vegetable coloring
|
Kids! You
Can Make These "Cookies"
At Home! Without
Your Mother!
It's Easy!
They will "keep" for many months without
spoiling! |
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 drin
ks
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.)
Click on the Coke image for a
blasting story about the origins of Coca Cola.
Return To Top
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.
Karl Note. Dr. Atkins is also a famous
intravenous chelation doctor!
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,
(psychiatrist) 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.’’
Return To Top
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.’’
I, Karl Loren, am NOT an
original researcher, but I bring an extraordinary
amount of intelligence and logic to my type of
research. When I first read Dr. Atkins, I just
figured this was "right" and said so in my Book on
heart disease, published in 1994. When I then,
later, learned of Aajonus Vonderplanitz, I again
figured that his diet concepts were a very useful
advance of those of Dr. Atkins.
Finally, I found this and that, here and there, and
actually did some "intuitive research" and designed
my own approach to diet. I think it is better
than any other, but you can judge. Click
HERE for my diet, and
click
here for more information about Aajonus
Vonderplanitz.
Return To Top
None of
thesestudies 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.
Return To Top
See more about Gary Taubes below.
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.
JOHN
W. FARQUHAR, professor of medicine and director of
the Stanford Wellness Center, is one of two
recipients of the 1999 Joseph Stokes Award in
Preventive Cardiology for outstanding achievement in
furthering education, research and the clinical
practice of preventive cardiology. He received the
award from the American Society of Preventive
Cardiology at the group's annual meeting in Orlando
in March.
source
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?’’
Copyright © May 20, 2008 6:25 AM by Karl Loren on behalf of Vibrant Life, ALL RIGHTS RESERVED.
Permission is granted for non-commercial downloading, copying, distribution or redistribution on two conditions:
One, that some form of copyright notice is included in every copy distributed or copied,
showing the copyright belonging to Vibrant Life, Burbank, CA, at
www.oralchelation.com .
The second condition is that the material is not to be used for any purpose contrary to
the purposes and objectives of this site.
This permission does not extend to materials on this site which are copyrighted by others.
Return To Top
Description
Freelance writer Gary Taubes won his third
Science-in-Society award with his Science magazine
story, "The soft science of dietary fat." Following his
prize winning technique of evaluating how inadequate
scientific tools are used to dictate important national
health issues—what people should eat—he once again
shows there is still much to be mined in a topic long
considered settled and indisputable. With painstaking
research and in-depth reporting, he challenges the
accepted wisdom on dietary fat and displays the chinks
in its armor. Many of his reported findings are still
controversial, yet judges lauded his risk-taking
reporting, making us think twice about obsessing about
our dietary choices.
Taubes, a freelance writer, spent a year on the story
mostly supported by other writing projects. Each story
in this vein takes longer than the last, he said. For
this one, He interviewed about 150 people. As a result,
in his own shopping Taubes ignores the nationally
approved health advice and hunts, sometimes in vain,
for yogurt made out of whole milk. When his friends ask
him for scientifically sound dietary advice, the only
thing he can tell them is still what his mother told
him: Eat your fresh fruits and vegetables, and watch
your weight.
Bio
Gary
Taubes has written about science, medicine and health
for Science, Discover, The Atlantic Monthly, The New
York Times Magazine, Esquire, GQ, and a host of other
publications. He is currently a contributing
correspondent with Science and a contributing editor
with Technology Review.
Taubes has won numerous awards for his reporting
including the National Association of Science Writers
Science-in-Society Journalism Award in both 1996 and
1999.
Taubes' most recent book, Bad Science, The Short
Life and Weird Times of Cold Fusion (Random House,
1993) was a New York Times Notable Book and a finalist
for the Los Angeles Times Book Awards.
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"You can
contribute to a groundswell of
people demanding that drug
companies, health organizations
and the government cease
following their own agendas and
listen to the people they are
supposedly interested in
helping."
— Dr. Atkins
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Sunday, July 7, 2002, was
one of the most gratifying
days of my life—and one that
validated the controlled
carbohydrate nutritional
approach to weight management
and good health. On that day
the New York Times
Magazine cover story
titled
What if It's All Been a Big
Fat Lie?, by Gary Taubes,
told millions of readers that
the low-fat hypothesis has
failed the test of time.
After hundreds of millions of
dollars and 20 years of
research, studies on low-fat
programs have not
proved to promote good health
and extend life. This
watershed article in a
mainstream consumer
publication accurately
describes the scientific
basis and effects of a
controlled carbohydrate
lifestyle, mirroring my
conclusions from 40 years of
clinical experience: The
low-fat belief system causes
individuals to over-consume
high carbohydrate foods,
which in turn has contributed
to the current epidemics of
both obesity and diabetes.
Taubes, a freelance
investigative science writer
who authored “The Soft
Science of Dietary Fat,”
which was published in the
respected journal Science
(March 30, 2001, Volume 291,
pages 2536-2545;
www.sciencemag.org) is one of
the growing number of
reporters who actually review
all the relevant research and
report the facts without
bias. He interviewed many of
the best researchers in the
field of medical nutrition,
including respected
scientists at Harvard,
Stanford, the University of
Pennsylvania, Tufts, the
University of Connecticut and
other institutions. All
agreed that the controlled
carb approach to weight
control and healthy living
has been neglected and the
subject should be studied
further. This is something
that I have advocated for the
last 20 years. |
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 Eggs
are such an efficient source of
nutrition that they're often called
the perfect food. One large egg
provides 70 calories, 6 grams of
protein, less than 1 gram of
carbohydrate, 4.5 grams of fat and
generous amounts of many vitamins and
minerals. In fact, the only nutrient
completely absent from the egg is
vitamin C—chickens, unlike humans,
manufacture all they need.
A large egg also contains 215
milligrams of cholesterol. But
dietary cholesterol does not
automatically become blood
cholesterol when you eat it. The
majority of the cholesterol in your
blood is actually made by your own
body. The quantity it makes is
determined by your weight and
hereditary factors. If you are
controlling your carbohydrate intake
by doing Atkins, the cholesterol in
eggs should pose no health risk.
Brown, organic, free-range, fertile
and a variety of nutritionally
enhanced eggs fill supermarket dairy
cases, and often cost twice as much
as generic eggs. |
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Source
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July 23, 2002
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Government's
Standard Lumps Hunks, Athletes With Truly Obese
By BETSY MCKAY
Staff Reporter of THE WALL STREET
JOURNAL
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Who's
overweight?
 Mel
Gibson, if you rely on the standard used by the
U.S. Centers for Disease Control and Prevention. By
their calculation, muscle-bound Arnold
Schwarzenegger and baseball star Sammy Sosa are
actually obese. So is any six-foot man who weighs
225 po unds
and a 5'5" woman weighing 180 pounds.
According to the
CDC, the country's most authoritative source of
statistics, an estimated 27% of American adults are
obese, while an additional 34% are overweight. The
CDC says the percentage of obese Americans has
nearly doubled over the past three decades, to a
level the U.S. Surgeon General calls "epidemic."
But those
numbers aren't exactly firm themselves. For
starters, the "body mass index" measurement used by
the CDC doesn't distinguish between muscle and fat,
so a number of athletes and Hollywood action heroes
can fit the definition of obese, depending on their
current weight. What's more, the most recent CDC
statistics -- oft-cited by the Surgeon General,
doctors and others -- come from a survey that even
the CDC says is too small to be conclusive.
Complicating matters further, a minor change in the
government's standard in 1998 made an extra 30
million Americans "overweight" overnight.
With obesity now
cited among the leading causes in the U.S. of
preventable disease, reliable statistics are in
heavy demand. Health officials use them to
galvanize support and dollars to fight the disease;
drug companies look at them when deciding where to
focus research money; hospitals, to buy equipment
for treatment. And right now, the government's
numbers are coming under criticism from the food
and restaurant industries, which some say have
contributed to the disease's surge.
Return To Top
"By changing the
calculations and the semantics, you create crises
where they aren't," asserts Rick Berman, executive
director of the Center for Consumer
Freedom, a Washington, D.C.-based group
representing casual-dining restaurants and other
food interests. The group is running an ad campaign
opposing proposed "twinkie taxes" on soda, snack
food, and restaurant meals that health advocates
and some legislators advocate as a means to curb
obesity. "That's not to say there aren't people who
are obese, but there's always a certain element of
hype and hyperbole designed to get people's
attention," adds Mr. Berman, who says he's athletic
and technically obese at 6'2" and 240 pounds.
The CDC says
that BMI, as it is called, is a suitable
measurement for large, national surveys because it
requires only a person's weight and height to make
the calculation. "Overweight" is defined as anyone
with a BMI over 25, such as a six-foot, 185-pound
man. Anyone with a BMI over 30 is defined as
"obese." (To calculate your BMI, see adjacent chart
or go to www.cdc.gov2)
Critics say
there are obvious problems with a standard that can
lump muscular Heisman Trophy winners and New York
Knicks stars in with the truly fat. "Using BMI puts
a lot of faith between weight and health risk,"
says Steven Heymsfield, deputy director of the
Obesity Research Center at St. Luke's-Roosevelt
Hospital Center in New York. As a result, he says,
at least 5% to 10% of people measured by BMI could
be mistakenly classified as overweight or obese.
"Five percent of 200-300 million is still a lot of
people," he says. And he adds, some people with low
BMIs -- such as the elderly -- can have more body
fat than they should.
CDC officials
stand by their numbers, even while conceding that
the over-muscular are sometimes unfairly labeled as
obese. The agency itself uses other tests that more
accurately measure body fat -- including a full
body scan during health surveys. Still, BMI is used
to calculate official obesity rates because it
matches international standards, says Katherine
Flegal, a CDC epidemiologist.
In the U.S., the
statistics are somewhat spotty historically. The
CDC began tracking the nation's weight in 1960, as
part of its first U.S. health survey. Participants
were chosen randomly through Census data and asked
if they could be interviewed at their homes by CDC
officials. The CDC then selected a group for
lengthy physical exams conducted in mobile tractor
trailers. Researchers studied much in addition to
weight: the growth charts that now line
pediatricians' walls arose from these surveys; so
did the discovery of high lead levels in Americans'
blood. The latter eventually inspired the
government to phase out leaded gasoline.
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The government
conducted the same health survey four times in
recent decades, each time spanning several years:
1960-62, 1971-74, 1976-80, 1988-94. There were
large gaps between the studies, primarily because
funding wasn't always available. During this time,
obesity didn't get much public attention -- mostly
because it wasn't perceived as a pressing health
issue. In fact, there wasn't even a uniform
standard for measuring the disease until 1985 when
the National Institutes of Health, the government's
health research arm, decided on BMI partly because
it would be efficient for researchers.
The BMI standard
made it possible to look back at the change in
obesity through the years. And after the 1988-94
results were released, doctors and researchers
became alarmed. The figures showed a significant
climb in the number of obese participants -- up 53%
from the prior survey taken from 1976 to 1980.
Experts speculated that lifestyles had changed
significantly in the 1980s: People had become more
sedentary and their diets had worsened.
Suddenly, what
had been a moderate health concern looked like a
crisis. Armed with the new data, obesity experts
began lobbying heavily for more funding to research
and treat the condition as a disease. In 1999
Congress granted annual funding for the survey. The
CDC, under pressure to provide more data -- fast --
last year released the only new numbers it had from
its continuing mobile-health survey. Those numbers,
based on a sample of only 1,446 people conducted
over seven months during 1999, are the standard
most experts use when talking about the nation's
current weight woes. By those numbers, an estimated
61% of American adults are either overweight or
obese.
"You need about
three years [of data] for a confident estimate,"
concedes Bill Dietz, director of the CDC's division
of nutrition and physical activity. The CDC also
tracks weight and height in an annual telephone
survey of 150,000 people. But those numbers aren't
as widely cited because the CDC believes people
underreport their weight and overreport height when
asked, says Dr. Dietz. For example, in its 1999
telephone survey, only 20% of respondents qualified
as obese compared to 27% in the widely cited van
survey.
There are other
concerns with the current weight data. For
instance, some obesity experts say the BMI
threshold for being "overweight" is too low. In
1998 the government lowered it to 25 from over 27
to bring the U.S. in line with World Health
Organization standards. Instantly, millions of
Americans became "overweight," including basketball
superstar Michael Jordan. Meantime, the switch
compounded the perception that the nation was
experiencing a weight crisis.
Given questions
about existing data, how does anyone know if
obesity is truly an epidemic? Certainly, the
anecdotal evidence is inescapable, from the boom in
large-sized clothing to hospitals needing to buy
more specialized bariatric equipment to accommodate
severely overweight patients. The precise dimension
of the problem "doesn't matter," argues Kelly
Brownell, director of Yale University's Center for
Eating and Weight Disorders. "No matter how you
count it, it's a staggering problem."
The CDC
maintains that even the seven-month figures are
accurate enough to gauge general levels of obesity,
although too small to analyze trends in depth by
sex, ethnicity or other factors. New obesity
statistics based on more BMI analyses are expected
later this year. CDC experts are also examining the
new body scan data for numbers on body fat.
Some health
experts are lobbying for different official
measurements than BMI. The American Heart
Association this month endorsed waistline
measurement as a good predictor of heart disease
risk. Others endorse measuring body fat, as in the
body scans the CDC uses. For instance, body fat can
be measured by immersion in a water tank in a
sports club or health clinic, although such tests
are expensive and cumbersome. What's more, there is
no official definition of obesity using body fat.
Body fat can
also be measured by a body fat caliper that
determines a person's level of body fat by pinching
and measuring skin folds in eight areas of the
body, such as the front upper thigh, abdomen, and
triceps. John Lollar, a 38-year-old former college
decathlete who invented a $19.99 body fat caliper,
says body fat measurements are far superior to BMI,
because they single out the fat from the muscle.
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"You have good
weight and bad weight," he says. "A lot of people
may think they need to lose weight, but really what
they need to do is lose body fat."
Celebrity BMIs
Using the
standard formula for calculating Body Mass Index,
or BMI*, several
muscular Hollywood hunks and star athletes could be
considered overweight or obese, according to weight
and height statistics posted on various celebrity
and sports Web sites. Meantime, many of their
female counterparts are normal or underweight,
according to these statistics.
[Madonna image on right]
|
Actor or
athlete |
Height |
Weight in lbs.)
|
BMI |
Actress or athlete
|
Height |
Weight (in lbs.)
|
BMI |
|
Sylvester Stallone
|
5'9" |
228 |
34 |
Rebecca Lobo |
6'4" |
185 |
22 |
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Arnold Schwarzenegger
|
6'2" |
257 |
33 |
Venus Williams
|
6'1" |
169 |
22 |
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Sammy Sosa |
6'0" |
220 |
30 |
Demi Moore |
5'5" |
130 |
22 |
|
Harrison Ford |
6'1" |
218 |
29 |
Lisa Leslie |
6'5" |
170 |
20 |
|
George Clooney |
5'11" |
211 |
29 |
Julia Roberts
|
5'9" |
121 |
18 |
|
Bruce Willis |
6'0" |
211 |
29 |
Hilary Swank |
5'7" |
118 |
18 |
|
Mike Piazza |
6'3" |
215 |
27 |
Nicole Kidman
|
5'10" |
120 |
17 |
|
Brad Pitt |
6'0" |
203 |
27 |
Madonna |
5'4" |
101 |
17 |
|
Michael Jordan |
6'6" |
216 |
25 |
Gwyneth Paltrow
|
5'10" |
111 |
16 |
*BMI = (Weight
in pounds ÷height in inches ÷height in inches) x
703. Scale: BMI of less than 18.5 = underweight;
18.5 to 24.9 = healthy weight; 25 to 29.9 =
overweight; 30 or more = obese
Sources:
Absolutepictures.com, actorarchives.com, NBA, WNBA,
New York Mets, Chicago Cubs, Washington Wizards,
ESPN
Write to Betsy
McKay at
betsy.mckay@wsj.com
3
Return To
Top
Updated
July 23, 2002 10:34 a.m. EDT
|
Copyright 2002 Dow Jones & Company, Inc. All Rights
Reserved
Printing, distribution, and use of this material is
governed by your Subscription agreement and
Copyright laws.
For information about subscribing go to http://www.wsj.com
|
Wall
Street Journal Editorial Article About the Caveman Diet
Source
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July 23, 2002
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Physicians Start
to Turn Focus To Fitness, Not Body Weight
By KEVIN HELLIKER
Staff Reporter of THE WALL STREET
JOURNAL
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When he started
running, Steve Blair was fat. After 35 years of
running more than 30 miles a week, he says he's
fatter -- nearly 25 pounds fatter.
Many would call
this a failure of exercise. But they would be
wrong, and nobody knows that as well as Dr. Blair.
As director of research at the renowned Cooper
Institute for Aerobics in Dallas, founded in 1970
by Kenneth Cooper, who is widely regarded as the
father of the aerobic-exercise movement. Dr. Blair
has led or participated in recent studies whose
conclusions suggest something revolutionary: that
being overweight, even obese, isn't as unhealthy as
being sedentary.
One study in
particular examined both the body composition and
fitness level of about 22,000 men over a period of
eight years. The purpose was to look especially
closely at those who died during that time, a
number that turned out to be 428. The study reached
this conclusion: The unfit lean -- as measured by
performance on a treadmill -- were nearly twice as
likely to die earlier as the fit, including the
obese fit. Indeed, despite the common assumption
that obesity is life-threatening, "we found that
obesity did not appear to increase mortality risk
in fit men," concluded the three authors of the
study, including Dr. Blair.
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About two dozen
studies support the notion that the standard
treatment for excessive weight -- dieting -- is
insufficient and perhaps even misguided, at least
for any individual who isn't working out. A more
effective treatment might be a healthful diet (lots
of fresh fruit and vegetables) and exercise --
though not for the purpose of weight loss. While
diets typically fail, exercise fails only when
participants set unrealistic goals, the most common
of which is weight loss.
[Karl Note: The "healthy diet" of lots of
fruits and vegetables certainly contradicts other
articles in this same newspaper, and certainly
contradicts my own diet suggestions!
Exercise? I certainly DO agree with the need
for that! I strongly recommend using the
mini-trampline.]
 A
half hour a day of exercise as moderate as brisk
walking has been shown to mitigate the dangers of
obesity -- including high blood pressure, diabetes,
cardiovascular disease, even cancer -- regardless
of whether the activity takes off pounds. If forced
to recommend only one course of action against
obesity, Ralph S. Paffenbarger Jr., professor
emeritus of epidemiology at the Stanford University
School of Medicine, says he would recommend
exercise over dieting. For one thing, "your
appetite may be reduced slightly by being active,"
says Dr. Paffenbarger, who has conducted numerous
studies showing the benefits of exercise among the
obese.
To be sure, the
healthiest option is to be fit and trim. Moreover,
exercise is no excuse for excessive or
non-nutritious eating. But even in cases where
exercise doesn't shed pounds, it still can limit
how much additional weight is gained. "I hate to
think how fat I'd be if I didn't run," Dr. Blair
says. Some studies suggest that weight control may
be more conducive to longevity than weight loss.
But getting
doctors to preach this message is difficult. Only a
small minority of the population exercises half an
hour a day, the surgeon general's recommended
amount, and physicians are no more rigorous about
it than anybody else. They are disinclined to nag
patients about something they themselves aren't
doing.
A larger problem
is the cultural obsession with appearance. Many
people work out not to get fit but to get thin, and
when that fails to happen -- and happen quickly --
they quit. The challenge for preventative medicine
experts: getting people to focus on feeling better
rather than looking thinner.
Sometimes a
health crisis can achieve that, as happened to Inga
Andriessen. The Toronto lawyer, 100 pounds
overweight, tried exercising, but invariably
stopped when the pounds failed to vanish fast
enough. "I was always focused on dress size," she
says.
Return To Top
Then she got
pregnant and developed pregnancy-related diabetes.
Under doctor's orders, she started swimming three
times a week for her health and that of her unborn
child. It left her feeling great -- and she paid no
attention to whether she lost any weight.
 Though
the diabetes disappeared after she gave birth, her
doctor told her she was now a serious candidate for
developing a chronic form of that disease. So she
set a new exercise goal that had nothing to do with
weight loss: the completion of a triathlon. Nine
months after giving birth, she did it, and now
she's a committed triathlete, exercising six days a
week. Of the 100 extra pounds she carried before
getting pregnant, she still carries about 70 and
wears a size 20 dress.
But her doctor's
visits are a delight. Her blood pressure, which was
borderline high before she became a regular gym
goer, now is fine, and her blood-sugar levels show
no danger of diabetes. "My doctor is amazed," she
says.
 It likely will
take years to dispel the myth that thin equals fit,
and fat unfit. But there are signs of change. A
5-year-old maker of fitness apparel for plus-size
women, A Big Attitude, is posting double-digit
growth. After a 240-pound woman sued Jazzercise
Inc. for refusing to let her become an instructor,
the national operator of fitness classes relented,
saying in a settlement that "Jazzercise has
determined that the value of 'fit appearance' as a
standard is debatable."
Then there is
7-year-old Team Clydesdale, a national organization
that seeks to level the racing field for large-size
participants in marathons, triathlons and such.
Instead of competing against others in their age
group -- which is how the typical race is
structured -- Clydesdales go up against others in
their weight group. The motto of Team Clydesdale:
You don't have to be thin to be fit. The truth of
that is becoming apparent as growing numbers of
large people cross the finish line at marathons,
triathlons and other endurance races.
Team Clydesdale
founder Guy East, a former college-football
lineman, notes that exercise offers an enormous
advantage over dieting. A moment of weakness late
at night can negate an entire day of disciplined
dieting. But nothing can taint a completed workout.
"I've been exercising for many, many years, and
I've never regretted a single workout," says the
42-year-old Indianapolis engineer.
Write to Kevin
Helliker at
kevin.helliker@wsj.com1
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URL for this article:
http://online.wsj.com/article/0,,SB1027369664581719320.djm,00.html
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Hyperlinks in this Article:
(1)
mailto:kevin.helliker@wsj.com
(2)
http://online.wsj.com/article/0,,SB102547289088320400,00.html
(3)
http://online.wsj.com/article/0,,SB1023994415867700040,00.html
(4)
http://online.wsj.com/article/0,,SB1023915818486451160,00.html
(5)
http://online.wsj.com/article/0,,SB1023915670931417880,00.html
|
Updated
July 23, 2002
|
Copyright 2002 Dow Jones & Company,
Inc. All Rights Reserved
Printing, distribution, and use of this material is
governed by your Subscription agreement and
Copyright laws.
For information about subscribing go to
http://www.wsj.com
|
Return To Top
|
Source
|
Fat doesn't kill...
carbohydrates do
If you think a
high-carbohydrate, low-fat diet will help you
lose weight, think again. This is because new
research is suggesting otherwise
THAT bowl of fat belly pork
might not be as sinful as you think.
For years, medical experts
around the world have been urging people to
embrace a low-fat, high-carbohydrate diet.
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Don't eschew the fat, like this dish of
pork belly. Some studies have found that
cutting back on fat could actually increase
the risk of heart disease instead. So, lard
it on because grease is the word. -- JOYCE
FANG |
Now, a report in the
July 7 issue of the New York Times
magazine, titled What If It's All Been A
Big Fat Lie?, suggests that people could have
been eating the wrong food all along.
Fat may not be as harmful as
many have come to believe. What may be really
causing obesity and heart disease, and killing
people are carbohydrates.
But this high-fat,
low-carbohydrate school of thought is nothing
new.
In 1972, Dr Robert Atkins, in
his best-selling book Dr Atkins' Diet
Revolution, said that people could lose weight
eating steak, eggs and butter. He blamed
obesity and coronary disease on carbohydrates
like pasta and sugar.
Return To Top
But the American Medical
Association brushed him off as a fraud for
advocating 'an unlimited intake of saturated
fats and cholesterol-rich foods'.
New evidence found in the
last five years, however, shows that perhaps Dr
Atkins' prescription may have been the
healthier choice after all.
Walter Willet, chairman of
the department of nutrition at the Harvard
School of Public Health, says: 'The idea that
all fat is bad for you - the exclusive focus on
adverse effects of fat may have contributed to
the obesity epidemic.'
He is the spokesman for the
ongoing longest-running, most comprehensive
diet and health study ever performed, involving
nearly 300,000 people.
There are many reasons which
suggest that the low-fat-is-good hypothesis is
untrue, says the magazine report. For starters,
the world is in the midst of an obesity
epidemic that started in the 1980s. Around that
time, medical experts were actively advocating
a low-fat diet.
Type Two diabetes, the most
common form of the disease, also increased
significantly during this period.
Research has also shown that
low-fat weight loss diets have failed both in
clinical trials and in real life.
The percentage of fat in the
American diet has been decreasing over the last
two decades. Cholesterol levels, and the number
of smokers, are also falling.
Yet, the incidence of heart
disease has not fallen along with them, as one
would have expected.
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So, the current worldwide
epidemic of obesity cannot be blamed on what
Yale psychologist Kelly Brownell describes as a
'toxic food environment' - cheap food, large
portions, pervasive food advertising and
sedentary lives - or, at least, not entirely on
it.
Fast food consumption did
grow steadily through the 1970s to the 1980s,
but not at the pace at which obesity surged.
Exercise and increasing
obesity rates also have little correlation.
The US Center for Disease
Control's 1990 data shows that obesity rates
continue to climb, even though the levels of
exercise remain unchanged.
Studies show that consuming
more carbohydrates makes your body produce
higher levels of insulin, which is needed to
break them down into sugar molecules to be
transported into the blood stream. And as long
as insulin levels are high, there is less
chance of the body burning its own fat.
When there is too much
insulin, blood sugar drops. This leads to
hunger pangs which, in turn, leads people to
eat more carbohydrates, produce more insulin
and so on, until they get fat or even
dangerously obese.
By contrast, if people had
more fat in their diets instead, they would not
be staying so hungry. Thus, they would not
consume as many carbohydrates, says the
eat-fat, stay-slim school of thought.
So, if carbohydrates create a
situation that is ripe for obesity, how did fat
become known as 'the greasy killer'?
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WHY A LOW-FAT DIET WAS ALL
THE RAGE
UNTIL the late 1970s, the
accepted wisdom indeed was that fat and protein
protected against overeating by making people
feel sated. Carbohydrates just made them fat.
But in 1977, a US Senate
committee published its Dietary Goals For The
United States, advising Americans to
drastically curb their fat intake to prevent an
epidemic of 'killer diseases' that was sweeping
the country supposedly.
In 1984, the National
Institutes of Health (NIH) recommended that
Americans over the age of two eat less fat.
Then, it spent several hundred millions of
dollars trying to show a connection between
eating fat and getting heart disease.
Nothing came out of their
research.
And so, the NIH latched on to
a study which found that reducing cholesterol
by drug therapy could prevent heart disease.
It then made its own
conclusion that if a cholesterol-lowering drug
could prevent heart attacks, then a low-fat,
cholesterol-lowering diet should do the same.
That led to the food industry
producing thousands of reduced-fat products to
meet this new dietary decree.
But foods like biscuits,
chips and yoghurt did not taste as good when
the fat had been removed. So. sugar, often
high-fructose corn syrup, was added to satisfy
the taste buds.
All these added up to more
calories, and subsequently, more cases of heart
disease, diabetes and obesity.
The Atkins' diet is back in
the limelight, not to be mocked as it was
before, but to be tested to see if it really
can help curb the obesity epidemic.
So far, five US studies have
shown that subjects on some form of the Atkins'
diet lost twice the weight as the subjects on a
low-fat, low-calorie diet.
Results also suggest that the
heart-disease risk could actually be reduced
when fat is added back into the diet, while
starches and refined carbohydrates are removed.
As Eleftheria Maratos-Flier,
director of obesity research at Harvard's
prestigious Joslin Diabetes Centre, told New
York Times Magazine: 'For a large percentage of
the population, perhaps 30 to 40 per cent,
low-fat diets are counter-productive.
'They have the paradoxical
effect of making people gain weight.'
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For now, more tests are
needed to find out if people are growing fatter
because of how they have been eating wrongly
all this time.
And to see if the health
authorities who have long promoted a low-fat,
high-carbohydrate diet will be forced to eat
humble pie.
Why some fat is needed in
the diet
IT'S A NUTRIENT
Fat is one of the three
nutrients, along with protein and
carbohydrates, that supply calories to the
body.
STORAGE SUBSTANCE
It serves as the storage
substance for the body's extra calories. It
fills the fat cells (adipose tissue) which help
insulate the body.
HELPS IN ABSORPTION
Fat helps in the absorption,
and transportation through the bloodstream, of
the fat-soluble vitamins A, D, E and K.
PROVIDES FATTY ACIDS
Return To Top
Fat is essential for the
proper functioning of the body. It provides the
essential fatty acids, which are not made by
the body and must be obtained from food.
Fatty acids provide the raw
materials that help in the control of blood
pressure, blood clotting, inflammation and
other body functions.
AN ENERGY SOURCE
It is an important energy
source. When the body has used up the calories
from carbohydrates, which occurs after the
first 20 minutes of exercise, it begins to
depend on the calories from fat.
Also, healthy skin and hair
are maintained by fat.
Facts provided by the
Nutrition Programme Management, Health
Promotion Board.
WHAT'S GOOD AND BAD
CARBOHYDRATES
Good:
Complex carbohydrates are a good
source of minerals, vitamins and fibre. They
can be found in bread, cereals, beans, lentils,
dried peas, legumes and pastas.
Return To Top
Some simple carbohydrates,
which also contain vitamins and minerals, can
be found in fruit, vegetables and milk
products.
Bad:
These are simple carbohydrates found in
processed and refined sugars, which provide
calories but lack vitamins, minerals and fibre.
They can be found in foods like candy, table
sugar, syrups (not including natural syrups
such as maple) and carbonated beverages.
FAT
Good:
Polyunsaturated and monounsaturated fat may
help to lower blood cholesterol. Foods high in
polyunsaturated fat include margarine,
vegetable oils (like corn oil, soy bean oil and
sunflower oil) and fatty fish like salmon and
mackerel. Foods high in monounsaturated fat
include olive oil, canola oil, groundnut oil
and avocado.
Bad:
Excessive consumption of saturated fat and
trans fat can raise blood cholesterol and
increase the risks of developing heart disease
and stroke. Foods high in such fat include
animal fats, butter, coconut cream, pastries
and biscuits.
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f article?? That is a milestone! Many people
will move toward a more healthy diet and life just
because of this one criticism of the low fat diet.
Note also, the validation of my major article on the
fraud in cholesterol claims. The vast majority of
doctors are still telling their patients the blatantly
false data that "high cholesterol" is dangerous -- is the
cause of heart disease. This is blithering tripe!
Read my article on the cholesterol fraud
HERE.
At the very moment
that the government started telling Americans to eat
less fat, we got fatter. The truths about why we
gain weight and why it is so hard to lose it just
might turn out to be much different from what we have
been led to think.
fat —particularly the saturated fat of meat and dairy
products—was the primary nutritional evil in the
American diet. Atkins managed to sell millions of
copies of a book promising that we would lose weight
eating steak, eggs and butter to our heart’s desire,
because it was the carbohydrates, the pasta, rice,
bagels and sugar, that caused obesity and even heart
disease. Fat, he said, was harmless. 
Atkins allowed his
readers to eat ‘‘truly luxurious foods without
limit,’’ as he put it, ‘‘lobster with butter sauce,
steak with béarnaise sauce...bacon cheeseburgers,’’
but allowed no starches or refined carbohydrates,
which means no sugars or anything made from flour.
Atkins banned even fruit juices, and permitted only a
modicum of vegetables, although the latter were
negotiable as the diet progressed.
