What if It's All Been a Big Fat Lie? (Part 2)
Few experts now deny that the low-fat message is radically oversimplified. If nothing else, it effectively ignores the fact that unsaturated
fats, like olive oil, are relatively good for you: they tend to elevate your good cholesterol, high-density lipoprotein (H.D.L.), and lower
your bad cholesterol, low-density lipoprotein (L.D.L.), at least in comparison to the effect of carbohydrates. While higher L.D.L. raises your
heart-disease risk, higher H.D.L. reduces it.
What this means is that even saturated fats -- a k a, the bad fats -- are not nearly as deleterious as you would think. True, they will elevate
your bad cholesterol, but they will also elevate your good cholesterol. In other words, it's a virtual wash. As Willett explained to me, you will
gain little to no health benefit by giving up milk, butter and cheese and eating bagels instead.
But it gets even weirder than that. Foods considered more or less deadly under the low-fat dogma turn out to be comparatively benign if you
actually look at their fat content. More than two-thirds of the fat in a porterhouse steak, for instance, will definitively improve your cholesterol
profile (at least in comparison with the baked potato next to it); it's true that the remainder will raise your L.D.L., the bad stuff, but it will also
boost your H.D.L. The same is true for lard. If you work out the numbers, you come to the surreal conclusion that you can eat lard straight
from the can and conceivably reduce your risk of heart disease.
The crucial example of how the low-fat recommendations were oversimplified is shown by the impact -- potentially lethal, in fact -- of low-fat
diets on triglycerides, which are the component molecules of fat. By the late 60's, researchers had shown that high triglyceride levels were at
least as common in heart-disease patients as high L.D.L. cholesterol, and that eating a low-fat, high-carbohydrate diet would, for many
people, raise their triglyceride levels, lower their H.D.L. levels and accentuate what Gerry Reaven, an endocrinologist at Stanford University,
called Syndrome X. This is a cluster of conditions that can lead to heart disease and Type 2 diabetes.
It took Reaven a decade to convince his peers that Syndrome X was a legitimate health concern, in part because to accept its reality is to
accept that low-fat diets will increase the risk of heart disease in a third of the population. ''Sometimes we wish it would go away because
nobody knows how to deal with it,'' said Robert Silverman, an N.I.H. researcher, at a 1987 N.I.H. conference. ''High protein levels can be
bad for the kidneys. High fat is bad for your heart. Now Reaven is saying not to eat high carbohydrates. We have to eat something.''
Surely, everyone involved in drafting the various dietary guidelines wanted Americans simply to eat less junk food, however you define it, and
eat more the way they do in Berkeley, Calif. But we didn't go along. Instead we ate more starches and refined carbohydrates, because calorie
for calorie, these are the cheapest nutrients for the food industry to produce, and they can be sold at the highest profit. It's also what we like
to eat. Rare is the person under the age of 50 who doesn't prefer a cookie or heavily sweetened yogurt to a head of broccoli.
''All reformers would do well to be conscious of the law of unintended consequences,'' says Alan Stone, who was staff director for
McGovern's Senate committee. Stone told me he had an inkling about how the food industry would respond to the new dietary goals back
when the hearings were first held. An economist pulled him aside, he said, and gave him a lesson on market disincentives to healthy eating:
''He said if you create a new market with a brand-new manufactured food, give it a brand-new fancy name, put a big advertising budget
behind it, you can have a market all to yourself and force your competitors to catch up. You can't do that with fruits and vegetables. It's
harder to differentiate an apple from an apple.''
Nutrition researchers also played a role by trying to feed science into the idea that carbohydrates are the ideal nutrient. It had been known, for
almost a century, and considered mostly irrelevant to the etiology of obesity, that fat has nine calories per gram compared with four for
carbohydrates and protein. Now it became the fail-safe position of the low-fat recommendations: reduce the densest source of calories in the
diet and you will lose weight. Then in 1982, J.P. Flatt, a University of Massachusetts biochemist, published his research demonstrating that, in
any normal diet, it is extremely rare for the human body to convert carbohydrates into body fat. This was then misinterpreted by the media
and quite a few scientists to mean that eating carbohydrates, even to excess, could not make you fat -- which is not the case, Flatt says. But
the misinterpretation developed a vigorous life of its own because it resonated with the notion that fat makes you fat and carbohydrates are
harmless.
As a result, the major trends in American diets since the late 70's, according to the U.S.D.A. agricultural economist Judith Putnam, have been
a decrease in the percentage of fat calories and a ''greatly increased consumption of carbohydrates.'' To be precise, annual grain consumption
has increased almost 60 pounds per person, and caloric sweeteners (primarily high-fructose corn syrup) by 30 pounds. At the same time, we
suddenly began consuming more total calories: now up to 400 more each day since the government started recommending low-fat diets.
If these trends are correct, then the obesity epidemic can certainly be explained by Americans' eating more calories than ever -- excess
calories, after all, are what causes us to gain weight -- and, specifically, more carbohydrates. The question is why?
The answer provided by Endocrinology 101 is that we are simply hungrier than we were in the 70's, and the reason is physiological more than
psychological. In this case, the salient factor -- ignored in the pursuit of fat and its effect on cholesterol -- is how carbohydrates affect blood
sugar and insulin. In fact, these were obvious culprits all along, which is why Atkins and the low-carb-diet doctors pounced on them early.
The primary role of insulin is to regulate blood-sugar levels. After you eat carbohydrates, they will be broken down into their component sugar
molecules and transported into the bloodstream. Your pancreas then secretes insulin, which shunts the blood sugar into muscles and the liver
as fuel for the next few hours. This is why carbohydrates have a significant impact on insulin and fat does not. And because juvenile diabetes is
caused by a lack of insulin, physicians believed since the 20's that the only evil with insulin is not having enough.
But insulin also regulates fat metabolism. We cannot store body fat without it. Think of insulin as a switch. When it's on, in the few hours after
eating, you burn carbohydrates for energy and store excess calories as fat. When it's off, after the insulin has been depleted, you burn fat as
fuel. So when insulin levels are low, you will burn your own fat, but not when they're high.
This is where it gets unavoidably complicated. The fatter you are, the more insulin your pancreas will pump out per meal, and the more likely
you'll develop what's called ''insulin resistance,'' which is the underlying cause of Syndrome X. In effect, your cells become insensitive to the
action of insulin, and so you need ever greater amounts to keep your blood sugar in check. So as you gain weight, insulin makes it easier to
store fat and harder to lose it. But the insulin resistance in turn may make it harder to store fat -- your weight is being kept in check, as it
should be. But now the insulin resistance might prompt your pancreas to produce even more insulin, potentially starting a vicious cycle. Which
comes first -- the obesity, the elevated insulin, known as hyperinsulinemia, or the insulin resistance -- is a chicken-and-egg problem that hasn't
been resolved. One endocrinologist described this to me as ''the Nobel-prize winning question.''
Insulin also profoundly affects hunger, although to what end is another point of controversy. On the one hand, insulin can indirectly cause
hunger by lowering your blood sugar, but how low does blood sugar have to drop before hunger kicks in? That's unresolved. Meanwhile,
insulin works in the brain to suppress hunger. The theory, as explained to me by Michael Schwartz, an endocrinologist at the University of
Washington, is that insulin's ability to inhibit appetite would normally counteract its propensity to generate body fat. In other words, as you
gained weight, your body would generate more insulin after every meal, and that in turn would suppress your appetite; you'd eat less and lose
the weight.
Schwartz, however, can imagine a simple mechanism that would throw this ''homeostatic'' system off balance: if your brain were to lose its
sensitivity to insulin, just as your fat and muscles do when they are flooded with it. Now the higher insulin production that comes with getting
fatter would no longer compensate by suppressing your appetite, because your brain would no longer register the rise in insulin. The end result
would be a physiologic state in which obesity is almost preordained, and one in which the carbohydrate-insulin connection could play a major
role. Schwartz says he believes this could indeed be happening, but research hasn't progressed far enough to prove it. ''It is just a hypothesis,''
he says. ''It still needs to be sorted out.''
David Ludwig, the Harvard endocrinologist, says that it's the direct effect of insulin on blood sugar that does the trick. He notes that when
diabetics get too much insulin, their blood sugar drops and they get ravenously hungry. They gain weight because they eat more, and the
insulin promotes fat deposition. The same happens with lab animals. This, he says, is effectively what happens when we eat carbohydrates --
in particular sugar and starches like potatoes and rice, or anything made from flour, like a slice of white bread. These are known in the jargon
as high-glycemic-index carbohydrates, which means they are absorbed quickly into the blood. As a result, they cause a spike of blood sugar
and a surge of insulin within minutes. The resulting rush of insulin stores the blood sugar away and a few hours later, your blood sugar is lower
than it was before you ate. As Ludwig explains, your body effectively thinks it has run out of fuel, but the insulin is still high enough to prevent
you from burning your own fat. The result is hunger and a craving for more carbohydrates. It's another vicious circle, and another situation ripe
for obesity.
The glycemic-index concept and the idea that starches can be absorbed into the blood even faster than sugar emerged in the late 70's, but
again had no influence on public health recommendations, because of the attendant controversies. To wit: if you bought the glycemic-index
concept, then you had to accept that the starches we were supposed to be eating 6 to 11 times a day were, once swallowed, physiologically
indistinguishable from sugars. This made them seem considerably less than wholesome. Rather than accept this possibility, the policy makers
simply allowed sugar and corn syrup to elude the vilification that befell dietary fat. After all, they are fat-free.
Sugar and corn syrup from soft drinks, juices and the copious teas and sports drinks now supply more than 10 percent of our total calories;
the 80's saw the introduction of Big Gulps and 32-ounce cups of Coca-Cola, blasted through with sugar, but 100 percent fat free. When it
comes to insulin and blood sugar, these soft drinks and fruit juices -- what the scientists call ''wet carbohydrates'' -- might indeed be worst of
all. (Diet soda accounts for less than a quarter of the soda market.)
The gist of the glycemic-index idea is that the longer it takes the carbohydrates to be digested, the lesser the impact on blood sugar and insulin
and the healthier the food. Those foods with the highest rating on the glycemic index are some simple sugars, starches and anything made from
flour. Green vegetables, beans and whole grains cause a much slower rise in blood sugar because they have fiber, a nondigestible
carbohydrate, which slows down digestion and lowers the glycemic index. Protein and fat serve the same purpose, which implies that eating
fat can be beneficial, a notion that is still unacceptable. And the glycemic-index concept implies that a primary cause of Syndrome X, heart
disease, Type 2 diabetes and obesity is the long-term damage caused by the repeated surges of insulin that come from eating starches and
refined carbohydrates. This suggests a kind of unified field theory for these chronic diseases, but not one that coexists easily with the low-fat
doctrine.
At Ludwig's pediatric obesity clinic, he has been prescribing low-glycemic-index diets to children and adolescents for five years now. He does
not recommend the Atkins diet because he says he believes such a very low carbohydrate approach is unnecessarily restrictive; instead, he
tells his patients to effectively replace refined carbohydrates and starches with vegetables, legumes and fruit. This makes a low-glycemic-index
diet consistent with dietary common sense, albeit in a higher-fat kind of way. His clinic now has a nine-month waiting list. Only recently has
Ludwig managed to convince the N.I.H. that such diets are worthy of study. His first three grant proposals were summarily rejected, which
may explain why much of the relevant research has been done in Canada and in Australia. In April, however, Ludwig received $1.2 million
from the N.I.H. to test his low-glycemic-index diet against a traditional low-fat-low-calorie regime. That might help resolve some of the
controversy over the role of insulin in obesity, although the redoubtable Robert Atkins might get there first. |
