Health Gallery Nutrition Center

Box 283, Gold Beach, Or 97444
1-541-247-7077

drhealth@getwel.com * drhealth's getwel.com Home Page http://www.getwel.com

Obesity Epidemic Caused By A Misinterpretation!

The confusion about fats and carbohydrates began in 1982, when 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 according to Flatt.

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, thus resulting in the Obesity Epidemic.

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 and I think they are, 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. 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 as ''the Nobel-prize winning question.''

Why do over weight people always feel like munching? 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 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 Viscous Cycle! The resulting rush of insulin stores the blood sugar away and a few hours later, your blood sugar is lower than it was before you ate. As Ludwig explains, your body effectively thinks it has run out of fuel, but the insulin is still high enough to prevent you from burning your own fat. The result is hunger and a craving for more carbohydrates. It's another vicious circle, and another situation ripe for obesity.

The glycemic-index concept and the idea that starches can be absorbed into the blood even faster than sugar emerged in the late 70's, but again had no influence on public health recommendations, because of the attendant controversies. To wit: if you bought the glycemic-index concept, then you had to accept that the starches we were supposed to be eating 6 to 11 times a day were, once swallowed, physiologically indistinguishable from sugars. This made them seem considerably less than wholesome.

Rather than accept this possibility, the policy makers simply allowed sugar and corn syrup to elude the vilification that befell dietary fat. After all, they are fat-free. Sugar and corn syrup from soft drinks, juices and the copious teas and sports drinks now supply more than 10 percent of our total calories.

The 80's saw the introduction of Big Gulps and 32-ounce cups of Coca-Cola, blasted through with sugar, but 100 percent fat free. When it comes to insulin and blood sugar, these soft drinks and fruit juices -- what the scientists call ''wet carbohydrates'' -- might indeed be worst of all. (Diet soda accounts for less than a quarter of the soda market.) The gist of the glycemic-index idea is that the longer it takes the carbohydrates to be digested, the lesser the impact on blood sugar and insulin and the healthier the food. Those foods with the highest rating on the glycemic index are some simple sugars, starches and anything made from flour.

Green vegetables, beans and whole grains cause a much slower rise in blood sugar because they have fiber, a nondigestible carbohydrate, which slows down digestion and lowers the glycemic index. Protein and fat serve the same purpose, which implies that eating fat can be beneficial, a notion that is still unacceptable. And the glycemic-index concept implies that a primary cause of Syndrome X, heart disease, Type 2 diabetes and obesity is the long-term damage caused by the repeated surges of insulin that come from eating starches and refined carbohydrates. This suggests a kind of unified field theory for these chronic diseases, but not one that coexists easily with the low-fat doctrine.

At Ludwig's pediatric obesity clinic, he has been prescribing low-glycemic-index diets to children and adolescents for five years now. He does not recommend the Atkins diet because he says he believes such a very low carbohydrate approach is unnecessarily restrictive; instead, he tells his patients to effectively replace refined carbohydrates and starches with vegetables, legumes and fruit. This makes a low-glycemic-index diet consistent with dietary common sense, albeit in a higher-fat kind of way. His clinic now has a nine-month waiting list. Only recently has Ludwig managed to convince the N.I.H. that such diets are worthy of study. His first three grant proposals were summarily rejected, which may explain why much of the relevant research has been done in Canada and in Australia.

In April, however, Ludwig received $1.2 million from the N.I.H. to test his low-glycemic-index diet against a traditional low-fat-low-calorie regime. That might help resolve some of the controversy over the role of insulin in obesity, although the redoubtable Robert Atkins might get there first. The 71-year-old Atkins, a graduate of Cornell medical school, says he first tried a very low carbohydrate diet in 1963 after reading about one in the Journal of the American Medical Association. He lost weight effortlessly, had his epiphany and turned a fledgling Manhattan cardiology practice into a thriving obesity clinic.

He then alienated the entire medical community by telling his readers to eat as much fat and protein as they wanted, as long as they ate little to no carbohydrates. They would lose weight, he said, because they would keep their insulin down; they wouldn't be hungry; and they would have less resistance to burning their own fat. Atkins also noted that starches and sugar were harmful in any event because they raised triglyceride levels and that this was a greater risk factor for heart disease than cholesterol.

Atkins's diet is both the ultimate manifestation of the alternative hypothesis as well as the battleground on which the fat-versus-carbohydrates controversy is likely to be fought scientifically over the next few years. After insisting Atkins was a quack for three decades, obesity experts are now finding it difficult to ignore the copious anecdotal evidence that his diet does just what he has claimed.

Why does such a low-calorie/low carb regimen 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.

An inevitable criticism of Atkins's diet has been that ketosis is dangerous and to be avoided at all costs. Ketosis experts, however, 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. The medical establishment always worried about diabetic ketoacidosis. But ketosis is a normal physiologic state. 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. History and research has proven the low carb diet does work and is safe if done correctly. A four to six per day multivitamin/mineral is required as well as six caps daily of Essential Fatty Acids. Most important are eight glasses of purified water daily. Detailed instructions and books are available at the Health Gallery or call 541-247-7077.

Thought For The Day : You create your thoughts, your thoughts create your intentions and your intentions create your reality! Our lives are what our thoughts create!