Curiously, what todayseems in our society to be a genetic predis position toward obesity functioned during the famines of prehistory as an effective method of survival.
Ironically, the ancestors of those who todayare most at riskfor type2 diabetes were, during prehistory, not the sickand dying, but the survivors.
If famine struck today in the UnitedStates, guess who would survive most easily?
The samepeople who are most at risk for type 2 diabetes.
For those livingin a harsh en vironment wherethe availability of food is uncertain, bodies that store fat most efficiently when food is available (for example, by being insulin-resistant and craving carbohydrate,like most type 2 diabetics) survive to reproduce.
If you give it some thought, it makes perfectsense: If a farmer wants to fatten up his pigs or cows, he doesn't feed them meat or butter and eggs, he feeds them grain.
If you want to fatten yourself up, just start loading up on bread, pasta, potatoes, cake, and cookies — all high- carbohydrate foods.
If you want to hasten the fattening process, con sume dietary fat with your carbohydrate.
Indeed, two recent studies showed that dietaryfat, whenconsumed aspart of a high-carbohydrate diet, was converted to body fat.
Fat consumed as part of a low-carbo hydrate diet was metabolized,or burned off.
The Insulin/Fat Connection The primary source of body fat for most Americans is not dietary fat but carbohydrate, which is converted to blood sugar and then, with the aid of insulin, to fat by fat cells.
Remember, insulin is our main fat- building hormone.
Eat a plate of pasta.Your blood sugar will rise and your insulin level (if you havetype 2 diabetes or are not diabetic) will also rise in order to cover, or prevent, the jump in blood sugar.
Allthe blood sugarthat is not burnedasenergy or storedasglycogen isturned into fat.
Soyou could, in theory, acquire more body fat from eating a high-carbohydrate "fat-free" dessert than youwouldfrom eatinga ten der steaknicely marbledwithfat.
Even the fatin the steakis more likely to be stored if it is accompanied by bread, potatoes, corn, and so on.
The fatty-acid building blocks of fats can be metabolized (burned), stored, or converted by your body into other compounds, depending on what it requires.
Consequently, fat is always in fluxin the body,be ing stored, appearing in the blood, and being converted to energy.The amount of triglycerides (the storage form of fat) in your bloodstream at any giventime willbe determined byyour heredity, your levelof ex ercise, your blood sugar levels, your diet, your ratio of visceral (ab-
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dominal) fat to lean body mass (muscle), and especially byyourrecent consumption ofcarbohydrate.
The slim and fit tend to be very sensitive (i.e., responsive) to insulin and have low serum levels not only of triglycerides but insulin aswell.
But even their triglyceride levels will increase after a high-carbohydrate meal, as excess blood sugar is con verted to fat.
The higher the ratioof abdominal fat (and, to a lesserde gree, total body fat) to lean body mass, the less sensitive to insulin you'll tend to be.
In the obese, triglycerides tend to be present at high levels in the bloodstream all the time. (This is sometimes exaggerated during weight loss because fat is appearing in the bloodstream as it comes out of storage to be converted into energy.) Not only are high triglyceride levels a direct cause of insulin resistance, but they also contribute to fatty deposits on the walls of yourbloodvessels (athero sclerosis).
Research demonstrates that if high concentrations of triglycerides are injected into the blood supply of the liver of a well- conditioned athlete, someone very sensitive to insulin, she will be come temporarily insulin-resistant. (The most important thing to note here is that insulin resistance, as well as other risk factors for dia betic complications, canbe reversed by eating less carbohydrate, nor malizing blood sugars, and slimming down, which we'll discuss in greaterdetail later on.) If you become overweight, you'll produce more insulin, become insulin-resistant (which will require youto produce yetmoreinsulin), and become even more overweight because you'llcreate more fat and store more fat.
You'll enterthe vicious circle depicted in Figure 1-1.
Consider that steak I mentioned earlier.
As youknow,the body can convert protein to blood sugar, but it does so at a very slow rate, and inefficiently.
Serum insulinlevels derived from the phase II insulin re sponse or even from insulin injected before a meal may thus be suffi cient to preventablood sugar rise from proteinconsumption by itself.
Dietary fat cannot be converted to blood sugar, and therefore it doesn't cause seruminsulinlevels or requirements for injected insulin to increase.
Say you eat a 6-ounce steak with no carbohydrate side dish — this won't require much insulin to keep your blood sugar steady, and the lower insulin level will cause only a small amount of the fat to be stored.
Now consider what would happen if you instead ate a "fat-free" dessertwith exactlythe same number of calories asthat steak.Your in sulin level will jump dramatically in order to cover the sugar and starches in the dessert.
Remember, insulin is the fat-building and fat-
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storage hormone.
Since it's dessert, youprobably won'tbe going out to run a marathon after eating, so the largest portion of your newly cre atedblood sugar won't getburned.
Instead much of it will be turned into fat and stored.
Interestingly enough,eating fat with carbohydrate canactually slow the digestion of carbohydrate, so the jump in your blood sugar level might thereby be slowed.
This would probably be relatively effective if you're talking about eating a green salad with vinegar-and-oil dress ing.
But if you're eating a regular dessert, or abaked potato with your steak, the slowdown in digestion would not prevent blood sugar ele vation in a diabetic.
Despite what the popular media would have us believe, fat is not evil.In fact, many researchers are becoming quite concernedabout the dangerous potential of "fatsubstitutes." Fat is absolutely necessary for survival.
Much of the brain is constructed from fatty acids.Without essential fatty acids — which, like essential amino acids, cannot be manufactured by the body and must be eaten — you would die.
Fat substitutes such as the FDA-approved olestra (sold under the brand name of Olean and present in such products as Frito-Lay WOW! potato chips) bring aboutthe specter of people trying to subsiston a no-fat diet, a diet that could kill them. (Olestra actually robs the body of important fat-soluble vitamins and essential fatty acids.
The FDA has required that it contain additives of those vitamins.
In test mar kets, some consumers havebeen made quite ill by the product, while others don't see any effect.
I don't recommend it — it's at best com pletely unnecessary.) Diabetics are affected disproportionately by diseases such as ather osclerosis.
This has led to the long-standingmyth that diabetics have abnormal lipid profiles because they eatmore fat than nondiabetics.* It was likewise once thought that dietary fat caused all the long-term complications of diabetes.
For many years, this was taken asgospel by most in the medicalcommunity.
In truth, however, the high lipid pro files in many diabetics with uncontrolled blood sugar havenothing to do with the fatthey consume.Most diabetics consume very little fat — they've been conditioned to fear it.
High lipid profiles are a symptom
*Alipidprofile isthe measuremenc of cholesterol, HDL (good cholesterol), LDL (bad cholesterol), and triglyceride levels in the blood. Somephysicians now con siderlipoprotein(a)to be an essential componentof the lipid profile. (See Chap ter 2.)
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not of excess dietary fat, but of high blood sugars.
Indeed, even in most nondiabetics, the consumption of fat has little if anything to do with their lipid profiles.
On the other hand, high consumption of carbohydrate, as we will discuss shortly, can cause "nondiabetics" to develop some of the com plications usuallyassociated with diabetes.
When I was on a very low fat, high-carbohydrate diet about forty years ago, I had high fasting triglycerides (usually over250mg/dl) and high serum cholesterol (usually over 300 mg/dl), and I developed a number of vascular complications.
When I went onto a very low car bohydrate diet and did not restrictmyfat,mylipidsplummeted.Now, in my midseventies, I have the lipid profile of an Olympic athlete, ap parently from eating a low-carbohydrate diet in order to normalize my blood sugars.
That I exercise regularly probably doesn't hurt my lipid profile, either— but I was also exercising when my lipid profile was abnormal.
Dare your physician.
Ask him or her if his or her lipid profile on a low-fat diet can remotely compare to mine, on a high-fat, low- carbohydrate diet: • LDL— the "bad" cholesterol — 53 (below 100 is considered normal) • HDL — the "good" cholesterol— 118 (above 39 is considered normal) • Triglycerides— 45 (below 150 is considered normal) • Lipoprotein(a) — undetectable (below 30 is considered normal) Contrary to popular myth,fat is not a demon.It's the body'swayof storing energy and maintaining essential organs such as the brain.
Without essential fatty acids, your body would cease to function.
CARBOHYDRATE
I've saved carbohydrate for last because it's the food group that ad versely affects blood sugarmost profoundly. Ifyou'relikemost diabet ics— or virtually everyone who fives in an industrialized society — you probably eat a diet that's mostly carbohydrate. Grains. Fruit. Bread. Cake. Beans. Snack foods. Rice. Potatoes. Pasta. Breakfast ce real. Bagels. Muffins. They look different, but dietarily speaking, they're essentiallythe same.
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