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Once you've started to follow a restricted-carbohydrate diet, you may find yourself pressured by well-meaning but uninformed friends or family, or even newspaper articles, to cease penalizing yourself and eat more "fun" foods, sweets, and treats. This chapter will provide you with specific scientific information that underpins my philosophy and will perhaps give you some ammunition for responding to this pressure. Even if you skip it now, you may want to come back to it later, or show it to your loved ones to lay their concerns to rest. As I don't expect most readers to be scientists, I've tried to keep all these explanations relatively simple. Some of the explanations may at this moment represent more theory than fact, but they're based on the latest information available to us.

How Did the Commonly Prescribed High-Carbohydrate Diet Come About?

Why is such advice being promulgated, when the major cause of such diabetic complications as heart disease, kidney disease, high blood pressure, and blindness is high blood sugar?

When I first developed diabetes, in 1947, little was known about why this disease, even when treated, caused early death and such distressing complications. Prior to the availability of insulin, about twenty-five years earlier, people with Type I diabetes usually died within a few months of diagnosis. Their lives could be prolonged somewhat with a diet that was very low in carbohydrate and usually high in fat. Sufferers from the milder Type II diabetes frequently survived on this type of diet, without supplemental medication. When I became diabetic, oral hypoglycemic agents were not available, and many people were still following very low carbohydrate, high-fat diets. It was at about this time that diets very high in saturated fats, with resultant high serum cholesterol levels, were experimentally shown to correlate with blood vessel and heart disease in animals. It was promptly assumed by many physicians that the complications of diabetes, nearly all of which related to abnormalities of large or small blood vessels, were caused by the high-fat diets. I and many other diabetics were therefore treated with a high-carbohydrate, low-fat diet. This new diet was adopted in the mid-1940s by the ADA, the New York Heart Association, and eventually by the American Heart Association (AHA) and other groups around the world. On the new diet, many of us had even higher serum cholesterol levels, and still developed the grave long-term complications of diabetes. Seemingly unaware of the importance of blood sugar control, the ADA raised the recommended carbohydrate content to 40 percent of calories, and then more recently to 60 percent.

Recent Developments Regarding Risk Factors for Heart Disease

A number of fatty substances have been found in the blood which relate to risk of heart attacks and vascular disease. These include HDL (high-density lipoprotein), LDL (low-density lipoprotein), triglyceride, fibrinogen, and lipoprotein(a). High serum levels of LDL, triglyceride, fibrinogen, and lipoprotein(a) tend to increase cardiovascular risk, while high levels of HDL tend to protect from cardiovascular disease. Cholesterol is a component of both LDL and HDL particles. The fraction of total cholesterol found in LDL particles is an index of risk, while the fraction of cholesterol found in HDL particles is an index of protection. Nowadays, when we want to estimate the effects of lipids upon the risk of coronary artery disease, we look at the ratio of total cholesterol to HDL and also at fasting triglyceride levels. Someone with high serum HDL can thus have a high total cholesterol and yet be at low statistical risk for a heart attack. Conversely, a person with low total cholesterol and very low HDL may be at high risk.

Recently a very large multicenter study (the Lipid Research Clinics Trial) investigated the effects of a low-fat, high-carbohydrate diet on middle-aged men. The study followed 1,900 people for seven years. Throughout this period, total cholesterol had dropped 5 percent from baseline in the low-fat group, but serum triglyceride went up about 10 percent! (Serum triglyceride rises very rapidly after a high-carbohydrate meal in nondiabetics, and moves up and down with blood sugar levels in most diabetics.) As with prior studies, no significant correlation was found between serum cholesterol levels and mortality rates.

On average, diabetics with chronically high blood sugars have elevated levels of LDL (the "bad" cholesterol) and depressed levels of HDL (the "good" cholesterol), even though the ADA low-fat diet has now been in use for many years. Of great importance is the recent discovery that the forms of LDL that harm arteries are small, dense LDL, oxidized LDL, and glycosylated LDL. All of these increase as blood sugar increases. In addition, independently of blood sugars, high serum insulin levels caused by high-carbohydrate diets bring about increased production of small, dense LDL particles and enlargement of the cells lining and surrounding arteries.

Under normal conditions, receptors in the liver remove LDL from the bloodstream and signal the liver to reduce its manufacture of LDL when serum levels rise even slightly. Glucose may bind to the surface of the LDL particle and also to liver LDL receptors, so that LDL cannot be recognized by its receptors. In people with high blood sugars, many LDL particles thus become glycosylated, and are therefore not cleared by the liver. They accumulate in the blood, where they can become incorporated into the walls of arteries, forming fatty deposits called atherotic plaques. Since liver LDL production cannot be turned off by the glycosylated LDL (and also the presence of glycosylated LDL receptors), the liver continues to manufacture more LDL, even though serum levels may be elevated.

The proteins in the walls of arteries can also become glycosylated, rendering them sticky. Other proteins in the blood then stick to the arterial walls, causing further buildup of plaque.

Serum proteins also glycosylate in the presence of glucose. White blood cells called macrophages ingest glycosylated proteins and glycosylated LDL. The loaded macrophages swell up, becoming very large. These transformed macrophages, loaded with fatty material, are called foam cells. The foam cells penetrate the sticky arterial walls, causing disruption of the orderly architecture of the artery, and narrow the channel through which blood can flow.

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