Fasting and Eating for Health (19 page)

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Authors: Joel Fuhrman; Neal D. Barnard

Tags: #Fasting, #Health & Fitness, #Nutrition, #Diets, #Medical, #Diet Therapy, #Therapeutic Use

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Forty thousand amputations per year are due to complications of diabetes. It is the leading cause of blindness in adults and of kidney failure.

Diabetics, regardless of the type, have abnormal blood lipids, meaning they have higher levels of triglycerides and lower levels of HDL (the "good"

cholesterol) in their blood than the general population. The overproduction of triglycerides in particular is probably related to the increased flux of glucose and fatty acid substrates to the liver.1 Unfortunately, at any given cholesterol or triglyceride level, diabetics have a much higher risk of coronary heart disease, compared to the nondiabetic population.

In both types of diabetes, the high glucose level in the blood damages the body. In conjunction with blood lipids, it inevitably causes a significant acceleration of the atherosclerotic process, hardening and narrowing the blood vessels: Atherosclerosis accounts for 80 percent of all diabetic deaths. Diabetics have more than four times as many heart attacks as nondiabetics. One third of all patients with insulin-dependent diabetes die of heart attacks before age 50.2

Diabetics should be made aware that they can protect themselves from becoming part of these morbid statistics. But diabetics are typically given the wrong recommendation by the professionals caring for them. You would expect that any dietary recommendations designed for diabetics would attempt to reduce the risk of a heart attack, stroke, or other cardiovascular event.

Unfortunately, this is not the case. In fact, the typical dietary recommendations suggested to diabetics by their doctors and dieticians have been shown to allow the advancement of athersclerosis in normal patients, let alone diabetics.3,4

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Both interventional studies and large epidemiologic (population-based) studies have shown conclusively that certain diets promote cardiovascular disease and diabetes, and that other nutritional practices can prevent and reverse them.

The Lifestyle Heart Trial is just one of several studies that document that the standard recommendations (utilizing a diet in which 30 percent of calories come from fat) allow the progression of heart disease even in nondiabetic patients. These recent studies were designed after it was noted in numerous population-based studies that cardiovascular deaths were virtually nonexistent in rural populations consuming vegetarian diets. In these same populations diabetes was unknown. Researchers noted that deaths from heart disease increased as populations gradually increased their consumption of animal-based foods, and that diabetes started to appear as animal foods and other rich foods were consumed.5

All animal foods are rich in fat and protein and deficient in fiber and the antioxidant nutrients that protect against heart disease and cancer. Many studies looking at populations consuming around 30 percent of calories from fat illustrate that such populations have a substantial amount of cardiovascular deaths, and all studies done on populations that consume less than 15 percent of calories from fat show that heart disease and diabetes are virtually nonexistent.6

Heart disease is the leading cause of death in diabetics. The point here is that the standard diabetic diet, which recommends 30 percent of calories from fat and usually includes salad oils, chicken, fish, and lower-fat dairy foods, is still too heavy in animal-based foods, which cause heart disease. Such a diet is risky for all people, but for the diabetic this degree of fat, cholesterol, and even protein is exceptionally hazardous. As the evidence indicates, it is a deadly diet for the diabetic.

A high-protein diet is especially risky for diabetic patients because such a diet places a significant stress on their kidneys, accelerating the progression of kidney failure.

Fat Is the Chief Enemy of the Diabetic

At in the diet of the diabetic not only accelerates the disease process but also interferes with the uptake of glucose by the cells, thus further raising the blood glucose level.

Experiments described in the medical literature have tested the effects of high-fat diets on insulin intolerance. In one study, healthy young medical students were fed a very high fat diet containing egg yolks, heavy cream, and butter, and within two days all of the students had blood sugar levels high enough to be labeled diabetic.7 Complex carbohydrates have been shown to have the opposite effect.8

Fat in the food we eat prevents the proper utilization of insulin, and more insulin is needed to process the glucose when fats are included in the meal.

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Additionally, the fat on one's body makes the cells resistant to insulin, and the pancreas must produce more insulin to compensate. This is due not only to the additional insulin demanded by the extra body mass of fat cells, but also to the fact that the fat in and around normal tissue, like muscle and internal organs, interferes with insulin uptake into these tissues. The major contributors to fat in the American diet are animal-source foods such as meat, fowl, fish, and dairy products, as well as cooking or salad oils.

Insulin Is the Accomplice in Crime

After World War I, when insulin was first discovered, the medical profession thought diabetes would be totally curable as a medical problem. Diabetes was believed to be due to insulin deficiency, and everyone thought that since insulin would now be given to patients there would be no more problems. It seemed this way for a few years, but terrible things started happening to patients with diabetes who were given insulin to control their blood sugar levels. They developed eye disease, kidney disease, and, most important, accelerating atherosclerosis leading to blood vessel disease and early heart attacks. Their problems were worse than ever.

Decades later, when the insulin assay became available and doctors were able to measure insulin levels in their patients' bloodstreams, they found most interesting results: the insulin levels of type I (childhood-onset) diabetics were indeed low, but the levels in type II (adult-onset) diabetics were not only not low, but also were higher than those of people without diabetes.

It became clear that type II diabetics is a disease of insulin resistance, not insulin deficiency. Type II diabetics produce plenty of insulin, but for some reason still not enough to drive the glucose from the bloodstream into the cells.

If we measured the insulin level in prediabetic people (those who will become diabetic years later), we would find insulin levels much higher than normal.

These persons consume excesses of fat, sugar, protein, and refined or processed foods and have excess fat on their bodies; as a result their pancreas must secrete increased amounts of insulin to overcome the insulin-blocking effects of their fat cells and the fat they ingest.

All overweight individuals, whether diabetic or not, have abnormally high levels of circulating insulin. In fact, being overweight can force one's body to manufacture up to four to five times as much insulin as a normal person. Many obese individuals eventually become diabetic. About 85 percent of adult diabetics are significantly overweight.

Some of the obese may never become diabetic because their pancreatic reserve may enable them to continue to produce this excessive amount of insulin for years. Even if they never become diabetic, however, the high levels of insulin contribute to their cardiovascular risk by increasing the process of atherosclerosis. Insulin increases the rate at which cholesterol-laden plaque builds up on arterial walls. The abnormally high levels of
insulin
produced by all overweight individuals, diabetic or not, is an independent risk factor for early 101

cardiac death.

After years of this unusual stress, the pancreas starts to tire out and eventually can secrete only normal amounts of insulin in response to the high demand by the body. This occurs because we all lose some beta cell function as we age (beta cells are the cells in the pancreas that secrete insulin) and excessive demand causes an acceleration of this process. Now, 8 to 20 years later, the pancreas finally says "enough is enough" and slowly stops producing high levels of insulin. At this point the glucose level in the blood begins to rise, and the person may notice the first signs that something is wrong, such as increased urination. Diabetes is then diagnosed. These are the major factors causing adult-onset diabetes.

The seeds of diabetes are planted by high insulin levels many years before a person becomes a diabetic. This is when the damaging effects of the elevated insulin begin to hurt the body, long before the disease is diagnosed. When a person first develops the signs and symptoms of type II (adult-onset) diabetes, the problem has existed for a long time. Typically the body has been battling with excessive insulin requirements and the pancreas has been overworked to exhaustion for more than ten years before the level of glucose rises in the bloodstream. If we could have tested insulin levels of an individual every year for ten years before diagnosis, we would have found high and rising insulin levels.

When the diagnosis of diabetes is first made, the individual may already have other related medical complications. In fact, many of these patients actually come to physicians because of these complications, such as a heart attack, and then the physician notices this person's glucose is a little high. But such individuals so often never knew they had diabetes until a medical complication of diabetes made them come to the doctor. This is because excess insulin is very damaging to the body—especially to the circulation, including the large blood vessels as well as the small ones in the eyes and kidneys. All those years of excessive insulin secretion take their toll, resulting in extensive damage to the body.

The tendency of the pancreas eventually to lose the ability to produce such excessive amounts of insulin may be influenced by genetics. Thirty to 40 years ago the Pima and Tohono O'odham Indian tribes of the American Southwest ate cactus, roots, berries, beans, corn, and greens. Diabetes was unknown in their ancestry. Eventually these Native American tribes adopted the standard American diet. As a result, more than half of these Indians presently become diabetic by the age of 35, although before 1945 diabetes was unknown in this population.9

Multiple other studies show similar patterns when societies adopt modern diets.10,11 Therefore, the inherited tendency to develop diabetes may be there, but that does not mean we have to stress our bodies so much that this inherited weakness becomes evident.

When Earl Ray, a Pima Indian who lives near Phoenix, switched back to a 102

more traditional Native American diet of mesquite meal, beans, and cactus fruit, his weight dropped from 239 pounds to less than 150 pounds and his severe diabetes was controlled without medication.

So fat and glucose are not the only villains. The high levels of insulin present in diabetics also promote hardening of the blood vessels and aging of the body.

Findings from numerous studies have shown that insulin blocks cholesterol removal, stimulates the formation of atherosclerotic plaques, and contributes to the delivery of cholesterol to the cells. Insulin also promotes other damage such as smooth muscle and connective tissue proliferation.12,13 This leads to even more blood vessel stiffness and damage, because the muscular wall of the blood vessel becomes thicker. and less elastic as the interior lining becomes laden with atherosclerotic plaque, thus increasing the diabetic's risk of stroke and heart attack.

So insulin is a great villain. In fact, if you want to have your blood taken for just one blood test that will be the best indicator of your risk for heart attack in the next ten years, get a serum insulin level, not a serum cholesterol.

Insulin obviously has some essential functions in the body. It allows the uptake of glucose by the cells, thus giving our cells energy, but it also drives the growth of fat and helps us store our excess nutrients in the form of body fat. Extra insulin also can slow down one's metabolic rate .as it efficiently aids the process of packing away more fat on the body. So the heavier one becomes, the more insulin the body needs to make, and the more insulin the body produces (or is given), the fatter—and the more diabetic, or insulin-resistant—one becomes.

So it is absolutely essential that type II diabetics maintain a slim physique.

Sometimes type II diabetics who think they are not overweight can loose ten pounds of fat they didn't think they had and, like magic, their glucose levels normalize.

Standard Recommendations for Diabetes

Now that you understand the mechanism that leads to the development of adult-onset, or type II, diabetes, let's look at the current methods for treating diabetes. The American Diabetic Association recommends restricting fat intake to 30 percent of

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calories from fat. Patients follow an exchange diet to keep daily calories constant. A low-protein diet is sometimes recommended only after the kidneys show damage.

The 30-percent-of-calories-from-fat recommendation is the same number used by the American Heart Association and other governmental authorities in this country. When this diet fails to adequately control blood sugar levels, oral medication is used to stimulate the pancreas to produce more insulin. When this fails, insulin injections are used to attempt to bring glucose levels near normal. When this fails, both insulin and oral medication are used.

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