~Obesity, Part 2 - Why Obese People Can't Lose Body Fat

~Obesity, Part 2 - Why Obese People Can't Lose Body Fat

  • Insulin's Insidious Dark Side
  • Why Diets Fail
  • Too Much Insulin Causes Severe Disease States
  • Why Insulin Makes People Hungry
  • JAMA Study Indicates Hyperinsulinemia Causes Hunger
  • Today's Diet Controversy
  • Cutting Calories

There are several hormones that impact how many ingested calories are stored as body fat. If any of these hormones are out of balance, a person can gain weight even though they may eat less food. One hormone that exerts a significant effect on hunger and fat storage is insulin.

Insulin is produced by beta cells in the pancreas mainly in response to high levels of glucose (sugar) in the blood. Insulin enables the liver to store excess serum glucose. Insulin also stimulates the liver to form fatty acids that are transported to adipose cells and stored as fat. The net effect of insulin is the storage of carbohydrate, protein, and fat in the body.

A poor diet can induce the pancreas to secrete large amounts of insulin. Aging people also experience metabolic disorders that cause the hypersecretion of insulin. Eventually the cells in the body become resistant to insulin (by decreasing the number of insulin receptors).

As cells become insulin resistant, the body stabilizes blood glucose by producing higher levels of insulin. The effect of high insulin production is weight gain. The long-term result is often Type II diabetes in which blood glucose levels become unstable even though insulin levels remain dangerously high.

As people accumulate excess body fat, they develop a chronic condition known as hyperinsulinemia, meaning the pancreas constantly secretes too much insulin and the body is unable to effectively utilize it.

A novel approach to fat loss has been developed based on the established fact that overweight people have too much insulin in their blood. Insulin causes sugar and dietary fats to be converted to body fat. Excess insulin prevents stored body fat from being released, even when a person undergoes severe calorie restriction, such as in crash dieting.

Poor diet, obesity, aging, and metabolic disturbances result in the excessive secretion of insulin, a factor in the development of Type II diabetes. Suppressing excess insulin production is a crucial and often overlooked component of a fat-loss program.

The role of excess insulin in causing weight gain has been an accepted scientific fact for years (Beeson et al. 1971; Woodward et al. 1989; Heller et al. 1994). Building on this observation, some scientists have postulated that it is impossible for people to lose significant body fat as long as they have insulin overload.

A noticeable effect of surplus serum insulin is constant hunger, which results in a vicious cycle in which overeating causes more and more body fat to accumulate, which in turn causes even greater amounts of unwanted insulin to be secreted from the pancreas. We now know that hyperinsulinemia predicts diabetes mellitus (Haffner et al. 1990; Kekalainen et al. 1999; Weyer et al. 2000). Even in children, serum insulin levels are far higher in obese than in non-obese children of the same age.

Insulin's Insidious Dark Side

Type I diabetes, characterized by a severe deficiency of pancreatic insulin secretion, was at one time universally fatal. In 1922, a young boy received the first form of supplemental insulin and experienced a reduction of blood sugar. Insulin was soon viewed as a wonder drug because it saved the lives of people who were previously doomed to die shortly after diagnosis. Since Type I diabetics do not produce enough insulin, supplemental insulin for these individuals is a life-saving therapy. Most people consider insulin to be a "healthy" hormone, but insulin has an insidious dark side.

Because the aging process and poor diet deprives cells of insulin sensitivity, many people produce excess levels of insulin to force serum glucose into cells. This excessive insulin production is a contributing cause to a host of degenerative diseases including cardiovascular disease and cancer.

However, the most immediate and noticeable effect of excess insulin production is unwanted weight gain. When the blood is saturated with insulin, the body will not release significant fat stores, even when a person restricts their calorie intake (diets) and exercises. Insulin drives fat into cells, prevents fat from being released from cells, and makes people chronically hungry. Not only do high insulin levels contribute to obesity, but chronic elevated insulin in and of itself also contributes to the multitude of disease states associated with being overweight.

Insulin saves the lives of Type I diabetics who are insulin-dependent, but it becomes a "death hormone" to aging people who secrete too much insulin. Reducing serum insulin is thus a critical component of a weight reduction program.

Why Diets Fail

The fact that 64.5% of Americans are overweight is dramatic testimony to the ineffectiveness of all existing weight loss treatments. On any given day of the year, at least half of these people are trying--earnestly trying--to lose weight.

We know that "dieting" (eating less of something than you usually do) only results in short-term loss of weight. Dieters typically lose lean tissue and not fat.

As early as 1968, the Cecil Textbook of Medicine observed: " Elevation of fasting insulin is the difference between thin and obese individuals" (Beeson et al. 1968). Because insulin blocks the release of fat from storage, most people will not lose stored fat by lowering food intake as long as any insulin is present in the blood.

Too Much Insulin Causes Severe Disease States

A surprising number of studies report that excess serum insulin (hyperinsulinemia) is a major health problem. It appears that excess insulin promotes hypertension by impairing sodium balance. Too much insulin harms the kidneys. The vascular system is also severely damaged by prolonged exposure to excess insulin. By acting as a catalyst in promoting cell growth, excess insulin increases the risk and progression of certain cancers. Excess insulin is even a contributory factor to benign prostate enlargement because of its effects in promoting overgrowth of prostate cells.

For people trying to reduce body fat, excess insulin suppresses the release of growth hormone in addition to preventing fat from being released from cells. High serum insulin is associated with the development of abdominal obesity and the number of health problems this induces, including atherosclerosis and impotence. Obesity is associated with excess insulin and reduced insulin sensitivity, both risk factors for Type II diabetes.

Perhaps the simplest method of evaluating the toxic effects of excess insulin is to look at its effects on human mortality. One early study showed that over a 10-year period, the risk of dying was almost twice as great for those with the highest levels of insulin compared to those with the lowest. The scientists stated that hyperinsulinemia is associated with increased all-cause and cardiovascular mortality, independent of other risk factors (NIH 1985).

Another study showed that the risk of developing coronary artery disease increased by 60% for each single-digit increase in fasting insulin level among men aged 45-76 years (after other risk factors were controlled) (Despres et al. 1996). In optimal health, fasting insulin levels should be in the range of 0-3. As people age, their fasting insulin levels normally increase several single digits. Fasting insulin levels in the obese often exceed 20.

Having too much insulin in the blood has become so commonplace that laboratory reference ranges now indicate that fasting insulin levels of 6-27 mcIU/mL are "normal." While it is normal for aging people to have high fasting insulin, it is by no means desirable. Aging people experience a wide range of degenerative diseases that are directly attributable to elevated insulin.

Standard laboratory reference ranges can sometimes be misleading. For instance, it was once considered normal to have a cholesterol reading of up to 300 (mg/dL). While it is true that a cholesterol count of 300 was normal at that time in history, so was an epidemic of heart attacks. Once the dangers of high cholesterol became known, laboratories reduced the high normal reference range to 200 for cholesterol. We expect that laboratory reference ranges for fasting insulin will eventually be changed to alert physicians to patients with dangerously high serum levels of insulin.

Why Insulin Makes People Hungry

One of the ways that excess insulin results in weight gain is that it causes people to be chronically hungry. A reason for this is that high insulin levels rapidly deplete glucose from the blood. This causes a state known as "reactive hypoglycemia," in which the blood becomes deficient in glucose because too much insulin is in the blood.

Low blood sugar-induced by hyperinsulinemia--produces a ravenous craving for glucose-producing foods. This hyperinsulin state promotes excess food intake and leads to a cycle where even greater amounts of insulin are produced to balance the increased calorie intake. The continuous consumption of glucose-producing foods leads to even more insulin secretion and contributes to the pathological accumulation of body fat.

Published studies show that even modest decreases in blood glucose concentrations are associated with hunger and the initiation of eating (Ludwig 2002). Indeed, insulin-induced hypoglycemia appears to provoke prolonged hunger, persisting long after restoration of normal blood glucose levels.

Furthermore, hyperinsulinemia (Kopf et al. 2001) and reactive hypoglycemia (Wursch et al. 1997) may preferentially stimulate consumption of high-glycemic index foods, leading to cycles of greater insulin secretion, followed by low blood sugar and the inevitable desire to rapidly consume more calories. Weight loss efforts (dieting) may exacerbate this phenomenon, as demonstrated by severe hypoglycemia after overweight subjects who were dieting consumed a high-glycemic index carbohydrate (Ludwig 2002). This helps to explain why so many diets fail, i.e., chronically high insulin levels cause people to crave the very carbohydrates that are making them fat. However, as you will learn later in this protocol, changing the type of food ingested is not a cure for obesity.

JAMA Study Indicates Hyperinsulinemia Causes Hunger

The anti-obesity potential of reducing serum insulin was reported in a study in the Journal of the American Medical Association (JAMA) that described the effects of serum insulin increase (hyperinsulinemia), hunger, and weight gain that ensues. The study concluded by stating: "It is possible that the hunger incident to hyperinsulinemia may be a cause of overeating, and therefore, the obesity that so often precedes diabetes" (Ludwig 2002).

Healthy people secrete enough insulin to efficiently metabolize glucose. Once enough glucose is taken up by the cells and removed from the blood, insulin then drops to very low levels in these metabolically balanced individuals. Overweight people, on the other hand, typically suffer from a metabolic disorder that results in elevated insulin secretion because the pancreas is attempting to overcome insulin insensitivity and drive excess glucose out of the blood.

There are serious misconceptions about why people accumulate so much body fat as they age. One overlooked factor is that overweight/obese people have startlingly high levels of insulin in their blood. When the blood is saturated with insulin, the body will not release significant fat stores, even when a person restricts their calorie intake and exercises.

Today's Diet Controversy

The role that excess insulin plays in inducing and maintaining obesity has not gone completely unnoticed. A number of popular weight loss books advocate dietary alterations that reduce or eliminate all high-glycemic food groups in order to suppress excess insulin secretion. Some of these diet programs go as far as to prohibit ingestion of healthy fruits.

Most obese individuals suffer from severe metabolic disorders that are not readily correctable by altering the amount or types of foods they consume. When we refer to the term "metabolic disorders," we are describing a host of pathological biochemical imbalances in an obese individual's body that precludes an individual from losing body fat. These same metabolic disorders also cause or contribute to the myriad of diseases associated with obesity. The information contained in this Obesity protocol explains how to correct the metabolic disorders responsible for inducing obesity and associated diseases.

The most compelling question confronting overweight Americans is: Why is no effective treatment available? Although scientific advances have been made in defining the metabolic mechanisms that occur in our bodies after we ingest calories, medicine has not progressed beyond the you-ate-too-much-so-you-got-fat concept.

The intrinsic difficulty with such simplistic explanations for weight gain is the fact that overeating does not automatically make a person become fat. We all know people with an unfair ability to eat anything and everything without gaining an ounce. There are published studies showing that dieting does not make an obese person thin over the long term (Toubro et al. 1998; Brand-Miller et al. 2002). Another study demonstrated no weight loss differences when obese individuals consume either high or low glycemic index diets (Astrup et al. 2002).

Blaming different types of food--or blaming the patient him or herself--may be popular, but it is monumentally unproductive. This attitude started in the early 1950s when scientists at the Rockefeller Foundation postulated that an increase in obesity that followed World War II was caused by excess protein consumption. Noting that 56% of the protein eaten enters the blood as glucose, they presumed this to be the source of excess sugar, which is easily stored as fat. However, restricting protein intake did not end the problem of obesity.

Caloric restriction "diets" and low carbohydrate diets have dominated for years because they do induce quick weight loss. Unfortunately, they do not cause significant fat loss. Too often, the weight that an obese person loses on a low carbohydrate diet not only comes back, but also will contain more fat than the weight lost through the painful diet.

One of the problems with modern diets is that they forget scientific principles that were long ago established relating to what happens when a person suddenly reduces their calorie intake. For example, if a person cuts calories from their normal diet, they initially lose a lot of protein, and its accompanying extracellular water, but almost no fat. The reason for the failure of diets to initially induce fat loss is that chronically high insulin levels preclude the release of fat from storage in the body. Since insulin blocks fat release, the body first burns up its protein reserves in response to dieting, which results in a quick reduction of body (protein) weight, but virtually no loss of body fat.

One early mathematical model showed that in response to cutting just 500 calories from one's daily diet, a weight loss of 620 grams (1.37 pounds) of protein tissue and water could occur as opposed to only 62 grams of body fat being lost (Albrick 1971). This model helps explain why people can easily lose total body weight when dieting, but fail to eliminate enough fat to resolve their obesity problem. When normal food intake is resumed, lost protein tissue is replaced with even more body fat. Taking into account these observations, Dr. Margaret Albrick, a prominent obesity researcher, concluded: ". . . available long-term studies show discouraging results on all diets. There is no basis for recommending any one diet over any other."

There are other metabolic adjustments that the body makes in response to lower food intake that can make it impossible to lose fat. People respond to a drop in food intake by immediately lowering production of the enzyme (5 -monodeiodinase) that converts the relatively inactive thyroxine to T3. It is the thyroid hormone T3 (triiodothyronine) that promotes the oxidation of glucose and its metabolites. Reduced levels of T3 cause conservation of calories, meaning that the body automatically burns fewer calories at rest. The minute a person cuts calories, whether from carbohydrate, fat, or protein, they turn down the rate at which calories are burned! (Braverman 1996). Overcoming a thyroid hormone (T3) deficiency will be discussed in more detail later in this protocol.

Cutting Calories/Carbohydrates Adds Fat

Reduction in caloric intake causes a decrease in T3 levels (Merimee et al. 1976; Carlson et al. 1977; Palmblad et al. 1977; Vagenakis et al. 1977; Beer et al. 1989; Wadden et al. 1990), even when the decrease is caused by bypass surgery of gut (Wilcox 1977). The lowering of T3 is equal whether caused by lowering total calories or lowering carbohydrates (Spaulding et al. 1976; Azizi 1978). T3 is the more calorigenic form of thyroid hormone. Lowering T3 automatically lowers the basal metabolic rate and favors conservation of energy--in other words, if excess calories are present fat storage!

Continued . . .

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