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Obesity
Protocol Carrying extra pounds has a profound impact on our health and well-being. Perhaps the most devastating emotional impact of being overweight comes from the frustration of continued dieting without success or ending up heavier than ever after following a diet. Many physicians fail to realize that no single fat reduction protocol will work for everyone. That is why overweight people must follow a custom-tailored program to modulate factors in their body that result in excess fat build-up. There are several common culprits that cause aging people to add body fat and to also prevent them from losing it. These missing links are often overlooked, and the result is that most weight loss programs fail. In this protocol, the mechanisms involved in age-associated weight gain will be discussed, and how an individual can circumvent these metabolic imbalances will be described as well. Most important, overlooked factors that preclude successful weight loss in the majority of people who try to "diet" will be revealed. Definition
The majority of adults in the United States are overweight (BMI over 25), with an increasing number being medically classified as obese (BMI over 30). Unfortunately, the trend is increasing. The prevalence of obesity in the United States has almost doubled compared to the year 1980 (NIH 1998; WHO 1998).
Obesity is associated with stress, incontinence, complications of pregnancy, menstrual irregularities, excess facial hair, increased surgical risk, and psychological disorders such as depression. Epidemiological evidence supports popular belief that the BMI associated with the lowest mortality falls within the range of 18.5-24.9, i.e., thinner people live much longer (Baird 1994; Stevens 2000). Weight gain in adulthood is associated with significant increased mortality. In the famous Framingham Heart Study, the risk of death increased by 1% for each extra pound (0.45 kg) increase in weight between 30 and 42 years of age and increased by 2% between 50 and 62 years of age (Solomon et al. 1997; Kopelman 2000). The subjects in the Framingham Heart Study were followed for 26 years. Another study found that fat loss was associated with a decrease in mortality rate (Allison et al. 1999).
According to the National Institutes of Health, adults who have a BMI of 25 or more are considered at risk for premature death and disability as a consequence of overweight and obesity. These health risks increase even more as the severity of an individual's obesity increases (NIH 1998). The statistics on obesity in the United States are alarming. To make matters worse, the prevalence of obesity has been steadily increasing over the past decades. Perhaps even more disturbing is that this increase often occurs simultaneously with a decrease in average fat intake and total calories, along with a dramatic rise in the consumption of low-fat products. There was no change in the prevalence of sedentary lifestyle. According to this report, people are adding more weight even though they are eating less fat and exercising regularly (Heini et al. 1997). More recent reports, however, indicate that many Americans are consuming too many calories, while simultaneously reducing physical activity (Serdula et al. 1999; Astrup 2001; Mokdad et al. 2001). As you will learn later, acutely cutting calorie intake is not the ideal way of achieving long-term weight control in the obese and in fact may preclude successful fat loss in many overweight individuals.
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.
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
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. Obesity
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These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease
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