~Obesity, Part 3 - Pathology and Treatment

THE PATHOLOGY OF OBESITY

  • The Insulin Trap


Although many people experience life-long weight problems, many more find themselves beginning to gain weight as they age. The underlying metabolic disorder is the same, but the existence of the pathological factors involved in this condition is more easily understood in studying individuals who were thin in their youth. The primary difference between the two groups is not in the functional manifestations of the condition, but in its origin.

Elegant research involving sets of identical twins has confirmed beyond question the role of genetic predisposition in the etiology of life-long obesity (Hainer et al. 2001; Koeppen-Schomerus et al. 2001; Poulsen et al. 2001; Kunesova et al. 2002a,b). If one of two parents is obese, the chances of their offspring developing obesity are 4 in 10 (40%). If both parents were overweight all their lives, the chances jump to 80% that the offspring will also be overweight. However, the metabolic changes that cause weight gain are virtually the same in both inherited and acquired obesity. Correction of these functional changes will result in normalization of weight whether the obesity is inherited or a consequence of aging.

Those who start out life being slim enjoy the seemingly unfair ability to eat as much as they want of whatever they want without ever gaining weight. They rarely pay any attention to their diets and take for granted that their clothing will always fit.

Most individuals begin a steady march into obesity during their late twenties. It is in the late twenties that most people begin to lose muscle mass--unless they work hard to retain it. Between the ages of 26 and 28 that loss of muscle mass can represent from 3-10% of lean tissue. Some are lucky enough to not see an increase in body fat replacing the lost muscle for 5 or so years. Those who are athletic may not notice that their slim days are behind them for 10 or 12 more years. However, by age 39 the vast majority of Americans are forced to face the fact that they are overweight.

The normal changes of aging that make it easy for people to gain weight include alterations in endocrine hormone levels. Unfortunately, insulin, cortisol, and estrogen (in men)--hormones that do not decrease as we grow older--favor fat gain. Later in the protocol, you will learn how each of these hormones plays a role in causing people to add fat and what can be done to restore a more youthful hormone balance that promotes calorie wasting rather than fat storage.

The Insulin Trap

Prior to the 1950s, scientists believed that stored fat was relatively inert and that once adipose (body fat) tissue was formed, very little metabolic activity took place in fat cells; however, it was then learned that the triglyceride stores of fat tissue are constantly turning over (Bjorntorp 1996). An enzyme called lipoprotein lipase controls the passage of fat precursors into the fat cell. The breakdown of stored fat and the passage of these breakdown products out of the fat cell are controlled by a different enzyme, hormone sensitive lipase. Insulin prevents the action of the second enzyme (hormone sensitive lipase).

As long as insulin is present in the blood, stored fat cannot be mobilized--it is locked into the cell. The bad news is that fasting insulin levels are elevated in obesity (Kolterman et al. 1980). In normal health, when glucose in blood drops below 83 mg/deciliter, insulin vanishes. When an individual is overweight, insulin never vanishes.

Insulin not only keeps fat in storage, but insulin also stimulates the production of new fat. It even lowers levels of the amino acid carnitine in the liver. Carnitine is needed to carry fat precursors into the mitochondria, where the fat precursors can be burned as heat to "waste" calories.

Overweight individuals have long been known to have high fasting insulin levels--in fact, Dr. Margaret Albrick observed that elevated fasting insulin is the critical difference between thin and obese persons (Albrick 1971).

As the undeniable role of insulin in causing and maintaining obesity has come to the attention of popular "diet" and "weight-loss" experts, many useless solutions have been suggested. The many attempts to lower fasting insulin by dietary restriction, either of carbohydrates or of high glycemic foods, arose from the observation that elevation in blood glucose is a primary stimulus of insulin release. However, it is not the only stimulus. Amino acids such as L-leucine have a strong effect on insulin release, as do many digestive hormones (Galabova et al. 1976; Malaisse et al. 1984; Giroix et al. 1999).

The early demonstration that glucose given orally produces a much greater insulin surge than the same amount of glucose given intravenously proved that elevation of blood glucose alone is not the source of hyperinsulinemia (Mclntyre 1978). This enhanced release of insulin is thought to be caused by gut hormones. No diet is effective in correcting fasting hyperinsulinemia in obese individuals.

Obesity and metabolic diabetes (in the early stages) are also associated with an increase in the mass of the tissue that produces insulin, the beta cells of the islets of Langerhans (Mclntyre 1978). Both high-carbohydrate and high-protein diets have the same stimulatory effect on increased islet cell mass.

As long as insulin is present in the blood, fat cannot be released from storage. Thus, the weight lost by overweight people in response to "dieting" is largely protein and water. "Dieting" or lowering food intake can be seen to have two disastrous effects on obesity:

1. Lowering of metabolic rate by turning down conversion of T4 to T3
2. Depletion of lean tissue

Exercise, the other popularly prescribed "treatment" modality, has only one disastrous consequence for obese individuals: exercise lowers the need for insulin (Kirwan et al. 2002; Reynolds et al. 2002). Obese individuals already have too much insulin. Therefore, exercise causes the excess to be that much more excessive!

Please note that all these statements refer to persons who are overweight. Caloric restriction and exercise are beneficial for individuals who are thin.

INITIAL TREATMENT FOR OBESITY

Although what an individual eats may not have a critical influence on weight gain, when an individual eats most certainly does (Taylor et al.1999). Early observations had also indicated that the majority of obese people take in most of their daily calories in a relatively short period in the evening (Dole et al. 1953; Stunkard et al. 1955, Hollifield et al. 1964). Based on these observations, a first step in treating obesity is changing the time of day when most calories are consumed. By shifting consumption of high-calorie foods from late in the day to earlier in the day, there is great potential that some of the fundamental metabolic disorders (disruptions in glucose, insulin, and leptin metabolism) that prevent obese people from losing body fat can be corrected (Taylor et al. 1999).

In clinical weight loss practice, overweight and obese patients were told to alter the time of day when they consumed their food. The result was rapid and sustained fat loss in those who adhered to the following instructions:

1. Immediately after awakening, eat a large breakfast. If you want a banana split, eat it at breakfast! Eat as much as you want of whatever you want. The reason we advocate a liberal breakfast is that you should follow this program for the rest of your life. If you are continuously deprived of the foods you like, at some point you might rebel and begin eating at the wrong time of the day. Ideally, breakfast will consist of fresh fruit and whole grains, but if you need to consume high calorie foods or prefer to do so, do so in the morning and not late in the day.

2. Late in the morning, have a snack equivalent in calories to a hamburger and potato fries. Healthier foods are recommended, but for the purposes of complying with this program, eat whatever you want at this time of the day instead of waiting until the evening when these calories readily convert to body fat.

3. Mid-afternoon, have another snack equivalent to the calories obtained from a tuna salad sandwich on whole wheat bread and some fruit.

4. No later than 6:30 p.m., have a modest dinner such as fish or lean chicken, potato, and several vegetable servings.

5. It is critical that no food be consumed after 6:30 p.m. This program is designed to achieve this critical purpose, i.e., to normalize fasting insulin so that body fat can be released from storage.

Most important of all is that you consume two to six capsules of PGX highly viscous fiber blend (1,000-3,000 mg) 5-10 minutes before each meal with 8-16 ounces of water. This recent discovery is described in greater detail later in this Protocol.

It may take a week for some obese individuals to wake up hungry (as they are supposed to do) and not have the desire to eat after 6:30 p.m. After 45 days of following this program that alters the time of day when calories are consumed, an improvement in several metabolic parameters should become evident, including a reduction in postprandial insulin levels. Enough fat loss should have occurred during this initial 45-day period to motivate an individual to reduce total calorie intake and begin to exercise.

Following this five-step program described has resulted in many overweight patients achieving a normal weight in a relatively short time period. Most obese individuals experienced sustained reductions in body fat, especially in the abdominal area. Some patients did require additional therapies to correct underlying metabolic disorders responsible for their inability to lose body fat. These supplementary therapies will be discussed later in the protocol, but first the beneficial mechanisms that occur when the calorie burden is shifted to early day eating will be explained.

THE SCIENTIFIC PREMISE BEHIND EARLY DAY EATING

The American Journal of Clinical Nutrition published a study reporting that food eaten early in the day generates more energy (diet-induced thermogenesis) than food eaten later in the day (Weststrate 1993). What this study demonstrated was that the metabolic rate of the body is high enough early in the day to burn off calories as energy, whereas these same calories consumed at night can be stored as fat. Based on these types of scientific findings, progressive physicians have advocated that overweight patients not eat anything after 6-7:00 p.m.

However, until recently it was difficult for obese individuals to avoid late night snacking.

In a presentation made at the 43rd Annual Conference of the American Heart Association (March 5, 2003), a study was described showing that people who eat breakfast daily are less likely to succumb to obesity and diabetes. In comparison to people who ate breakfast twice per week or less often, those eating breakfast every day had 35%-50% lower rates of developing obesity and insulin resistance syndrome (Pereira 2003). Dr. Mark A. Pereira, one of the scientists involved in the study, stated that breakfast might reduce the risk of obesity, Type II diabetes, and cardiovascular disease by controlling appetite and thus reducing the likelihood of overeating later in the day. The study included 2681 young adults who were followed for 8 years. Those who ate whole grain breakfast cereals were associated with a reduction in risk, whereas refined grain breakfast cereals were not. The study did not evaluate the nighttime eating habits of these individuals. (Remember: The key to weight loss for severely overweight people is to consume the bulk of their calories for breakfast and avoid eating all food after 6:30 p.m.)

TODAY'S DIET FALLACIES

  • The Forgotten Science


There are so many overweight Americans that the diet industry has exponentially grown over the past 15 years. Each diet book, clinic, food, supplement, and infomercial claims to have discovered the "real" reason for today's obesity epidemic. However, a cursory review of published scientific literature indicates that the causes of weight gain are multi-factorial. Fortunately, there are established fundamental factors that can be used to induce significant and sustained fat loss. The diet "trap" to avoid is to believe that any one solution is the key to losing weight.

Age-associated weight gain is the end result of numerous degenerative changes that are at least partially reversible. Most Americans with excess body fat were not overweight in their youth. Young people can often consume as much food as they want and efficiently burn off excess calories, but aging results in an excess accumulation of body fat stores, even though the person might be consuming fewer calories. The problem in aging is that healthy metabolic function is impaired and ingested food accumulates as body fat.

There is an epidemic of childhood and adolescent obesity in the United States. In many of these cases, a premature metabolic disorder is induced by poor diet, genetic predisposition, and sedentary lifestyle. Relatively simple steps that induce a healthy metabolic profile can correct many of the causes of obesity in younger people.

Hyperinsulinemia (too much insulin in the blood) is one of the culprits in the obesity epidemic today. According to some popular diet books, one way to reduce excess insulin is to eat a low-glycemic diet. Authors of these books advocate that obese people should avoid foods that induce the pancreas to over-secrete insulin. In reading the many diet books that extol the role of high-glycemic foods in causing weight gain, one is led to believe that it is an absolute fact that individuals become overweight because they consume too many of the wrong kinds of (high-glycemic) food or drink. However, a review of the published scientific literature reveals contradictions in the hypothesis that an obese individual can switch to a low-glycemic diet and obtain meaningful body fat loss. Some studies show no weight loss in individuals consuming low glycemic rather than high glycemic diets (Astrup et al. 2002). Other studies report moderate weight loss benefits to those consuming lower glycemic diets (Morris et al. 1999; Brand-Miller et al. 2002).

The only way to reverse obesity is to correct the multiple metabolic disorders that induce the body to store ingested calories as fat rather than to burn them as energy. By failing to alter an individual's biochemistry, severely overweight people suffer through agonizing diets, only to attain mediocre or no fat loss results.

The Forgotten Science

This Obesity protocol has been written to address the failure of both conventional and alternative medicine to develop a program for inducing sustained fat loss in obese individuals.

In reviewing medical works published in the 1960s and 1970s, it is apparent that great progress was being made toward discovering the specific underlying metabolic abnormalities that cause excess fat gain (Bray 1969). Today however, one of these same medical works (Cecil-Loeb Textbook of Medicine) omits this crucial information. The premises espoused in the early textbook have by no means been refuted--they have only been forgotten. For example, an early work revealed the mechanism by which normal, non-obese people handled excess calories--without gaining weight--and also provided a giant step toward developing meaningful obesity treatment modalities (Bray 1969). By itself, an increased understanding of the role of insulin in storing excess fat (Felig et al. 1969) should have ended use of today's flawed "diet" concept. These early works emphasized that an individual cannot mobilize fat from storage if insulin is present in the blood--and if an individual is overweight, insulin levels are elevated.

Physicians today are largely unaware of these long-ago established facts. The result is that they treat diseases associated with obesity (cardiovascular, cancer, diabetes, cartilage breakdown), but do not effectively treat obesity itself. Physicians tell obese patients to eat less and exercise more; yet the obesity epidemic worsens every year. This protocol will present the forgotten science and combine it with breakthrough approaches that have never been utilized outside a small clinical setting.

Continued . . .


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