Obesity Protocol

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. With the advent of standardized avocado extract (to be described later in the protocol), it is possible to curb one's appetite late in the day so that food is ingested only early in the day.

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

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, infomercial, etc. 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 predispositions, 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 oversecrete 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 (high-glycemic) of 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; Albrick 1971). 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, fasting 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, etc.), 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.

How to Regulate Excess Insulin

The avocado fruit contains a sugar called mannoheptulose, which has been shown to inhibit both synthesis and release of insulin. Consumption of the proper amount of this avocado sugar would thus appear to be a natural, dietary solution to the problem of hyperinsulinemia (excess blood insulin levels).

The History of Avocado Sugar
Mannoheptulose was first isolated in 1917. Mannoheptulose has been proven to be present in many foods, but is found most abundantly in the avocado (La Forge 1916-1917). In 1957, the first research was published in the Archives of Biochemistry and Biophysics (Volume 69, page 592), suggesting that avocado extract blocked normal insulin secretion. In 1963, it was demonstrated that avocado extract blocks glucose-stimulated release of insulin (Nature, Volume 197, page 1264). By 1967, low doses of avocado extract were found to inhibit both pancreatic secretion and synthesis of insulin without eliciting measurable hyperglycemia (high blood sugar) (Nature, Volume 214, page 276). This finding was significant because it demonstrated that a controlled dose of avocado extract could suppress pancreatic production of insulin without inducing a diabetic state.

Based on these findings, in 1968 an oral dose of avocado extract was administered to a child who had severe leucine-sensitive hypoglycemia. Severe leucine-sensitive hypoglycemia is a type of hypoglycemia that occurs because a genetic defect induces the amino acid leucine to produce abundant amounts of insulin. This study was published in The Annals of the New York Academy of Science and reported that a small oral dose of avocado extract effectively lowered blood insulin levels in the child without any impairment in glucose utilization (Paulsen 1968). Because it was necessary to administer the avocado extract by stomach tube, it was not practical to continue this therapy, but physicians did establish that a small amount of avocado extract could suppress excess serum insulin without provoking a hyperglycemic event.

Another early report in the journal Nutrition Review (1969) stated that avocado extract may be an "effective therapeutic agent in man for the treatment of chronic or recurrent hypoglycemic conditions" (Anon. 1969). Hypoglycemia (low blood sugar) occurs when the pancreas secretes too much insulin, thus driving serum glucose levels down to uncomfortable or dangerous levels. Suppressing excess insulin secretion would thus preclude hypoglycemic episodes.

The 1969 article in Nutrition Review pointed out that the reason why standardized avocado extract had not been made available as a therapy was the difficulty and uncertainty of oral administration. The problem is that avocado extract readily converts to mannitol in the stomach and is not readily absorbed into the bloodstream. As a result, much of the work (conducted in animals) to substantiate the ability of avocado extract to reduce serum insulin was done by intravenous administration. These studies in animals showed that the effects of avocado extract are dose-dependent and the effects are reversible upon cessation of avocado extract. This finding is crucial if people are to take a standardized avocado extract as a weight-reducing agent.

Also in 1969, an article in the journal Metabolism described a human study in which varying doses of avocado extract were given to nine volunteers. No significant changes in blood glucose were seen, but in five of the nine subjects, serum insulin levels declined by an astounding 60%. The average group percentage reduction in insulin levels after 6 hours was statistically significant. This study showed that the oral administration of avocado extract could drastically reduce insulin levels in humans without causing a corresponding increase in serum glucose (Viktora et al. 1969). If avocado extract is to be safely and effectively ingested by humans, it must suppress excess insulin without causing a corresponding increase in serum glucose.

In 1983, a study that evaluated the effects of avocado extract on food consumption by rats was reported in the journal Behavior and Neurological Biology. In a series of studies, the rats were administered avocado extract injections and then were allowed to eat either high-carbohydrate (cornstarch) or high-fat (animal fat) foods. In each of the experiments, avocado extract significantly reduced the rats' desire to eat carbohydrates, but not fat (Langhans et al. 1983).

The 1983 experiment showed that rats administered avocado extract consumed 35% less carbohydrate-rich (cornstarch) food compared to a group of rats that were administered saline. In another group of rats administered avocado extract, but fed a high-fat diet, there was no effect on the quantity of high-fat food consumed. This result was expected because excess insulin has been shown to cause only intense sugar craving. The experiment also showed a substantial decrease in the size and duration of the first two high-carbohydrate meals consumed after avocado extract injection. The study corroborated observations that when humans ingest standardized avocado tablets, they develop an aversion for high-carbohydrate foods (Langhans et al. 1983).

In another experiment in this series, water intake was restricted for 7 days in groups of rats. After 7 days, one group was injected with avocado extract, while the other served as the control group (injected with saline). The thirsty rats were then given free access to regular water or to water sweetened with saccharine. The results showed that the avocado extract-injected rats displayed a strong aversion to the saccharine-sweetened water, while the control group eagerly consumed the sweetened saccharine water. The scientists stated that this experiment demonstrated that "food becomes distasteful after avocado extract injection in rats." They noted that the taste aversion was more pronounced in rats fed a high-carbohydrate diet compared to a high-fat diet. This experiment showed that avocado extract suppressed appetite in rats fed a high-carbohydrate diet. The significance of this finding is that many individuals become overweight because of uncontrolled carbohydrate craving. Case history reports show that overweight humans who consume avocado extract develop an aversion to high-glycemic (sugary) foods. Some scientists believe that overconsumption of high-glycemic foods is a cause of body fat accumulation. Therefore, avocado extract shows potential as an anti-obesity agent via this mechanism alone (Langhans et al. 1983).

How Mannoheptulose Regulates Insulin
One of the means by which insulin is secreted by pancreatic beta cells is through the activation of the hexokinase enzyme pathway. Avocado extract
(d-mannoheptulose) functions as a competitive inhibitor of the hexokinase enyzme, thus inducing a temporary block of glucose-stimulated release of insulin. In addition, avocado may interfere with the leucine-provoked synthesis of insulin.
The inhibition of both synthesis and secretion of insulin by mannoheptulose can be seen in studies in which small doses of mannoheptulose fail to elicit measurable hyperglycemia, but do suppress glucose-stimulated increases in serum insulin.

Based on the findings that avocado extract inhibits excess insulin production and might be a therapeutic agent in treating hypoglycemia, another series of studies was conducted in 1969 to assess the effects of administering massive oral doses of avocado extract to humans. These studies were reported in the journal Metabolism (Johnson et al. 1970).

In the first pilot study, six people fasted overnight. Their blood was drawn to measure baseline levels of glucose and insulin and indicators of toxicity such as liver and kidney function. Two subjects received 5,000 mg of avocado extract and two subjects received 10,000 mg, while the other two subjects were given 20,000 mg. Blood glucose, insulin, and mannoheptulose levels were determined at 1, 2, 4, 6, and 10 hours after administration.

The results showed that blood concentrations of mannoheptulose were related to the ingested dose. Mannoheptulose blood levels peaked 2-4 hours after ingestion and then fell slowly during the next 6 hours. In all subjects given these extremely high doses of avocado extract, there was a reduction in fasting insulin. The elevation in fasting glucose was approximately 15% and returned to normal 6 hours after avocado extract ingestion. Throughout the 10-hour study, there was a continuous decline in fasting insulin of the subjects. All subjects remained fasting throughout the study and none of them showed any change in blood test results used to ascertain if toxicity were occurring. Both subjects who received the 20,000-mg dose developed nausea and diarrhea. This pilot study showed no toxicity when the subjects received up to 100 times the amount of avocado extract that has been used to treat obesity (Johnson et al. 1970).

The second study in this series was a double-blind cross-over design involving 12 fasting volunteers who consumed 10,000 mg of avocado extract or placebo. An intravenous (IV) glucose tolerance test was performed 2 hours and 4 hours after consumption of either the avocado extract or placebo. Multiple blood tests were performed and toxicity was assessed as in the pilot study. In the placebo group, the glucose infusion resulted in the expected increase in serum glucose and insulin. In the group receiving the very high dose of avocado extract, there was a reduction in insulin with a corresponding moderate increase in average serum glucose (Johnson et al. 1970).

The findings of these studies showed that high doses of avocado extract reduced both fasting and glucose-provoked insulin levels in man, while only inducing a moderate and temporary increase in serum glucose. There was considerable variation between test subjects, but no toxicity was detected other than a reduction in blood potassium levels in response to the very high doses of avocado extract.

The conclusion by the scientists was that while avocado extract induces an insulin-suppressing effect in man similar to animals, "it is unlikely to have any clinical value." In 1970, the only disease that scientists were seeking to treat was hypoglycemia. They did note that if more than 20,000 mg a day of avocado extract could be administered to subjects, it might work better. What these scientists lacked in 1970 was a controlled delivery system to enable avocado extract to be consistently absorbed into the bloodstream. They suggested that regular injections of avocado extract might be an effective hypoglycemia therapy (Johnson et al. 1970).

Why Diets Do Not Work
The failure of today's dietary guidelines (designed to reduce body fat) was reported in a study described in the July 2002 issue of the American Journal of Clinical Nutrition. The scientists who conducted this study stated: "Current dietary guidelines have not prevented weight regain or population-level increases in obesity and overweight. Many high-carbohydrate, low-fat diets may be counterproductive to weight control because they markedly increase postprandial hyperglycemia and hyperinsulinemia (excess serum insulin)" (Brand-Miller et al. 2002).

In a 1970 study described in the Journal of Endocrinology, a male physician and female volunteer were given a glucose intravenous infusion for 10 continuous hours with a high-dose avocado extract infusion being administered after 70 minutes. The intravenous avocado extract induced an immediate drop in serum insulin and a reversible spike in blood glucose. The purpose of this study was to reproduce the many animal studies that had shown a similar effect. This study helped to establish the safety of avocado extract because such a high dose had been administered intravenously with no toxicity (Lev-Ran et al. 1970).

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