Insulin-Control Life Extension Program
Lose Weight, Feel Great and Live Longer

Studies have shown that lower insulin levels can promote rapid fat loss, increase energy, enhance mental clarity, slow aging, lower blood pressure, improve cholesterol and overall health, and generate a feeling of euphoric wellness.

The Insulin-Aging Equation

Announcing Syndrome X

What Causes Insulin Resistance?

How Insulin Causes Obesity

The Cardiovascular-Insulin Connection

Diabetes: End Stage Insulin Resistance

The Solution Begins With The Low Glycemic Diet

Dietary Ketosis Accelerates Results

Ending the Fat Myth

Exercise Enhances Results

Metformin - The Most Under-Appreciated Life Extension Drug?

Life Extension, Weight Loss, Mental Clarity and Energy

One of the most significant medical breakthroughs of the end of this century is the discovery of insulin's role in health and disease. While many are familiar with the diabetic's insulin plight, few realize the amazing life-extending potential that optimally low insulin levels can have. Studies have shown that lower insulin levels can promote rapid fat loss, increase energy, enhance mental clarity, slow aging, lower blood pressure, improve cholesterol and overall health, and generate a feeling of euphoric wellness.

 

How can this be achieved? Through a simple approach to diet, exercise, supplements and a life extension drug called metformin. Combined, these steps allow insulin levels to drop and life expectancy to rise. But before the how comes the why, along with some important background information.

The Insulin-Aging Equation

The last several decades of research have confirmed that consistently high insulin levels can be deadly. This fact is most evident in the diabetic population, who must constantly monitor blood sugar and insulin levels in order to survive. Extensive trials now show that elevated insulin levels are intimately linked with symptoms of aging, including obesity, non-insulin dependent diabetes mellitus (NIDDM), cardiovascular disease, and even cancer.1,2, 3,4

Insulin, sometimes referred to as the sugar-processing hormone, is critical for glucose metabolism, storage and maintenance. When food is consumed, the digestive process converts carbohydrates into glucose, a simple sugar, which is absorbed into the blood stream. The pancreas releases insulin in response to blood glucose. Insulin then enters certain cells and triggers a set of events that causes the cells to absorb glucose from the blood. The hormone also helps other nutrients get inside the cells, including vitamins, minerals, amino- and fatty-acids. While this is the normal mechanism that should occur, gerontologists are noticing an alarming increase in the breakdown of this metabolic process in our aging population.

Announcing Syndrome X

A condition characterized by hypertension, abnormal blood lipid profile, glucose intolerance or diabetes, insulin resistance, obesity and coronary artery disease has been proposed by Dr. Gerald Reaven to be termed Syndrome X.5

Although this syndrome has been recently popularized in the west, it was first described and characterized by professor V. Dilman in 1968.6

The central feature of this syndrome is insulin resistance, the gradual loss of sensitivity by many peripheral tissue cells, to insulin. The body responds by producing even more insulin, which results in high levels of insulin, glucose, and other unabsorbed nutrients circulating in the blood stream.5

Insulin resistance can go unnoticed for up to 40 years, until either serious complications begin to surface or the pancreas can't keep up with the demand for insulin. This results in NIDDM or type II diabetes. Such diabetics often produce two, three or four times the normal amounts of insulin, yet because of insulin resistance, they require even more insulin to maintain normal glucose levels. When the pancreas can't keep up, hyperglycemia occurs and the diagnosis of diabetes often follows.

Some experts estimate that as many as 50 percent of Americans may have insulin resistance without knowing it. It can remain effectively hidden for years, masquerading as symptoms of other conditions. These may include fatigue, poor mental concentration, abdominal (apple-shaped) obesity, edema and an intense craving for sweets. In advanced stages, such as in the 80-year old insulin resistant person who is producing up to four times the normal amount of insulin, a dangerous cascade of other metabolic imbalances and illnesses can follow.1,2,3,5

Syndrome X encompasses insulin resistance itself, along with the resulting imbalances, which often occur together in the same patient. These can include cardiovascular disease, type II diabetes, obesity, hypertension, hyperuricemia (high uric acid, and mental decline.1,2,3,4,5
 

What Causes Insulin Resistance?

While aging is perhaps the most universal cause of insulin resistance, our modern western lifestyle does much to accelerate its progression via excessive sugar consumption. Less than two hundred years ago, the per capita sugar consumption averaged just five pounds a year. Today Americans eat over 20 times that amount, at about 115 pounds per person per year. Other factors contributing to the condition include overeating, mineral deficiencies, consumption of processed and refined foods, alcohol , smoking and lack of physical exercise.

 

Table 1

  • Factors Contributing to
  • Insulin Resistance
  • Aging
  • Alcohol Consumption
  • High Sugar & Refined
  • Carbohydrate Diet
  • Mineral Deficiencies
  • Processed Foods
  • Sedentary Lifestyle
  • Smoking

 

How Insulin Causes Obesity

Despite the national obsession with weight control, we are fatter today than ever. In fact, more than a third of American adults are obese; yet its major cause, insulin resistance, remains largely overlooked by the medical community and an unsolved mystery to those suffering from it.

When high insulin and blood sugar levels prevail, lipogenesis (fat production and storage) and triglyceride synthesis are also stimulated. To compound the problem, there is evidence that high insulin levels trigger the hypothalamus (the "master gland") to send hunger signals. As a result, the insulin resistant person not only feels hungry more often, but produces and deposits fat more readily than healthy individuals.6

The problem can be exacerbated by what is known as the Randle effect: the competition between glucose and fatty acid utilization. Professor Vladimir Dilman described it as follows: "While fats burn in the flame of carbohydrates, carbohydrates do not burn in the flame of fats."6 According to Dilman, when macro-nutrients are consumed together, fatty acids are used as fuel, while the body acts quickly to convert the carbohydrates into glucose, and glucose into stored fat. Thus the obese, insulin-resistant person is often caught in an endless cycle of hunger, carbohydrate cravings, excessive food consumption, followed by the inevitable increase in blood glucose, insulin, body fat deposits, and the vicious cycle begins once again.6

 

The Cardiovascular-Insulin Connection

Major studies show that high levels of circulating insulin are linked to the devastating epidemic of heart disease. The Helsinki Finnish Policeman study, one of the first epidemiological studies demonstrating an association between high insulin levels and the risk of coronary heart disease (CHD), followed 970 men between the ages of 34 to 64 years who were initially free of CHD, other cardiovascular disease, or diabetes. During the 22-year follow-up, 164 men had had a major cardiovascular event (fatal or nonfatal heart attack), which corresponded directly with the highest insulin levels.7 The Paris Prospective Study, which followed 7,152 men for an average of 63 months, also found a direct relationship between elevated insulin and coronary heart disease. This relationship was even more pronounced in those who were obese.8

Another study in The New England Journal of Medicine showed that people with normal glucose tolerance and high insulin levels were at a greater risk for coronary artery disease, when compared with a group of healthy people.2 Other trials further demonstrate the link between insulin resistance and other cardiovascular risk factors, including atherosclerotic cardiovascular disease, elevated cholesterol and triglycerides, and hypertension.1,2,3,4,5

 

Table 2

  • Follow the Insulin Life Extension Program to Avoid The Risks of:
  • Atherosclerosis
  • Cardiovascular Disease
  • Cancer (certain types)
  • Elevated Triglycerides
  • Elevated Uric Acid
  • Glucose Intolerance
  • High cholesterol
  • Hypertension
  • Low HDL, High LDL
  • Non-Insulin-Dependent Diabetes
  • Mellitus (NIDDM)
  • Obesity

 

Diabetes: End Stage Insulin Resistance

Diabetes afflicts over 135 million people worldwide, and every three minutes an American dies of the disease. The number of Americans with NIDDM or type II diabetes has tripled in the last 15 years, and accounts for up to 95 percent of all diabetic cases. Reactive hypoglycemia, hyperglycemia (pre-diabetes), and NIDDM may all be different stages of the same condition, insulin resistance.

Largely the result of diet and lifestyle, NIDDM has also been called advanced, extreme, or end stage insulin resistance, and scientists are increasingly classifying the condition as early onset or premature aging. Since the glucose tolerance gradually declines with age, by age 70 almost everyone develops some level of diabetes.6

The Type II patient often produces massive amounts of insulin, which are still not enough to let glucose into the peripheral cells. The resulting elevated glucose penetrates non-insulin dependent tissues (lens of the eye, nerve and artery), causing a damaging trail of biological breakdowns, including blindness, nerve damage, poor circulation, arterial damage, kidney failure, gangrene, limb amputations and ultimately a premature death.

The Solution Begins With The Low Glycemic Diet

The solution to insulin resistance begins with a fairly recent development in food evaluation called the glycemic index. The index is a food rating system based on the effect a particular food has on blood sugar. Foods that cause a rapid rise in blood sugar and therefore an excessive release of insulin, are "high glycemic." Conversely, "low glycemic" foods promote a slower, sustained release of glucose and insulin.9,10

The glycemic index (GI) is not an exact science since the numbers are compiled from a wide range of research studies. However, in general, glucose is given a value of 100, and other carbohydrate foods are evaluated relative to it. For example, ice cream has a GI of 50, which means it produces half the rise in blood sugar as glucose.9,10

It might seem that all simple and refined carbohydrate foods have a high glycemic index, while all complex carbohydrate foods (especially those high in fiber) have a low glycemic index. But this is not the case. In fact, some vegetables and grains such as carrots, peas, potatoes, and rice exhibit a surprisingly high glycemic index. These foods produce a rapid rise in blood glucose similar to table sugar. Equally unexpected is the fact that some simple sugars such as fructose have a lower glycemic index than many vegetables, grains, and legumes (See Table 3). It is important to note that while fructose does have a low glycemic rating, it can still induce insulin resistance, increase triglycerides, and promote fat storage.

 

Table 3

Glycemic Index of Select Foods (With Glucose as the Standard of Comparison)

FOOD Glycemic Index
Glucose

Potato, baked

Carrots, cooked

White rice, instant

Cornflakes

Honey

Bread, white

Bread, wheat

Table sugar

Beets

Banana

Green peas

Ice cream

Pinto beans

Pasta

Apples

Tomatoes

Yogurt, plain

Peanuts

Fructose

100

98

92

91

84

74

72

69

65

64

53

51

50

42

41

39

38

38

23

20

The low glycemic diet emphasizes foods with a lower glycemic rating. In general, non-starchy vegetables have a low glycemic index and should be a cornerstone of a balanced life extension program. Proteins and fats are also optimal choices because they contain no carbohydrates and therefore have no glycemic index.

* For more information on the glycemic index of foods, contact the Glycemic Research Institute at 601 Pennsylvania Avenue, N.W., Washington, D.C. 20004.

Dietary Ketosis Accelerates Results

Some life extension experts are taking the low glycemic approach to an extreme with excellent results. Very low carbohydrate diets such as the well-known Atkins diet produce a state of benign dietary ketosis (BDK), which has been found to have an exceptionally rejuvenating effect on the biological terrain. The consumption of about thirty or fewer carbohydrates a day may promote a myriad of advantages, including longevity and weight loss, and the reversal of many of the conditions associated with aging. The BDK diet has all the benefits of the low glycemic diet, and also offsets cravings, discourages yeast infections (candida), balances mood disorders and reverses heart disease.4

Being in ketosis is one of the quickest, safest and healthiest ways to control hyperinsulinism and burn off excess body fat. The key to its effectiveness is a shift in the body's fuel supply. Several studies have shown that as carbohydrate intake is sufficiently lowered, the metabolism shifts from a glucose-based energy supply to one that utilizes the body's own fat. This mechanism, called lipolysis, occurs during sleep, fasting, and when insulin levels are low.6

After two days without carbohydrates, the absence of glucose induces lower insulin levels, which cause the desirable metabolic shift. As lipolysis begins, the body enters into ketosis. First, fats (triglycerides) are split into glycerol and free fatty acids. These are then broken down into simple compounds called ketone bodies, which in turn are used as fuel by the brain and muscle.

The degree of fat utilization can be inferred by measuring blood or urine levels of ketones. The level of ketones in the urine can be measured at home with KetostixTM, which are available over-the-counter (OTC) at any pharmacy. A slight state of ketosis is reflected by a light peach color. The more ketones that are released, the deeper the state of ketosis, and the darker the shade of the stick. Purple, which reflects the deepest state of ketosis, also indicates that maximum fat loss is occurring. However since insufficient water intake can cause concentrated urine (and the false impression of elevated ketones), it is important to drink plenty of water when following this diet.

The basis of the BDK diet is proteins, fats and very low carbohydrate-containing foods, with meals consisting of eggs, fish, fowl, meat, cheese, dairy cream, non-starchy vegetables, herbs and spices. Breakfast might consist of an egg and cheese omelette with a side of bacon; lunch, a tuna salad with greens and creamy dressing; and for dinner, steak and lobster drenched with butter and a side of sauteed broccoli. It is surprisingly simple to follow, and is satisfying as well.4

 Ending the Fat Myth

With all the hoopla over low fat diets, Americans have been brainwashed that any amount of fat is hazardous to health, body weight and longevity. This is not entirely true. In fact, it is becoming increasingly clear that refined carbohydrates are the real offenders, while many fats (especially in the absence of carbohydrates) can actually improve and extend life.

In fact, most fats are an ally on this diet. They impart flavor and satiation, and induce ketosis. Some saturated fats, such as coconut oil may actually accelerate weight loss. Coconut oil is naturally rich in medium chain triglycerides (MCTs), which have been shown to accelerate fat loss. Fats to be avoided are trans-fatty acids produced during hydrogenation (Crisco and margarine), as well as those that are oxidized (excessively heated or spoiled).

Since not all nutritional requirements are satisfied by the scope of this diet, the following supplements are recommended: calcium, vitamin C, chromium, vanadyl sulfate, dietary fiber (psyllium), homocysteine regulators, GLA, omega-3 oils, lecithin, and a full spectrum multivitamin-mineral formula. These should be taken daily with meals for best results.4

 Exercise Enhances Results

Regular physical exercise can replenish vitality and promote a longer healthier life by increasing insulin sensitivity and promoting glucose uptake in the skeletal muscles. This has been confirmed by numerous studies, including a recent trial performed in Sweden. This study demonstrated that younger people exhibited improved insulin sensitivity after only a single exercise session! For those who were middle-aged or older, the same benefit was confirmed after just a few training sessions.11,12

The study also showed that both aerobic and strength training enhance whole-body insulin sensitivity to a similar extent. The authors explain that exercise may stimulate certain sex hormones, which in turn potentiates insulin response. Exercise also increases the levels of a glucose transporter protein called GLUT-4, enhances the muscle capillary network; and reduces body fat, blood pressure, and LDL-cholesterol.12

 Dietary Supplements That Improve Insulin Sensitivity

Chromium and vanadium are two trace minerals which have been shown to have a remarkably positive effect on insulin and blood sugar levels. Studies increasingly show that when plasma chromium levels are low, glucose intolerance increases; and low chromium levels are directly related to hyperglycemia, hyperinsulinemia, and cardiovascular disease.

Chromium is the unique component of the blood sugar regulating molecule called Glucose Tolerance Factor (GTF). GTF works intimately with insulin to facilitate the uptake of glucose into the cells, actually helping it to be more effective.

Adequate chromium supplementation considerably improves insulin sensitivity, blood sugar levels, and longevity (in laboratory rats). It may also be an effective agent against serum lipid disorders. While several types of chromium supplements are available, the most convincing research is on chromium picolinate and chromium polynicotinate. The best results are obtained by taking 400-800 micrograms (mcg) per day.

Vanadium is important because it has been shown to effectively mimic insulin. According to research conducted at the University of British Columbia in Vancouver, sufficient doses of vanadyl sulfate (one form of the mineral) completely eliminated diabetes in laboratory animals.3 Other human studies show similar therapeutic benefits in the treatment of diabetes.

Vanadium supplementation seems to have other beneficial effects as well. When laboratory animals were fed large amounts of fructose, insulin levels increased. Following vanadium supplementation, not only did their plasma insulin concentrations decrease significantly, but the animals also exhibited improved glucose tolerance and inhibited cholesterol synthesis. Vanadium can be found in whole grains, soybeans, shellfish, mushrooms, black pepper, dill and parsley; however, dietary levels found in food don't seem to be relevant to glucose utilization. In order to derive the therapeutic benefits, daily supplementation of 50 to 150 mcg is necessary.13,14 

Metformin - The Most Under-Appreciated Life Extension Drug?

According to Ward Dean, M.D., metformin may be the "most effective and under-appreciated life extension drug." Recently introduced in the United States for the treatment of Type II diabetes, this biguanide drug works by restoring insulin-sensitivity to the cells. Its action is similar to vanadyl sulfate, with a stronger, more predictable action.15

Unlike the sulfonylueas, which force insulin output from the pancreas (eventually destroying the organ), metformin increases the sensitivity of peripheral tissues to the effects of insulin. Dean notes that a "potential side-effect in long term users of metformin, is that it may cause malabsorption of vitamin B12." He goes on to recommend "that anyone taking metformin also supplement their diet liberally with vitamin B12."15

Metformin is chemically related to phenformin, an anti-diabetic drug that was discontinued in the United States in 1976 after a number of deaths in diabetic patients. While phenformin was safe for most diabetics, ill-informed doctors contributed to its downfall by administering it to patients with compromised liver and kidney function.

Metformin, a newer, much safer drug, carries many of the same benefits as phenformin. According to Dilman, these include lowered blood cholesterol, triglycerides and beta lipo-proteins, reduced development of atherosclerosis, reduced insulin levels, increased hypothalamo-pituitary sensitivity (which normally declines with age), improved cellular immunity, reduced incidence of chemically induced cancer in rats, reduced growth of some tumors, and enhanced action of certain anti-cancer medications. Most significantly, phenformin (and presumably metformin) increased the lifespan of laboratory animals. According to Dean, most adults suffer from "subclinical" diabetes. He recommends the drug to all of his life extension patients over 40 at a dose of 500 mg two to four times per day.4,14 Metformin is structurally related to Guanidine, a substance that is found in the herb goat's rue. (Gallega officinalis, which has been traditionally used to treat diabetes.)

 

Life Extension, Weight Loss, Mental Clarity and Energy

A total approach to insulin resistance requires an understanding of its multifaceted aspects and the increased necessity for nutritional and lifestyle interventions. The use of diet, exercise, nutritional supplements and medications such as metformin are central not only to restoring metabolic balance, but for biological age reversal and life extension as well. The following program is recommended for optimal results.

1. Follow a low glycemic or BDK diet

2. Exercise regularly

3. Take 200-800 mcg of chromium and 50-150 mcg of vanadium daily

4. Take 500 mg of metformin two or three times per day or five to six capsules of VRP's GluControl.

 

Alpha-lipoic Highly recommended source of nutrients and supplements. vitamins antioxidants supplements

How did we qualify them ?

References

1. DeFronzo, R, Ferrannini, E. Insulin Resistance - a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease, Diabetes Care. 1991; 4(3):173-94.

2. Zavoroni, I. et al.Risk factors for coronary artery disease in healthy persons with hyperinsulinemia and normal glucose tolerance. The New England Journal of Medicine. 1989;320:702-6.

3. Reaven, G. Role of insulin resistance in human disease. Diabetes. 1988;37, 1595-1607.

4. Atkins, R. Dr. Atkins' New Diet Revolution. New York, NY: M. Evans and Company Inc.; 1992.

5. Reaven, G. Syndrome X. Clinical Diabetes. 1994;3-4, 32-52.

6. Dilman, V, Dean,W. The Neuroendocrine Theory of Aging and Degenerative Disease. Pensacola, FL: The Center for Bio-Gerontology, 1992.

7. Pyorala M, Miettinen H, Laakso M, Pyorala K. Hyperinsulinemia predicts coronary heart disease risk in healthy middle-aged men: the 22-year follow-up results in the Finnish Helsinki Policeman Study. Circulation. 1998;4;98(5): 398-404.

8. Fontbonne A, Thibult N, Eschwege E, Ducimetiere, P. Body fat distribution and coronary heart disease mortality in subjects with impaired glucose tolerance or diabetes mellitus: the Paris Prospective Study, 15-year follow-up. Diabetologia. 1992;35 (5):464-8.

9. Jenkins, D, Wolever, T. Glycemic index of foods: a physiologic basis for carbohydrate exchange. The American Journal of Clinical Nutrition. 1981; 34:362-366.

10. Podell, R.The G-Index Diet. New York, NY: Warner Books Inc.; 1993.

11. Endre, T. Insulin resistance is coupled to low physical fitness in normotensive men with a family history of hypertension. Journal of Hypertension. 1994; 12, 81-88.

12. Henriksson J. Influence of exercise on insulin sensitivity. J. Cardiovasc. Risk. 1995; 4:303-309.

13. McNeill, J. Enhanced in vivo sensitivity of vanadyl-treated diabetic rats to insulin. Canadian Journal of Physiology and Pharmacology 1996. 68 (4):486-91.

14. Poucheret P, Verma S, Grynpas M, McNeill J. Vanadium and diabetes. Mol Cell Biochem 1998;188(102):73-80.

15. Dean, W. Metformin, the most effective and under-appreciated life extension drug. Vitamin Research News. November 1998;12 (9).

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