All hormones including thyroid, testosterone, insulin, growth hormone, melatonin, cortisol, etc. are powerful regulators of the body’s metabolism and cellular functions. It has been observed that hormones can cause health problems when occurring either in deficient or excess quantities. For example, when thyroid hormone is deficient, depression, dry hair, dry skin, constipation, lassitude and weight gain may occur. When thyroid hormone occurs in excess, anxiety, heart palpitations, moist skin, and inability to gain weight may result. It is a most curious observation that until very recently, no one has considered the effects on human health of excess insulin secretion, even though the deficiency of insulin, diabetes, has been recognized for decades. This is because the effects of elevated insulin levels are often silent for years.
Insulin is a hormone secreted by specialized cells of the pancreas. One of insulin’s main functions in human biochemistry is to transport blood sugar (glucose) across the cell membrane to ultimately be burned as fuel in the energy making part of the cell called the mitochondria. This function of insulin is critical to human health, as evidenced by Type I Diabetes, a condition in which the pancreas is unable to produce insulin-the affected person must take insulin by injection. However there are other lesser known but very important effects of insulin in human biochemistry that will be addressed in this article.
In a 1988 article in the journal Diabetes, Dr. Gerald Reaven of Stanford University, described a cluster of metabolic disorders, including but not limited to adult onset diabetes, typically found in association with insulin resistance. The term insulin resistance implies the inability of insulin receptor sites on one’s cell membranes to take up insulin, whether that insulin is secreted by the pancreas or taken by injection. He dubbed this cluster Syndrome X.
In order to understand what happens when someone becomes resistant to insulin, we must review the role insulin and its balancing hormone, glucagon, play in the body. When we eat, our bodies break down the food into its basic components – protein (amino acids), carbohydrate (glucose), fat (fatty acids), which are then absorbed into the bloodstream. It is important to realize that carbohydrate has a far greater effect on raising blood sugar (glucose) than fat or protein. A rise in blood sugar signals the pancreas to make and release insulin. Insulin secretion should promptly return blood sugar levels to a normal fasting level within two hours after eating. This occurs as insulin transports glucose out of the blood stream, across the cell membrane, and into cells where it is either burned for energy, stored as fat in fat cells or stored as glycogen (a storage form of glucose) in muscle. Fat travels in the blood in the form of a molecule called triglyceride. A triglyceride is composed of three fatty acid molecules. When a triglyceride in the blood reaches a cell, enzymes at the surface of the cell break down the molecule and the fatty acids can enter the cell. Once inside the cell, an amino acid, L-carnitine helps shuttle the fatty acids into a fat burning factory inside the cell called the mitochondria. Although fat is able to enter the cell without using insulin to transport it like glucose must, insulin blocks this fat-carnitine system and thereby keeps the fat from entering the mitochondria where it would be burned for energy production. Insulin pushes the fatty acids back into triglycerides and out of the cell encouraging the storage of fat in adipose (fatty) tissue. In short, excess insulin directly creates obesity.
When there is no insulin secretion (as in Type I Diabetes) blood sugar rises dramatically and glucagon activity is unopposed by insulin, allows fat to pour into the blood stream. This fat has to be burned in the body’s back-up fat burning system in liver cells. The end result of this “default” process is the production of excessive amounts of acidic ketone bodies, a by-product of fat burning in the liver. Diabetic ketoacidosis, a life threatening condition may result. (It should be noted that while diabetic ketoacidosis is a serious problem, the mere presence of ketones in the blood in a non-diabetic, simply called ketosis, is not serious and in fact provides proof of fat burning for dieters.)
Years of high dietary carbohydrate intake, especially in genetically predisposed individuals, stresses insulin receptors which in turn malfunction. The normal amount of insulin then cannot maintain a normal blood sugar, and the body must then produce more and more insulin to keep blood sugar in the normal range. This higher level of insulin can often control blood sugar levels adequately, at least for a while, but the other lesser-known effects of insulin now come into play. These effects include:
* encouraging storage rather than burning of fat, thus leading to obesity
* enhancing the synthesis of cholesterol, especially LDL, increasing the risk of vascular disease
* thickening arterial walls making blood vessels more stiff leading to increased blood pressure and increased risk of vascular disease
* retention of sodium (salt) and fluid with subsequent rise in blood pressure
* increased secretion of norepinephrine increasing blood pressure as well as pulse rate.
These effects explain all the abnormalities Dr. Reaven described in his article on Syndrome X years ago.
Some individuals will eventually lose the ability to keep their blood sugar levels normal even in the presence of very high levels of insulin. This is the cause of adult onset, Type II or non-insulin dependent diabetes. This type of diabetes when treated early can be completely controlled with dietary intervention and need never lead to dependence on blood sugar lowering pills or insulin injections. Controlling Type II diabetes by diet can also prevent, to a large degree, many complications of the disease. These include heart disease, peripheral vascular disease (which can lead to amputation of extremities), peripheral neuropathy (burning and numbness in the hands and feet), retinopathy (which can lead to blindness) and kidney disease.
Some insulin resistant individuals may never lose enough control over blood sugar levels to be considered diabetic. These individuals represent another population group at risk for Syndrome X: American adults in their 40′s, 50′s and 60′s who may feel well, yet have elevated insulin levels which, unfortunately are rarely measured at screening exams. Their elevated insulin levels put them at much higher than average risk for high blood pressure, obesity, heart disease, elevated triglycerides and “bad cholesterol” (LDL). The sooner a problem with insulin resistance or excess insulin is diagnosed, the sooner it can be remedied with appropriate dietary changes. It is for this reason that glucose tolerance tests (GTTs) (which measure blood glucose response to carbohydrate ingestion) are inadequate for assessing the risk of diabetes.
Years before blood sugar measurements are clearly abnormal, the problem that leads to Type II diabetes can be diagnosed by measuring an individual’s blood insulin response to carbohydrate ingestion, a glucose/insulin tolerance test (GITT). Such evaluation is indicated in anyone with a family or personal history of high blood pressure, obesity, diabetes, heart disease, vascular disease in the legs, cerebrovascular disease, high blood triglycerides or cholesterol. It is important to remember that someone having elevated insulin levels in response to carbohydrate ingestion need not have all the side effects associated with high insulin levels. Because we are each individually unique, one person may only have high blood pressure and fluid retention, another may only have obesity and high triglycerides. They may look different and feel different from each other and yet the underlying cause of their problems may be the same. Likewise, not everyone with high blood pressure or high cholesterol or obesity has insulin resistance. The only way to know is to be tested.
Government figures released in 1994 indicate that despite reduced consumption of fat, the incidence of Americans who are significantly overweight jumped by 30% in one ten year period. This should be a hint that decreasing fat in the diet is not the answer for being overweight. The information reviewed above reveals that for those whose obesity is related to elevated insulin levels (hyperinsulinemia), the solution is to drastically reduce carbohydrate in the diet since carbohydrates stimulate insulin and suppress glucagon.
(Glucagon, the other hormone secreted by the pancreas, stimulates the opposite effect of insulin: the movement of fatty acids out of adipose tissue and into the mitochondria for burning.)
Interestingly enough, even for those who are not insulin resistant but want to lose weight and keep it off, decreasing carbohydrate intake is still necessary. Long ago in the history of man, it was probable that weight loss stimulated activity of an enzyme, LPL, which was protective against starvation. Weight loss via dieting in modern times still stimulates this enzyme and encourages the storage of fat. We are well designed for famine, but poorly designed for affluence. In our presently over-fat society this is a metabolic reality that makes it easier to re-gain weight shortly after it is lost. Therefore, no matter what approach someone takes to losing weight, they need to do whatever they can to suppress this enzyme activity. This is accomplished by three strategies:
* Eating meals lower in carbohydrate and richer in fat and protein
* Eating protein to supply amino acids which stimulate glucagon production (a reason to have adequate fat and protein in every snack)
* Stimulating norepinephrine activity by exercise, which in turn stimulates glucagon production. Exercise is important in controlling obesity, hypertension and elevated blood fats.
A metabolic evaluation to define glucose/insulin tolerance is necessary for anyone with a family history of diabetes or any of the health problems mentioned above that are associated with hyperinsulinemia.