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The Truth About Type 2 Diabetes Therapy

Before discussing therapy for type 2 diabetes, it is important to understand the logic behind conventional therapy and to understand why this logic is flawed. Type 2 diabetics are routinely told they need to boost their insulin levels, which will help drive blood glucose into their cells and lower their blood glucose levels. Unfortunately, this assumption defies common sense.

In the early stages of type 2 diabetes, insulin levels are already elevated (hyperinsulinemia). This is because the problem is not with insulin production; rather, a metabolic defect of insulin utilization. The delicate insulin receptors on cell membranes are less responsive to the insulin than are the receptors of people without type 2 diabetes, which means that less glucose is absorbed from the blood stream than would be normally, and glucose levels slowly rise.

This elevation in glucose upsets the body’s natural balance, prompting the pancreas to discharge copious amounts of insulin to normalize glucose levels. This short-term, biological fix successfully drives glucose into cells, thereby lowering blood glucose levels, but it also hastens the progression of the disease. Eventually, the fragile insulin receptors become less sensitive (insulin resistant), which means that the pancreas must secrete even more insulin to keep clearing the blood of glucose. In later stages of the disease, the pancreas becomes “burned out” and can no longer produce adequate insulin. Insulin levels drop far below normal, allowing blood glucose to rise even higher and inflict greater damage.

Unfortunately, many early-stage diabetics are prescribed drugs (e.g., sulfonylureas) designed to boost insulin levels. Considering that insulin levels are already high, this strategy is counterproductive and may actually serve to hasten the disease by further exhausting the insulin receptors on cell membranes. Also, insulin itself is a powerful hormone that, in high levels, can inflict damage. Evidence suggests that high levels of insulin may suppress growth hormone synthesis and release among obese and overweight people (who are prone to hyperinsulinemia) (Luque 2006). There is also evidence that increased levels of insulin contribute to the proliferation of colorectal cells, which suggests that high levels of insulin may be a factor in the development of colorectal cancer (Tran 2006).

A Program For Early Diabetics

There are acute differences between early and advanced stages of diabetes. Thus, it doesn’t make sense to treat all people with type 2 diabetes the same. In the early stages of the disease, people suffer from both hyperglycemia and hyperinsulinemia. Rather than take drugs that further increase the level of insulin in the blood, people with type 2 diabetes would do better to pursue therapies that increase the sensitivity of insulin receptors on the cell membranes.

One of the best defenses against mild to moderate type 2 diabetes and hyperinsulinemia is improved diet and exercise. Although the disease has a genetic component, many studies have shown that diet and exercise can prevent it (Diabetes Prevention Program Research Group 2002; Diabetes Prevention Program Research Group 2003; Muniyappa 2003; Diabetes Prevention Program Research Group 2000). One study also showed that while some medications delay the development of diabetes, diet and exercise work better. Just 30 minutes a day of moderate physical activity, coupled with a 5 to 10 percent reduction in body weight, produces a 58 percent reduction in the incidence of diabetes among people at risk (Sheard 2003). The American Diabetes Association recommends a diet high in fiber, unrefined carbohydrates, and low in saturated fat (Sheard 2004). Foods with a low glycemic index are especially recommended because they blunt the insulin response. For more information on glycemic index, see the Obesity protocol.

The high-carbohydrate, high-plant-fiber (HCF) diet popularized by James Anderson, MD, has substantial support and validation in the scientific literature as the diet of choice in the treatment of diabetes (Anderson 2004; Hodge 2004). The HCF diet is high in cereal grains, legumes, root vegetables, and restricts simple sugar and fat intake. The diet consists of 50 to 55 percent complex carbohydrates, 12 to 16 percent protein, and less than 30 percent fat, mostly unsaturated. The total fiber content is between 25 and 50 grams daily. The HCF diet produces many positive metabolic effects, including the following: lowered post-meal hyperglycemia and delayed hypoglycemia, increased tissue sensitivity to insulin, reduced low-density lipoprotein (LDL) cholesterol and triglyceride levels, increased high-density lipoprotein (HDL) cholesterol levels, and progressive weight loss.

A healthy diet for diabetics is also rich in potassium. Potassium improves insulin sensitivity, responsiveness, and secretion. A high potassium intake also reduces the risk of heart disease, atherosclerosis, and cancer. Insulin administration induces potassium loss (Khaw 1984; Norbiato 1984).

Obese people have a far greater tendency to develop type 2 diabetes than slim people. Therefore, weight loss accompanied by increased exercise and a healthy diet is effective for diabetes prevention and treatment (Mensink 2003; Sato 2000; Sato 2003).

Metformin: Increasing Insulin Sensitivity

In addition to diet and exercise, the prescription drug metformin has been proven to increase insulin sensitivity in people with mild to moderate hyperglycemia. Metformin is now the most commonly prescribed oral antidiabetic drug worldwide. It works by increasing insulin sensitivity in the liver (Joshi 2005). It also has a number of other beneficial effects, including weight loss, reduced cholesterol-triglyceride levels, and improved endothelial function.

Metformin is better tolerated than many other antidiabetic prescription drugs, but people with congestive heart failure, kidney or liver disease are not candidates for metformin therapy. Neither are people who consume alcohol in excess. A benchmark assessment of kidney function, followed by an annual renal evaluation, is essential. Vitamin B12 levels should also be checked regularly because chronic use of metformin can cause a folic acid and B12 deficiency, resulting in neurological impairment and disruption in homocysteine clearance. Also, metformin should not be used for two days before or after having an x-ray procedure with an injectable contrast agent because of the rare risk of lactic acidosis.

Metformin is effective on its own, but it may also be prescribed in combination with another class of insulin sensitizers called thiazolidinediones (TZDs; e.g., pioglitazone or Actos®, and rosiglitazone or Avandia®). TZDs increase insulin sensitivity and stimulate release of insulin from β-cells in the pancreas. TZD treatment also improves blood pressure and relieves vascular and lipid defects (Meriden 2004). However, TZDs have potentially serious side effects, including liver toxicity, which requires regular monitoring of liver function (Isley 2003; Marcy 2004).

In addition to these two prescription drugs, many nutrients have been shown to increase insulin sensitivity, protect vulnerable cell membranes, and reduce the damaging effects of elevated glucose (see “Nutritional Supplementation for Diabetics,” below). Ideally, a combination of improved diet, exercise, supplementation, and insulin-sensitizing prescription drugs can reverse mild to moderate hyperglycemia before stronger drugs are needed and permanent damage is done.

Drug Therapy For Advanced Diabetics

Some people, however, will not have the benefit of this knowledge before their type 2 diabetes advances to a more dangerous stage. In severe hyperglycemia, the pancreas becomes burned out after producing high levels of insulin for a long time. Insulin levels drop as a result of decreased production, and blood glucose levels are allowed to rise to very high, toxic levels. Although diet and exercise, along with supplementation, are still strongly recommended, prescription drugs might also be necessary.

Sulfonylurea drugs stimulate pancreatic secretion of insulin. Unfortunately, they are often prescribed as first-line treatment for mild to moderate type 2 diabetics, even when their use is inappropriate. By increasing levels of insulin, which are already raised, sulfonylurea drugs actually hasten the progression of early type 2 diabetes by exhausting insulin receptors faster, which causes the pancreas to burn out more quickly. Sulfonylurea drugs should really be considered a “last resort” for people with severe hyperglycemia.

Insulin replacement therapy is also a last resort for type 2 diabetics. While insulin therapy is universal and essential among type 1 diabetics, it is reserved for severe, refractory (nonresponsive to treatment) type 2 diabetics only. Proper dosing and monitoring of blood glucose are essential as too much insulin causes low blood sugar and coma, and too little insulin creates hyperglycemia. A new delivery system for insulin was recently approved by the US Food and Drug Administration. This new system allows for inhaled insulin.

What You Have Learned So Far

  • Diabetes is caused by abnormal metabolism of glucose, either because the body does not produce enough insulin or because the cells become desensitized to the effects of insulin.
  • Type 1 diabetes is caused by an autoimmune reaction that destroys insulin-producing β-cells in the pancreas. Type 2 diabetes is caused by decreased insulin sensitivity.
  • Type 2 diabetes has reached epidemic proportions in America. The incidence of this disease, which is caused by obesity and genetic predisposition, has increased dramatically over the past five years. It is more common among older people than in other segments of the population, although it is also affecting children at increasing rates.
  • People with mild to moderate type 2 diabetes should avoid drugs and therapies that increase levels of insulin. Their disease is characterized by elevated levels of both insulin and glucose. Instead, therapy should focus on strategies to increase insulin sensitivity.
  • Possible complications in diabetes arise from damage to enzymes and other proteins that impair their function and from resulting damage to blood vessels. The subsequent decreased blood flow, increased vulnerability to oxidant stress, and decreased antioxidant capacity all interact to produce end-organ damage to the eyes, nerve tissue, kidneys, and cardiovascular system.
  • Type 1 diabetics always require insulin therapy to replace their lost insulin.