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Diabetes Mellitus, Type 2

Introduction

What should I know about Type 2 Diabetes Mellitus?

Diabetes mellitus, a term that means “the running through of sugar," was first identified in the 1st century AD. (1) The disease was described in old books as “the melting down of flesh into urine." Diabetes mellitus is a chronic condition where there is less insulin than what the body needs. This can be low insulin, a problem with the release of insulin, insulin that cannot work in the cells that need it, or insulin that is inactivated before it is able to function. Diabetes mellitus is a disease in which the body does not produce or does not use insulin effectively. It is not simply hyperglycemia, or too much glucose (sugar) in the blood.

Insulin is a hormone produced in the pancreas by the beta cells in the Islets of Langerhans. The release of insulin by these special cells is regulated by the amount of glucose in the blood. It is responsible for transporting glucose (from carbohydrates) into the cells for energy production. After a meal, when blood sugar increases, insulin release increases. Between meals, when blood sugar is low, insulin release is low. Insulin is released from the pancreas directly into the liver where some is used and some is broken down and eliminated from the body. The rest is released into the general blood circulation. By helping to move glucose into the cells, insulin decreases blood sugar. Insulin also decreases the breakdown of stored fat and builds triglycerides. Insulin is involved in the production of protein. The proper growth and development of children is dependent on insulin.

Diabetes can affect people of any age. It increases the risk of chronic conditions like heart disease, retinopathy (a disease of the retina) and blindness, peripheral neuropathies (a disease of the nervous system), circulation problems that can lead to amputation, problems with the immune system, and skin ulcers and poor wound healing.

Diabetes is diagnosed by lab tests, either a fasting plasma glucose (FPG) or a two-hour plasma glucose (OGTT – oral glucose tolerance test). There are two forms of diabetes mellitus: type 1 (also called IDDM, insulin dependent diabetes mellitus, or juvenile onset) and type 2 (NIDDM, non-insulin dependent diabetes, or adult onset).

Ninety percent of individuals with diabetes have type 2. Most of these individuals are over 40 years old. One in five patients is over the age of 65, and 80 percent are overweight. (2) Many patients have increased blood sugar seven to ten years before symptoms occur.

When something is wrong with a person’s blood sugar regulation even if insulin is being produced by their pancreas, the individual probably has type 2 diabetes. People with type 2 do not need to depend on insulin injections to survive. Type 2 diabetes is not fully understood. Three physical abnormalities usually occur in type 2: insulin resistance, increased glucose production in the liver, and poor beta cell function. These can occur individually or in combination.

Insulin resistance appears to be the first stage of the disease. It means that insulin cannot help glucose go from the blood into the cells. (3) While the beta cells are able to release normal or even higher than normal amounts of insulin, glucose movement into the cells is sluggish and blood glucose slowly begins to rise. Therefore, blood sugar remains increased even with insulin being produced by the pancreas. Then the pancreas releases even more insulin, and hyperinsulinemia (too much insulin in the blood) begins.

This is likely due to a genetic defect that affects how insulin is used or the way it is transported to the cells. Insulin resistance is due to high insulin levels, not high glucose levels. Therefore, the individual is always hyperglycemic. Eventually, the beta cells “burn out" and insulin resistance may turn into diabetes.

Many people with type 2 diabetes also produce a large amount of glucose in the liver. This increase in liver glucose production is likely related to fat breakdown. When the body is not efficiently using glucose as an energy source, stored fat becomes an important source of fuel. The breakdown of fat makes the liver produce glucose. Because patients with type 2 diabetes are insensitive to the effects of insulin, which normally stops the production of glucose in the liver, this condition continues. This situation also appears to be related to weight and physical activity.

In type 2 diabetes, the ability of the beta cells to release the first amount of insulin needed after eating a meal (postprandial insulin release) deteriorates early on in the disease. Therefore, blood glucose remains increased for one to two hours after a large meal. As the disease gets worse, the insulin release that continues following a meal also worsens, resulting in something called pancreatic beta cell exhaustion.

Type 2 diabetes appears to be caused by genetic defects that at first make a person not able to respond to the actions of insulin and, over time, the beta cells in the pancreas will stop releasing insulin. However, new evidence points to diet and lifestyle as important factors that may be responsible for the development of the disease. A person over the age of 45 and overweight is a likely candidate for developing type 2 diabetes. About 30-39 percent of Americans are obese, and many more are overweight. Research has shown a strong connection between upper body obesity (people with “apple shapes") and the development of type 2 diabetes mellitus. (4)

The long-term complications associated with diabetes are serious, often life-threatening, and diagnosed in the late stages of the disease. These complications are due to continuous hyperglycemia from poor glucose control. Many of these chronic complications can be traced to changes in blood vessels that cause a decreased blood flow. These changes include coronary heart disease and peripheral vascular disease, retinopathy, nephropathy, and neuropathy.

Heart disease is the leading cause of diabetes-related deaths, with adults having two to four times higher heart disease death rates than adults without the disease. The risk of stroke is two to four times higher in people with diabetes. Patient with diabetes develop more atherosclerosis (hardening of the arteries) than people without diabetes, and some 60-65 percent of patients with diabetes have high blood pressure.

When high amounts of blood glucose are present in tissues such as the lens of the eye and nerve cells, the body finds other ways to handle the extra glucose in these cells. Enzymes (proteins that stimulate chemical reactions to occur in the body) work to breakdown the extra glucose, causing an increase in sorbitol and fructose (types of sugars). This excess sugar in these cells will then take on extra fluid, eventually damaging these cells.

Retinopathy is the leading cause of new cases of blindness among adults 20 to 74 years of age. Because of increased glucose, blood vessels weaken and microaneurysms (small swellings in the blood vessel) occur in the capillaries of the retina. The retinal cells can then burst and hemorrhage (bleed). This blurs vision and can lead to detachment of the retina.

Nephropathy (kidney disease) is the leading cause of kidney failure requiring dialysis. The first sign is microalbuminuria (a type of protein in the urine), which leads to proteinuria (protein in the urine), and eventually end stage kidney disease.

Neuropathy (disease of the nervous system) causes numbness and tingling in the arms, legs, hands, and feet, eventually leading to injury and the development of diabetic ulcers (wounds) in these areas. Diabetes is the leading cause of amputations in the U.S. Other changes that occur with neuropathies include GI problems, such as gastroparesis (a paralysis in the gastrointestinal tract), chronic constipation, or diarrhea; loss of sexual function, bladder function, and heart problems.

Statistic

International Diabetes Federation, 2007.

  • Diabetes currently affects 246 million people worldwide and is expected to affect 380 million by 2025.
  • Diabetes is the fourth leading cause of global death by disease.
  • In 2007, the five countries with the largest numbers of people with diabetes are India (40.9 million), China (39.8 million), the United States (19.2 million), Russia (9.6 million) and Germany (7.4 million).
  • Each year a further 7 million people develop diabetes.
  • Each year 3.8 million deaths are attributable to diabetes.
  • Every 10 seconds two people develop diabetes.
  • Up to 80% of type 2 diabetes is preventable by adopting a healthy diet and increasing physical activity.
  • Type 2 diabetes has become the most frequent condition in people with kidney failure in countries of the Western world.
  • It is estimated that more than 2.5 million people worldwide are affected by diabetic retinopathy.
  • Cardiovascular disease is the major cause of death in diabetes, accounting for some 50% of all diabetes fatalities, and much disability.

Persatuan Diabetes Malaysia, 2007.

  • Of the nearly 1.2 million Malaysians with diabetes, more than 98% have type 2 diabetes.

Sudaram Medical Foundation, 2007.

  • It is currently estimated that there are 35 million diabetics in India. The number is expected to increase by another 60% by the year 2025.

Diabetes New Zealand, 2006.

    • Approximately 105,000 people in New Zealand have been diagnosed with Type 2 diabetes. It is estimated that 115,000 are undiagnosed.

The Center of Disease Control, National Diabetes Fact Sheet, 1998.

    60-65% of people with diabetes have High Blood Pressure (HBP). 15.7 million people have diabetes or about 5.9% of population. 10.3 million have been diagnosed with diabetes. 5.4 million people are undiagnosed. There are 798,000 new cases of diabetes diagnosed each year. 6.3 million age 65 or over or 18.4% of all people in this age group have diabetes.

Center for Disease Control and Prevention, 2003.

    Over a million adults between 18 and 79 years of age were diagnosed with diabetes in 2000.

Signs and Symptoms

The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.

Initial symptoms of diabetes include frequent urination, thirst, fatigue, and irritability. Dizziness, lethargy, irritability, loss of coordination, and perspiration are marked during episodes of low blood sugar (blood glucose 250mg/dl) among insulin-dependent diabetics can lead to ketoacidosis, characterized by increased thirst, nausea, vomiting, and an acetone or "fruity" odor to the breath.

General

  • Frequent urination
  • Thirst
  • Fatigue
  • Irritability
  • Episodes of low blood sugar (blood glucose 250mg

Treatment Options

Conventional

Treatment for patients with type 2 diabetes includes diet, exercise, and drug therapy. Diet is considered to be the first treatment to try. Maintaining ideal body weight can help the patient to control the disease. Exercise can help the insulin that is available to work better and help regulate glucose production in the liver. Even with diet and exercise, however, within the first five years after diagnosis, over 60 percent of patients will need oral antidiabetic drugs. It is also estimated that approximately 40 percent of patients will eventually need insulin injections to control their blood sugar.

Oral Antidiabetic Drugs

Oral drug therapy for the management of type 2 diabetes now includes more choices in several drug classes, most of which work differently. Sulfonylureas cause release of insulin from the pancreas and help insulin to work better; biguanides work in the liver; thiazolidenedones work in muscles; glucosidase inhibitors work in the small intestine; and meglitinide causes release of insulin from the pancreas.

Oral Drugs for Treating Diabetes

First Generation
Tolbutamide 250mg, 500mg
Acetohexamide 125mg, 250mg
Tolazamide 100mg, 250mg, 500mg
Chlorpropamide 100mg, 250mg

Second Generation
Glipizide 5mg, 10mg
Glipizide extended release 2.5mg, 5mg, 10mg
Glyburide 1.25mg, 2.5mg, 5mg
Glyburide Micronized 1.5mg, 3mg, 6mg
Glimepiride 1mg, 2mg, 4mg

Alpha-Glucosidase Inhibitors
Acarbose 50mg, 100mg
Miglitol 25mg, 50mg, 100mg

Biguanides
Metformin 500mg, 850mg, 1,000mg
Metformin extended release 500mg

Meglitinides
Repaglinide 0.5mg, 1mg, 2mg

Thiazolidinediones
Rosiglitazone 2mg, 4mg, 8mg
Pioglitazone 15mg, 30mg, 45mg

Combination Products
Glyburide and Metformin 1.25/250mg, 2.5/500mg, 5/500mg

Sulfonylureas
Oral sulfonylureas are related to sulfa antibiotics but do not have antibacterial action. They stimulate insulin release, increase the amount of insulin circulating in the bloodstream, and make the beta cells more sensitive to the actions of glucose. (5) They are used along with diet and exercise. They are only effective in patients that can produce insulin. They don’t prevent beta cell loss. Therefore, sulfonylureas can become less effective over time. The newer agents in this group of drugs have less drug interactions than the first drugs that were marketed in this group. About 50 percent of patients will successfully control their diabetes with the use of sulfonylureas. These agents can also be used in combination with injectable insulin.

All of the sulfonylureas can be taken with food except for glipizide. Food slows down glipizide absorption, so it is recommended that this drug be taken 30 minutes before meals.

Biguanides
Metformin is a member of the biguanide group of antidiabetic drugs and not related to the sulfonylureas. It makes the insulin that is available work better – it doesn’t increase the amount of insulin that is released. By not increasing insulin release, it does not cause hyperinsulinemia. It also decreases blood glucose without producing hypoglycemia. It can be used with diet or in combination with other drugs. It does not produce weight gain. (6) Metformin is the only antidiabetic drug ever shown to extend the life of patients with type 2 diabetes.

Thiazolidinediones
Troglitazone, a member of the thiazolidinedione drug class became available in January, 1997, and was reported to lower blood glucose by decreasing insulin resistance, not by increasing insulin release. It could be used alone, with insulin, or along with oral sulfonylureas. By December of that year, the FDA announced new guidelines to be followed to monitor patients for signs of liver injury. This was due to 35 reports of liver injury in U.S. and Japanese patients, including one liver transplant and one death. The manufacturer removed the drug from the market in March, 2000.

In May, 1999, the FDA approved rosiglitazone, the second drug in this class of antidiabetic drugs. It does not seem to have the same liver problems that were seen with troglitazone. No significant drug-drug interactions have been reported. However, caution is still needed and watching patients on this drug is still recommended.

The third drug in this group to receive FDA approval is pioglitazone. It has advantages over the other two drugs in this group. Most patients will have lower triglycerides, increased HDL cholesterol, and no changes in LDL cholesterol with this drug. This may be important for those patients with type 2 diabetes that are at high risk for heart disease. Watching patients on this drug is still recommended.

Alpha-Glucosidase Inhibitors
Acarbose and miglitol are alpha-glucosidase inhibitors. They lower postprandial blood glucose by slowing down the digestion and absorption of carbohydrates. These agents do not affect the absorption of simple sugars, such as glucose and lactose. Unlike sulfonylureas, they do not cause hypoglycemia, hyperglycemia, or weight gain. They do not increase insulin release. They can be used with diet alone or combined with sulfonylurea or biguanide agents. They have been reported to decrease triglycerides and LDL cholesterol. These drugs are most useful for patients in the early stages of the disease who have high blood glucose after meals, but have normal fasting blood glucose lab results.

Meglitinides
Repaglinide belongs to a drug class known as the meglitinides, not related to the sulfonylureas. It decreases blood glucose by increasing the release of insulin from the pancreas. It needs to have functioning beta cells to work effectively. Repaglinide can be used alone or in combination with metformin. When it is used along with metformin, the results are better than with using either drug alone. It must be taken multiple times daily, usually within 15 minutes of each meal. Patients who have not done well with a sulfonylurea will probably not do well with repaglinide.

Use of Insulin in Type 2 Diabetes
In patients with type 2 diabetes, it is important to make sure that the drug therapy is special for each patient. When there is little or poor response to a drug from one class, a drug from another class can be substituted to see how that works in the patient. For those patients who need it, a second drug from another class can be added. However, control of blood glucose is likely to decrease over time, as type 2 diabetes is a progressive disease – that is, it does get worse with time.

Even with the use of oral agents, postprandial hyperglycemia still is a problem for 60 percent of patients. The failure of oral agents to control blood sugar is common. More than 25 percent of type 2 patients will require insulin to adequately control their blood sugar. Blood sugar monitoring and taking all antidiabetic drugs properly are extremely important.

Nutritional Suplementation


Chromium

The way that chromium affects blood sugar was first discovered in animal studies in the 1950's. In the 1970's, it was discovered that chromium is important in special intravenous (IV) feeding solutions called total parenteral nutrition (TPN solutions). It was discovered that when chromium was missing from the TPN solution, after several months, blood sugar increased in patients. Chromium was added and blood sugar in TPN patients returned to normal. Various studies support that chromium has a positive effect on blood glucose. (7)

It is thought that chromium helps insulin by moving glucose and other nutrients into the cells of the body. (8) This helps to maintain muscle mass during times when the diet does not provide enough calories. Chromium also stabilizes the body’s metabolism. Chromium can lower cholesterol and triglycerides. Chromium may also decrease hunger and limit food cravings. Insulin is involved in the regulation of the center in the brain the makes one feel full and stop eating. Insulin is also important in the development of a brain chemical linked to the craving for carbohydrates.

Most Americans are at risk for low chromium because of a diet rich in refined sugars. Individuals who eat diets high in refined sugars tend to eliminate 300 percent more chromium in their urine than those whose diets are low in refined sugars. Individuals who live in countries with high levels of chromium that comes from diets rich in unrefined grains have a lower rate of diabetes and atherosclerosis (hardening of the arteries). People who exercise regularly eliminate two to six times the normal amount of chromium in their urine on days of exercise. (9) Many athletes make this problem worse by using high-carbohydrate supplements. The elderly also are at risk for low chromium due to not enough chromium in the diet and poor absorption. Women can have a drop in chromium levels during the third trimester (seventh, eighth, and ninth months) of pregnancy. (10)

There is a disagreement among healthcare professionals over what is the best chromium to use. Chromium is only active in certain forms. The most important of these forms is glucose tolerance factor (GTF). Dr. Walter Mertz of the United States Department of Agriculture did research with GTF chromium. He found that chromium was a crucial part of the process where insulin attaches to cells. GTF chromium is safe and usually does not cause side effects.

Chromium picolinate is another popular form of chromium that is used to regulate blood sugar levels. (11) , (12) Even though chromium picolinate is considered safe, a recent study in lab animals at Dartmouth College and The George Washington Medical Center reported that certain doses of chromium picolinate caused damage to chromosomes. (13) More information is needed about this supplement because other studies have reported that it is safe and effective.

For diabetics, adding chromium or other blood sugar regulating agents to their diet should be done slowly, especially if they are on other medication to control their diabetes. With lifestyle and dietary changes, only a small dose of chromium may be needed.


Magnesium

Magnesium is involved in the breakdown of glucose in the body and release of insulin. (14) Low magnesium may make diabetes worse in some people. (15) Hypomagnesemia (low magnesium in the blood) happens in about 25 percent of diabetic patients. (16) Many Americans are below the RDA (Recommended Dietary Allowance) for magnesium. Many experts feel that the RDA for magnesium needs to be increased.

Magnesium is eliminated from the body by the kidneys. Individuals with kidney disease should consult a healthcare professional before using a magnesium supplement. Too much magnesium may cause diarrhea.


Vanadium

Vanadium is a trace mineral that is very important for plant nutrition, but what it does for human nutrition is not clear. It works with enzymes in the body. High amounts of vanadium are found in the kidneys, liver, and bone. Fat cells temporarily store vanadium for quick release into the body. Supplementing with vanadyl sulfate and other forms of vanadium has been reported to improve diabetes. (17) , (18)

Animal studies have reported that when vanadium was given to diabetic rats, their increased blood glucose returned to normal. Other studies have reported that vanadyl sulfate not only lowers blood glucose in diabetic animals, but also decreases cholesterol and triglycerides. (19) In one study in diabetic rats, researchers found that vanadium may protect the pancreatic beta cells. (20)

Human studies are encouraging. Type 2 diabetics given oral vanadyl sulfate had a nearly 20 percent drop in fasting blood glucose in one study. (21) Minor gastrointestinal upset was the only reported side effect. In another study, supplementation with vanadyl sulfate daily for three weeks resulted in improved insulin action. (22)

Vanadium pentoxide and vanadyl sulfate are active forms of vanadium that are easily absorbed by the body. Vanadium appears to be safe even at high doses. Doses should be increased gradually, especially if it is given with GTF chromium.


Alpha-Lipoic Acid (ALA)

Alpha-lipoic acid (ALA) is an antioxidant made by the body. ALA is also known as alpha-lipoate or thiotic acid. Lipoates are small water and fat-soluble molecules that are easily absorbed from the gastrointestinal tract. It is also used in heart disease and for AIDS patients. (23) Alpha-lipoic acid affects insulin and blood sugar in type 2 diabetics. (24) , (25) , (26) ALA may be effective in the treatment of diabetic neuropathy. (27) In a recent study, about 97 percent of diabetic patients treated with ALA daily for three weeks reported an improvement in their neuropathy symptoms. (28) There are no known toxicities with ALA. It is important to monitor blood glucose closely in diabetics supplementing their diet with ALA.


Zinc

Zinc deficiency is found in patients with problems in blood glucose control. (29) In clinical studies, diabetic animals and humans with zinc deficiencies improved when supplemented with zinc. (30) , (31) Zinc helps to regulate insulin production by the pancreas and glucose use by muscle and fat cells. Very high doses of zinc may cause diarrhea, dizziness, lethargy, vomiting, and loss of muscle coordination.


Cyclo (His-Pro)

Cyclo hispro may be a useful agent in improving blood sugar regulation in individuals with hypoglycemia, diabetes, and impaired glucose tolerance (IGT). (32) It has been reported that individuals with diabetes have problems with absorbing zinc from the intestines, causing low zinc levels in the blood. Both animal and human studies report that cyclo hispro may affect the absorption of zinc from the intestines. This extract also contains high levels of zinc. For the diabetic patient, zinc is important for wound healing, proper functioning of the immune system, and for the skin. There are no reported side effects with the use of cyclo hispro.

In a recent clinical study, cyclo hispro was given to 22 male subjects with type 2 diabetes. After three months, the treatment group reportedly decreased fasting blood glucose levels and fasting plasma insulin levels. In addition, the treatment group had slight decreases in cholesterol and LDL and increased plasma zinc concentrations. The results of the study demonstrated the benefit of the use of cyclo hispro extract with zinc in type 2 diabetics. (33)

Herbal Suplementation


Evening Primrose

Evening primrose oil (EPO) contains gamma-linolenic acid, which is an omega-6 fatty acid. (34) , (35) Omega-6 fatty acids may decrease inflammation. Using essential fatty acids such as EPO may prevent zinc deficiency, possibly improving the immune system. (36) Fatty acids are an important part of the normal functions of the human body. The human body can produce all of the fatty acids it needs except for omega-3 and omega-6 fatty acids. Both of these must come from the diet or with the use of supplements. A balance of these two fatty acids is very important. Essential fatty acids are needed for building cells and hormones. Modern diets often do not provide enough fatty acids.

Diabetics who cannot make gamma-linolenic acid (GLA) from linoleic acid will need a quality GLA supplement. (37) , (38) This is very important for proper nerve function and for the prevention of diabetic neuropathy. (39) , (40) Evening primrose oil has been reported to be beneficial for patients with diabetic neuropathy. (41) , (42)


Gymnema

Gymnema is a rain forest vine found in Central and Southern India, which has a long tradition in the treatment of diabetes. The Indian name is Gurmar, which means, “sugar destroyer." Its use has been documented in Ayurvedic medical texts for over 2,000 years in the treatment of “sweet urine." The leaves of gymnema are thought to increase insulin secretion, and several studies report control of hyperglycemia in diabetic laboratory animals. (43) , (44) A decrease in body weight has also been reported.

Human studies have reported decreased blood glucose during therapy with gymnema. (45) , (46) Improved lab test results and the need for less prescription medications have also been reported. In some studies, patients with diabetes were able to stop taking prescription diabetes medication and control their blood glucose with gymnema alone. (47) Researchers report that beta cells may be repaired in type 2 diabetics taking gymnema supplements. (48) Other studies report that gymnema controls blood glucose by decreasing the absorption of glucose in the intestines. (49)

Because gymnema leaf powder acts like an anesthetic on the taste buds that can last for several hours, some researchers feel that gymnema may be a possible agent to use for weight control and to decrease the craving for sweets. (50) A recent study also reports decreases in cholesterol with the use of gymnema. (51) Gymnema may be useful for athletes who want to develop more lean muscle mass compared to body fat. Another study suggested that gymnema may be safe and effective for weight reduction, BMI and promoting healthy blood lipids. (52)


Bitter Melon

Bitter melon or karela fruit has been used in South America and the Orient as a food and also as a febrifuge (fever reducer), abortifacient (an agent that causes abortion), emmenagogue (increases menstruation), anthelmintic and vermifuge (agents that remove intestinal worms), antiviral, emetic (induces vomiting), and agent for diabetes. (53) Recent studies have looked at the benefits of the fruit in diabetes and hyperinsulinemia, HIV viral infection (AIDS), and certain cancers. (54) , (55)

Bitter melon has been reported to improve glucose control in humans. (56) , (57) Research reports that molecules with insulin-like activity may be present in bitter melon seeds. (58) A few studies say that bitter melon may increase glucose use in the liver rather than having any effect on insulin release. (59) Bitter melon has also been reported to lower cholesterol and triglycerides in diabetic patients. Some reports have said that bitter melon extracts did not lower blood sugar in laboratory animals. (60) , (61) It is recommended that a standardized extract of bitter melon always be used.

Diet & Lifestyle

Diet: Diabetes and obesity have increased over the past 50 years in the United States. People don’t eat enough fresh foods, and there are fewer micronutrients in the soil (like chromium and vanadium) where food is grown. Fad diets of high protein, low or high fat, and low or no carbohydrates are not the answer. While this type of diet may help take weight off at first, it is not a long-term answer. Carbohydrates alone are not the cause because humans were eating carbohydrates long before these problems arose. It is true, however, that people are eating excessive amounts of carbohydrates, and it would be better to moderate that habit.

There are several ways to support and improve insulin regulation by using natural agents, but the real key is to change the selection of foods in the diet. In general, the American diet is made up of a large amount of carbohydrates, especially refined carbohydrates. People limit their intake of fresh vegetables and fruits, and quality sources of protein and legumes, and they do not take in enough essential fats. As of 1985, the typical American diet was 46 percent carbohydrates, 43 percent fat (poor quality), and only 11 percent protein. With the average American eating approximately 150 pounds of sugar a year, there is a continuous demand for more insulin to be released. The average person drinking two “big gulp" drinks a day is receiving about 54 teaspoons of sugar. Using diet drinks does not work either because they contain sodium. This is particularly a problem for diabetics with hypertension (high blood pressure). While current research shows that dietary fat and cholesterol are definite problems, this situation is only made worse by the continuous, increased amount of carbohydrates along with the fat. Dietary fat is then stored because of excess insulin that is released while eating a high amount of carbohydrates.

Many experts over the years have praised the low-fat, high-carbohydrate diet. The problem with this diet has been that it does not cause weight loss. In fact, a diet with too many carbohydrates has been linked to increased LDL cholesterol and triglycerides. (62) The other thing to be aware of is that many prepared foods may be labeled low fat, but are loaded with refined sugars, which increase insulin release, and therefore, fat storage.

The obvious first step is to eat foods that will cause the least amount of insulin to be released. This will not only benefit the diabetic, but many individuals wanting to lose weight will benefit from this approach as well. The first concept to understand is the glycemic index - the fact that certain foods actually cause a sharper rise in insulin release than others. The glycemic index was first developed to help diabetics control postprandial (after meals) insulin blood sugar regulation, since this is the most difficult part of controlling blood sugar. Foods that do not cause a rapid rise in blood sugar will not cause increased insulin release. For example, in the past, it was thought that all complex carbohydrates were equal. It is now known that grains have different glycemic indexes. It is valuable to look at glycemic index when choosing foods that contain different amounts of carbohydrates. Proteins and fats do not have a glycemic index.

Legumes: Almost all legumes have a moderate glycemic index. They also provide a source of water-soluble fiber that is valuable for lowering cholesterol. They also provide phytoestrogens, which may provide health benefits.

Vegetables: Some vegetables have a high glycemic index and should be used in moderation if one is trying to actively control blood sugar. These include white potatoes (baked), carrots, beets, and turnips. However, if an individual is eliminating other sources of refined sugar in the diet and is decreasing the amount of complex carbohydrates (breads and pastas), he/she should be able to eat these vegetables with moderation.

Dairy products: Most dairy products have a low glycemic index. However, some people do not tolerate dairy very well.

Fruits: Fruits are generally in the middle of the road in terms of glycemic index; but dried fruits, which are concentrated, have a higher index. Drinking fruit juices will definitely increase blood sugar release. Therefore, fruit juices should be limited or diluted with three-fourths water.

Most sweeteners such as honey, molasses, sugar, and white grape juice concentrate tend to have a high glycemic index. Rice syrup and granulated rice sweeteners may be used instead. The artificial sweetener aspartame may increase insulin resistance over time.

Grains: Grains such as rice, wheat, and corn tend to have a high glycemic index, but grains such as buckwheat, millet, barley, rye, and bulgur are actually quite low. For successful weight loss and blood sugar control, this group of foods should be used in moderation. Also, the addition of fats such as olive oil or butter (in moderation) can lower the glycemic index.

Fiber: Fiber is an important part of the diet for a number of reasons. It is well known that fiber helps prevent constipation. However, fiber also controls sugar and cholesterol and helps in the prevention of colon cancer and diverticulitis. Most individuals with diabetes or insulin resistance do not realize that they run a 75 percent risk for developing atherosclerosis. Decreasing cholesterol levels with the use of fiber is one way to combat this problem.

Fiber is the indigestible part of plant food that acts as roughage for the body. There are two types of fiber. Water-soluble fiber is found in fruits, vegetables, and legumes in the form of guar, pectin, and gums. These products form a gel in the gastrointestinal tract that allows for a food to be held there longer, causing in a slow rise in blood sugar. This type of fiber also helps to lower cholesterol. Insoluble fiber is made of cellulose, hemicellulose, and lignins, and can be found in grains and bran. This food also takes longer to be broken down and used for energy, but its main value is in adding bulk and preventing constipation.

Food Nutrient Groups and Their Importance in Insulin Regulation

Proteins: Protein is important in every individual’s diet. It is needed for growth and for building tissues. Proteins are made of amino acids. These amino acids are absorbed through the small intestine and used by the body as needed. The body can manufacture most amino acids, but there are eight essential amino acids that must come from the diet. These eight can best be found in eggs, poultry, fish, and meat. Nuts, seeds, legumes, and grains can provide some of these essential amino acids as well. Protein intake is needed for tissue healing and body functions.

Carbohydrates: Carbohydrates is the class of foods that are likely to be eaten in excess. They are easy to get, are filling, and tend to be satisfying (like desserts). They are an energy source that eventually gets broken down into sugar. There are complex and simple sugars. Simple sugars are found in fruit and fruit products, white and brown sugar, maple syrup, and honey. These simple sugars increase insulin release. Carbohydrates are the main reason for the late night craving for sweets that occurs for so many individuals. Because of its fiber content, fruit, however, does have the advantage of being broken down in the stomach, with the sugar released over time. However, fruit should not be overeaten, since it does contain, in some cases, a large amount of fructose, a type of sugar. Complex carbohydrates provide the advantage of fiber, but too many complex carbohydrates are not good for the metabolism. Carbohydrates should come from vegetables.

Fats: Fats are an important part of the diet. Americans eat poor sources of dietary fat for the most part. Most of the fats come from margarine, partially hydrogenated oils, or oils that have been commercially heated. Monounsaturated fats, such as olive oil, benefit by helping to control cholesterol. The use of omega-3 fatty acids, especially from vegetable sources (flax seed), can provide benefits. Because of the shortage of quality oils in the diet, most people actually need more essential fatty acids, in particular, the omega-3 fatty acids. These fatty acids are important as anti-inflammatories, for the health of nerve tissue, as well as being key nutrients for the health of every cell in the body.

Exercise: Along with diet, exercise is the most important step diabetics can take toward blood sugar control. Today, there is more stress and less physical activity than even a generation ago. Exercise can decrease the risk for heart problems in diabetic patients. Regular exercise can improve heart and lung health, make insulin work better, and increase HDL cholesterol while decreasing LDL cholesterol. (63) Exercise also helps to regulate blood sugar. At a minimum, diabetics should get 30 minutes of some form of exercise at least four days a week, but more would be beneficial. Anyone who is over 40, or a brittle diabetic, and has not been exercising, should check with their health care professional before starting any exercise program.

References

  1. Porth CM. Pathophysiology. Philadelphia: JB Lippincott Co; 1990.
  2. View Abstract: Tuomilehto J, Wolf E. Primary prevention of diabetes. Diabetes Care. Mar1987;10(2):238-48.
  3. Brindley DN. Introduction: Perspective on molecular mechanisms of insulin action. Canadian Journal of Diabetes Care. 1998;22(3s):31s.
  4. View Abstract: Legato MJ. Gender specific aspects of obesity. J Fertil. May1997;42:184-97.
  5. Freeman Clark JB, Queener SF, Burke Karb V. Pharmacologic Basis of Nursing Practice. St. Louis: Mosby; 1993.
  6. View Abstract: Mudaliar S, Edelman SV. Insulin therapy in type 2 diabetes. Endocrinol Metab Clin North Am. Dec2001;30(4):935-82.
  7. Studies presented at the Annual Scientific Sessions of the American Diabetes Association. San Francisco, CA. 1996.
  8. View Abstract: Vincent JB. Mechanisms of chromium action: low-molecule-weight chromium-binding substance. J Am Coll Nutr. 1999;18(1):6-12.
  9. View Abstract: Anderson RA. Chromium as an essential nutrient for humans. Reg Tox Pharmacol. 1997;26:S35-S46.
  10. View Abstract: Saner G. Urinary chromium excretion during pregnancy and its relationship with intravenous glucose loading. Am J Clin Nutr. Sep1981;34(9):1676-9.
  11. Evans GW. The effect of chromium picolinate on insulin controlled parameters in humans. Int J Biosocial Med Research. 1989;11(2):163-80.
  12. View Abstract: Ghosh D, Bhattacharya B, Mukherjee B, et al. Role of chromium supplementation in Indians with type 2 diabetes mellitus. J Nutr Biochem. Nov2002;13(11):690-697.
  13. View Abstract: Stearns DM, et al. Chromium (III) picolinate produces chromosomal damage in chinese hamster ovary cells. FASEB J. 1995;9(15):1643-8.
  14. View Abstract: Elamin A, et al. Magnesium and insulin-dependent diabetes mellitus. Diabetes Res Clin Pract. 1990;10(3):203-9.
  15. View Abstract: Lal J, Vasudev K, Kela AK, Jain SK. Effect of oral magnesium supplementation on the lipid profile and blood glucose of patients with type 2 diabetes mellitus. J Assoc Physicians India. Jan2003;51:37-42.
  16. View Abstract: Tosiello L. Hypomagnesemia and diabetes mellitus: a review of clinical implications. Arch Int Med. 1996;156(11):1143-8.
  17. View Abstract: Brichard SM, et al. The role of vanadium in the management of diabetes. Trends Pharmacol Sci. 1995;16(8):265-70.
  18. View Abstract: Orvig C, et al. Vanadium compounds as insulin mimics. Met Ions Biol Syst. 1995;31:575-94.
  19. View Abstract: Poucheret P, et al. Vanadium and diabetes. Mol Cell Biochem. 1998;188(1,2):73-80.
  20. View Abstract: Cam MC, et al. Partial preservation of pancreatic beta cells by vanadium: evidence for long-term amelioration of diabetes. Metabolism. 1997;46(7):769-78.
  21. View Abstract: Boden F, et al. Effects of vanadyl sulfate on carbohydrate and lipid metabolism in patients with non-insulin dependent diabetes mellitus. Metabolism. 1996;45(9):1130-5.
  22. View Abstract: Cohen N, et al. Oral vanadyl sulfate improves hepatic and peripheral insulin sensitivity in patients with non-insulin dependent diabetes mellitus. J Clin Invest. 1995;95(6):2501-9.
  23. View Abstract: Suzuki YJ, Aggarwal BB, Packer L. Alpha-lipoic acid is a potent inhibitor of NF-kappa B activation in human T cells. Biochem Biophys Res Commun. Dec1992;189(3):1709-15.
  24. View Abstract: Nagamatsu M, et al. Lipoic acid improves nerve blood flow, reduces oxidative stress, and improves distal nerve conduction in experimental diabetic neuropathy. Diabetes Care. 1995;18:1160-7.
  25. View Abstract: Khanna S, et al. Cytokine-induced glucose uptake in skeletal muscle: redox regulation and the role of alpha-lipoic acid. Am J Physiol. 1999;276(5 pt 2):R1327-33.
  26. View Abstract: Evans JL, Goldfine ID. Alpha-lipoic acid: a multifunctional antioxidant that improves insulin sensitivity in patients with type 2 diabetes. Diabetes Technol Ther. Sep2000;2(3):401-13.
  27. View Abstract: Ziegler D, et al. Alpha-lipoic acid in the treatment of diabetic peripheral and cardiac autonomic neuropathy. Diabetes. 1997;46(supp2):S62-S66.
  28. View Abstract: Strokov IA, et al. The efficacy of the intravenous administration of the trometamol salt of thioctic (alpha-lipoic) acid in diabetic neuropathy. Zh Nevrol Psikhiatr Im SS Korsakova. 1999;99(6):18-22.
  29. Song MK, et al. Animal prostate extract ameliorates diabetic symptoms by stimulating intestinal zinc absorption in rats. Diabetes Res. 1996;31:157-70.
  30. View Abstract: Tobia MH. The role of dietary zinc in modifying the onset and severity of spontaneous diabetes in the BB Wistar rat. Mol Genet Metab. Mar1998;63(3):205-13.
  31. View Abstract: Gupta R. Oral zinc therapy in diabetic neuropathy. J Assoc Physicians India. Nov1998;46(11):939-42.
  32. View Abstract: Tobia MH. The role of dietary zinc in modifying the onset and severity of spontaneous diabetes in the BB Wistar rat. Mol Genet Metab. Mar1998;63(3):205-13.
  33. View Abstract: Song MK, et al. Effects of bovine prostate powder on zinc, glucose, and insulin metabolism in old patients with non-insulin dependent diabetes mellitus. Metabolism. 1998;47(1):39-43.
  34. View Abstract: Chapkin RS, et al. Dietary Influences of Evening Primrose and Fish Oil on the Skin of Essential Fatty Acid-deficient Guinea Pigs. J Nutr. 1987;117(8):1360-70.
  35. View Abstract: Dutta-Roy AK, et al. Effects of Linoleic and Gamma-linolenic Acids (Efamol Evening Primrose Oil) on Fatty Acid-binding Proteins of Rat Liver. Mol Cell Biochem. 1990;98(1-2):177-82.
  36. View Abstract: Dib A, et al. Effects of Gamma-linolenic Acid Supplementation on Pregnant Rats Fed a Zinc-deficient Diet. Ann Nutr Meta. 1987;31(5):312-19.
  37. View Abstract: Takahashi R, et al. Evening Primrose Oil and Fish Oil in Non-Insulin-Dependent-Diabetes. Prostaglandins Leukot Essent Fatty Acids. 1993;49(2):569-71.
  38. View Abstract: Stevens EJ, et al. Essential Fatty Acid Treatment Prevents Nerve Ischaemia and Associated Conduction Anomalies in Rats with Experimental Diabetes mellitus. Diabetologia. 1993;36(5):397-401.
  39. View Abstract: Cameron NE, et al. Metabolic and Vascular Factors in the Pathogenesis of Diabetic Neuropathy. Diabetes. 1997;46 (Supp 2):S31-S37.
  40. Jamal GA, et al. Gamma-Linolenic Acid in Diabetic Neuropathy. Lancet. May1986:1098.
  41. View Abstract: Keen H, et al. Treatment of Diabetic Neuropathy with Gamma-linolenic Acid. The gamma-Linolenic Acid Multicenter Trial Group. Diabetes Care. Jan1993;16(1):8-15.
  42. View Abstract: Jack AM, Keegan A, Cotter MA, Cameron NE. Effects of diabetes and evening primrose oil treatment on responses of aorta, corpus cavernosum and mesenteric vasculature in rats. Life Sci. Sep2002;71(16):1863-77.
  43. Srivastava Y, et al. Hypoglycemic and Life-prolonging Properties of Gymnema sylvestre Leaf Extract in Diabetic Rats. Isr J Med Sci. Jun1985;21(6):540-42.
  44. View Abstract: Okabayashi Y, et al. Effect of Gymnema sylvestre, R.Br. On Glucose Homeostasis in Rats. Diabetes Res Clin Pract. May1990;9(2):143-48.
  45. View Abstract: Baskaran K, et al. Antidiabetic Effect of a Leaf Extract from Gymnema Sylvestre in Non-insulin-dependent Diabetes Mellitus Patients. J Ethnopharmacol. Oct1990;30(3):295-300.
  46. View Abstract: Shanmugasundaram ER, et al. Use of Gymnema sylvestre Leaf Extract in the Control of Blood Glucose in Insulin-dependent Diabetes Mellitus. J Ethnopharmacol. Oct1990;30(3):281-94.
  47. View Abstract: Shanmugasundaram ER, et al. Use of Gymnema sylvestre Leaf Extract in the Control of Blood Glucose in Insulin-dependent Diabetes Mellitus. J Ethnopharmacol. Oct1990;30(3):281-94.
  48. View Abstract: Shanmugasundaram ER, et al. Possible Regeneration of the Islets of Langerhans in Streptozotocin-Diabetic Rats Given Gymnema sylvestre Leaf Extracts. J Ethnopharmacol. Oct1990;30(3):265-79.
  49. View Abstract: Shimizu K, et al. Suppression of Glucose Absorption by Extracts From the Leaves of Gymnema inodorum. J Vet Med Sci. Sep1997;59(9):753-57.
  50. View Abstract: Brala PM, et al. Effects of Sweetness Perception and Caloric Value of a Preload on Short Term Intake. Physiol Behav. Jan1983;30(1):1-9.
  51. View Abstract: Preuss HG, et al. Comparative Effects of Chromium, Vanadium and Gymnema sylvestre on Sugar-Induced Blood Pressure Elevations in SHR. J Am Coll Nutr. Apr1998;17(2):116-23.
  52. View Abstract: Preuss HG, Bagchi D, Bagchi M, Rao CV, Dey DK, Satyanarayana S. Effects of a natural extract of (-)-hydroxycitric acid (HCA-SX) and a combination of HCA-SX plus niacin-bound chromium and Gymnema sylvestre extract on weight loss. Diabetes Obes Metab. May2004;6(3):171-80.
  53. View Abstract: Zhu ZJ, et al. Studies on the active constituents of Momordica charantia L. Yao Hsueh Hsueh Pao. 1990;25(12):898-903.
  54. View Abstract: Khanna P, et al. Hypoglycemic Activity of Polypeptide-P From a Plant Source. J Nat Prod. Nov1981;44(6):648-655.
  55. View Abstract: Lee-Huang S, et al. Anti-HIV and Anti-Tumor Activities of Recombinant MAP30 From Bitter Melon. Gene. Aug1995;161(2):151-156.
  56. View Abstract: Leatherdale BA, et al. Improvement in Glucose Tolerance Due to Momordica Charantia (Karela). Br Med J(Clin Res Ed). Jun1981;282(6279):1823-1824.
  57. View Abstract: Welihinda J, et al. Effect of Momordica Charantia on the Glucose Tolerance in Maturity Onset Diabetes. J Ethnopharmacol. Sep1986;17(3):277-282.
  58. View Abstract: Ng TB, et al. Insulin-Like Molecules in Momordica Charantia Seeds. J Ethnopharmacol. Jan1986;15(1):107-117.
  59. View Abstract: Sarkar S, et al. Demonstration of the Hypoglycemic Action of Momordica Charantia in a Validated Animal Model of Diabetes. Pharmacol Res. Jan1996;33(1):1-4.
  60. View Abstract: Platel K, et al. Effect of Dietary Intake of Freeze Dried Bitter Gourd (Momordica charantia) in Streptozotocin Induced Diabetic Rats. Nahrung. 1995;39(4):262-8.
  61. View Abstract: Ali L, et al. Studies on Hypoglycemic Effects of Fruit Pulp, Seed, and Whole Plant of Momordica charantia on Normal and Diabetic Model Rats. Planta Med. Oct1993;59(5):408-12.
  62. View Abstract: Baum CL, Brown M. Low-fat, high-carbohydrate diets and atherogenic risk. Nutr Rev. May2000;58(5):148-51.
  63. View Abstract: Lehmann R, et al. Impact of physical activity on cardiovascular risk factors in IDDM. Diabetes Care. 1997;20(10):1603-11.