Articles

Diabetes Mellitus, Type 1

Introduction

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 historical text as “the melting down of flesh into urine." Diabetes mellitus is a chronic condition of insufficient insulin availability in relation to need. This can represent an absolute insulin deficiency, impaired insulin secretion, defective insulin receptors on target cells, 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.

Insulin is a hormone produced in the pancreas by the beta cells in the Islets of Langerhans. Insulin secretion is regulated by blood glucose levels. It is responsible for transporting glucose (from carbohydrates) into the cells to fuel cellular metabolism and energy production. After a meal, when blood sugar increases, insulin levels rise. Between meals, when blood sugar is low, insulin levels remain low. Insulin is secreted from the pancreas directly into the liver where some is utilized and some is degraded. The rest is released into the general circulation. By facilitating the transport of glucose into the cells, insulin reduces blood sugar. Insulin also decreases the catabolism of fat stores and stimulates triglyceride synthesis. Insulin is involved in the active transport of amino acids into the cell, increasing protein synthesis. The growth and development of children is dependent on insulin.

Diabetes can affect people of any age. It increases the risk of chronic, debilitating conditions, including cardiovascular disease, retinopathy and blindness, peripheral neuropathies, vascular insufficiency and amputation, immune deficiencies, skin ulceration and wound healing disturbances, and kidney disease. The discovery of insulin in the early 20th century has afforded much progress in the diagnosis and treatment of the disease.

Diabetes is diagnosed when there is a fasting plasma glucose (FPG) of greater than 126mg/dL, or a two-hour plasma glucose (OGTT – oral glucose tolerance test) of greater than 200mg/dL. There are two forms of diabetes mellitus recognized today: type 1 (formerly referred to as IDDM, insulin dependent diabetes mellitus, or juvenile onset) and type 2 (previously called NIDDM, non-insulin dependent diabetes, or adult onset).

Type 1 diabetes is a condition in which the pancreatic beta cells fail to secrete insulin. This is known as an absolute insulin deficiency, characterized by hyperglycemia and the breakdown of fats and protein in order to meet the energy demands of the body. The catabolism of fats and protein predisposes insulin dependent diabetics to an accumulation of ketone bodies and subsequent ketoacidosis. Insulin dependent diabetics require a continuous supply of insulin to prevent ketoacidosis and maintain a stable blood sugar concentration.

Type 1 diabetes typically occurs in people younger than 30 years of age. It is thought that the disease is a caused by a genetic predisposition for an abnormal immune response to beta cells in the Islets of Langerhans. Islet cell antibodies have been detected in 60-95 percent of persons with type 1 diabetes. (2) Some of the potential triggers to this autoimmune response include Coxsackie virus, vaccination, other viral loads, and fungal mycotoxins.

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.

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 11,000 people in New Zealand have Type 1 diabetes.

Persatuan Diabetes Malaysia, 2007.

  • There are an estimated 24,000 people with type 1 diabetes in Malaysia today.

National Diabetes Information Clearinghouse, National Institute of Health. 2002.

  • Type 1 Diabetes accounts for 5 to 10% of all diabetes cases in the US
  • One in every 400 to 500 children and adolescents has type 1 diabetes

Signs and Symptoms

[span class=alert]The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.[/span]

Initial symptoms of diabetes include frequent urination, thirst, weight loss despite increased appetite, fatigue and irritability. Dizziness, lethargy, irritability, loss of coordination and perspiration are marked during hypoglycemic episodes (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.

Diabetic coma, or ketoacidotic coma, is a life threatening complication of type 1 diabetes. As the plasma becomes hyperosmolar, water is transported from the tissues. Severe water and electrolyte imbalances occur. Symptoms include abdominal pain, nausea, vomiting and shortness of breath (Kussmaul breathing). Signs include flushing, absent reflexes and acetone breath.

General

  • Frequent urination
  • Thirst
  • Weight loss despite increased appetite
  • Fatigue
  • Irritability
  • Hypoglycemic episodes
  • Hyperglycemia

Treatment Options

Conventional

Treatment goals for diabetes include avoiding the acute consequences of hyperglycemia, avoiding hypoglycemia, and minimizing, delaying, or avoiding the long-term complications of the disease. Positive treatment results should approximate the non-diabetic state as closely as possible. Therapy should be individualized to meet the unique patient condition. It is important to realize that the disease will progressively worsen throughout the patient’s lifetime, and that the treatment plan may need to be modified to control blood sugar levels and avoid other health problems.

The treatment of diabetes is directed at maintaining adequate insulin levels to control blood sugar. Along with a program of a healthy diet and exercise, insulin is the therapy of choice for the patient with type 1 diabetes. Intensive glucose control is the cornerstone of type 1 diabetes treatment including self-monitoring of blood glucose to minimize the risk of future complications.

Insulin is composed of two amino acid chains, A (acidic) and B (basic), joined together by disulfide linkages. All commercially available insulins are derived from animal or biosynthetic sources. Animal-derived products are being phased out, although a few purified pork insulins are still available. Human insulin is a biosynthetic product produced through recombinant DNA technology using a nonvirulent strain of E. coli or baker’s yeast. Insulin analogs, lispro and aspart, are also available. They are prepared by recombinant DNA technology and distinguished from human insulin by the reversal of two amino acids, lysine and proline (in the lispro product) and aspartic acid for proline (in the aspart product).

Insulin is administered by subcutaneous injection in a highly individualized dosing regimen to achieve glucose control. Insulin must be injected because it is a protein and can be digested in the GI tract. Insulin can be measured and injected via the traditional insulin syringe or with a pen-injection system. Insulin administration by continuous subcutaneous infusion pumps is an alternative to multiple daily injections. The following list summarizes the various insulin formulations currently on the market.

Commercially Available Insulin Formulations
Rapid-acting
Human Insulin Lispro
Human Insulin Aspart

Short-acting
Human Insulin (rDNA)
Pork Purified Insulin

Intermediate-acting
Isophane Human Insulin (rDNA)
Pork Purified Isophane Insulin
Human Insulin Zinc Suspension (rDNA)
Pork Purified Insulin Zinc Suspension

Long-acting
Human Insulin Zinc Suspension (rDNA), Extended
Insulin Glargine

Human Insulin (rDNA) Mixtures
Isophane Insulin + Insulin 50/50
Isophane Insulin + Insulin 70/30
Insulin Lispro + Protamine 0.19mg (50/50 Mix)
Insulin Lispro + Protamine 0.28mg (75/25 Mix)

Nutritional Supplementation


Chromium

The influence of chromium on blood sugar regulation was first recognized in animal studies in the 1950s. In the 1970s, chromium’s importance was discovered in TPN solutions. When TPNs void of chromium were administered over a period of months, insulin resistance and elevated blood sugar levels appeared in patients. Chromium was added and blood sugar levels in TPN patients returned to normal. Various studies support that chromium has a positive effect on blood glucose levels, and recent studies report that chromium may positively impact hemoglobin A1c as well. (3)

It is thought that chromium facilitates insulin by activating the protein kinase molecules in receptor cells, therefore enhancing the uptake of glucose and other nutrients. (4) By aiding insulin utilization in the body, chromium helps to maintain muscle mass during hypocaloric dietary intake, stabilizing the basal metabolic rate. Because of the influence of insulin on thyroid hormone conversion, it has a lowering effect on cholesterol and triglycerides. By improving insulin regulation, chromium may also reduce hunger and limit food cravings. Insulin is involved in the regulation of the hypothalamic satiety center. Improving insulin response should improve satiety signals. Insulin is also vital in serotonin synthesis, a neurotransmitter linked to the craving for carbohydrates.

Several groups are at risk for reduced chromium levels. First of all, most Americans are at risk because of a diet rich in refined sugars. Individuals who eat diets high in refined sugars tend to excrete 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 incidence of diabetes and atherosclerosis. People who exercise regularly excrete two to six times the normal amount of chromium in their urine on days of exercise. (5) Many athletes compound this problem with high-carbohydrate supplements. The elderly also tend to be at risk due to reduced absorption and inadequate intake of chromium. It is interesting to note that women tend to have a drop in chromium levels during the third trimester of pregnancy. (6)

There is a great deal of controversy over what is the best chromium to use. Chromium is biologically active only in the trivalent state in which it forms complexes with organic compounds. The most important of these complexes is glucose tolerance factor (GTF), which is comprised of trivalent chromium, niacin, glycine, glutamic acid, and cysteine. Dr. Walter Mertz of the United States Department of Agriculture researched GTF chromium. He found that chromium was a crucial part of the binding complex that allowed insulin to attach to cells. Organically bound GTF chromium is thought to be safe and well tolerated.

Chromium picolinate is another popular form of chromium that has clinical support for blood sugar regulation. (7) The majority of evidence points to the safety of the picolinate form. A recent study in lab animals reported different findings. Researchers at Dartmouth College and The George Washington Medical Center discovered that exposing ovarian cells of laboratory animals to certain doses of chromium picolinate resulted in chromosomal damage. (8) More information is needed before any true conclusion can be drawn regarding this supplement, in light of the fact that there have been studies reporting safety and efficacy.

For diabetics, adding chromium or other blood sugar regulating agents to their supplement list should be done gradually, especially if they are currently controlled on medication. With lifestyle and dietary changes, there may not be a need for an aggressive chromium dosage. If another agent is being used, its complementary activity may allow for a reduced dose of chromium.


Magnesium

Magnesium is involved in glucose metabolism and insulin secretion. (9) It is well documented that low magnesium may aggravate diabetic conditions. (10) Hypomagnesemia occurs in approximately 25 percent of diabetic patients and has been reported in type 1 diabetics. (11) Many Americans tend to be below the RDA for magnesium intake by 70-80mg. Many experts feel that the RDA for magnesium needs to be significantly increased from the current level of 350mg to as much as 700mg per day.


Vanadium

Vanadium is a trace mineral essential for plant nutrition, but its role in human nutrition remains unclear. It is a known co-factor in enzymatic functions. High concentrations of vanadium are found in the kidneys, liver, and bone. Fat cells temporarily store vanadium for quick release into the body. Supplementation with vanadyl sulfate and other vanadium compounds has been reported to markedly improve a number of clinical measures of diabetes. It appears that vanadium mimics the effects of insulin, resulting in decreased gluconeogenesis, an increase in the activity of glycolytic enzymes, and an increase in glycogen production. (12) , (13)

Animal studies have demonstrated that vanadium administered to diabetic rats restores elevated blood glucose to normal ranges. Subsequent studies have reported that vanadyl sulfate not only lowers blood glucose in diabetic animals, but cholesterol and triglycerides as well. (14) Furthermore, the hypoglycemic effect of vanadium may have a sustained effect. In one study, diabetic rats remained euglycemic for as long as 20 weeks after withdrawal from treatment, indicating that vanadium may exert a protective role over the pancreatic beta cells. (15)

Vanadium pentoxide and vanadyl sulfate are active, absorbable forms of vanadium.


Alpha-Lipoic Acid (ALA)

Alpha-lipoic acid (ALA) is an antioxidant substance produced 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 has been recognized recently for its role in cardiovascular disease, as well as a potential adjunctive therapy for AIDS patients. (16) Alpha-lipoic acid has also demonstrated a positive effect on insulin and blood sugar metabolism for type 1 diabetics. (17) ALA reportedly improved glucose metabolism in insulin-resistant skeletal muscle in one study, indicating its potential in restoring glucose availability. (18)

ALA may also be a promising antihyperglycemic agent for diabetics who suffer glucose overproduction by inhibiting hepatic fatty acid oxidation and gluconeogenesis. (19) In addition, ALA’s antioxidant properties are reportedly effective in the treatment of diabetic neuropathy. (20) In a recent single blind, placebo-controlled study, 97.5 percent of diabetic subjects treated with a 200 ml intravenous solution daily for three weeks reported an improvement of neuropathy symptoms. The response rate of the control group was 40 percent. (21) These mechanisms are enhanced over several weeks of intake and can be used in conjunction with other glycemic agents.


Zinc

Zinc deficiency is associated with a number of metabolic disorders, including impaired glucose tolerance, insulin degradation, decreased insulin potency, and reduced pancreatic insulin content. (22) In clinical studies, diabetic animals and humans with zinc deficiencies have demonstrated improved glucose tolerance when supplemented with zinc. (23) , (24) Zinc plays a role in the regulation of insulin production by the pancreas and glucose utilization by muscle and fat cells. Zinc also serves as a component in glucose transport and in gene expression of insulin receptors.


Vitamin E

Although vitamin E does not directly treat this condition, it is an extremely important substance to help reduce the cardiovascular complications that are so common in this patient population. In a double-blind trial, patients with type 1 diabetes who took 250 IU of vitamin E three times daily for one year experienced a 30% to 60% decline in the production of thiobarbituric acid-reactive substances (TBARS). This represents a significant reduction in the peroxidizability of LDL and VLDL lipoproteins. Based on these results, the authors of this study stated that, "life-long supplementation with vitamin E should be considered in patients with type 1 diabetes." (25) In an 8-month randomized double-blind placebo-controlled crossover study, 36 patients and 9 healthy subjects were evaluated. The results suggest that vitamin E supplementation may reduce the risks for developing diabetic retinopathy and/or nephropathy in patients with type 1 diabetes. (26)


Vitamin C

Individuals with type 1 and type 2 diabetes were found to have significantly lower levels of serum ascorbic acid compared to controls. These results suggest that the difficulty diabetics have in preventing oxidative damage may be due to lower ascorbic acid concentrations. (27) Another study reported finding that patients with type 1 diabetes have approximately a 50% reduction in ascorbic acid tissue storage capabilities. It is suggested that this may cause intracellular scurvy, which contributes to the chronic degenerative afflictions that commonly develop in patients with diabetes. (28)


Cyclo (His-Pro)

Cyclo hispro, a thyrotropin releasing hormone metabolite, is thought to be a useful agent in improving blood sugar regulation. (29) Cyclo hispro has potential for individuals with hypoglycemia, diabetes, and impaired glucose tolerance (IGT). It has been documented that individuals with diabetes have impaired intestinal zinc absorption and low plasma zinc levels. Both animal and human studies suggest that this extract influences intestinal zinc absorption mechanisms. Zinc deficiency has been associated with reduced pancreatic insulin content, decreased insulin potency, IGT, and increased insulin degradation. (30) This extract not only contains high levels of zinc, but also several cofactors reported to stimulate intestinal zinc absorption.

Improving zinc utilization is important because it plays a role in over 300 different enzymatic functions. Most importantly for the diabetic, it is involved in wound healing, immune function, and skin integrity.

Herbal Supplementation


Evening Primrose

Evening primrose oil (EPO) is rich in gamma-linolenic acid which is an omega-6 fatty acid. (31) , (32) Omega-6 fatty acids reportedly reduce the arachidonic acid cascade and decrease inflammation through inhibiting the formation of inflammatory mediators in this process. Supplementation with essential fatty acids such as EPO has been reported to prevent zinc deficiency, thereby potentially improving immunity. (33) Fatty acids are an important part of normal homeostasis. The human body can produce all but two fatty acids - omega-3 and omega-6 fatty acids. Both must be obtained through the diet or by the use of supplements. Obtaining a balance of these two fatty acids is essential. Essential fatty acids are needed for building cell membranes, and are precursors for production of hormones and prostaglandins. Modern diets tend to be lacking in quality sources of fatty acids.

Diabetics who do not convert linoleic acid to gamma-linolenic acid will need a quality source of GLA. (34) , (35) This is said to be essential for proper nerve function and for the prevention of diabetic neuropathy. (36) , (37) Evening primrose oil was reported to be beneficial in effecting the course of diabetic neuropathy by decreasing microvascular problems associated with diabetes. (38)


Gymnema

Gymnema is a rain forest vine found in Central and Southern India, which has a long tradition in the treatment and management 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." Gymnema is gaining popularity with clinicians utilizing natural therapy protocols in the management of diabetes, hyperinsulinemia, and impaired glucose tolerance. The leaves of gymnema are thought to increase insulin secretion, and several studies report control of hyperglycemia in moderately diabetic laboratory animals. (39) , (40) A decrease in body weight was also reported. Gymnema reportedly produced blood glucose homeostasis and increased the activity of the enzymes involved in the utilization of glucose by insulin dependent pathways. (41)

Human studies have reported a significant reduction in blood glucose during therapy with gymnema. (42) , (43) A reduction in glycosylated hemoglobin and glycosylated plasma proteins has also been reported, with a reduction in conventional drug dosage. In studies, patients with diabetes were able to discontinue conventional drugs and maintain their blood glucose homeostasis with gymnema alone. (44) Other studies report that gymnemic acids suppress the elevation of blood glucose levels by inhibiting glucose uptake in the intestine. (45)

Gymnema has also been reported to selectively suppress the neural responses to sweet taste stimuli. (46) , (47) , (48) Because gymnema leaf powder has an anesthetizing effect on the taste buds which can last for several hours, some researchers feel that gymnema may be a potential agent in weight reduction and sweet cravings. (49) A recent study reports significant serum cholesterol lowering effects of gymnema. (50) Gymnema may potentially be used in athletes to develop a higher ratio of lean muscle mass to body fat. This may be due to the reported increase of insulin output associated with long-term use of gymnema. Increased insulin output and utilization encourages the uptake of amino acids into muscle tissue. Another study found that gymnema was effective and safe for the reduction of excess weight, BMI and also promoted healthy blood lipid levels. (51)


Bitter Melon

Bitter melon or karela fruit has long been used in South American and the Orient as not only a food but also as a febrifuge, abortifacient, emmenagogue, vermifuge, antiviral, emetic, anthelmintic, and antidiabetic agent among other uses. (52) Recent studies have focused on the beneficial properties of the fruit in diabetes and hyperinsulinemia, HIV viral infection, and certain cancers. (53) , (54)

Bitter melon has been reported to significantly improve glucose tolerance in humans. (55) , (56) The currently accepted hypotheses regarding hypoglycemic activity is claimed to be mediated through an insulin secretagogue effect, or through an influence on enzymes involved in glucose metabolism. (57) Research indicates that molecules with insulin-like bioactivity may be present in bitter melon seeds. (58) A few studies suggest that the hypoglycemic mechanism of action of bitter melon could be partly attributed to increased glucose utilization in the liver rather than an insulin secretion effect. (59) A recent laboratory study reported a significant reduction of fasting blood glucose levels observed in diabetic rats, but no hypoglycemic activity in the treated normal rats. (60) Bitter melon also demonstrated considerable lowering of serum cholesterol and triglycerides in the treated diabetic group. There was a significant improvement in hepatic glycogen level in treated diabetic rats, with a return of close to normal levels after the treatment with bitter melon. There have been negative reports as to the ability of bitter melon extracts to lower blood sugar levels in laboratory animals. (61) , (62) It is recommended that a standardized extract of bitter melon always be used.

Diet & Lifestyle

Diet: Diabetes and obesity have increased significantly 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 initially, it is not a long-term answer. Carbohydrates alone are not the culprit, 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 intake.

There are several ways to support and potentially improve insulin regulation through natural agents, but the real key is to modify the dietary selection of foods. In general, the American diet consists 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 adequate sources of 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, it is apparent that there is a continual demand for more insulin production. The average person drinking two “big gulp" drinks a day is receiving approximately 54 teaspoons of sugar. Using diet drinks does not work either because of their sodium content. This is particularly a problem for diabetics with hypertension. While current research shows that dietary fat and cholesterol are definite problems, this situation is compounded by the continuous, elevated intake of carbohydrates simultaneously with fats. Dietary fat is stored under the influence of excessive insulin release during a repeated high-carbohydrate load.

Many experts over the years have acclaimed the low-fat, high-carbohydrate diet. The problem with this diet has been that it does not result in weight loss. In fact, excessive carbohydrate intake has been linked to elevated LDL cholesterol and triglycerides. (63) This conclusion makes sense when realizing what mechanisms are involved metabolically under a continuous high-carbohydrate load. The other deceiving aspect is that many prepared foods may be labeled low fat, but are loaded with refined sugars, which aggravate the insulin response mechanism, and therefore, fat storage.

The obvious first step is to eat foods that will least aggravate insulin response. This will not only benefit the diabetic, but many individuals wanting to lose weight will notice a positive effect 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 insulin blood sugar regulation, since this is the most difficult aspect of controlling blood sugar. Foods that do not cause a rapid rise in blood sugar will not aggravate the insulin response. For example, in the past, it was thought that all complex carbohydrates were equal. It is now known that different grains have varying glycemic responses. It is valuable to consider the glycemic index when looking at foods that contain varying amounts of carbohydrates. Proteins and fats have virtually no glycemic factor.

Legumes: Virtually 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. The most prominent of these are white potatoes (baked), carrots, beets, and turnips. However, if an individual is eliminating other sources of refined sugar in the diet and is reducing the amount of complex carbohydrates (breads and pastas), he/she should be able to use these vegetables with moderation.

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

Fruits: Fruits are generally in the middle of the road in terms of glycemic index, but dried fruits, which are concentrated, rank higher. Drinking fruit juices will definitely aggravate blood sugar response and is known to contribute to triglyceride response. 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 are also acceptable alternatives. There is some evidence that aspartame may aggravate insulin resistance over time.

Grains: Many of the grain sources 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 slow 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 levels and aids in the prevention of colon cancer and diverticulitis. Most individuals with diabetes/insulin resistance do not realize that they run a 75 percent risk of developing atherosclerosis. Reducing cholesterol levels through 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 digestive tract that allows for a food to be held longer, resulting in a slow rise in blood sugar. This type of fiber also aids in lowering 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 a vital part of every individual’s diet. It is needed for the growth and rebuilding of tissues. Proteins are made of amino acids. These amino acids are absorbed through the small intestine and distributed as needed. The body can manufacture most amino acids, but there are eight essential amino acids that must be obtained through the diet. These eight can best be found in sources such as eggs, poultry, fish, and meat. Nuts, seeds, legumes, and grains can provide some of these essential amino acids as well. For the sedentary individual, an average of about 0.8 grams/kilogram body weight is normal; for the more active individual or aerobic enthusiast, 1.2 grams/kilogram may be needed. For the individual who engages in anaerobic or weight or strength-related exercises, as much as 1.7 to 1.8 grams/kilogram body weight may be needed. Protein intake is invaluable for tissue healing and maintaining anabolic function in the body.

Carbohydrates: Carbohydrates is the class of foods that tend to be overconsumed. They are easy to obtain, are filling, and tend to be gratifying (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 definitely tend to aggravate insulin response. Carbohydrates are the main fuel for serotonin production and a principle 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. Complex carbohydrates provide the advantage of fiber, but too many complex carbohydrates, especially the high glycemic index ones, will have a negative effect on metabolism. Significant carbohydrate intake should come from vegetable sources.

Fats: Fats are an essential 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 and are oxidized. 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 are actually deficient in essential fatty acids. In particular, the omega-3 fatty acids seem to be an issue. These fatty acids are important as regulators of inflammatory pathways and for the health of nerve tissue, as well as being key nutrients for the health of every cell in the body.

Exercise: Along with dietary responsibility, exercise is the most important step diabetics can take toward tighter blood sugar control. Today, there is more stress and less physical activity than even a generation ago. As Diabetes Care recently reported, exercise improves cardiovascular risk in diabetic patients. Regular exercise improved cardio-respiratory endurance, insulin sensitivity, and HDL cholesterol, while decreasing LDL cholesterol levels. (64) Of course, it is well established that exercise also helps to regulate blood sugar levels. 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 seek medical advice and supervision before initiation of any exercise program.

Clinical Lab Assessment

Some of the following laboratory testing can provide information necessary for diagnosis and treatment. In addition, the tests listed may also give insight to functional metabolism and functional nutrient status in the body.

Organic Acids

Organic acids analysis is a useful method for measurement of biochemical intermediates in urine. These intermediates can offer information about key enzyme functions and nutrient competence (amino acids, nutrient cofactors, minerals and fatty acids). Several examples can be cited:

    Elevations of pyruvate, lactate, á-hydroxybutyrate, and â-hydroxybutyrate indicate impairment in enzyme functions relative to carbohydrate metabolism.

    Elevation of tricarballylate suggests functional magnesium deficiency, which can impact glycemic response mechanisms due to bacterial pathogens.

    Elevation of vanilmandelate reflects elevations in epinephrine, an aggressive antagonist of insulin.

    Detoxication and dysbiosis markers in organic acids suggest the relative competence of the liver and gastrointestinal tract to detoxify insulin, a critical process in carbohydrate metabolism.

Fructosamine

This is a measure of glycosylated serum proteins (primarily albumin) implicated in the formation of glycosylated hemoglobin. Because albumin has a circulatory half-life of 20 days, the amount of fructosamine reflects hyperglycemic periods within the previous few weeks. Thus, blood or urine glucose provides information about immediate diabetic control, fructosamine about short-term control, and HbA1c about long-term control.

Glucose

High blood glucose is suggestive of type 1 insulin-dependent diabetes mellitus (IDDM). Type 2 non-insulin-dependent diabetes mellitus (NIDDM) is often associated with a lower glucose, but with an increased fasting insulin level in serum. Blood glucose levels vary in response to food intake, stress, physical exertion, and various disorders. Elevations of serum glucose should lead to confirmatory testing such as fasting insulin, serum phosphorus, magnesium, hemoglobin A1c, and/or fructosamine.

Glucose Tolerance Test (GTT)

This evaluation is sometimes employed when a diagnosis is uncertain. The GTT can be performed with an oral glucose load, or in cases where gastrointestinal absorption may be variable (gastroenterostomy, thyrotoxicosis, or sprue and other malabsorption syndromes), it can be performed with an intravenous loading dose. Pretreatment with glucocorticoids (e.g., cortisone) can increase the GTT sensitivity; this is known as the Cortisone-Glucose Tolerance Test. Measuring insulin at the same time as glucose can offer significant additional information regarding insulin response, further contributing to a more accurate assessment of function in carbohydrate metabolism. The Glucose-Insulin Tolerance Test (GITT) can be useful in contrasting insulin deficiency with cellular insulin insensitivity abnormalities.

Hemoglobin A1c (glycosylated hemoglobin)

When exposed to high glucose levels, the hemoglobin molecule irreversibly acquires a glucose-derived segment on the beta chain. Elevated HbA1c levels reflect poor diabetic control in the previous three to five weeks. Following the stabilization of glycemic levels, HbA1c levels will return to normal in about three weeks. HbA1c can provide information missed in spot checks of urine or serum glucose. Insulin-sensitive IDDM individuals may have undetected periods of hyperglycemia, alternating with post-insulin periods of normoglycemia or hypoglycemia. Episodic or chronic hemolysis will result in low HbA1c values. Old red cells have higher A1c levels than young cells. Any condition that results in a higher proportion of young RBCs will result in an A1c value that is not necessarily a true reflection of glucose management.

Urine Glucose

Screening of random or postprandial urine specimen for reducing substances is the most widely used and simplest procedure used to diagnose diabetes. Clinitest color reactions are semiquantitative, while glucose oxidase test strips provide a gross assessment of urine glucose. If reducing substances are present, a check for ketone bodies is usually done to determine if diabetic acidosis is present.

Clinical Notes

Dietary changes must be emphasized for the diabetic patient. In addition, there are multiple considerations such as nutrient status for magnesium, essential fatty acids, zinc, and organic acids testing to determine fungal involvement in the gut, circulatory support, antioxidant support, and cardiovascular support. These all need to be considered in addition to suggesting nutritional support for maintaining tighter control of blood sugar. When recommending any agent that may alter blood sugar metabolism, it is best to titrate the dose slowly over a few weeks so that blood sugar regulation is gradually altered.

References

  1. Porth CM. Pathophysiology. Philadelphia: JB Lippincott Co; 1990.
  2. Eisenbarth GS. Type I diabetes mellitus: A chronic autoimmune disease. N Engl J Med. 1986;310:1360.
  3. Studies presented at the Annual Scientific Sessions of the American Diabetes Association. San Francisco, CA. 1996.
  4. View Abstract: Vincent JB. Mechanisms of chromium action: low-molecule-weight chromium-binding substance. J Am Coll Nutr. 1999;18(1):6-12.
  5. View Abstract: Anderson RA. Chromium as an essential nutrient for humans. Reg Tox Pharmacol. 1997;26:S35-S46.
  6. 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.
  7. Evans GW. The effect of chromium picolinate on insulin controlled parameters in humans. Int J Biosocial Med Research. 1989;11(2):163-80.
  8. View Abstract: Stearns DM, et al. Chromium (III) picolinate produces chromosomal damage in chinese hamster ovary cells. FASEB J. 1995;9(15):1643-8.
  9. View Abstract: Elamin A, et al. Magnesium and insulin-dependent diabetes mellitus. Diabetes Res Clin Pract. 1990;10(3):203-9.
  10. 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.
  11. View Abstract: Tosiello L. Hypomagnesemia and diabetes mellitus: a review of clinical implications. Arch Int Med. 1996;156(11):1143-8.
  12. View Abstract: Brichard SM, et al. The role of vanadium in the management of diabetes. Trends Pharmacol Sci. 1995;16(8):265-70.
  13. View Abstract: Orvig C, et al. Vanadium compounds as insulin mimics. Met Ions Biol Syst. 1995;31:575-94.
  14. View Abstract: Poucheret P, et al. Vanadium and diabetes. Mol Cell Biochem. 1998;188(1,2):73-80.
  15. 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.
  16. 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.
  17. 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.
  18. 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.
  19. View Abstract: Khamaisi M, et al. Lipoic acid acutely induces hypoglycemia in fasting nondiabetic and diabetic rats. Metabolism. 1999;48(4):504-10.
  20. 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.
  21. 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.
  22. Song MK, et al. Animal prostate extract ameliorates diabetic symptoms by stimulating intestinal zinc absorption in rats. Diabetes Res. 1996;31:157-70.
  23. 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.
  24. View Abstract: Gupta R. Oral zinc therapy in diabetic neuropathy. J Assoc Physicians India. Nov1998;46(11):939-42.
  25. View Abstract: Engelen W, Keenoy BM, Vertommen J, et al. Effects of long-term supplementation with moderate pharmacologic doses of vitamin E are saturable and reversible in patients with type 1 diabetes. Am J Clin Nutr. Nov2000;72(5):1142-9.
  26. View Abstract: Bursell SE, Clermont AC, Aiello LP, et al. High-dose vitamin E supplementation normalizes retinal blood flow and creatinine clearance in patients with type 1 diabetes. Diabetes Care. Aug1999;22(8):1245-51.
  27. View Abstract: Jennings PE, Chirico S, Jones AF, et al. Vitamin C metabolites and microangiopathy in diabetes mellitus. Diabetes Res. Nov1987;6(3):151-4.
  28. View Abstract: Cunningham JJ, Ellis SL, McVeigh KL, et al. Reduced mononuclear leukocyte ascorbic acid content in adults with insulin-dependent diabetes mellitus consuming adequate dietary vitamin C. Metabolism. Feb1991;40(2):146-9.
  29. 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.
  30. Song MK, et al. Animal Prostate Extract Ameliorates Diabetic Symptoms by Stimulating Intestinal Zinc Absorption in Rats. Diabetes Research. 1996;31:157-70.
  31. 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.
  32. 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.
  33. 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.
  34. 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.
  35. 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.
  36. View Abstract: Cameron NE, et al. Metabolic and Vascular Factors in the Pathogenesis of Diabetic Neuropathy. Diabetes. 1997;46 (Supp 2):S31-S37.
  37. Jamal GA, et al. Gamma-Linolenic Acid in Diabetic Neuropathy. Lancet. May1986:1098.
  38. 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.
  39. 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.
  40. 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.
  41. View Abstract: Shanmugasundaram KR, et al. Enzyme Changes and Glucose Utilization in Diabetic Rabbits: The Effect of Gymnema sylvestre, R.Br. J Ethnopharmacol. Mar1983;7(2):205-34.
  42. 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.
  43. 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.
  44. 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.
  45. 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.
  46. View Abstract: Kamei K, et al. Amino Acid Sequence of Sweet-taste-suppressing Peptide (Gurmarin) from the Leaves of Gymnema sylvestre. J Biochem (Tokyo). Jan1992;111(1):109-12.
  47. View Abstract: Imoto T, et al. A Novel Peptide Isolated from the Leaves of Gymnema sylvestre - I. Characterization and Its Suppressive Effect on the Neural Responses to Sweet Taste Stimuli in the Rat. Comp Biochem Physiol A. 1991;100(2):309-14.
  48. View Abstract: Kurihara Y. Characteristics of Anti-sweet Substances, Sweet Proteins, and Sweetness-inducing Proteins. Crit Rev Food Sci Nutr. 1992;32(3):231-52.
  49. 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.
  50. 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.
  51. 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.
  52. View Abstract: Zhu ZJ, et al. Studies on the active constituents of Momordica charantia L. Yao Hsueh Hsueh Pao. 1990;25(12):898-903.
  53. View Abstract: Khanna P, et al. Hypoglycemic Activity of Polypeptide-P From a Plant Source. J Nat Prod. Nov1981;44(6):648-655.
  54. 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.
  55. 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.
  56. 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.
  57. View Abstract: Platel K, et al. Plant Foods in the Management of Diabetes Mellitus: Vegetables as Potential Hypoglycaemic Agents. Nahrung. Apr1997;41(2):68-74.
  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: Rao BK, et al. Antidiabetic and Hypolipidemic Effects of Momordica cymbalaria Hook. Fruit Powder in Alloxan-diabetic Rats. J Ethnopharmacol. Oct1999;67(1):103-9.
  61. 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.
  62. 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.
  63. View Abstract: Baum CL, Brown M. Low-fat, high-carbohydrate diets and atherogenic risk. Nutr Rev. May2000;58(5):148-51.
  64. View Abstract: Lehmann R, et al. Impact of physical activity on cardiovascular risk factors in IDDM. Diabetes Care. 1997;20(10):1603-11.