Type 2 Diabetes and Its Natural Care

TYPE 2 DIABETES

This page is still under construction....so keep checking back.

There is a lot of information on this page. Some is very technical, some is easy to follow. Take your time to "digest" it all. You may find that you will know more than your doctor about the nutritional side of diabetes. This page will continue to be updated as newer and better options are evaluated. Also, this information will do wonders for your infliction through the natural approach to treating diabetes if it is followed correctly.

ARTICLE #1 Diabetes Mellitus (CMDT)

ARTICLE #2 Eat Whole, Eat Fresh, Eat to Live

ARTICLE #3 Nutrients That Control Blood Sugar

ARTICLE #4 Coconut Oil and Diabetes

ARTICLE #5 Natural Therapy for Type 2 Diabetes

ARTICLE #6 Pedometer Against Glucometer

ARTICLE #7 Glycemic Index

ARTICLE #8 Track Your Blood Sugar

ARTICLE #9 Recipes for Diabetes Type 2

Diabetes Mellitus

CMDT (the technical side)

Type 2 Diabetes represents a heterogeneous group comprising milder forms of diabetes that occur predominantly in adults but occasionally in juveniles. More than 90% of all diabetics in the USA are included under this classification. Circulating endogenous insulin is sufficient to prevent ketoacidosis, but is inadequate to prevent hyperglycemia in the face of increased needs owing to tissue insensitivity. In most cases of this type of diabetes, the cause is "unknown".

Tissue insensitivity to insulin has been noted in most type 2 patients irrespective of weight and has been attributed to several interrelated factors. These include a putative genetic factor, which is aggravated in time by additional enhancers of insulin resistance such as again, a sedentary lifestyle, and abdominal-visceral obesity. In addition, there is an accompanying deficiency in the response of pancreatic Beta cells to glucose. Both the tissue resistance to insulin and the impaired Beta cell response to glucose appear to be further aggravated by increased hyperglycemia, and both defects are ameliorated by treatment that reduces the hyperglycemia toward normal.

In non-obese type 2 patients, there is generally an absent or blunted early phase of insulin release in response to glucose; however, it can be elicited in response to other insulinogenic stimuli such as acute intravenous administration of sulfonylureas, glucagon, or arginine.

Although insulin resistance may be detected with special tests, it does not seem to be clinically relevant to the treatment of most nonobese type 2 patients, who generally respond to appropriate therapeutic supplements such as lipoatrophy or acanthosis nigricans.

Among this heterogeneous subgroup of patients with non-obese type 2 diabetes, the majority are idiopathic. However, with increasing frequency, a variety of etiologic genetic abnormalities have been documented in a subset of these of these patients who have recently been reclassified within a group designated "other specific types". (see chart)

Factors Reducing Response to Insulin

Prereceptive Inhibitors	Anti-insulin antibodies
Receptive Inhibitors	Insulin receptor antibodies "Down-regulation" of receptors by hyperinsulinism: primary hyperinsulinsim (B cell adenoma), Hyperinsulinism secondary to a postreceptor defect (obesity, Cushing's syndrome, acromegaly, pregnancy) or prolonged glycemia (diabetes mellitus, post-glucose tolerance test)
Postreceptive Inhibitors	Poor responsiveness of principal target organs; obesity; hepatics disease; muscle inactivity; sustained hyperglycemia Hormonal excess: glucocorticoids, growth hormone, oral contraceptive agents, progesterone, human chorionic somatomammotropin, catecholamines, thyroxine

Other Specific Types of Diabetes Mellitus

1. Maturity-onset diabetes of the young (MODY) This subgroup is a relatively rare monogenic disorder characterized by non-insulin-dependent diabetes with auotsomal dominant inheritance and an age at onset of 25 years or younger. Patients are non-obese and their hyperglycemia is due to impaired glucose-induced secretion of insulin. Five types of MODY have been described, with single gene defects localized to chromosomes 20, 7, 12, 13, and 17. Except for MODY 2, all types involve mutations of a nuclear transcription factor that regulates islet gene expression.

a. MODY 1 includes 74 members of a pedigree known as the R-W family, who are descendants of a German couple who immigrated to Michigan in 1861. Their extremely rare genetic defect was shown to be a nonsense mutation of a nuclear transcription factor found in liver as well as in pancreatic B cells. This gene has been termed hepatocyte nuclear factor 4 alpha and is found on chromosome 20. How it reduces glucose-induced insulin secretion has not yet been clarified. Six families with mutations of this gene have been reported.

b. MODY 2 has been described in all parts of the world, and at least 26 different mutations of the glucokinase gene on chromosome 7 have been identified. Reduced sensitivity of pancreatic Beta cell glucokinase to plasma glucose causes impaired insulin secretion, resulting in fasting hyperglycemia and mild diabetes. Most of these patients have a benign course without long-term complications and respond will to diet or oral agents.

c. MODY 3 is caused by mutations of the hepatocyte nuclear factor-1alpha, whose gene is located on chromosome 12. Approximately two-thirds of all known cases of MODY are due to MODY 3, with 41 different mutations reported in 61 families. this transcription factor is expressed in pancreatic Beta cells as well as in liver and is a weak transactivator of the insulin gene. this may explain how mutations of hepatocyte nuclear factor-1 alpha impair glucos-induced insulin secretion. Unlike most type 2 diabetes, there is no associated insulin resistance, but the clinical course of these two disorders is otherwise similar regarding prevalence of microangiopathy and failure to continue to respond to oral agents with time.

d. MODY 4 results from mutation of a pancreatic nuclear transcription factor known as inulin promoter factor-1 (IPF-1), whose gene is on chromosome 13. It mediates insulin gene transcription as well as regulates expression of other Beta cell-specific genes such as glucokinase and the glucose transporter-2. When both alleles of this gene are nonfunctioning, agenesis of the entire pancreas results; but in the presence of a heterozygous mutation of IPF-1, a mild form of MODY has been described in a family in whom affected individuals developed diabetes at a later age (mean onset at 35 years) than occurs with the other forms of MODY in which onset generally occurs before the age of 25 years.

e. MODY 5 has recently been reported in a Japanese family with a mutation of hepatic nuclear transcription factor-1 Beta, which acts with the 1 alpha factor to regulate gene expression in pancreatic islets. This mutation caused a moderately severe form of MODY with progression to insulin treatment and severe diabetic complications in those affected. In addition, a nephropathy was seen in affected individuals prior to the onset of diabetes, suggesting that decreased levels of this transcription factor in the kidney, where it is also normally expressed in high levels, may contribute to renal dysfunction.

2. Diabetes due to mutant insulins . This is a very rare subtype of non-obese type 2 diabetes, with no more than ten fmailies having been described. Since affected individuals were heterozygous and possessed one normal insulin gene, diabetes was mild, did not appear until middle age, and showed autosomal dominant genetic transmission. There is generally no evidence of clinical insulin resistance and these patients respond will to standard therapy.

3. Diabetes due to mutant insulin receptors. Defects in the insulin receptor gene have been found in more than 40 people with diabetes, but most have extreme insulin resistance associated with acanthosis nigricans.

4. Diabetes mellitus associated with a mutation of mitochondrial DNA. Since sperm do not contain mitochondria, only the mother transmits mitochondrial genes to her offspring. Diabetes due to a mutation of mitochondrial DNA that impairs the transfer of leucine into mitochondrial proteins has been described in Japanese families as well as in isolated case reports in Caucasians. Most patients have a mild form of diabetes that responds to oral hypoglycemic agents, some a nonimmune form of type 1 diabetes. Two-thirds of patients with this subtype of diabetes have a hearing loss, and a smaller proportion had a syndrom of myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). A lusine transfer defect has also recently been found in a family with maternally transmitted diabetes.

5. Obese type 2 patients. This most common form of diabetes is secondary to extrapancreatic factors that produce insensitivity to endogenous insulin. When an associated defect of insulin production prevents adequate compensation for this insulin resistance, nonketotic mild diabetes occurs. The primary problem is a "target organ" disorder resulting in ineffective insulin action that can secondarily influence pancreatic Beta cell function. Hyperplasia of pancreatic Beta cells is often present and probably accounts for the fasting hyperinsulinism and exaggerated insulin and proinsulin responses to glucose and other stimuli seen in the milder forms of this disorder. In more severe cases, especially after several years' duration of diabetes, failure of Beta cell secretion may result. Chronic deposition of amyloid in the islets may combine with inherited genetic defects to progressively impair Beta cell function. Obesity is generally associated with abdominal distribution of fat, producing and abnormally high waist-to-hip ratio. This "visceral" obesity, due to accumulation of fat in the omental and mesenteric regions, correlates with insulin resistance; subcutaneous abdominal fat has little if any association with insulin insensitivity. Visceral metabolites released into the portal circulation alter liver metabolism and increase hepatic glucose output more than peripheral fat mobilizatio into systeic veins. Exercise may affect the deposition of visceral fat as suggested by CT scans of Japanese wrestlers, whose daily vigorous exercise program prevents accumulation of visceral fat, and they have normal serum lipids and euglycemia despite daily intakes of 5000-7000 kcal and development of massive subcutaneous obesity.

A major cause of the observed resistance to insulin in target tissues of obese patients is believed to be a postreceptor defect in insulin action. This is associated with overdistended visceral fat deposits, and there is a reduced ability to clear nutrients from the circulation after meals. The resulting hyperinsulinism can further enhance insulin resistance by down-regulation of insulin receptors. Moreover, when hyperglycemia develops, hexosamines accumulate in the muscle and fat tissue to further inhibit glucose transport. This contributes to further defects in postreceptor insulin action, thereby aggravating hyperglycemia.

When exercise increases blood flow to muscle as well as increasing muscle mass, and when overfeeding is corrected so that storage depots become less saturated, the cycle is interrupted. There is improvement in insulin sensitivity, which is further restored toward normal by a reduction of both the hyperinsulinism and the hyperglycemia.

Recently, a new factor termed "resistin" has been identified in animal models of obesity; it is a peptide specifically expressed in and secreted by fat cells. Its serum levels are increased markedly in both genetic and diet-induced obesity. Neutralization of this factor with antibodies improves insulin action in obese animals, and injection of resistin into normal mice impairs insulin action. This novel peptide may have the key to better understanding of the relationship of insulin resistance to obesity.

Signs and Symptoms

While many patients with type 2 diabetes present with increased urination and thirst, many others have an insidious onset of hyperglycemia and are asymptomatic initially. This is particularly true in obese patients, whose diabetes may be detected only after glycosuria or hyperglycemia is noted during routine laboratory studies. Occasionally, type 2 patients may present with evidence of neuropathic or cardiovascular complications because of occult disease present for some time prior to diagnosis. Chronic skin infections are common. Generallized pruritis and symptoms of vaginitis are frequently the initial complaints of women. Diabetes should be suspected in women with chronic candidal vulvovaginitis as well as in those who have delivered large babies (>9 lbs, or 4.1 kg) or have had polyhydramnios, preeclampsia, or unexplained fetal losses.

Obese diabetics may have any variety of fat distribution; however, diabetes seems to be more often associated in both men and women with localization of fat deposits on the upper segment of the body (particularly the abdomen, chest, neck, and face) and relatively less fat on the appendages, which may be quite muscular.

Laboratory Findings

1. Urinalysis

a. Glucosuria—A specific and convenient method to detect glucosuria is the paper strip impregnated with glucose oxidase and a chromogen system (Clini stix, Diastix), which is sensitive to as little as 0.1 % glucose in urine. Diastix can be directly applied to the urinary stream, and differing color responses of the indicator strip reflect glucose concentration. A normal renal threshold for glucose as well as reliable bladder emptying is essential for interpretation.

b. Ketonuria—Qualitative detection of ketone bodies can be accomplished by nitroprusside tests (Acetest or Ketostix). Although these tests do not detect B-hydroxybutyric acid, which lacks a ketone group, the semiquantitative estimation of ketonuria thus obtained is nonetheless usually adequate for clinical purposes.

2. Blood testing procedures

a. Glucose tolerance test—

(1) Methodology and normal fasting glucose— Plasma or serum from venous blood samples has the advantage over whole blood of providing values for glucose that are independent of hematocrit and that reflect the glucose concentration to which body ussues are exposed. For these reasons, and because plasm and serum are more readily measured on automated equipment, they are used in most laboratories. If serum is used, samples should be refrigerated and separated within 1 hour after collection.

(2) Criteria for laboratory confirmation of diabetes mellitus—If the fasting plasma glucose level is 126 mg/dL or higher on more than one occasion, further evaluation of the patient with a glucose challenge is unnecessary. However, when fasting plasma glucose is less than 126 mg/dL in suspected cases, a standardized oral glucose tolerance test may be done.

For proper evaluation of the test, the subjects should be normally active and free from acute illness, Medications that may impair glucose tolerance include diuretics, contraceptive drugs, glucocorticoids, niacin, and phenytoin.

Because of difficulties in interpreting oral glucose tolerance tests and the lack of standards related aging, these tests are being replaced by documentation of fasting hyperglycemia.

Since fasting plasma glucose is known to increase with aging, clinicians should be more tolerant of slight abnormalities of fasting glucose values ira older people (over 70 years of age) and not deprive patients of occa sional sugar—containing snacks when symptoms are not evident. However, an occasional elderly patient may benefit from the diagnosis of mild diabetes in that macular edema may be detected earlier and laser treatment initiated before vision deteriorates permanently.

b. Glycosylated hemoglobin (hemoglobin A1) measurements—Glycoslated hemoglobin is abnormally high in diabetics with chronic hyperglycemia and reflects their metabolic control. It is produced by nonenzymatic condensation of glucose molecules with free amino groups on the globin component of hemoglobin. The higher the prevailing ambient levels of blood glucose, the higher will be the level of glycosylated hemoglobin. The major form of glycohemoglobin is termed hemoglobin A1c which normally comprises only 4—6% of the total hemoglobin. The remaining glycohemoglobins (2—4% of the total) consist of phosphorylated glucose or fructose and are termed hemoglobin A1a and hemoglobin A1b. Some Laboratories measure the sum of these three glycohemoglobins and report it as hemoglobin A1, but more laboratories are converting to the more intricate but highly specific HhA1c assay. There are now monoclonal immunoassays for measuring HbA1c Machines based on this technology can be used in clinicians' offices. They use capillary blood and give a result in about 9 minutes, allowing immediate feedback to the patient regarding their glycemic control.

Since glycohemoglobins circulate within red blood cells whose life span lasts up to 120 days, they generally reflect the state of glycemia over the preceding 8-12 weeks, thereby providing an improved method of assessing diabetic control. Glycohemoglobins are extremely useful in monitoring the progress of patients. Measurements should he made in patients with either type of diabetes mellitus at 3 to 4 month intervals so that adjustments in therapy can be made if glycohemoglobin is either subnormal or if it is more than 2% above the upper limits of normal for a particular laboratory. In patients monitoring their own blood glucose levels, glycohemoglobin values provide a valuable check on the accuracy of monitoring. In patients who do not monitor their own blood glucose levels, glycohemoglobin values are essential for adjusting therapy. Use of glycohemoglobin for screening is controversial. Sensitivity in detecting known diabetes cases by hemoglobin A1c measurements is only 85%, indicating that diabetes cannot be excluded by a normal value. On the other hand, elevated hemoglobin A1c assays are quite specific (91%) in identifying the presence of diabetes.

Occasionally, fluctuations in hemoglobin A1 are due to an acutely generated, reversible, intermediary (aldimine-linked) product that can falsely elevate glycohemoglobins when measured with "short-cut"chromatographic methods. This can be eliminated by using specific HPLC methods that detect HbA1c or by dialysis of the hemolysate before chromatography. When hemoglobin variants are present, such as negatively charged hemoglobin F, acetylated hemoglobin from high-dose aspirin therapy, or carbamoylated hemoglobin produced by the compiexing of urea with hemoglobin in uremia, falsely high "hemoglobin A1" values are obtained with commonly used chromatographic methods. In the presence of positively charged hemoglobin variants such as hemoglobin S or C, or when the life span of red blood cells is reduced by in creased hemolysis or hemorrhage, falsely low values for "hemoglobin A1" result.

Serum fructosamine is formed by nonenzymatic glycosylation of serum proteins (predominantly albumin). Since serum albumin has a much shorter halflife than hemoglobin, serum fructosamine generally reflects the state of glycemic control for only the preceding 2 weeks. Reductions in serum albumin (eg, nephrotic state or hepatic disease) will lower the serum fructosamine value. When abnormal hemoglobins or hemolytic states affect the interpretation of glycohemoglobin or when a narrower time frame is required, such as for ascertaining glycemic control at the time of conception in a diabetic woman who has recently be come pregnant, serum fructosamine assays offer some advantage. Normal values very in relation to the serum albumin concentration and are 1.5—2.4 mmol/L when the serum albumin level is 5 g/dL.

c. Self-monitoring of blood glucose—Capillary blood glucose measurements performed by patients themselves, as outpatients, are extremely useful. In type 1 patients in whom 'tight' metabolic control is attempted, they are indispensable. A portable battery—operated glucometer provides a digital readout of the intensity of color developed when glucose oxidase paper strips are exposed to a drop of capillary blood for up to 45 seconds. Second-generation glucometers automatically time the reaction as soon as a drop of blood is applied to the previously inserted test strip. This relieves patients of the need to wipe off the strip after an exact interval of time and eliminates technical errors from improper blotting or timing.

3. Lipoprotein abnormalities in diabetes—Circulating lipoproteins are just as dependent on insulin as is the plasma glucose. In type I diabetes, moderately deficient control of hyperglycemia is associated with only a slight elevation of LDL cholesterol and serum triglycerides and little if any change in HDL cholesterol. Once the hyperglycemia is corrected, lipoprotein levels are generally normal. However, in obese patients with type 2 diabetes, a distinct 'diabetic dyslipidemia' is characteristic of the insulin resistance syndrome. Its features are a high serum triglyceride level (300—400 mg/dL), a low HDL cholesterol (less than 30 mg/dL), and a qualitative change in LDL particles, producing a smaller dense LDL whose membrane carries supranormal amounts of free cholesterol. Since a low HDL-cholesterol is a major feature predisposing to macrovascular disease, the term 'dyslipidemia' has preempted the term 'hyperlipidemia,' which mainly denoted the elevated triglycerides. Measures designed to correct the obesity and hyperglycemia, such as exercise, diet, and hypoglycemic therapy, are the treatment of choice for diabetic dyslipidemia, and in occasional patients in whom normal weight was achieved, all features of the lipoprotein abnormalities cleared. Since primary disorders of lipid metabolism may coexist with diabetes, persistence of lipid abnormalities after restoration of normal weight and blood glucose should prompt a diagnostic workup and possible pharmacotherapy of the lipid disorder.

Treatment

I will not include this portion of the medical text because it includes outdated and inaccurate information. It also includes all medications used in the treatment of diabetes....this is too vast for the purpose of this page. The goal here is toward the natural management of type 2 diabetes with new and correct forms of treatment. If you are interested in how the condition is treated medically, you can find this in any medical textbook.

Eat Whole, Eat Fresh, Eat to Live

If your wish is to prevent or reverse Diabetes Type 2 then a whole food diet is the only option. There are many studies and example of this being the case. In a famous study called the Harvard Physicians Health Study a group of 42,000 male physicians were categorized according to their diets. One group was called "prudent" and the other group was called "Western". In the "Prudent" group the diets contained high amounts of vegetables, fruits, fish, poultry and whole grains. In the "Western" diet group they ate foods like red meats, processed meat, french fries, high fat dairies, refined grains, and sweets.

On completion of this study, it was found that the group eating the "Western" diet had an increased risk of developing Diabetes Type 2 by 50%. When this diet was combined with low physical activity, the risk increased to nearly 100%. Also noted was that if the men were obese to begin with, this added another increase of 11 times. So if you were obese, inactive, and ate processed foods you increased your risk by 1,100%.

Between 1990 and 2001	* A 62% increase in the number of people with diabetes had been reported. *An increase of 76% in people that were in their 30's was also seen
Diabetes Type 2 in Children	* there are now 800,000 new cases occurring annually * that means that 1 out of every 3 children born will become diabetic in their lifetime.

Withour a change in lifestyle, eating habits, and nutritional behavior, it is expected that these numbers will DOUBLE by the year 2020.

The Harvard study is one of many studies that prove a whole food diet is the only healthy way humans should eat.

With all the technical advances and new medications on the market, why are we still seeing a rise in diabetes? The treatment of diabetes is a huge investment for the medical field. "Curing" this infliction is not what the medical community cares about. According to the WHO in the year 2000 the total annual cost of treating diabetes was estimated at $65,216 million (that is $65 billion). In 2002 the total cost of treating diabetes was estimated at $132 billion. The cost doubled in 2 years. That was a cost out of your pockets.

A large part of a General Practitioner's income comes from treating diabetes in conjunction with that of an Endocrinologist. Do you think these doctors want to give up such a sizable percentage of their income? What would be the cost of naturally treating diabetes?

Committing to natural foods is more effective than medication for preventing and treating diabetes type 2. In another study reported by the New England Journal of Medicine (2002; 346:393-403) the group that simply included wieght loss and exercise was found to be twice as safe from developing diabetes than that of the medicated group. In addition, they had no drug side effects to be concerned about.

It has been proved over and over again that diet and lifestyle change work the best and cost less.

Plant based diets like vegetarian, Mediterranean, and Asian are the diets that are the healthiest for diabetics.....or for anyone who cares about being disease free. Why? Simply, the correct carbohydrates, higher fiber, olive and coconut oils, and the lack of processed foods.

The human body was not designed to consume refined, processed foods like most sugars, white flour, hydrogentaed fats and other dead products that come in bags, boxes, and bottles. It was designed to eat whole, fresh, and raw foods which are loaded with nutrition.

Vegetables contain the widest range of nutrients of any food class. They have vitamins, minerals, the right type of carbohydrates, proteins, fiber, phytochemicals, and antioxidants. For example, the simple raw tomato has around 10,000 ingredients.

Fiber! In the Western diet? To make a significant effect on glycemic control, a required fiber intake of 35-50 grams is needed daily. This is a lot of fiber! About the amount in a vegan diet. Most people aren't vegans though. There are good fiber supplements on the market to make up for a lack of intake. There are two kinds of fiber for which you need to be aware. Insoluble fiber, this doesn't expand in liquid and it lessens bowel transit time. Soluble fiber, the does expand in liquid and slows the uptake of glucose into the blood.

Be sure to build your fiber intake slowly. Gas is formed by bacteria when they act on fiber. Gradually increase your intake to allow for the adjustments.

Bottom Line! Eat whole foods, live foods, and fresh foods. Stay away from fast foods, processed foods and anything artificial and you will be amazed at how your diabetic infliction will do an about face.

Nutrients That Control Blood Sugar

To help control diabetes, you will find that foods, supplements, and herbs will be very important. Nature gives us nutrients for very good reasons. Many answers to correcting and maintaining health come from natural sources. some of these natural remedies will either help control your blood sugar or will lessen complications. If you add these nutrients to your diet, make sure that your doctor is aware of them. The reason being, these supplements may lower your requirement for insulin.

Some Supplements That Control Blood Sugar

Chromium- In order for the cells to open their doors and let the glucose in, it must have a few keys to do this. One is insulin and another is chromium. Without chromium, the glucose builds up in the blood and eventually leads to diabetes. There is much evidence that doses of 400 micrograms (mcg) per day is effective in reducing blood sugar levels. Chromium's best forms for absorption are chromium picolinate and chromium histidine. A combination of chromium picolinate and vanadyl sulfate work sinergistically to regulate blood sugar. Further studies show that Chromium can shorten harmful heart rhythms, which may lower cardiovascular risk in diabetics as well! Over 30 years of biological studies in both humans and animals confirms Chromium as a safe and effective nutritional supplement. Current estimates show that 90% of North Americans are lacking in this essential mineral nutrient.

Food sources: beer, brewer's yeast, brown rice, cheese, meat, whole grains, blackstrap molasses, chicken, corn, dulse, eggs, mushrooms, and potatoes.

Magnesium- Low levels are seen most commonly in diabetes. It has been shown that as many as one out of every three people with diabetes has low levels of magnesium. As levels of magnesium go up, the risk of developing diabetes goes down. It has also been shown that supplementing with 350 mg per day will improve insulin resistnace and blood sugar control. The best way to control the amount is by supplement and magnesium citrate is the most readily absorbed form.

Food sources: blackstrap molasses, apples, apricots, avocados, bananas, brown rice, cantalope, figs, garlic, grapefruit, kelp, lemons, lima beans, peaches, black-eyed peas, salmon, sesame seeds, green leafy vegetables, legumes, nuts, lemons, wheat germ, and whole grains.

Manganese- Manganese is an important cofactor in the key enzymes of glucose metabolism. A deficiency of manganese was found to result in diabetes in guinea pigs. It also resulted in the frequent birth of offspring who develop pancreatic abnormalities or no pancreas at all. Diabetics have been shown to have only one-half the manganese of normal individuals.

Food sources: avocados, nuts and seeds, seaweed, whole grains, blueberries, egg yolks, legumes,dried peas, pineapples, and green leafy vegetables.

Potassium- Potassium supplementation yields improved insulin sensitivity, responsiveness and secretion in diabetics. Insulin administration often causes a potassium deficiency.

Food sources: dairy foods, fish, fruit, legumes, poultry vegetables, whole grains, apricots, avocados, bananas, lima beans, blackstrap molasses, brewer's yeast, brown rice, dates, dulse, figs, garlic, nuts, potatoes, raisins, spinach, winter squash, yams, and yogurt.

Zinc- Zinc is involved in virtually all aspects of insulin metabolism -synthesis, secretion and utilization. Zinc also has a protective effect against beta cell destruction, and has well-known anti-viral effects. People with Type 1 diabetes (IDDM) tend to be zinc deficient, which may impair immune function. Zinc supplements have lowered blood sugar levels in people with IDDM. People with Type 2 diabetes (NIDDM) also have low zinc levels, caused by excess loss of zinc in their urine. People with NIDDM are recommended to supplement their diet with moderate amounts of zinc (15-50 mg per day) as a way to correct for the deficit. Note: Take zinc with food to prevent stomach upset. If you take over 30 milligrams of zinc on a daily basis for more than one or two months, you should also take 1 to 2 milligrams of copper each day to maintain a proper mineral balance.

Food sorces: brewer's yeast, dulse, egg yolks, fish, kelp, lamb, legumes, lima beans, mushrooms, oysters, pecans, poultry, pumpkin seeds, sardines, seafood, soy lecithin, sunflower seeds, and whole grains. Various herbs also contain some levels of zinc.

Banaba- This simple plant has been documented for its ability to lower blood sugar in diabetics. The extract is a concentrated form of the active ingredient found in the leaf. The scientific name for this active ingredient is colosolic acid, or corosolic acid. It has been found that colosolic acid activates glucose transport in biological cells and that it also lowers the glucose levels in laboratory animals. Colosolic acid is technically known as 2alpha-hydroxyursolic acid, also known as "botanical insulin".

Bitter Melon- The scientific name is Momordica charantia. This plant benefits us in amazing ways, but is especially noted for its regulative abilities in helping with blood sugar levels. The reason it is so effective against diabetes mellitus (Type 2) is that within the juice of the unripe Bitter Melon are found key factors- Charanti; more effective than the oral drug, tolbutamide, in reducing sugar. Insulin-like polypeptides called polypeptide P; lowers blood sugar in Type 1 diabetes and alkaloids noted to also have sugar controlling effects. It has been confirmed in scientific studies that Bitter Melon can significantly improve glucose tolerance without increasing blood insulin levels, and also improves fasting glucose levels.

Cinnamon- Cinnamon (Cinnamomum verum) was used by ancient China to treat health conditions as early as 2700 B.C. USDA researchers indicate that cinnamon reduces the amount of insulin necessary for glucose metabolism in diabetics. According to a recent study cinnamon improves blood glucose as it reduces triglycerides, total cholesterol, and LDL, the bad cholesterol, in patients with diabetes.

Gymnema Sylvestre- Gymnema sylvestre is a woody climbing vine indigenous to the rain forests of central and southern India. Indian medical texts dating back 2,000 years mention the use of Gymnema in the treatment of diabetes. The notable Harvard Medical School in conjunction with Natural Standard, an organization that produces scientifically based reviews of natural medicine topics, states; “There is evidence to suggest that gymnema sylvestre can lower blood sugar levels in people with Type 1 and Type 2 diabetes.” The Yale University states; “Gymnema sylvestre will often improve blood sugar control in diabetes. Finally, the Journal of Endocrinology November 1999 at the School of BioMedical Sciences, King’s College, London, England, state, “Results confirm the stimulatory effects of gymnema sylvestre on insulin release indicate that this herb acts by increasing cell permeability.” Again, we are talking about Type I diabetes, the kind of diabetes that normally requires the patient to inject insulin for life. Now we have the notable Harvard University and King’s College telling us that gymnema sylvestre lowers blood sugar in Type I diabetics through potential regenerating beta cells!

Cayenne- Cayenne has been revered since 7000 B.C. for its impressive healing benefits. We know that the root cause of diabetes is directly related to the digestive processes, and we also know that Cayenne helps fortify this system while lowering blood cholesterol, increasing circulation which then boosts the immune system and stimulates organ secretions.

Juniper Berries- Juniper helps increase urine volume without a loss of electrolytes such as potassium. Juniper also warms the digestive system, has antiviral qualities and stimulates the kidneys.

Huckleberry- Huckleberry is an important ingredient in diabeticine™ as it helps all the little capillaries in the body to improve circulation to the hands and feet. We know that poor circulation is one of the symptoms of diabetes. The fruits are especially valuable in the botanical support and balance of the digestive process. Huckleberry's unique nutritional properties assist in strengthening the immune system. It is also helpful in the relief of stress, inflammation, and anxiety.

Vitamin E- This powerful antioxidant reduces free radical damage that can lead to complications from diabetes, such as heart disease and nerve damage. When given 1,200 IU per day, people with diabetes reduce the tendency of LDL cholesterol to become oxidized and therefore lead to atherosclerosis. This is important because nearly 70% of diabetic related deaths are due to damaged and clogged arteries. Food sources include: avocados, nuts, sunflower seeds, brown rice, cornmeal, sweet potatoes, watercress, alfalfa, dandelion, flaxseeds, rose hips, and wheat germ.

Food sources: cold pressed vegetable oils, dark green leafy vegetables, legumes, nuts, seeds, whole grains, brown rice, cornmeal, dulse, eggs, kelp, milk, oatmeal, sweet potatoes, watercress, wheat germ. Some herbs contain vitamin E as well.

Alpha-Lipoic Acid- This is also a powerful antioxidant. It is used, especially in Germany, for treatment of peripheral nerve damage in diabetic patients. It also helps control blood sugar levels. There are some food sources, but in order to get the therapeutic levels you must supplement with doses ranging from 600-1,200 mg per day.

Vitamin B6 (Pyridoxine)- Diabetics with neuropathy have been shown to be deficient in vitamin B6 and benefit from supplementation. Peripheral neuropathy is a known result of pyridoxine deficiency and is indistinguishable from diabetic neuropathy. Vitamin B6 supplements improve glucose tolerance in women with diabetes caused by pregnancy. Vitamin B6 is also effective for glucose intolerance induced by the birth control pill. 1,800 mg per day of a special form of vitamin B6-pyridoxine alpha-ketoglutarate-improves glucose tolerance dramatically. Pyridoxine is also important in preventing other diabetic complications because it is an important coenzyme in the cross-linking of collagen and inhibits platelet aggregation.

Food sources: brewer's yeast, carrots, chicken, eggs, fish, peas, spinach, sunflower seeds, walnuts, wheat germ, avocado, bananas, beans, blackstrap molasses, brocolli, brown rice, cabbage, cantaloupe, corn, dulse, plantains, potatoes, rice bran, tempeh.

Vitamin B12- Vitamin B12 is needed for normal functioning of nerve cells. Vitamin B12 taken orally, intravenously, or by injection reduces nerve damage caused by diabetes in most people. Oral supplementation may be sufficient, but intramuscular vitamin B12 may be necessary in many cases. Take up to 500 mcg of Vitamin B12 three times per day.

Food sources: brewer's yeast, clams, eggs, herring, kidney, liver, mackerel, milk, seafood, dulse, kelp, kombu, nori, and soybeans.

Biotin- Biotin is a B vitamin needed to process glucose. It has been shown to work synergistically with insulin and independently in increasing the activity of glucokinase. This enzyme is responsible for the first step in glucose utilization. Glucokinase is present only in the liver, where, in diabetics, its concentration is very low. Supplementation with large quantities of biotin may significantly enhance glucokinase activity, thereby improving glucose metabolism in diabetics. When people with Type 1 diabetes (IDDM) were given 16 mg of biotin per day for just one week, their fasting glucose levels dropped by 50%. Similar results have been reported using 9 mg per day for two months in people with Type 2 diabetes (NIDDM). Biotin may also reduce pain from diabetic nerve damage. Take 16 mg of biotin for a few weeks to see if blood sugar levels will fall.

Food sources: brewer's yeast, cooked egg yolks, meat, milk, poultry, saltwater fish, soybeans, and whole grains.

Niacin- High levels-several grams per day-of niacin, a form of vitamin B3, impair glucose tolerance . So, avoid it if you are diabetic. Smaller amounts (500-750 mg per day for one month followed by 250 mg per day) of niacin may help some people with Type 2 diabetes (NIDDM).

Food sources: beef liver, brewer's yeast, brocolli, carrots, cheese, corn flour, dandelion greens, dates, eggs, fish, milk, peanuts, potatoes, tomatoes, wheat germ, and whole wheat. Many herbs contain niacin also.

Coenzyme Q10- People with diabetes cannot adequately process carbohydrates. Coenzyme Q10, or CoQ10, is needed for normal carbohydrate metabolism. In one trial, blood sugar levels fell substantially in 30% of people with diabetes after they supplemented with 120 mg of CoQ10 per day. Another reason to supplement with CoQ10 is because the eye contains tiny blood vessels and supplementing with CoQ10 will aid in preventing retinopathy. Take 50 miligrams of coenzyme Q10 twice daily for up to three months, then reduce the dosage to 30 milligrams daily.

Food sources: Mackerel, salmon, sardines, beef, peanuts, and spinach.

Inositol- Inositol is needed for normal nerve function. Diabetes can cause nerve damage, or diabetic neuropathy. Some of these abnormalities have been reversed by inositol supplementation (500 mg taken twice per day).

Food sources: brewer's yeast, fruits, lecithin, legumes, meats, milk, unrefined molasses, raisins, vegetables, and whole grains

GLA- Gamma-linolenic acid (GLA), has been shown to be helpful for improving damaged nerve function, which is common in diabetes. Take 500 to 1,000 milligrams of any of these oils twice daily.

Food sources: Borage oil, black currant seed oil, flaxseed oil, and primrose oil

Carnitine- Proper use of fat for energy is important in diabetics. Supplementing with carnitine improves the breakdown of fatty acids, possibly playing a role in preventing diabetic ketoacidosis.When diabetics are given carnitine, around 1 mg per 2.2 pounds of body weight, high blood levels of both cholesterol and triglycerides dropped by 25-40% in just ten days.

Food sources: meats

Taurine- Taurine is an amino acid found in protein containing foods. Low levels of Taurine leads to a higher viscosity blood, a condition which increases the risk of heart disease and stroke. Supplementing with taurine,1500 mgs per day, will help restore taurine levels to normal and corrects the problem of blood viscosity within about three months.

Food sources: eggs, fish, meat, and milk

Coconut Oil and Diabetes

A book by Bruce Fife is a must read for anyone that is concerned about their health. This book entitled The Coconut Oil Miracle is a wonderful source many ailments and health concerns. I have include below his chapter on diabetes for your reference. In my opinion, the only oils that should be consumed are cold pressed olive oil, unrefined coconut oil, and unrefined palm kernel oil. No vegetable oils whatsoever should pass your lips. This means that fast foods and restaurant food are out of the question as far as diabetes is concerned.

"One of the many plagues of modern society is diabetes. The incidence of diabetes has risen over the last century to make it the sixth biggest killer in America. Diabetes not only can cause death, but also can lead to kidney disease, heart disease, high blood pressure, stroke, catarats, nerve damage, hearing loss, and blindness. It is estimated that 45% of the population is at risk of developing diabetes.

Diabetes is all about sugar in our bodies, otherwise known as blood glucose. Every cell in our bodies must have a constant source of glucose in order to fuel metabolism. Our cells use glucose to power processes such as growth and repair. When we eat a meal, the digestive system converts much of our food into glucose, which is released into the bloodstream. The hormone insulin, which is secreted by the pancreas gland, moves glucose from the blood and funnels it into the cells so it can be used as fuel. If the cells are unable to get adequate amounts of glucose, asi is the case in diabetes, they can literally starve to death and cause tissues and organs to degenerate.

There are two major forms of diabetes: Type I and Type II. Type I, also referred to as insulin-dependent or juvenile diabetes, usually begins in childhood and results from the inability of the pancreas to make adequate amounts of insulin. Type II diabetes is known as non-insulin-dependent or adult-onset diabetes because it usually appears in older adults. In Type II diabetes the pancreas may secrete a normal amount of insulin, but the cells are unable to absorb it. Insulin acts like a key to a lock. It goes to the cells and unlocks the door to allow glucose to enter. If the lock is made of cheap materials and breaks, the key no longer works, and the door remains locked. This is essentially what happens with Type II diabetes. In bot types of diabetes the level of glucose in the blood is elevated, while cells are deprived.

In Type I the pancreas is incapable of producing enough insulin to adequately shuttle glucose to all the cells in the body. Treatment involves insulin injections one or more times a day, along with adherence to a strict low-sugar diet. About 90 % of diabetes are of Type II, and 85% of them are overweight. Diet plays a key role in both the onset and the disease and its control. The types of food we eat can either promote or protect us from diabetes.

In the Pacific Islands, diabetes is unheard of among those people who eat traditional diets. But when they abandon their native foods and adopt Western ways, the incidence of diabetes rises. An interesting example of this has occurred on the island of Nauru in the South Pacific. Subsisting for centuries on a diet composed primarily of bananas, yams, and coconuts, the people lived totally free from diabetes. Phosphate deposits discovered on the island brought an influx of wealth and a change in lifestyle. The islanders replaced the coconut and yams they had eaten for centuries with foods made from refined flour, sugar, and processed vegetable oils. The result was the emergence of a never-before-seen-disease--diabetes. According to the World Health Organization, up to half of the urbanized Nauru population age 30-64 are now diabetic.

Doctors have been able to help patients control diabetes by putting them on a low-fat, high-carbohydrate diet. the diet restricts total fat intake to 30% or less of calories. Complex carbohydrates such as whole grains and vegetables make up 50% to 60% of calories. Simple carbohydrates such as refined flour and sugar are to be avoided. The reason for this is because simple carbohydrates can put undue strain on the pancreas and quickly raise blood sugar to dangerous levels. The reason for reducing fat as well as sweets is to promote weight loss. Since excess weight is of primary concern with diabetes, losing it is a priority. Another reason for the low-fat diet is to reduce the risk of heart disease, which is a common consequence of diabetes. Probably the best reason for keeping fat to a minimum is that some fats, particularly oxidized fats, not only promote diabetes but may actually cause it.

Researchers have discovered that the overconsumption of refined vegetable oils leads to diabetes. As far back as the 1920s, Dr. S. Sweeney produced reversible diabetes in all of his medical school students by feeding them a high-vegetable-oil diet for 48 hours. None of the students had previously bee diabetic. More recently, researchers have been able to cause test animals to develop diabetes by feeding them diets high in polyunsaturated fat (Parekh, 1998). Simply restricting fat intake in diabetic animals has shown to reverse Type II diabetes. Likewise, clinical studies with humans on low-fat diets also show reversal of the disease. Many studies have shown low-fat diets to be effective in controlling diabetes.

The current recommendation is to limit all fats. Monounsaturated fats, such as olive oil, don't seem to adversely affect diabetes and so are allowed in moderation, but because all fats, including olive oil, are high in calories, they are discouraged. Saturated fat is restricted because it is believed to increase the risk of heart disease. The biggest culprit, however, seems to be polyunsaturated oil. Studies have shown that when polyunsaturated fats from the diet are incorporated into cellular structure, the cell's ability to bind with insulin decreases, thus lowering its ability to get glucose. In other words, the "locks" on the cells that open the door for glucose to enter degrade when too much polyunsaturated oil is consumed in the diet. Insulin is then unable to open the door. Polyunsaturated oils are easily oxidized and damaged by free radicals. Fats of all types, including polyunsaturated fats in the cell membrane can adversely affect the cell's function, including its ability to allow hormones, glucose, and other substances to flow in and out of the cell. Therefore, a diet high in refined polyunsaturated vegetable oils promotes diabetes. A diet low in such oils helps to alleviate symptoms. Because all fats also promote weight gain, it's best to avoid them as much as possible.

There is one fat that diabetics can eat without fear. That fat is coconut oil. Not only does it not contribute to diabetes but it helps regulate blood sugar, thus lessening the effects of the disease. MCFA (medium chain fatty acids- which is what coconut oil is) can supply needed energy to cells without adversely affeting blood sugar or insulin levels. Because coconut oil can also help regulate metabolism, it can help the body burn more calories, causing weight loss and helping to regulate diabetes.

As mentioned earlier in this chapter, coconut oil puts less of a demand on the enzyme production of the pancreas. This lessens the stress on the pancreas during mealtime when insulin is produced most heavily, thus allowing the organ to function more efficiently. Coconut oil also helps supply energy to cells because it is easily absorbed without the need of enzymes or insulin. It has been shown to improve insulin secretion and utilization of blood glucose. Coconut oil in the diet enhances insulin action and improves binding affinity compared to other oils. The Jounal of the Indian Medical Association has reported that Type II diabetes in India has increased as the people have abandoned traditional oils, like coconut oil, in favor of polyunsaturated vegetable oils, which have been promoted as "heart-friendly". The authors comment on the link between polyunsaturated oils and diabetes and recommend increasing coconut oil consumption as a means to prevent diabetes."

As one can see, the information contained in this book is very valuable and is ahead of its time. The current medical and nutritional advice given to diabetics today is outdated. Most nutritional advice given today is just a blanket prescription given to patients. For example, the comment on following a "low-fat" diet is not entirely correct. As you have seen, it is more important to know which type of fat you are consuming. Another example are the comments made about weight loss. What is important about weight loss is its ability to make cells "upregulate" glucose receptors. Exercise does this also. Lastly, on oxidized fats. It is very important to consume foods and take supplements that are high in antioxidants. This is for the prevention of cellular destruction. When cell membrane are properly structured and intact, they function better.

The book The Coconut Oil Miracle has many recipes for the use of coconut oil. It is an excellent investment for someone who is truely concerned about the prevention or control of diabetes.

Natural Therapy for Type 2 Diabetes

Warning! If you are already on insulin, do not stop taking it. If you follow this advice, let your doctor slowly lower your dosage.

This natural therapy will take several months for the effects to be seen and felt. If the advice is followed correctly, you may find yourself never having to buy medications again.

The trick is to eliminate partially hydrogenated oils and trans fatty acids from your diet. This includes your typical store-bought and restaurant used vegetable oils and margarine. Replace these rancid non-functioning oils with better choices. For example, choose natural oils like flax seed oil, olive oil, real butter, lard, coconut oil, etc. Along with these better sources you must consume Omega-3 fatty acids (if you take the omega-3's with cottage cheese it will convert the fatty acids from a lipid soluble to water soluble form- which is good).

In addition to the above advice, try adding the following:

Reasons

Fatty acids and cholesterol are incorporated into every cell membrane. They require a certain structure to function correctly. If the structure of a fatty acid molecule is not correct, the cell will notwork properly. Since the body cannot tell the difference in these structures they still get incorporated into the cell membrane. If a trans-fatty acid becomes part of the cell structure, it reduces the ability of the cell to perform its duty. The trans-fatty structure makes the cell membrane more brittle. In other words, the cell loses its fluidity. Also, if a trans-fat becomes part of a membrane channel (the door that opens into the cell), then the door will not open correctly or it will not be the size to allow its molecules to pass through. As is the case in diabetes. The defective glucose channel will not allow the glucose to be transported into the cell. When insulin binds with a cell wall receptor that causes a transport molecule to come to the wall and escort the glucose into the cell to where it is needed. The trouble is that it can't easily come through a port made of the wrong fatty acids. The cell may still have some good ports (channels) so increasing insulin will still help. Over time, the glucose that remains outside the cell continues to get stored as triglyceride in fat cells and doesn't have a chance to burn off and the person becomes obese--just look around you, it's everywhere. Most diets are low-fat and the fats they do contain are bad fats and the problem just gets worse. This is why it is particularly important to have the correct types of fats...not just to make a blind statement of using low fat.

A type 2 diabetic should absolutely avoid any food that contains trans-fatty acids. This includes margarine, peanut butter, french fries, and virtually every other processed food (including restaurants). It will take about 7 years for your body to gradually purge all of the trans-fatty acids from the cells. However, it won't take that long to cure diabetes if you eat the good fats and omega 3, and stop eatting the bad fats.

The reason for cinnamon has been shown to be because of a compound called methylhydroxychalcone polymer (MHCP). MHCP can stimulate glucose uptake by our cells. It can even help in the synthesis of glycogen, a polymer of glucose that our bodies produce as a means of storing energy for later use, when it is depolymerized back to glucose. Most of our glycogen is found in the liver, but some is found in our muscles - a handy place to be when we start exercising and need quick energy. Producing adequate amounts of glycogen is a principal function of blood sugar metabolism, and MHCP can help.

MHCP has effects similar to those of insulin and works almost as well. Both of these substances work by chemically modifying our cells' insulin receptors in a manner that activates them to do their job, which is to allow glucose molecules to pass through the cell wall into the insulin cascade--the series of molecular events triggered by insulin's interaction with its receptor-is also triggered by MHCP. It has been discovered that when MHCP and insulin act together, the effect is synergistic, meaning tha the total effect is greater than the sum of its parts.

Pedometer Against Glucometer

You may be surprised that the simple act of walking can lower your glucose levels. By using a pedometer to keep track of your steps you can lower the scored on your glucometer by up to 20% to 30%.

Most of us have a very busy life and find it hard to do additional exercise programs. But walking is an easy way to get great exercise. By using a simple pedometer you can set goals that will easily improve your health. Whether using the pedometer for long walks, strolls down the hallway at work, taking the stares instead of the elevator, or by parking a little farther from the grocery store entrance, you can use the regimen to change your life.

Many studies show that people who are sedentary become more active when trying to reach goals with a pedometer. Just by increasing your everday activities can make a big difference. It is inexpensive and doesn't require any level of expertise. You just hook it on your belt and take a look every now and then.

Below is a sample chart to follow. The Printable Version includes instructions.

Starting Weight__________

Starting blood Sugar______

Starting Steps__________

Goal Per Day____________

# of steps Weekly Totals

	M	T	W	Th	F	Sat	Sun	Weight/sugar/steps
Week 1	.	.	.	.	.	.	.	.
Week 2	.	.	.	.	.	.	.	.
Week 3	.	.	.	.	.	.	.	.
Week 4	.	.	.	.	.	.	.	.
Week 5	.	.	.	.	.	.	.	.
Week 6	.	.	.	.	.	.	.	.
Week 7	.	.	.	.	.	.	.	.
Week 8	.	.	.	.	.	.	.	.

Ending Weight__________

Ending Blood Sugar______

Ending Steps___________

The use of the pedometer has the amazing ability to motivate. When you start filling in the chart you can see results and the satisfaction that you are accomplishing your goals. There are many testimonials as to the benefits of this simple way of becoming more active. These include the dropping of 100 points on the glucose test in 2 weeks to dropping pant sizes every few weeks.

This can be fun and rewarding at the same time. Involve your family members in it like a game. Kids love gadgets and love to compete with parents.

Pat yourself on the back once you've reached your goals. You will feel better and look better as a result of this tiny step you have taken. You will improve your health for you and your loved ones.

So pit your pedometer against your glucometer and see which one wins.

GLYCEMIC INDEX

The glycemic index is a chart that makes low carb eating very simple. The glycemic index is a measure of how fast your food is likely to raise your blood sugar levels which can be helpful in maintaining the correct glucose levels.

Low-glycemic foods (less than 55) produce a gradual rise in blood sugar and helps prevent that "spiking" that can occurs with other foods. Intermediate-glycemic foods are those that range from 55 to 70 in the index. High glycemic foods (those above 70) are the ones that cause blood sugar to "spike" rapidly.

Therefore, the glycemic index is a table of foods that measure how fast a carbohydrate will break down and enter the blood stream as glucose.

Below is a sample index:

Low-Glycemic Index Foods (<55)
Low-fat yogurt	14
Peanuts	14
Fructose	23
Plum	24
Grapefruit	25
Pearled Barley	25
Peach	28
Canned Peaches in Natural Juice	30
Dried Apricots	31
Soy Milk	31
Baby Lima Beans, Frozen	32
Fat-Free Milk	32
Fettuccine	32
Low-Fat Yogurt, Sugar Sweetened	33
Apple	36
Pear	36
Whole Wheat Spaghetti	37
Tomato Soup	38
Apple Juice	41
Spaghetti	41
All-Bran	42
Canned Chickpeas	42
Custard	43
Grapes	43
Orange	43
Canned Lentil Soup	44
Canned Pinto Soup	45
Macaroni	45
Pineapple Juice	46
Banana Bread	47
Long-Grain Rice	47
Parboiled Rice	47
Bulgar	48
Canned Baked Beans	48
Grapefruit Juice	48
Green Peas	48
Old-Fashioned Oatmeal	49
Cheese Tortellini	50
Canned Kidney Beans	52
Kiwifruit	52
Banana	53
100% Stone-Ground Whole Wheat Bread	53
Special K	54
Sweet Potato	54

Intermediate-Glycemic Index Foods (55 to 70)
Brown Rice	55
Canned Fruit Cocktail	55
Linguine	55
Oatmeal Cookies	55
Popcorn	55
Sweet Corn	55
White Rice	56
Orange Juice from Frozen Concentrate	57
Pita	57
Canned Peaches, Heavy Syrup	58
Mini Shreaded Wheats	58
Multi-Bran Chex	58
Blueberry Muffin	59
Bran Muffin	60
Cheese Pizza	60
Hamburger Bun	61
Quaker Chewy Granola Bar	61
Beets	64
Canned Apricots, light Syrup	64
Canned Black Bean Soup	64
Macaroni and Cheese	64
Raisins	64
Couscous	65
Quick-Cooking Oatmeal	65
Rye-Crispbread	65
Canned Green Pea Soup	66
Instant Oatmeal	66
Pineapple	66
Angel Food Cake	67
Grape-Nuts	67
Stoned Wheat Thins	67
American Rye Bread	68
Taco Shells	68
Whole Wheat Bread	69
Life Savers	70
Melba Toast	70
White Bread	70

High-Glycemic Index Foods (>70)
Carrots	71
Golden Grahams	71
Bagel	72
Corn Chips	72
Watermelon	72
Honey	73
Kaiser Roll	73
Mashed Potatoes	73
Bran Flakes	74
Bread Stuffing Mix	74
Cheerios	74
Cream of Wheat, Instant	74
Graham Crackers	74
Saltine Crackers	74
Doughnuts	75
French Fries	76
Frozen Waffles	76
Total Cereal	76
Vanilla Wafers	77
Grape-Nuts Flakes	80
Jelly Beans	80
Rice Cakes	82
Rice Krispies	82
Corn Chex	83
Mashed Potatoes, instant	83
Pretzels	83
Cornflakes	84
Baked Potato	85
Rice Chex	89
Rice, instant	91
French Bread	95
Parsnips	97
Dried Dates	103
Tofu Frozen Dessert	115

You should not avoid foods in any glycemic categorie solely for the reason of the index number. Many foods in each group are very nutritious and contain vitamins and minerals that you need to maintain a balanced diet. The goal is to control your blood sugar.

For a more detailed database of foods and their glycemic values visit this link:

Glycemic Index

click on the "GI Database"

Track Your Blood Sugar

If you have Microsoft Excel you can use this template to keep track of your blood sugar over time.