Overview 

Diabetes is a metabolic disorder characterized by chronic hyperglycemia. That is, serum glucose (blood-sugar) levels are elevated above normal range. Either the pancreas doesn’t produce enough of the hormone insulin, which breaks down sugar in the blood, or the body fails to use insulin properly because the cells have become resistant to its effects. 

Diabetes is a disease with many potential secondary complications, but the mechanism behind it is easily understood. When you eat, your body converts food into glucose (sugar) to fuel cells for energy.  In order for this process to work, sufficient amounts of insulin must be present to transport glucose from the blood to the cells.  In people who produce little or no insulin, glucose builds up in the blood instead.  When blood sugar remains too high, the patient is said to be hyperglycemic. 

Approximately 20.8 million American children and adults currently struggle with diabetes, with the rate of incidence increasing in recent years at an alarming pace. In addition, about one-third of those afflicted with diabetes are unaware that they have the disease. 

Diabetes can lead to serious health complications, such as heart disease, blindness, kidney failure and the loss of limbs.  In fact, more than 200,000 deaths each year in the US are attributed to diabetes-related complications. The total cost of medical care and related expenses in treating diabetes in 2007 has been estimated to be more than $170,000,000. 

In order to successfully control diabetes, it is essential that the patient is tested at the earliest indication of the presence of the disease and that aggressive treatment and management be maintained.  

Complications of Diabetes 

Diabetes is associated with serious health complications, including a significantly increased risk for heart disease, stroke, blindness, kidney failure and nerve damage that can lead to limb loss. 

Heart Disease 

The complications of diabetes can largely be blamed on glycation, the same process that causes food to brown in the oven. Normally, cells utilize simple sugars as fuel for energy. However, glycation occurs when sugar molecules bind to proteins to create radical proteins called advanced glycation endproducts (AGEs). Many AGEs are harmless, but others are not and promote oxidative stress. Harmful AGEs can promote high levels of free radicals that can further damage cellular proteins and reduce nitric oxide levels, leading to compromised arteries and blood supply throughout the body. In fact, an adult diabetic is at two to four times higher risk for stroke and heart disease. This risk is further driven when glucose molecules bind to cholesterol-transporting low-density lipoprotein (LDL) molecules. The LDL molecules are then inhibited from binding to liver receptor sites that normally signal a cease in the production of cholesterol. In effect, the liver is tricked into thinking there’s a shortage of cholesterol and keeps producing and transporting more into the bloodstream. 

Retinopathy 

According to the American Diabetes Association, diabetic retinopathy is the leading cause of new blindness in adults aged 20 to 74 years, with 12,000 to 24,000 cases being reported each year. Since the tiny blood vessels in the eye are especially vulnerable to high levels of blood glucose, they can hemorrhage and blurred vision may result. In an advanced stage, blood vessels may leak lipids (fats) into the macular portion of the retina and newly formed vessels grow along the retina and in the vitreous gel that fills the inside of the eye. Without treatment, these rogue vessels can destroy the retina, causing permanent blindness.

Kidney Disease 

Diabetes is also the leading cause of kidney disease and renal failure in the US. The medical term for this condition is known as nephropathy, and is caused by blood vessel damage and excess levels of albumin (protein) in the urine that disrupts the kidney’s natural filtering system. Unfortunately, symptoms may not develop until the late stage of this condition. However, increased blood pressure, along with raised cholesterol and triglyceride levels, are common indicators.

Neuropathy and Vascular Disease 

Oxidative stress and glycation associated with diabetes also contributes to dysfunction of the endothelial cells, the cells that line arterial walls. In a manner similar to the development of atheriosclerosis, the adhesion of white blood cells to the endothelium occurs. The effect of this is two-fold—the release of inflammatory mediators increases, which further damages the endothelium, and the restricted blood flow can lead to blood clot formation. 

Since diabetics typically suffer from impaired blood circulation, more than half of those with this disease will experience neuropathy, or nerve damage. The most common type is peripheral neuropathy, which usually affects the lower extremities and is characterized by a tingling ‘pins and needles’ sensation. However, complete numbness of the region could put the patient at risk for amputation simply because an ulcer may develop and remain undetected and untreated.

Types of Diabetes 

There are two major types of diabetes – type I and type II.  The former, also known as diabetes mellitus, or juvenile onset diabetes, is an autoimmune disorder in which the immune system attacks and destroys insulin-producing beta cells in the pancreas.  It’s not clear why this cellular genocide occurs, but it’s believed that abnormal antibodies, and possibly viral infections, may be involved. Type I accounts for 5-10% of diagnosed diabetes, occurring most commonly in children and young adults, and requires daily insulin intake.  Without this intervention, the body is forced to break down fats for energy, a process that produces ketones (waste products) in the blood, which can result in diabetic ketoacidosis, a highly toxic state that can lead to a life-threatening coma. Type I diabetics remain insulin-dependent and require lifetime replacement of insulin, usually via daily injections. However, the US Food and Drug Administration has recently approved a new delivery system for insulin that uses an inhaler. 

In Type II, or adult onset diabetes, the pancreas may produce adequate insulin, but for some reason the body ignores it, setting up insulin resistance.  In response, the pancreas pumps out even more insulin to force glucose into the cells, resulting in elevated blood glucose. This form of diabetes is more common, occurring in up to 95% of diabetics and is associated with age, family history, obesity, and certain ethnic groups.  The good news is that type II is largely preventable--even reversible--with proper care.

    
Risk Factors 

The following risk factors may mean an increased risk of diabetes: 

The risk of diabetes type II increases after age 45.

A family history of diabetes is present.

Giving birth to a baby weighing more than nine pounds. In addition, some women develop gestational diabetes during pregnancy.

Obesity, especially carrying excess weight around the middle.

Lack of physical activity.

Serum levels of triglycerides in excess of 250 mg/dL.

High levels of HDL cholesterol.

High blood pressure.

Ethnicity. The incidence of diabetes is higher among African Americans, Hispanics, and Native Americans. 

Symptoms and Diagnosis 

If diabetes is present, there will be indications of hyperglycemia that can be confirmed by measuring the amount of glucose in the urine. Certain physical symptoms may suggest that testing is necessary, such as: 

Excessive thirst.

Increased urination.

Blurred vision.

Dizziness.

Fatigue

The appearance of skin tags.

Sweet smelling breath, which indicates ketosis, or an elevation of ketones in the blood. 

Standard testing for diabetes is a measurement of blood glucose after a short period of fasting. Prediabetes may be indicated if glucose measures more than 100 mg/dL. Diabetes is confirmed if this measurement exceeds 125 mg/dL. 

Glucose tolerance and insulin response may be determined by measuring glucose levels in the blood after the subject is given glucose. Prediabetes may be indicated if serum glucose levels are higher than 140 mg/dL. Diabetes is confirmed if glucose levels exceed 200 mg/dL. 

In addition, a HbA1c test may be used to measure the average blood glucose level present during the previous two to four months. A normal range is within 60 and 120 mg/dL, with the ideal level for a diagnosed diabetic being 150 mg/dL or less. 

Treatment Goals for Diabetics 

Obviously, not all diabetic patients can be treated in the same manner. Treatment depends on the severity and progression of the disease, as well as individual insulin response. For instance, while all type I diabetics require insulin replacement therapy, not all type II diabetics benefit from boosting serum insulin levels. For one thing, simply increasing blood insulin levels doesn’t solve the problem of the body underutilizing this hormone. In fact, the pancreas may be stimulated to produce even more of the hormone in a futile attempt to complete this task. Yet, high levels of glucose remain and even more insulin is released, leading to increased oxidative damage and overtaxing of the pancreas. Therefore, a better treatment goal for type II diabetes is to stimulate insulin receptors in cell membranes to be more sensitive to insulin.  

Following this line of thought, several new drug therapies designed to promote insulin sensitization have emerged, including a class of drugs known as thiazolidinediones (TZDs). TZDs not only improve insulin sensitivity at receptor sites, but also increase insulin release from pancreatic beta cells. In addition, TZDs also provide protection from vascular damage and can lower blood pressure. However, these drugs can also pose a risk of liver damage and necessitate regular monitoring of liver enzymes. 

The most commonly prescribed oral drug for diabetics today, Metformin, also increases insulin sensitivity and is better tolerated than many TZDs, but is not without risks. Metformin therapy can lead to a deficiency of vitamin B12 and folic acid, as well as elevated levels of the amino acid homocysteine, which is also associated with the development of atheriosclerosis. In addition, treatment with this drug is not appropriate for individuals with kidney disease or congestive heart failure. 

Advanced diabetes translates to severe hyperglycemia, in which the pancreas has been overloaded with trying to keep up with insulin production over a long period of time. Without aggressive intervention, serum levels of glucose can rise to very dangerous levels in these patients. In fact, glucose levels must be carefully monitored several times a day.  

Diet and exercise are of concern to both type I and type II diabetics. In fact, diet and exercise may play a larger role in managing type II diabetes than medication. According to the American Diabetes Association, the diet should consist of foods low in saturated fats and high in fiber and unrefined carbohydrates. 

Recommended Supplements in the Treatment of Diabetes 

Vitamin C 

Studies indicate that vitamin C supplementation may inhibit aldose reductase, the enzyme that converts glucose to sorbitol. Normally, some of this sorbitol is converted to fructose and any excess sorbitol is excreted. However, if there isn’t enough cellular glucose available, this conversion doesn’t take place and an accumulation of sorbitol occurs. This accumulation is a major contributor to diabetes-related complications. In fact, high concentrations of sorbitol can be found in the nerve, eye and kidney cells diabetics. Further, since the delivery of vitamin C to cells is insulin-driven, diabetics may be deficient in this important antioxidant.  

Vitamin E 

Vitamin E has consistently shown to be helpful in preventing the development of diabetes type II. Vitamin E also improves insulin sensitivity and may help to deter the development of certain diabetes-related complications, including peripheral neuropathy.  

Quercetin 

Plant-based flavonoids such as quercetin naturally increase insulin production. Quercetin also helps to inhibit the effects of glycation, as well as help prevent the accumulation of sorbital. 

Carnitine 

Numerous studies show that carnitine, often found to be deficient in type II diabetics, reduces blood glucose and HbA1c levels while improving insulin sensitivity and carbohydrate conversion. In addition, a large trial showed evidence that carnitine provides positive benefit to diabetics by inhibiting damage to nerves that supply blood to the heart, a condition known as cardiac autonomic neuropathy. 

Coenzyme Q10 (CoQ10) 

Several studies indicate that CoQ10 may reduce blood pressure, improve blood circulation and help to deter cellular damage from oxidative stress. There is also evidence to suggest that this nutrient improves blood sugar control as evidenced by a reduction in HbA1c levels. In addition, this nutrient, which is often deficient in diabetics, can help to lower triglycerides and increase HDL cholesterol levels. 

Biotin  

Biotin is a water-soluble member of the B-complex family, sometimes referred to as vitamin H or B7. Some studies show that biotin may provide several benefits for type II diabetes patients, including improved glucose tolerance and insulin sensitivity. Biotin also enhances the action of glucokinase, an enzyme involved in the metabolism of glucose in the liver. 

Alpha Lipoic Acid (ALA) 

Also known as thiotic acid, ALA is used by every cell of the body. Its primary action is to increase glucose uptake in skeletal muscles, as well as improve glucose metabolism. In addition, the results of a preliminary study showed that daily supplementation with ALA for 18 months slowed the progression of kidney damage in both type 1 and type 2 diabetics. Researchers have also found that ALA can significantly decrease the frequency and severity of pain associated with neuropathy. In fact, ALA has been the standard treatment for diabetic neuropathy in Europe for more than 30 years.  

Herbs Used in the Treatment of Diabetes 

French Maritime Pine

French maritime pine tree bark yields a powerful antioxidant known as pycnogenol, which has been the subject of more than 180 studies over a span of four decades. Researchers have discovered that this agent has the ability to reduce high blood pressure, LDL cholesterol and blood glucose without affecting insulin levels. Of particular interest to researchers is a demonstrated ability to inhibit leakage into the retina associated with diabetic retinopathy. In fact, this very substance is the leading prescription for diabetic retinopathy in France. 

Cinnamon 

Cinnamon is currently being evaluated for its ability to improve glucose metabolism in type II diabetics. Its water-based polyphenols, namely proanthocyanidins, stimulate cell membrane insulin receptors, significantly increasing glucose uptake and reducing blood glucose levels.  In one recent study, cinnamon also reduced triglyceride levels by 18% and lipoprotein (LDL) by 7%, indicating that it may also lower the risk of cardiovascular disease, a condition closely linked to diabetes. Of particular note, is the recent finding that cinnamon-based proanthocyanidins inhibit the formation of AGEs. 

Coffee 

Coffee berries also show promise in blood glucose management.  Coffee berries contain caffeic and chlorogenic acids, which inhibit the action of the glucose-6-phospatase enzyme to reduce excess glucose production from liver-stored glycogen.  Like cinnamon-derived proanthocyanidins, caffeic acid also increases cellular glucose uptake, and is available in supplemental form. 

Green Tea 

A new study published in the American Journal of Clinical Nutrition examined the effects of green tea extract on glucose tolerance and fat oxidation during moderate-intensity exercise (stationary cycling) in men. Since the results revealed an average fat oxidation rates were 17% higher and an increase of 13% in insulin sensitivity, the researchers concluded that supplementation with green tea extract helps to promote insulin sensitivity and glucose tolerance. In addition, the compounds found in green tea, epigallocatechins, have been shown to deter beta cell destruction and to regulate inducible nitric oxide synthase, the latter of which may slow the progression of diabetes-related complications. 

Bitter Melon  

Bitter melon is a tropical fruit that has earned the common name of vegetable insulin. Extracts obtained from the unripe fruit have been shown to increase glycogen metabolism by stimulating GLUT4 expression, a transporter of glucose that has been compared to the drug Metformin in efficacy. In addition, bitter melon extract increases insulin secretion from the pancreas as effectively as treatment with sulfonylureas. It also appears to exhibit anti-hyperglycemic effects by inhibiting alpha-glucosidase, an enzyme required to digest carbohydrates and for the intestinal absorption of glucose.

Safety Precautions 

Vitamin C 

Do not take if you have kidney disease or a history of kidney stones. 

Consult with a physician before supplementing if you have sickle cell anemia, sideroblastic anemia, hemochromatosis, or erythrocyte glucose-6-phosphate dehydrogenase (G6PD) deficiency due to the risk of iron toxicity. 

Vitamin E 

Consult with a physician if you have liver disease, peptic ulcers, a vitamin K deficiency, or if you are taking warfarin (Coumadin). 

Coenzyme Q10 

Monitor blood glucose levels regularly. 

CoQ10 may be depleted by the use of statin drugs. 

Biotin 

May interact with certain anti-seizure medications. 

French Maritime Pine 

May interfere with the effects of immunosuppressants and chemotherapy agents. 

Green Tea 

Consult with a physician if you are taking warfarin (Coumadin or other blood thinners before supplementing. 

Discontinue use two weeks before and after any surgical procedure. 

Bitter Melon 

References


Corti A, Ferrari SM, et al. UV light increases vitamin C uptake by bovine lens epithelial cells. Mol Vis. 2004 Aug 6;10:533–6.

Will JC, Byers T. Does diabetes mellitus increase the requirement for vitamin C? Nutr Rev. 1996 Jul;54(7):193–202.

Antoniades C, Tousoulis D, et al. Vascular endothelium and inflammatory process, in patients with combined type 2 diabetes mellitus and coronary atherosclerosis: The effects of vitamin C. Diabet Med. 2004 Jun;21(6):552–8.

Manzella D, Barbieri M, et al. Chronic administration of pharmacologic doses of vitamin E improves the cardiac autonomic nervous system in patients with type 2 diabetes. Am J Clin Nutr. 2001 Jun;73(6):1052–7.

Tutuncu NB, Bayraktar M, et al. Reversal of defective nerve conduction with vitamin E supplementation in type 2 diabetes: A preliminary study. Diabetes Care. 1998 Nov;21(11):1915–8.

Mingrone G. Carnitine in type 2 diabetes. Ann N Y Acad Sci. 2004 Nov;1033:99–107. Review.

Turpeinen AK, Kuikka J, et al. Long-term effect of acetyl-L-carnitine on myocardial 123I-M IBG uptake in patients with diabetes. Clin Auton Res. 2005;10:13–6.

Watts GF, Playford DA, et al. Coenzyme Q(10) improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus. Diabetologia. 2002 Mar;45(3):420–6.

Montonen J, Knekt P, et al. Dietary antioxidant intake and risk of type 2 diabetes. Diabetes Care. 2004 Feb;27(2):362–6.

Al-Thakafy HS, Khoja SM, et al. Alterations of erythrocyte free radical defense system, heart tissue lipid peroxidation, and lipid concentration in streptozotocin-induced diabetic rats under coenzyme Q10 supplementation. Saudi Med J. 2004 Dec;25(12):1824–30.

Playford DA, Watts GF, et al. Combined effect of coenzyme Q10 and fenofibrate on forearm microcirculatory function in type 2 diabetes. Atherosclerosis. 2003 May;168(1):169–79.

Hodgson JM, Watts GF, et al. Coenzyme Q10 improves blood pressure and glycaemic control: A controlled trial in subjects with type 2 diabetes. Eur J Clin Nutr. 2002 Nov;56(11):1137–42.

Kucharska J, Braunova Z, et al. Deficit of coenzyme Q in heart and liver mitochondria of rats with streptozotocin-induced diabetes. Physiol Res. 2000;49(4):411–8.

Furukawa Y. [Enhancement of glucose-induced insulin secretion and modification of glucose metabolism by biotin]. Nippon Rinsho. 1999 Oct;57(10):2261–9. Review.

Zhang H, Osada K, et al. A high biotin diet improves the impaired glucose tolerance of long-term spontaneously hyperglycemic rats with non-insulin-dependent diabetes mellitus. J Nutr Sci Vitaminol (Tokyo). 1996 Dec;42(6):517–26.

Song KH, Lee WJ, et al. Alpha-lipoic acid prevents diabetes mellitus in diabetes-prone obese rats. Biochem Biophys Res Commun. 2005 Jan 7;326(1):197–202.

Doggrell SA. Alpha-lipoic acid, an anti-obesity agent? Expert Opin Investig Drugs. 2004 Dec;13(12):1641–3.

Melhem MF, Craven PA, et al. Alpha-lipoic acid attenuates hyperglycemia and prevents glomerular mesangial matrix expansion in diabetes. J Am Soc Nephrol. 2002 Jan;13(1):108–16.

Ametov AS, Barinov A, et al. The sensory symptoms of diabetic polyneuropathy are improved with alpha-lipoic acid: The SYDNEY trial. Diabetes Care. 2003 Mar;26(3):770–6.

Kamuren ZT, McPeek CG, Sanders RA, et al. Effects of low-carbohydrate diet and Pycnogenol treatment on retinal antioxidant enzymes in normal and diabetic rats. J Ocul Pharmacol Ther. 2006 Feb;22(1):10-8.

Spadea L, Balestrazzi E. Treatment of vascular retinopathies with Pycnogenol.
Phytother Res. 2001 May;15(3):219-23.

Anderson RA. Chromium and polyphenols from cinnamon improve insulin sensitivity.
Proc Nutr Soc. 2008 Feb;67(1):48-53.

Peng X, Cheng KW, Ma J, et al. Cinnamon bark proanthocyanidins as reactive carbonyl scavengers to prevent the formation of advanced glycation endproducts. J Agric Food Chem. 2008 Mar 26;56(6):1907-11. Epub 2008 Feb 20.

Solomon TP, Blannin AK. Effects of short-term cinnamon ingestion on in vivo glucose tolerance. Diabetes Obes Metab. 2007 Nov;9(6):895-901.

Cao H, Polansky MM, Anderson RA. Cinnamon extract and polyphenols affect the expression of tristetraprolin, insulin receptor, and glucose transporter 4 in mouse 3T3-L1 adipocytes.

Charles-Bernard M, Kraehenbuehl K, et al. Interactions between volatile and nonvolatile coffee components. 1. Screening of nonvolatile components. J Agric Food Chem. 2005 Jun 1;53(11):4417–25.

Basu R, Chandramouli V, et al. Obesity and type 2 diabetes impair insulin-induced suppression of glycogenolysis as well as gluconeogenesis. Diabetes. 2005 Jul;54(7):1942–8.

Cheng JT, Liu IM. Stimulatory effect of caffeic acid on alpha1A-adrenoceptors to increase glucose uptake into cultured C2C12 cells. Naunyn Schmiedeberg’s Arch Pharmacol. 2000 Aug;362(2):122–7.

Hsu FL, Chen YC, et al. Caffeic acid as active principle from the fruit of Xanthium strumarium to lower plasma glucose in diabetic rats. Planta Med. 2000 Apr;66(3):228–30.

Hemmerle H, Burger HJ, et al. Chlorogenic acid and synthetic chlorogenic acid derivatives: Novel inhibitors of hepatic glucose-6-phosphate translocase. J Med Chem. 1997 Jan 17;40(2):137–45.

Venables MC, Hulston CJ, Cox HR, et al. Green tea extract ingestion, fat oxidation, and glucose tolerance in healthy humans. Am J Clin Nutr. 2008 Mar;87(3):778-84.

Hung PF, Wu BT, et al. The antimitogenic effect of green tea (-)-epigallocatechin gallate on 3T3-L1 preadipocytes depends on the Erk and Cdk2 pathways. Am J Physiol Cell Physiol. 2005 May;288(5):C1094–108.

Kim MJ, Ryu GR, et al. Inhibitory effects of epicatechin on interleukin-1beta-induced inducible nitric oxide synthase expression in RINm5F cells and rat pancreatic islets by down-regulation of NF-kappaB activation. Biochem Pharmacol. 2004 Nov 1;68(9):1775–85.

Crespy V, Williamson G. A review of the health effects of green tea catechins in vivo animal models. J Nutr. 2004 Dec;134(12 Suppl):3431S–3440S.