Diabetes

The consequences of uncontrolled diabetes are severe blindness, kidney failure, increased risk of heart disease, and painful peripheral nerve damage. Today, most practitioners focus treatment on strict blood sugar control. While diabetes is characterized by excess blood glucose (the form of sugar used by cells as energy), this simplified approach can actually hasten the progression of the most common form of diabetes and does nothing to address the damage it causes.

A new approach to diabetes recognition and treatment is needed because the conventional wisdom has failed us. America is in the midst of a diabetes epidemic. Over the past 20 years, the number of adults diagnosed with diabetes has more than doubled, and children are being diagnosed with diabetes in alarming numbers. Diabetes has rapidly emerged as a leading culprit in the epidemic of heart disease, as well as being a leading cause of amputation and blindness among adults.

It is crucial that diabetics (and those predisposed to diabetes) understand the ways in which blood glucose causes damage and take active steps to interrupt these processes. The most notorious process is glycation (i.e., sugar molecules reacting with proteins to produce nonfunctional structures in the body). Glycation compromises proteins throughout the body, thus is a key feature of diabetes-related complications (e.g., nerve damage, heart attack, and blindness).

Oxidative stress is also central to the damage caused by diabetes. Diabetics suffer from high levels of free radicals that damage arteries throughout the body. It is important that diabetics understand the need for antioxidant therapy to help reduce oxidative stress and lower the risk of diabetic complications.

The Difference Between Type 1 And Type 2 Diabetes

There are two types of diabetes: type 1 and type 2. Underlying both forms of diabetes is a disorder of insulin production, use, or both. Insulin is a hormone responsible for transporting glucose into cells. When there is excess glucose in the blood, insulin is secreted from the pancreas and signals the liver and muscles to store glucose as glycogen. Insulin also stimulates adipose tissue to store glucose as fat for long-term energy reserves. Insulin receptors are found in all cells throughout the body. In a healthy person, blood glucose levels are extremely stable (Kumar 2005). Normal fasting glucose levels range between 70 and 100 mg/dL.

Type 1 diabetes. Type 1 diabetes, formerly known as insulin-dependent diabetes, is an autoimmune condition that occurs when the body attacks and destroys the cells (called beta-cells or β-cells) that make insulin. Type 1 diabetes accounts for about 5 to 10 percent of cases. Because type 1 diabetics can no longer make insulin, insulin replacement therapy is essential.

Type 2 diabetes. Type 2 diabetes, formerly known as non-insulin-dependent diabetes, occurs when the body is no longer able to use insulin effectively and gradually becomes resistant to its effects. It is a slowly progressing disease that goes through identifiable stages. In the early stages, both insulin and glucose levels are elevated (conditions called hyperinsulinemia and hyperglycemia, respectively). In the later stages, insulin levels are reduced, and blood glucose levels are very elevated. Although few people are aware of this crucial distinction, therapy for type 2 diabetes should be tailored to the stage of the disease.

Risk factors for type 2 diabetes include aging, obesity, family history, physical inactivity, ethnicity, and impaired glucose metabolism. Type 2 diabetes is also a prominent risk of metabolic syndrome, a constellation of conditions that includes insulin resistance along with hypertension, lipid disorders, and overweight.

Glycation and oxidative stress are central to the damage caused by diabetes. Unfortunately, neither of them figures into conventional treatment for diabetes, which is generally concerned only with blood sugar control.

Glycation occurs when glucose reacts with protein, resulting in sugar-damaged proteins called advanced glycation end products (AGEs) (Kohn 1984; Monnier 1984). One well-known AGE among diabetics is glycated hemoglobin (HbA1c). HbA1c is created when glucose molecules bind to hemoglobin in the blood. Measuring HbA1c in the blood can help determine the overall exposure of hemoglobin to glucose, which yields a picture of long-term blood glucose control.

Glycated proteins damage cells in numerous ways, including impairing cellular function, which induces the production of inflammatory cytokines (Wright 2006) and free radicals (Forbes 2003; Schmidt 2000). In animal studies, inhibiting glycation protects against damage to the kidney, nerves, and eyes (Forbes 2003; Sakurai 2003). In a large human trial, each 1 percent reduction in HbA1c correlated with a 21 percent reduction in risk for any complication of diabetes, a 21 percent reduction in deaths related to diabetes, a 14 percent reduction in heart attack, and a 37 percent reduction in microvascular complications (Stratton 2000).

High levels of blood glucose and glycation also produce free radicals that further damage cellular proteins (Vincent 2005) and reduce nitric oxide levels. Nitric oxide is a potent vasodilator that helps keep arteries relaxed and wide open. Oxidative stress in diabetes is also linked to endothelial dysfunction, the process that characterizes atherosclerotic heart disease. According to studies, diabetes encourages white blood cells to stick to the endothelium (i.e., the thin layer of cells that line the inside of arteries). These white blood cells cause the local release of pro-inflammatory chemicals that damage the endothelium, accelerating atherosclerosis (Lum 2001). Diabetes is closely associated with severe coronary heart disease and increased risk of heart attack.

Common symptoms of diabetes include increased thirst and urination, unusual weight changes, irritability, fatigue, and blurry vision. Clinical abnormalities include hyperglycemia and glucose in the urine. The breath might smell sweet because of ketones in the blood (ketosis), which are naturally sweet smelling. Dark outgrowths of skin (skin tags) may also appear.

The most common clinical tests used to diagnose diabetes are measures of blood glucose. The fasting plasma glucose (FPG) test measures the amount of glucose in the blood after fasting. Prediabetes is diagnosed if the fasting blood glucose level is between 100 and 125 mg/dL. Diabetes is diagnosed if the fasting blood glucose level rises to 126 mg/dL or above.

The oral glucose tolerance test (OGTT) is used to measure insulin response to high glucose levels. During this test, patients are given glucose, and the rise in blood glucose levels is measured. Prediabetes is diagnosed if the glucose level rises to between 140 and 199 mg/dL. Diabetes is diagnosed if blood glucose levels rise to 200 mg/dL or higher.

The HbA1c test is also helpful in diagnosing less severe cases of diabetes. From this test, clinicians can estimate the average blood glucose level during the preceding two to four months. Normally 4 to 6 percent of hemoglobin is glycosylated, which corresponds to average blood glucose between 60 and 120 mg/dL. Mild hyperglycemia increases HbA1c to 8 to 10 percent (or 180 to 240 mg/dL), while severe hyperglycemia increases HbA1c values up to 20 percent. For diabetics, a healthy HbA1c level is less than 7 percent, which corresponds to an average blood glucose level of 150 mg/dL or less.

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

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

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

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

A Program For Early Diabetics

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

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

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

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

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

Metformin: Increasing Insulin Sensitivity

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

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

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

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

Drug Therapy For Advanced Diabetics

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

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

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

What You Have Learned So Far

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

Type 1 diabetics will need to be on insulin therapy for life, although the supplements mentioned in this section may help offset some of the complications caused by diabetes (e.g., reduced antioxidant capacity and glycation) as well enhance glucose metabolism. Type 2 diabetics can counteract the progression of their disease by improving insulin sensitivity, enhancing glucose metabolism, and attempting to mitigate the complications of diabetes. The following supplements have been shown to improve blood sugar control or limit diabetic damage:

Lipoic acid. As a powerful antioxidant, lipoic acid positively affects important aspects of diabetes, including blood sugar control and the development of long-term complications such as disease of the heart, kidneys, and small blood vessels (Jacob 1995, 1999; Kawabata 1994; Melhem 2002; Nagamatsu 1995; Song 2005; Suzuki 1992).

Lipoic acid plays a role in preventing diabetes by reducing fat accumulation. In animal studies, lipoic acid reduced body weight, protected pancreatic β-cells from destruction, and reduced triglyceride accumulation in skeletal muscle and pancreatic islets (Doggrell 2004; Song 2005).

Lipoic acid has been approved for the prevention and treatment of diabetic neuropathy in Germany for nearly 30 years. Intravenous and oral lipoic acid reduces symptoms of diabetic peripheral neuropathy (Ametov 2003). Animal studies have suggested that lipoic acid is more effective when taken with gamma-linolenic acid (GLA) (Cameron 1998; Hounsom 1998).

Diabetes also damages deep nerves that control vital organs, such as the heart and digestive tract. In a large clinical trial, diabetics (with symptoms caused by nerve damage affecting the heart) showed significant improvement without significant side effects from 800 mg oral lipoic acid daily (Ziegler 1997a,b).

Biotin. Biotin enhances insulin sensitivity and increases the activity of glucokinase, the enzyme responsible for the first step in the utilization of glucose by the liver. Glucokinase concentrations in diabetics are very low. Animal studies have shown that a high biotin diet can improve glucose tolerance and enhance insulin secretion (Zhang 1996; Furukawa 1999).

Carnitine. An extensive body of literature supports the use of carnitine in diabetes (Mingrone 2004). Carnitine lowers blood glucose and HbA1c levels, increases insulin sensitivity and glucose storage, and optimizes fat and carbohydrate metabolism. Carnitine deficiency is common in type 2 diabetes. In a large human trial, acetyl-L-carnitine helped prevent or slow cardiac autonomic neuropathy in people with diabetes (Turpeinen 2005).

Carnosine. Carnosine is a glycation inhibitor that has been shown to exhibit protective effects against diabetic nephropathy and reduce the formation of AGEs (Janssen 2005; Yan 2005).

Studies show that diabetics’ cells have lower-than-normal carnosine levels, similar to levels in older adults (McFarland 1994). Carnosine lowers elevated blood sugar levels, limits oxidant stress and elevated inflammation, and prevents protein cross-linking in diabetics and otherwise healthy aging adults (Jakus 2003; Hipkiss 2005; Nagai 2003; Hipkiss 2001; Aldini 2005). Additionally, carnosine works ‘behind the scenes’ to offer the following protection (for diabetics) against the physiological destruction caused by high blood sugar:

  • Carnosine reduces oxidation and glycation of low-density lipoprotein (LDL), which helps decrease the incidence of diabetes-induced atherosclerosis (Lee 2005; Rashid 2007).
  • Carnosine reduces protein cross-linking in the lens of the eye and helps to reduce the risk of cataract (a common diabetic complication) (Yan 2005; Yan 2008).
  • Carnosine supplementation also prevents the microscopic blood vessel damage that produces diabetic retinopathy, a major cause of blindness in diabetics (Pfister 2011).
  • Carnosine supplements prevent loss of sensory nerve function (neuropathy) in diabetic animals (Kamei 2008).

Chromium. Chromium is an essential trace mineral that plays a significant role in sugar metabolism. Chromium supplementation helps control blood sugar levels in type 2 diabetes and improves metabolism of carbohydrates, proteins, and lipids. Several studies have shown encouraging results from chromium supplementation:

  • A controlled human study of type 2 diabetics compared two forms of chromium (brewer’s yeast and chromium chloride) (Bahijiri 2000). Both forms of chromium significantly improved blood sugar control. Positive results were also seen in two smaller human trials (Ghosh 2002; Jovanovic 1999).
  • A large human trial compared the effects of 1000 mcg chromium, 200 mcg chromium, and placebo (Anderson 1997). HbA1c values improved significantly in the group receiving 1000 mcg after two months and in both chromium groups after four months. Fasting glucose was also lower in the group taking the higher dose of chromium. Chromium is a highly reactive metal ion, requiring balance through additional organic materials in order to stabilize and enhance its effects.Amla(Indian gooseberry) and shilajit have more recently been shown to synergistically enhance chromium’s beneficial action. In a randomized clinical trial of 150 individuals with type 2 diabetes, 200 mcg twice per day of this novel chromium compound in addition to standard medication induced a greater reduction in fasting blood glucose than placebo (6%on average) and lowered postprandial blood glucose (14.2%) after just two months (Bhattacharyya 2010).

Coenzyme Q10. Coenzyme Q10 (CoQ10) improves blood sugar control, lowers blood pressure, and prevents oxidative damage caused by disease. In a controlled human trial, type 2 diabetics given 100 mg CoQ10 twice daily experienced improved glycemic control as measured by lower HbA1c levels and blood pressure (Hodgson 2002). In a separate study, CoQ10 improved blood flow in type 2 diabetics, an outcome attributed to CoQ10’s ability to lower vascular oxidative stress (Watts 2002). In a third study, improved blood flow correlated with decreased HbA1c (Playford 2003).

In animal studies, CoQ10 quenched free radicals, improved blood flow, lowered triglyceride levels, and raised HDL levels, suggesting a role for CoQ10 in preventing and managing complications of diabetes (Al-Thakafy 2004). Animal studies have also shown that CoQ10 levels are depleted by diabetes (Kucharska 2000).

Dehydroepiandrosterone. Recent studies have yielded very encouraging results supporting dehydroepiandrosterone (DHEA) supplementation in diabetics. DHEA has been shown to improve insulin sensitivity and obesity in human and animal models (Yamashita 2005). Although its mechanism of action is poorly understood, it is thought that DHEA improves glucose metabolism in the liver (Yamashita 2005).

Animal studies have also demonstrated that DHEA increases β-cells on the pancreas, which are responsible for producing insulin (Medina 2006).

In humans, DHEA levels are sensitive to elevated glucose; thus, higher glucose levels tend to be associated with decreased DHEA levels (Boudou 2006). One proposed mechanism of action in humans is linked to DHEA’s metabolism into testosterone. DHEA is an adrenal hormone that can be converted into either testosterone or estrogen. Studies have shown that testosterone improves insulin sensitivity in men, suggesting that DHEA’s conversion into testosterone may be responsible for its beneficial effects in improving insulin sensitivity (Kapoor 2005).

Essential fatty acids. In human experiments, omega-3 fatty acids lowered blood pressure and triglyceride levels, thereby relieving many of the complications associated with diabetes. In animals, omega-3 fatty acids cause less weight gain than other fats do; they have also been shown to have a neutral effect on LDL, while raising HDL and lowering triglycerides (Petersen 2002). There are two types of essential fatty acids:

  • Omega-3. Marine oil contains omega-3 fatty acids. The research on omega-3 fatty acids stems from studies of the Inuit (Eskimo) people, who seldom suffer from heart attacks even though their diets contain an enormous amount of fat from fish, seals, and whales, presumably because these are very high in omega-3 fatty acids. Omega-3 fatty acids found in marine oil lower blood triglyceride levels, contribute to “thinning” blood, and decrease inflammation (Ebbesson 2005). These effects partially explain many of fish oil’s benefits.
  • Omega-6. Diabetic neuropathy is a gradual degeneration of peripheral nerve tissue. There is some evidence that GLA, an omega-6 fatty acid, can be helpful if given long enough to work. In one double-blind, placebo-controlled study, 111 people with mild diabetic neuropathy received either 480 mg daily of GLA or placebo. After 12 months, the group taking GLA was doing significantly better than the placebo group in 13 out of 16 measures of nerve function, with patients whose diabetes was under control doing best (Keen 1993). There is also evidence that GLA is more effective for diabetic neuropathy when combined with lipoic acid (Hounsom 1998).

Fiber. Eating a diet rich in high-fiber foods prevents and reduces the harm caused by chronically elevated blood glucose.

One study reported the results of diabetic individuals consuming a diet supplying 25 grams of soluble fiber and 25 grams of insoluble fiber (about double the amount currently recommended by the American Diabetes Association). The fiber was derived from foodstuffs, with no emphasis placed on special or unusual fiber-fortified foods or fiber supplements. A high-fiber diet reduced blood glucose levels by an average of 10 percent (Chandalia 2000).

Fiber is also valuable because it produces a feeling of satiety, reducing the desire to overeat. Because high-fiber foods are digested more slowly than other foods, hunger pangs are forestalled. For the most part, fibrous foods are healthful (nutrient dense and low-fat).

Fiber should be added slowly, gradually replacing low-fiber foods, for the following reasons: (1) insulin and prescription drugs may have to be adjusted to accommodate lower blood glucose levels, and (2) without a gradual introduction of the new material, intestinal distress could occur, including bloating, flatulence, and cramps.

Some individuals prefer to bolster fiber volume by adding supplemental fiber in the form of pectin, gums, and mucilages to each meal. Calculate the amount of fiber gained from foodstuffs and supplement with enough to compensate for shortfalls. Monitor blood glucose levels closely to assess gains and adjust oral or injectable hypoglycemic agents.

Propolmannan. Specially processed, propolmannan is a polysaccharide fiber derived from a plant (Amorphophallus konjac) that grows only in the remote mountains of Northern Japan.

Used throughout Asia as a source of bulk in the diet, it creates a viscous barrier that impedes carbohydrate digestion, suppressing postprandial (after-meal) blood sugar surges. Propolmannan also slows “gastric emptying”—the passage of food from the stomach into the small intestine—impeding carbohydrate overexposure in the digestive tract. Propolmannan’s power to safely suppress postprandial glucose surges has generated compelling results. In a group of 72 diabetics given konjac foods, postprandial glucose levels fell by an average of 84.6% (Huang 1990).

In placebo-controlled human studies, those taking propolmannan before meals lost 5.5 to 7.92 pounds after eight weekswithout changing their diets. The placebo groups in these studies showed no significant weight loss. The propolmannan groups also showed reductions in blood lipid/glucose levels (Walsh 1984; Biancardi 1989).

Flavonoids. Flavonoids are antioxidants that help reduce damage associated with diabetes. In animal studies, quercetin, a potent flavonoid, decreased levels of blood glucose and oxidants. Quercetin also normalized levels of the antioxidants superoxide dismutase, vitamin C, and vitamin E. Quercetin is more effective at lower doses and ameliorates the diabetes-induced changes in oxidative stress (Mahesh 2004).

Magnesium. Diabetics are often deficient in magnesium, which is depleted by medications and the disease process (Eibl 1995; Elamin 1990; Tosiello 1996). One double-blind study suggested that magnesium supplementation enhanced blood sugar control (Rodriguez-Moran 2003).

N-acetylcysteine. N-acetylcysteine (NAC) is a powerful antioxidant that is used to treat acetaminophen overdose. Among diabetic rats, it has also demonstrated the ability to protect the heart against endothelial damage and oxidative stress that is associated with heart attacks among diabetics. In one study, NAC was able to increase the availability of nitric oxide in diabetic rats, thus improving their blood pressure as well as reducing the level of oxidative stress in their hearts (Xia 2006). In a human study examining the effects of broad-based antioxidants, NAC, in addition to vitamins C and E, was able to reduce oxidative stress after a moderate-fat meal (Neri 2005).

Silymarin. In animal studies, silymarin was shown to improve insulin levels among induced cases of diabetes (Soto 2004). A small, controlled clinical study evaluated type 2 diabetics with alcohol-induced liver failure (Velussi 1997). Those receiving 600 mg silymarin daily experienced a significant reduction in fasting blood and urine glucose levels. Fasting glucose levels rose slightly during the first month of supplementation but declined thereafter from an average of 190 mg/dL to 174 mg/dL. As daily glucose levels dropped (from an average of 202 mg/dL to 172 mg/dL), HbA1c also substantially decreased. Throughout the course of treatment, fasting insulin levels declined by almost one-half, and daily insulin requirements decreased by about 24 percent. Liver function improved. A lack of hypoglycemic episodes suggests silymarin lowered as well as stabilized blood glucose levels.

Vitamin B3. Vitamin B3 (niacin) is required for the proper function of more than 50 enzymes. Without it, the body is not able to release energy or make fats from carbohydrates. Vitamin B3 is also used to make sex hormones and other important chemical signal molecules.

In the past, the use of niacin was discouraged in diabetic individuals because it was found to increase insulin resistance and degrade glycemic control, particularly at high doses (Sancetta 1951). However, emerging clinical evidence shows that niacin is both safe and effective for diabetics (Meyers 2004).

There is evidence that niacin reduces the risk of developing type 1 diabetes (Pocoit 1993; Pozzilli 1993). Niacinamide helps restore β-cells, or at least slow their destruction. Because niacin can disrupt blood sugar control in diabetics, individuals taking any form of niacin, including inositol hexaniacinate, must closely monitor blood sugar levels and discontinue treatment in the event of worsening of diabetic control. Inositol hexaniacinate has long been used in Europe to lower cholesterol levels and improve blood flow in individuals with intermittent claudication.

Vitamin C. Several preclinical studies evaluated vitamin C’s role during mild oxidative stress. The aqueous humor of the eye provides surrounding tissues with a source of vitamin C. Since animal studies have shown that glucose inhibits vitamin C uptake, this protective mechanism may be impaired in diabetes (Corti 2004). Supplementation with antioxidant vitamins C and E plays an important role in improving eye health (Peponis 2004). High vitamin C intake depresses glycation, which has important implications for slowing diabetes progression and aging (Krone 2004).

Vitamin C, through its relationship to sorbitol, also helps prevent ocular complications in diabetes. Sorbitol, a sugar-like substance that tends to accumulate in the cells of people with diabetes, tends to reduce the antioxidant capacity of the eye, with a number of possible complications. Vitamin C appears to help reduce sorbitol buildup (Will 1996).

Vitamin C also has a role in reducing the risk of other diabetic complications. In one clinical study, vitamin C significantly increased blood flow and decreased inflammation in patients with both diabetes and coronary artery disease (Antoniades 2004). Three studies suggest that vitamin C, along with a combination of vitamins and minerals (Farvid 2004), reduces blood pressure in people with diabetes (Mullan 2002) and increases blood vessel elasticity and blood flow (Mullan 2004).

Vitamin E. Vitamin E has been shown to significantly reduce the risk of developing type 2 diabetes (Montonen 2004). One double-blind trial found a reduction in the risk of cardiac autonomic neuropathy, or damage to the nerves that supply the heart, which is a complication of diabetes (Manzella 2001). Additional evidence documented benefits for diabetic peripheral neuropathy (Tutuncu 1998), blood sugar control (Kahler 1993; Paolisso 1993a,b; Paolisso 1994), and cataract prevention (Paolisso 1993a,b; Paolisso 1994; Seddon 1994). In addition, vitamin E enhances sensitivity to insulin in type 2 diabetics (Paolisso 1993a,b).

Botanical Supplements For Diabetes

Before insulin, botanical medicines were used to treat diabetes. They are remarkably safe and effective. However, because many botanical medicines function similarly to insulin, people taking oral diabetes medications or insulin should use caution to avoid hypoglycemia. Botanical medicines should be integrated into a regimen of adequate exercise, healthy eating, nutritional supplements, and medical support.

Cinnamon. Cinnamon has been used for several thousand years in traditional Ayurvedic and Greco-European medical systems. Native to tropical southern India and Sri Lanka, the bark of this evergreen tree is used to manage conditions such as nausea, bloating, flatulence, and anorexia. It is also one of the world’s most common spices, used to flavor everything from oatmeal and apple cider to cappuccino. Recent research has revealed that regular use of cinnamon can also promote healthy glucose metabolism.

Astudy at the US Department of Agriculture’s Beltsville Human Nutrition Research Center isolated insulin-enhancing complexes in cinnamon that are involved in preventing or alleviating glucose intolerance and diabetes (Anderson 2004). Three water-soluble polyphenol polymers were found to have beneficial biological activity, increasing insulin-dependent glucose metabolism by roughly 20-fold in vitro (Anderson 2004). The nutrients displayed significant antioxidant activity as well, as did other phytochemicals found in cinnamon, such as epicatechin, phenol, and tannin. Moreover, scientists determined that these polyphenol polymers are able to upregulate the expression of genes involved in activating the cell membrane’s insulin receptors, thus increasing glucose uptake and lowering blood glucose levels (Imparl-Radosevich 1998).

The problem with long-term cinnamon use is the presence of highly reactive aldehyde compounds. These toxic fat-soluble compounds accumulate in the body over time. An aqueous extract of cinnamon has been identified and through a patented process, delivers cinnamon’s beneficial water-soluble nutrients while removing deleterious fat-soluble toxins.

In a recent double-blind, placebo-controlled trial (Stoecker 2010), a group of individuals (average age 61) with high blood sugar taking 500 mg daily of this form of cinnamon extract experienced an average decline of 12 mg/dL in fasting blood glucose after just two months. It also produced a significant decrease in postprandial glucose spikes (by an average of 32 mg/dL) after ingestion of 75 grams of carbohydrates. These findings support previous clinical data on similar aqueous cinnamon extracts, in which diabetic patients saw their fasting glucose drop an average of 10.3% after four months (Mang 2006).

Brown seaweed and bladderwrack. Another approach in managing glucose levels is to blunt the conversion of starches into their component sugars in the gastrointestinal tract. This can be accomplished safely and effectively by introducing natural enzyme inhibitors that halt carbohydrate metabolism in the gut. The most attractive targets are the sugar-producing alpha-amylase and alpha-glucosidase enzymes.

Extracts from a variety of seaweeds have inhibitory effects on these enzymes (Kim 2010; Apostolidis 2010; Kim 2008; Zhang 2007). Animal studies have revealed that inhibiting these enzymes lowers blood sugar levels (Heo 2009; Lamela 1989). In a recent double-blind, placebo-controlled clinical trial, a single dose of 500 mg daily of bladderwrack and seaweed significantly increased insulin sensitivity while inducing a 48.3% decline in postprandial glucose levels in healthy individuals (Lamarche 2010).

Irvingia gabonensis. Published studies show that extract of the African mango Irvingia gabonensis inhibits alpha-amylase-mediated conversion of carbohydrates into sugar (Oben 2008).

In 2006, researchers studied the effect of Irvingia in rats who were artificially induced to develop diabetes. A single oral dose of Irvingia lowered plasma glucose two hours after treatment (Ngondi 2006).

In 1990, researchers studied the effects of Irvingia on eleven human type 2 diabetics. Compared to baseline, there were significant reductions in blood triglyceride levels (16%), total cholesterol (30%), LDL (39 %), and glucose (38%), while HDL-cholesterol levels were increased by 29% after four-weeks of supplementation. These desirable biochemical effects were accompanied by improved clinical states (Adamson 1990).

Adiponectin is a hormone that plays a critical role in metabolic abnormalities associated with type 2 diabetes, obesity, and atherosclerosis (Berger 2002; Fasshauer 2004; Shand 2003; Yamauchi 2001; Kadowaki 2005; Kershaw 2004; Hotta 2001; Arita 1999; Ryo 2004; Yatagai 2003; Yamamoto 2004). Higher levels of adiponectin enhance insulin sensitivity; enhancing insulin sensitivity as we age is important to long-term metabolic health. Adipogenic transcriptional factors involved with adiponectin are also involved in the formation of new adipocytes, fat burning and endothelial function (Rosen 2000; Gustafson 2003; Oben 2008). Irvingia increases beneficial adiponectin levels and inhibits adipocyte differentiation mediated through the suppression of adipogenic transcription factors (Oben 2008).

White kidney bean. Extracts from the common white kidney bean, Phaseolus vulgaris, are powerful blockers of the enzyme alpha-amylase (Mosca 2008; Obiro 2008). White bean extract shows enormous potential for preventing the blood sugar and insulin spikes associated with many chronic health disorders (Preuss 2007).

Amylase inhibition with white bean extract has proven particularly effective in reducing glycemia (sugar load in the blood) in studies on diabetic animals. Supplementation in diabetic rats not only substantially lowered mean blood sugar levels, but it also reduced the animals’ total food and water intake (water intake is increased in untreated diabetes because of the amount lost in sugar-laden urine) (Tormo 2006).

White bean extract has yielded equally compelling results in human studies. It has been shown to diminish the effects of high-glycemic index foods (like white bread) that are notorious for producing sharp, potentially dangerous postprandial blood sugar spikes, helping to alleviate metabolic burden throughout the body (Udani 2009).

In one notable study, postprandial blood sugar levels were measured in a group of healthy subjects after consuming 50 grams of carbohydrate in the form of wheat, rice, and other high-carbohydrate plant foods (Dilawari 1981). Phaseolus vulgaris inhibited the average post-ingestion spike in blood sugar by 67%.

Green coffee extract. Coffee contains some well-studied phytochemicals such as chlorogenic acid, caffeic acid, ferulic acid, and quinic acid (Charles-Bernard 2005). Some of coffee’s most impressive effects can be seen in blood glucose management. Chlorogenic acid and caffeic acid are the two primary nutrients in coffee that benefit individuals with high blood sugar. Glucose-6-phosphatase is an enzyme crucial to the regulation of blood sugar. Since glucose generation from glycogen stored in the liver is often overactive in people with high blood sugar (Basu 2005), reducing the activity of the glucose-6-phosphatase enzyme leads to reduced blood sugar levels, with consequent clinical improvements.

Chlorogenic acid has been shown to inhibit the glucose-6-phosphatase enzyme in a dose-dependent manner, resulting in reduced glucose production (Hemmerle 1997). In a trial at the Moscow Modern Medical Center, 75 healthy volunteers were given either 90 mg chlorogenic acid daily or a placebo. Blood glucose levels of the chlorogenic acid group were 15 to 20 percent lower than those of the placebo group (Abidoff 1999). Chlorogenic acid also has an antagonistic effect on glucose transport, decreasing the intestinal absorption rate of glucose (Johnston 2003), which may help reduce blood insulin levels and minimize fat storage.

In another trial, researchers gave different dosages of green coffee bean extract, standardized for chlorogenic acid, to 56 people. Thirty-five minutes later, they gave the participants 100 grams of glucose in an oral glucose challenge test. Blood sugar levels dropped by an increasingly greater amount as the test dosage of green coffee bean extract was raised (from 200 mg to 400 mg). At the 400 mg dose, there was a full 24% decrease in blood sugar—just 30 minutes after glucose ingestion (Nagendran 2011).
Green coffee bean extract found in unroasted coffee beans, once purified and standardized, produces high levels of chlorogenic acid and other beneficial polyphenols that can suppress excess blood glucose levels. Roasting destroys much of the coffee bean’s beneficial content.

Garlic. Allium is the active component in garlic and onions. Allium compounds are sulfur-donating compounds that help reconstitute glutathione, a major internal antioxidant. This mechanism is probably responsible for allium’s positive effects. Allium has a number of positive effects that may help reduce the risk of diabetic complications, including the following:

  • Reducing the risk of cardiovascular disease, including atherosclerosis (Breithaupt-Grogler 1997; Efendy 1997; Koscielny 1999; Turner 2004)
  • Decreasing oxidative stress (Dhawan 2004)
  • Promoting weight loss and insulin sensitivity in animal models of diabetes (Elkayam 2003)
  • Lowering blood pressure (Auer 1990; Sharifi 2003; Silagy 1994; Wilburn 2004)
  • Improving cholesterol profile (Durak 2004; Gardner 2001; Holzgartner 1992; Isaacsohn 1998; Kannar 2001; Kris-Etherton 2002; Mader 1990; Neil 1996; Silagy 1994; Steiner 1996; Superko 2000; Warshafsky 1993)

Green tea. The compounds in these plants, including epicatechin, catechin, gallocatechin, and epigallocatechin, are powerful antioxidants, particularly against pancreas and liver toxins (Okuda 1983). Animal studies have shown that epigallocatechins, in particular, may have a role in preventing diabetes (Crespy 2004). In studies with rats, epigallocatechins prevented cytokine-induced β-cell destruction by downregulating inducible nitric oxide synthase, which is a pro-oxidant (Kim 2004; Song 2003). This process could help slow the progression of type 1 diabetes. In vitro studies have also shown that green tea suppresses diet-induced obesity (Murase 2002), a key risk factor in developing diabetes and metabolic syndrome (Hung 2005).

Vitamin D. Vitamin D has far-reaching implications that extend beyond promoting bone health. Over the past 40 years, research has shed light on the intersecting pathways of vitamin D and many other aspects of health.

Evidence from animal experiments and human observational studies suggests that vitamin D may help prevent type I diabetes, perhaps by acting as an immune system modulator (Zittermann 2007). Researchers demonstrated that the pancreatic β-cells of mice contain receptors for 1,25-dihydroxyvitamin D. When they administered this active form of vitamin D to mice early in life, the animals demonstrated a reduced incidence of type I diabetes. However, diabetes incidence was not affected when 1,25-dihydroxyvitamin D was administered to mice later in life. Vitamin D appears to limit the expression of certain cytokines, which may prevent the autoimmune attack on pancreatic cells that can lead to diabetes (Targher 2006).

Human studies likewise suggest that vitamin D may have a protective effect against type I diabetes. In a large-scale investigation, more than 12,000 pregnant women in Finland enrolled in a trial studying the relationship between vitamin D intake and type I diabetes in infants. After one year, children who supplemented with the suggested study dose of vitamin D (2000 IU daily) had a much lower risk of type I diabetes than children who did not supplement (Levin 2005).

Vitamin D supplementation may reduce susceptibility to type II diabetes by slowing the loss of insulin sensitivity in people who show early signs of the disease. Researchers studied 314 adults without diabetes and gave them either 700 IU of vitamin D and 500 mg of calcium daily or a placebo for three years (Pittas 2007). Among subjects who had impaired (slightly elevated) fasting glucose levels at the study’s onset, those taking the active supplement had a smaller rise in glucose levels over three years than did the controls, as well as a smaller increase in insulin resistance. The researchers concluded that for older adults with impaired glucose levels, supplementing with vitamin D and calcium may help avert metabolic syndrome and type II diabetes.

Ginkgo biloba. Animal studies demonstrate that ginkgo improves glucose metabolism in muscle fibers and prevents atrophy (Punkt 1999). Animal studies also show that ginkgo biloba extracts significantly inhibit post-meal sugar levels and act as anti-hyperglycemic agents (Tanaka 2004).

Ginkgo biloba extract has been shown to prevent diabetic retinopathy in diabetic rats, suggesting a protective effect in human diabetics (Doly 1988). In a preliminary clinical trial (Huang 2004), type 2 diabetics were given ginkgo extract orally for three months, which significantly reduced free radical levels, decreased fibrinogen levels, and improved blood viscosity. Ginkgo extracts also improved retinal capillary blood flow rate in type 2 diabetic patients with retinopathy.

Ginkgo has also been observed to lower blood glucose levels. It was studied in type 2 diabetics at a dose of 120 mg for three months. Ginkgo supplementation produced an increase in liver metabolism of insulin and oral hypoglycemic medications, which corresponded to a reduction in plasma glucose levels (Kudolo 2001). Type 2 diabetics with pancreatic exhaustion received the most benefit. Ginkgo does not appear to increase beta cell production; rather it enhances liver uptake of existing insulin, thereby reducing high insulin levels.

Blueberries. Native to North America, blueberries have long been used in food preparation and for therapeutic purposes (Prett 2005). Many of the health benefits attributed to blueberries have been linked to their potent antioxidant properties. Scientists attribute these powerful antioxidant properties to polyphenols in blueberries known as anthocyanins
In published studies, blueberries block carbohydrate metabolism in the intestine by up to 90% compared with the prescription drug acarbose (Johnson 2011; Melzig 2007).

Additionally, blueberries have been shown to lower baseline blood sugar levels in those diagnosed with type 2 diabetes by 37% (Vuong 2009; Abidov 2006; Takikawa 2010).

In a double-blind, placebo-controlled study, 32 obese, insulin-resistant (pre-diabetic) adult men and women drank smoothies made with freeze-dried blueberry powder for six weeks. A placebo control group consumed smoothies without blueberry extracts (Stull 2010). Fasting blood samples were obtained with a clamp technique considered state-of-the-art for precise determination of insulin sensitivity. With no changes in body weight or composition compared to controls, the blueberry group showed a statistically significant and much greater improvement in insulin sensitivity (22.2% plus or minus 5.8%) versus the placebo arm (4.9% plus or minus 4.5%).

Vaccinium myrtillus (bilberry). Studies of diabetic rats show that bilberry decreases vascular permeability (Cohen-Boulakia 2000). Studies of diabetic mice receiving an herbal extract containing bilberry demonstrated significantly decreased blood glucose levels (Petlevski 2001; Petlevski 2003).

A double-blind, placebo-controlled trial of bilberry extract in 14 people with diabetic retinopathy or hypertensive retinopathy (damage to the retina caused by diabetes or hypertension, respectively) found significant improvements in the treated group (Bone 1997). Other open clinical trials in humans also showed benefits. A preliminary study of 31 people with retinopathy documented that bilberry reduced vascular permeability and reduced hemorrhage (Scharrer 1981).

Under no circumstances should people suddenly stop taking diabetic drugs, especially insulin. A type 1 diabetic will never be able to stop taking insulin. However, it is possible to improve glucose metabolism, control, and tolerance with the following supplements:

  • R-lipoic acid: 240 – 480 mg daily
  • L-carnitine: 500 – 1000 mg twice daily
  • Carnosine: 500 mg twice daily
  • Chromium: 500 – 1000 mcg daily
  • CoQ10(in the form of ubiquinol): 100 to 300 mg daily
  • DHEA: 15 – 75 mg early in the day, followed by blood testing after three to six weeks to ensure optimal levels
  • EPA/DHA: 1400 mg EPA and 1000 mg DHA daily
  • Fiber(guar, pectin, propolmannan, or oat bran): 20 to 30 g daily at least, up to 50 g daily.
  • Propolmannan: 2 grams twice daily
  • GLA: 900 – 1800 mg daily
  • Quercetin: 500 mg daily
  • Magnesium: 140 mg daily as magnesium L-threonate; 320 mg daily as magnesium citrate
  • NAC: 500 – 1000 mg daily
  • Silymarin: containing 750 mg Silybum marianum standardized to 80 percent Silymarin, 30 percent Silibinin, and 8% Isosilybin A and Isosilybin B
  • Vitamin C: at least 2000 mg daily
  • Vitamin E: 400 IU daily (with 200 mg gamma tocopherol)
  • Garlic: 1200 mg daily
  • Green tea extract: 725 mg green tea extract (minimum 93 percent polyphenols)
  • Ginkgo biloba: 120 mg daily
  • Bilberry extract: 100 mg daily
  • B complex: Containing the entire B family, including biotin and niacin
  • Cinnamon extract: 175 mg (Cinnamomum cassia) standardized to 2.5% (4.375 mg) A-type polymers three times daily
  • Green coffee bean extract: 200 – 400 mg (standardized to contain chlorogenic acid) three times a day
  • Vitamin D: 5000 – 10 000 IU daily
  • Brown seaweed and bladderwrack: 100 mg three times a day
  • Irvingia gabonensis: 150 mg twice a day
  • White kidney bean: 445 mg twice a day
  • Blueberry:standardized to contain 50 mg 3,4 – caffeoylquinic (chlorogenic) acid, and 50 mg myricetin) or 22.5 g blueberry bioactive freeze dried powder

In addition, the following blood testing resources may be helpful:

  • Fasting glucose
  • Postprandial glucose test
  • HbA1C
  • Fasting insulin
  • Vitamin D
  • CoQ10
  • Omega Score®