The dietary solution to diabetes

Insulin dysfunction has reached epidemic proportions, and the most practical, cost-efficient solutions centre around diet and nutraceuticals. Dan Lukaczer, ND, offers both macronutrient and micronutrient approaches to solving the crisis of metabolic syndrome and type 2 diabetes

More than 60 years ago, Dr HP Himsworth put forth the notion that diabetes did not result from a lack of insulin, as was commonly believed, but rather appeared in the presence of near-normal insulin levels. The problem, as he saw it, was the diminished ability of the tissues to utilise glucose, which he termed ?insulin insensitivity.? The idea was considered heretical at the time, and it took 40 years before the medical community finally began to accept this hypothesis.1 It is now well understood that the vast majority of subjects with type 2 diabetes have insulin insensitivity or resistance.2

Insulin resistance results when normal insulin action is impaired. It can occur for a variety of reasons: lack of the appropriate numbers of insulin receptors, altered insulin binding, and/or an inability of the insulin receptor to respond and send a signal across the cell?s membrane. Whatever the reason, the cell does not ?hear? the message of the insulin molecule.

During the initial stages, the pancreas tries to overcome the insulin insensitivity and maintain normal glucose levels by secreting larger and larger amounts of insulin. This then results in a hyperinsulinaemic state. If the pancreas can continue to secrete large amounts of insulin, and the cells respond to this high level, an individual may continue to maintain normal, or near-normal glucose levels. In a percentage of hyperinsulinaemic individuals, the pancreas cannot maintain this compensatory mechanism, leading to a decrease in insulin secretion and the development of glucose intolerance or diabetes.

The diagnosis of type 2 diabetes is based on both World Health Organization and American Diabetes Association guidelines. According to these criteria, diabetes can be diagnosed either by a two-hour oral glucose tolerance test with a value of 200mg/dL or greater, or by a fasting glucose concentration of 126mg/dL or greater.

In addition, there are intermediate categories of glucose tolerance. Impaired glucose tolerance is diagnosed by a two-hour post-load oral glucose tolerance test of 140-200mg/dL, and impaired fasting glucose is diagnosed by a fasting glucose tolerance test of 100-125mg/dL. Both individuals with impaired glucose tolerance and impaired fasting glucose are at high risk of developing diabetes and are often considered ?prediabetic.?

Notably, not all individuals who are insulin resistant ultimately develop diabetes, but this chronic hyperinsulinaemia is itself associated with significant morbidity and mortality. This prediabetic or potentially prediabetic state, in which near-normal glucose levels are maintained at the expense of high insulin secretion, has been termed metabolic syndrome or Syndrome X. This condition is present in as many as 47 million Americans, or 25 per cent of the non-diabetic population.3,4 Research over the past 10 years has shown a significant relationship between metabolic syndrome and coronary heart disease (CHD),5 hypertension,6 polycystic ovary syndrome, and colon and breast cancers.7,8,9

Diet and lifestyle
Evidence points strongly to diet, exercise and nutritional supplementation as primary clinical strategies for individuals with diabetes. Diet and exercise can have a profound effect in preventing diabetes for those who are at the highest risk. In a landmark article published just two years ago, lifestyle intervention was shown to be more effective than metformin (Glucophage) in preventing diabetes.10

Research has shown that all carbohydrates are not equally problematic for diabetics

This was just the most prominent of a number of recent studies to show that intensive lifestyle changes can have significant preventive effects. For instance, an earlier lifestyle intervention trial resulted in a 58 per cent reduction in the incidence of diabetes in high-risk subjects. 11 And intervention does not necessarily have to result in dramatic changes. It has been shown that even modest weight loss (4.5kg over two years or 4.5 per cent of initial body weight) can substantially decrease the risk of developing diabetes. 12 In individuals who already have diabetes, most studies show that intensive lifestyle changes help as well, improving blood-sugar control and some of the complications associated with diabetes. 13,14,15 While exercise and diet should be undertaken together, a recent meta-analysis suggested that exercise will improve blood-sugar control even without weight loss. 16

Carbs and fats: the great debate
An enormous amount of publicity has been given to the issue of carbohydrates and fats and their effects on blood sugar and weight loss. Clearly, the relative amount and type of carbohydrate and fat are important factors that influence glucose availability and insulin secretion. Yet the dietary prescription remains somewhat controversial, with duelling diets and authors.

While the research is not completely clear, the emerging consensus is that high-carbohydrate, low-fat diets may not be the optimal diet for diabetics. For instance, some studies have shown that diets high in carbohydrates can decrease insulin receptor numbers and increase triglycerides, very low-density lipoprotein cholesterol and concentrations of insulin and glucose in type 2 diabetics.17,18,19

However, research has shown that all carbohydrates are not equally problematic for diabetics. The concept of the glycaemic index (GI) was developed as a result of research showing that similar amounts of carbohydrates in foods do not elicit similar postprandial glycaemic responses. GI is defined as the incremental area under the blood glucose curve in response to a standardised carbohydrate load. It is therefore an index of the blood glucose raising potential of the available carbohydrate in a food. The glycaemic index for a particular food is derived by expressing the individual glycaemic index as a percentage of a reference food, typically white bread or glucose. The GI of a food depends on a number of factors besides just the absolute amount of carbohydrate, including type of starch, physical form of the food, food processing, and the amount and type of protein, fat and fibre.

Studies indicate a low-GI diet helps control blood-sugar levels, leads to decreased caloric intake, and is associated with a lower risk of type 2 diabetes and CHD

Studies indicate a low-GI diet helps control blood-sugar levels, leads to decreased caloric intake, and is associated with a lower risk of type 2 diabetes and CHD. 20,21,22 Epidemiological studies suggest that higher GI diets are associated with increased risk for diabetes. 23,24 Prospective studies have shown a low-GI diet compared to a high-GI diet improved blood glucose and lipid control in overweight diabetic subjects. 25,26 Additionally, a low-GI diet can lower the glucose and insulin responses throughout the day and improve the lipid profile in type 2 diabetic subjects. 27 Studies have also shown that high-GI meals promote excessive food intake. 28 As most diabetics are overweight, this may be another important reason to incorporate this approach.

Even with the abundance of supporting data, the concept of glycaemic index is not well accepted by the conventional medical establishment in the United States. However, it is so well acknowledged worldwide that the UN?s World Health Organization has recommended that all people base their diets on low-GI foods.

While many factors can affect a food?s glycaemic index, two in particular deserve specific mention: fibre and starch type

While many factors can affect GI, two in particular deserve specific mention: fibre and starch type. High fibre, independent of total carbohydrates, has a beneficial effect on blood-glucose control. A recent study showed a diet rich in soluble and insoluble fibre (50g/day of a 50:50 blend) improved glycaemic control and decreased lipid concentrations in diabetic subjects. 29 Soluble fibres in particular improve blood glucose control in diabetics by slowing gastric emptying and, to a lesser extent, inhibiting starch degradation in the upper small intestine. 30 One study showed 10g of the highly soluble psyllium fibre improved glycaemic and lipid control; 31 in another, 20g guar gum improved blood glucose, haemoglobin A1C (HA1C) and LDL cholesterol. 32

Fenugreek is of interest here as it may have other components in it—aside from the soluble fibrethat result in improved glucose control. In one study, 15g fenugreek seed powder significantly reduced postprandial glucose levels in diabetic subjects.33 Yet in another study, 1g of the hydroalcoholic extract of fenugreek seeds (far too little actual fibre to have an effect) improved glycaemic control in 25 subjects with mild type 2 diabetes.34

Another factor in carbohydrates? effects on blood sugar is the type of starch found in those carbohydrates. The amylose form of starch, as opposed to the more common amylopectin, has a significant positive influence on insulin response.35,36 This appears to be due to the way the starch molecules are configured. Because of this configuration, amylose is digested slower; therefore, the blood-sugar rise is blunted. One study showed insulin and triglyceride levels were reduced in individuals placed on a high-amylose diet.37 Foods high in amylose include legumes, whereas potatoes are high in amylopectin.

Resistant starch sources are high in amylose and only partially digested in the small intestine. Incorporation of resistant starch into processed foods, such as flour substitutes, reduces the glycaemic index of that food and will assist in maintaining healthy blood sugar levels and insulin sensitivity.38,39 Research suggests that this may reduce the risk of type 2 diabetes.

Fat and essential fatty acids
Fat has little effect on glucose stimulation, and therefore is generally given a free ride. In fact, some diet gurus have said you can eat as much fat as you want. However, while it appears eating fat does not cause blood sugar to rise, fat has other important physiological actions that make it a bit more complicated than once thought.

Once ingested, fats are incorporated into the membrane of all cells. Because the cell membrane is the gateway into the cell, changes in its composition can change the membrane?s fluidity and therefore influence important cellular functions. Thus the kind of fat one eats plays a major role in determining the composition of cell membranes and thus how a cell may function.

Studies suggest type 2 diabetics have altered cell membrane dynamics. Since the insulin receptor is bound in the cell membrane, altered membrane fluidity may negatively affect insulin receptor function.40,41

It has been shown that long-chain polyunsaturated fatty acids (PUFAs) can modulate the function of insulin receptors. In cultured cells, increasing the PUFA cell membrane content increases membrane fluidity, insulin binding to receptors and insulin action.42 In animal models, the specific omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have been shown to have beneficial effects on serum insulin and lipids levels.43

Conversely, saturated fats and transfatty acids decrease membrane fluidity and the binding of insulin to its receptor.43,44 In animal trials, when omega-3 fatty acids are substituted into a high-fat diet, insulin resistance in skeletal muscle may be attenuated.45 In human trials, monounsaturated fatty acid (MUFA) diets appear to mitigate against these adverse changes as well.17

Thus eating more fat, but not just any fat, may be important in improving glucose control in diabetics.

Studies show a lower carbohydrate, higher MUFA/PUFA diet results in decreased fasting glucose, insulin and triglycerides.46,47 A meta-analysis supports the idea that high-MUFA diets are more advantageous than high-carbohydrate diets for diabetic subjects.48

However, there may be an upper limit to a good thing. One study showed that favourable effects of substituting a MUFA diet for a saturated fat diet were seen only at a total fat intake below 37 per cent.49 There has been some suggestion in the past that omega-3 fatty acids may cause some problems for diabetics related to tryglycerides, haemoglobin and blood-sugar levels. But another meta-analysis suggests that EPA and DHA lower triglycerides by 30 per cent in diabetic subjects, with no adverse effects on HbA1C and blood-sugar control.50

Micronutrients In addition to dietary and exercise changes, research has shown that certain vitamins, minerals and phytonutrients have the potential to improve insulin sensitivity and thus help stabilise blood-glucose levels. There are many nutrients that have shown value. We will concentrate on those with the strongest research to date.

Chromium has enjoyed a great deal of work on its relationship to glucose tolerance.51,52 Certain lipophilic forms of chromium have been shown to increase membrane fluidity and insulin-mediated glucose uptake in cultured cells and animal models. Chromium at 200mcg and 1,000mcg significantly improved HA1C, glucose, insulin and cholesterol in diabetic subjects. The higher dose appeared more effective.53 Chromium may be beneficial in individuals who are prediabetic and those who have overt diabetes.54

Magnesium plays an important role in glucose homeostasis by altering both insulin secretion and action. Adequate intracellular magnesium concentrations may therefore allow for improved glucose handling. Tissue levels of magnesium are often low in diabetics (as well as normal subjects).55 It has been shown that low intracellular magnesium results in impaired insulin action and a worsening of insulin resistance in hypertensives and type 2 diabetics.56 Daily magnesium supplements appear to improve hormone receptor response and glucose transport into the cell.57

The research is somewhat mixed concerning magnesium supplementation, however. For instance, 400mg/day supplemental magnesium lowered blood pressure but did not improve glycaemic control or other CVD risk factors in 28 diabetic subjects after 16 weeks.58 It appears that diabetic individuals may benefit if they have insufficient intake of magnesium. Because magnesium insufficiency is so ubiquitous, and magnesium has so many other important functions, increasing magnesium through diet or supplementation seems reasonable.

Alpha-lipoic acid (ALA) used in both animal and human studies suggest that it increases insulin-stimulated glucose disposal, possibly by improving glucose transport, increasing the number or activation of glucose transporter proteins, or increasing non-oxidative or oxidative glucose disposal.59,60 Clinical trials suggest oral ALA (600-1,800mg/day for four weeks) can improve insulin sensitivity in subjects with type 2 diabetes, and doses of 600mg/day may improve diabetic polyneuropathy.61,62 ALA might exert some of its beneficial effects by improving microcirculation as well.61

Co-enzyme Q10 research on diabetes is mixed at this point. There are four recent controlled trials that have looked at glycaemic control and co-Q10 supplementation. The first suggested that 120mg/day co-Q10 improved blood-sugar levels and blood pressure in 30 patients after eight weeks.63 However, another trial published concurrently suggested no significant improvement among 23 patients taking 100mg/day.64

Two trials published more recently also failed to agree. The first, in 2002, showed improved blood pressure and haemoglobin A1C levels after 12 weeks on 200mg co-Q10.65 Yet in a second study that year, again using 200mg daily, 40 patients did not show improved glycaemic control after 12 weeks.66

While these were all placebo-controlled trials, the number of participants was small, with differences in the types of subjects recruited in each trial that could create confounding variables. Unfortunately, this is the state of our current knowledge. In the absence of more compelling findings, it would seem that if a person has diabetes with elevated blood pressure, then supplementing with 150-200 mg/day co-Q10 seems reasonable.

Vitamin C has been overlooked somewhat in diabetic nutritional formulas. Beneficial effects have been noted in type 2 diabetics in both glycaemic control and blood lipids at 2g/day.67 In another study, 1g vitamin C had beneficial effects upon glucose and lipid metabolism.68 In another study, 1.25g/day lowered urinary albumin excretion rate, a marker of progression to end-stage renal disease,69 while in another study a lesser dose of 1g vitamin C lowered the urinary albumin excretion.70 Other findings indicate that 100mg or 600mg/day vitamin C reduces sorbitol accumulation and therefore may be useful in preventing diabetic retinopathy complications.71

Antioxidants might help slow the process of free radical generation, which occurs more rapidly in diabetics. Accordingly, while single nutrients can positively influence glucose control, some of these nutrients do double duty by working as antioxidants.

Vitamin E has been used in diabetes to improve insulin sensitivity, generally at 600IU or more,72,73,74 and it clearly has a beneficial effect through its antioxidant activity as well. Clinical trials have demonstrated reduced oxidative stress in type 2 diabetic subjects receiving 400IU/day vitamin E.75 Vitamin E can reduce LDL-cholesterol oxidation, a likely mechanism in the battle against free radicals.76

Vitamin C has also been shown to attenuate oxidative stress in hyperinsulinaemics and to have beneficial effects on oxidative stress markers and insulin sensitivity in type 2 diabetics.68,77

Combining antioxidants may be most effective. In one study, 20 type 2 diabetics who supplemented for 12 weeks with an antioxidant combination (24mg beta-carotene, 1g vitamin C and 800IU vitamin E) showed decreased LDL oxidation.74 In another study, supplementation with 30mg/day zinc gluconate and 400mcg/day chromium pidolate improved lipid perioxidation.78

The economic costs for society of treating diabetes are obviously enormous. Early treatment is, therefore, essential. Recognition of the underlying biochemical defect, loss of insulin sensitivity and resistance to glucose disposal is of central importance. While genetic background may determine propensity to the disorder, modifiable factors such as weight, exercise, diet and individual nutrient intake appear to play critical roles.

A comprehensive strategy of lifestyle and dietary modifications, along with nutrient supplementation, is an important step in clinical management of type 2 diabetes. Significant progress could be made against this rising epidemic if these specific interventions were aggressively pursued.

Dan Lukaczer, ND, is director of clinical research at the Functional Medicine Research Center, the clinical research arm of Metagenics Inc in Gig Harbor, Wash.

Respond: [email protected]
All correspondence will be forwarded to the author.

Science Viewpoint
The costs of the disease: $132 billion
According to the World Health Organization, 30 million people worldwide had diabetes in 1985. By 2000, this number shot up to 177 million. The curve is estimated to continue unabated. In the US alone, direct medical costs and indirect expenditures attributable to diabetes in 1997 were estimated at $132 billion. Each year in the US, diabetic complications result in the following statistics:

  • 12,000-24,000 develop blindness
  • 43,000 develop kidney failure
  • 82,000 have leg and foot amputations

Additionally, it is estimated that heart disease and stroke cause about 65 per cent of deaths among people with diabetes. Overall, direct medical expenditures attributable to diabetes in 2002 totalled $92 billion. Attributable indirect costs (premature mortality and disability) totalled $40 billion. In 1998, medical expenditures for people with diabetes totalled $10,071 per capita, compared with $2,669 for non-diabetics.

With all that, the full burden of diabetes is probably under-reported; death records often fail to reflect the role of diabetes, and the costs related to undiagnosed diabetes are unknown. It should be clear from these statistics that the economic burden of diabetes in the US is staggering. For more information, visit


Science Viewpoint
Vanadium: Studies suggest caution needed
In both animal and human studies, vanadium has demonstrated insulinlike effects on glucose metabolism. It appears to activate cellular insulin receptors, which leads to an increase in glucose uptake by transporter proteins in the cell membrane.1,2 A number of diabetes supplemental formulations include vanadium, but significant caveats accompany its use, and responsible formulators should probably steer away from large dosages.

In human trials, vanadium at dosages of 100-125mg/day have been shown to improve insulin sensitivity in type 2 diabetes. However, these were short-term trials of only a few months. Also, this amount caused cramps and loose stools in 23 of 25 patients and fatigue in a minority.1,3,4 There is currently no RDA for vanadium. The upper safe limit for adults has been set by the US Food and Nutrition Board at 1.8mg/day; therefore, ingesting 50-100mg long-term may be dangerous.

In fact, a recent study suggested chronic exposure to high levels of vanadium reduces cognitive abilities.5 While this was not from oral ingestion of vanadium, caution is called for in long-term supplementation with high levels of vanadium.


1. Halberstam M, et al. Oral vanadyl sulfate improves insulin sensitivity in NIDDM but not in obese nondiabetic subjects. Diabetes 1996; 45(5):659-66.
2. Shechter Y, et al. Insulin-like actions of vanadate are mediated in an insulin-receptor-independent manner via non-receptor protein tyrosine kinases and protein phosphotyrosine phosphatases. Mol Cell Biochem 1995; 153(1-2):39-47.
3. Boden G, et al. Effects of vanadyl sulfate on carbohydrate and lipid metabolism in patients with non-insulin-dependent diabetes mellitus. Metabolism 1996; 45(9):1130-5.
4. Goldfine AB, et al. In vivo and in vitro studies of vanadate in human and rodent diabetes mellitus. Mol Cell Biochem 1995; 153(1-2):217-31.
5. Barth A, et al. Neurobehavioral effects of vanadium. J Toxicol Environ Health Part A 2002; 65(9):677-83.

Science Viewpoint
Green tea and cinnamon: spices on the rise
Green tea seems to be good for everything. Major phytonutrients in green tea are the catechins and/or epicatechins.

In vitro and animal studies have shown catechins are an insulin sensitizer, are a pancreatic protectant, help in the delay of glucose absorption and repress hepatic glucose production.1,2,3,4,5 While the dose is unclear, as there are only animal data thus far, 200-400mg/day catechins have been used in various studies and have been shown to be therapeutic in other areas.

The work on cinnamon began a few years ago with in vitro data that suggested this common spice had bioactive compounds that might have insulin-like effects.6 Other in vitro work seemed to confirm this.7,8

Follow-up animal experiments suggest that long-term use of cinnamon bark might provide benefit against diabetic conditions.9

In 2003, the first human clinical trial was published. In this placebo-controlled study, diabetic subjects given as little as 1g/day cinnamon for six weeks showed improvements in fasting glucose (18-29 per cent), triglycerides (23-30 per cent), LDL cholesterol (7-27 per cent) and total cholesterol (12-26 per cent).10


1. Mori M, Hasegawa N. Superoxide dismutase activity enhanced by green tea inhibits lipid accumulation in 3T3-L1 cells. Phytother Res 2003; 17(5):566-7.
2. Kim MJ, et al. Protective effects of epicatechin against the toxic effects of streptozotocin on rat pancreatic islets: in vivo and in vitro. Pancreas 2003; 26(3):292-9.
3. Han MK, Epigallocatechin gallate, a constituent of green tea, suppresses cytokine-induced pancreatic beta-cell damage. Exp Mol Med 2003; 35(2):136-9.
4. Murase T, et al. Beneficial effects of tea catechins on diet-induced obesity: stimulation of lipid catabolism in the liver. Int J Obes Relat Metab Disord 2002; 26(11):1459-64.
5. Anderson RA, Polansky MM. Tea enhances insulin activity. J Agric Food Chem 2002; 50(24):7182-6.
6. Imparl-Radosevich J, et al. Regulation of PTP-1 and insulin receptor kinase by fractions from cinnamon: implications for cinnamon regulation of insulin signalling. Horm Res 1998; 50(3):177-82.
7. Broadhurst CL, et al. Insulin-like biological activity of culinary and medicinal plant aqueous extracts in vitro. J Agric Food Chem 2000; 48(3):849-52.
8. Anderson RA, et al. Isolation and characterization of polyphenol type-A polymers from cinnamon with insulin-like biological activity. J Agric Food Chem 2004; 52(1):65-70.
9. Onderoglu S, et al. The evaluation of long-term effects of cinnamon bark and olive leaf on toxicity induced by streptozotocin administration to rats. J Pharm Pharmacol 1999; 51(11):1305-12.
10. Khan A, et al. Cinnamon improves glucose and lipids of people with type 2 diabetes. Diabetes Care 2003;26(12):3215-8.

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