Recent studies indicate that an inadequate supply of vitamin D could be involved in the onset of numerous chronic diseases like diabetes mellitus types 1 and 2 (21, 22). Study data indicate that a lack of vitamin D represents a risk factor for type 2 diabetes and for metabolic syndrome, since it increases insulin resistance and reduces insulin secretion from pancreatic beta cells (23). Higher blood vitamin D levels could be linked to lower blood sugar readings. In this context a reduction in the pro-inflammatory tumor necrosis factor alpha, a signaling substance (cytokine), in the immune system appears to play an important part. In one randomized controlled study with insulin-resistant women having a mean blood vitamin D concentration lower than 10 ng/mL, daily administration of 4000 IU for six months led to a significant improvement in insulin sensitivity and a reduction in insulin resistance (24). Insulin resistance was optimized with vitamin D values around 32 to 48 ng/mL (80 to 120 nmol/L). It thus appears that patients with a distinct vitamin D deficiency benefit especially from supplementation with vitamin D.
A sufficient intake of vitamin D also seems to have a positive influence on the mortality risk for patients having type 2 diabetes as an element of a metabolic syndrome: In a study of patients with metabolic syndrome, a vitamin D status over 30 nanograms per milliliter was associated with a 75% reduction in total mortality and a 66% reduction in mortality from cardiovascular diseases(e.g., cardiac insufficiency) as compared to patients with severe vitamin D deficiency (under 10 ng/mL) (25). Supplementary intakes of vitamin D seem to lead to an improvement in lipid metabolism in type 2 diabetes sufferers, especially in combination with physical exercise (26).
Experimental research produced evidence that vitamin D can help prevent the destruction of insulin-producing pancreatic beta cells and thus combat the onset of type 1 diabetes (27). It is assumed that this is due primarily to the immunomodulatory action of the vitamin via T-helper cells and to the reduction of pro-inflammatory cytokines.
Omega-3 fatty acids
Apart from hypertension, elevated triglyceride levels (hypertriglyceridemia), which are regarded as an indicator for insulin resistance, are the most important risk factor for myocardial infarction. In some studies elevated blood levels of omega-3 fatty acids were found to be associated with increased sensitivity to insulin (28) and reduced resistance to insulin (29). The long-chain, polyunsaturated omega-3 fatty acids appear to possess lipid-lowering, antithrombotic and endothelium-protective properties (30). Diabetes sufferers could therefore especially benefit from omega-3 fatty acids for the prevention of diabetic micro- and macroangiopathies. Further, a supplementary intake of omega-3 fatty acids appears to improve the composition of essential fatty acids in the cell membrane and myelin sheath of nerve cells and hence combat the onset of diabetic neuropathy (31). A meta-analysis showed that a supplementary intake of the omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) can significantly raise the concentration of adiponectin in the blood (32). Adiponectin is an important hormone that controls metabolic processes such as blood sugar regulation and the containment of inflammatory processes in the body.
Aerobic energy metabolism depends on an adequate supply of coenzyme Q10. Blood levels of coenzyme Q10 are frequently lower than normal in type 2 diabetics (33). For example, patients with diabetic disease of the myocardium (cardiomyopathy) may have low serum levels. In patients with diabetic retinopathy the ratio of reduced to oxidized coenzyme Q10 is substantially lower – a sign of increased oxidative stress (34). Coenzyme Q10 concentrations in the pancreas fall with increasing age. In studies, targeted administration of coenzyme Q10 to diabetes sufferers have optimized the energy balance of the heart, increased the protection of lipoproteins against oxidation, reduced lipid peroxidation and improved vascular endothelium function (35, 36). Clinical studies also indicated that coenzyme Q10 could lower diastolic and systolic blood pressure in type 2 diabetics (37).
An insufficient concentration of intracellular magnesium is viewed as a major cause of the onset of insulin resistance. Magnesium appears to be able to improve glycemic control via a positive influence on the activity of the insulin receptor and signal conduction (38). In diabetics, magnesium status is often unsatisfactory due to increased renal elimination (39). This in turn leads to poor glucose utilization, increased insulin resistance, higher blood glucose and HbA1C levels and progression of diabetic complications (40). Further, treatment with frequently used antidiabetic medication (e.g., metformin) and diuretics can often lower magnesium concentrations in the blood (41). When magnesium levels are low, a rise in the concentration of C-reactive protein (CRP) – an important risk factor for vascular complications like thrombosis and heart attack – can be observed (42).
One extensive epidemiological study showed that the risk for both diabetes mellitus type 2 and for metabolic syndrome as a diabetes precursor rises as magnesium intake falls. According to a meta-analysis the risk for diabetes was reduced by 15% per 100 mg of additional magnesium intake (43). A more recent meta-analysis reported an approximately 60% lower risk for diabetes in study participants with the highest dietary and supplementary magnesium intakes compared to subjects with the lowest intakes (44). According to one new study, the preventive effect of an adequate magnesium intake for type 2 diabetes appears to vary depending on genetic variations and ethnic origin (45). Magnesium (Mg2+) is taken up via ion channels that are coded by genes for which the different single nucleotide polymorphisms are known. These ion -channel-related gene variants can significantly influence the body’s magnesium status and its glucose metabolism, and are associated with the risk of developing type 2 diabetes. A sufficient intake of magnesium could partially compensate for the magnesium deficiency caused by these genetic mutations.
A poor magnesium status is frequently observed in diabetes sufferers with diabetic retinopathy as well as in patients with diabetic polyneuropathy; in studies, a supplementary intake of magnesium was found to bring about a significant improvement (46). Supplementation with magnesium was also effective in diabetic patients with inadequate magnesium values and newly diagnosed depression: the symptoms of depression improved to the same extent as with antidepressant treatment (47).
Zinc is an important element of insulin structure; it has a stabilizing effect and protects against oxidative damage. Zinc deficiency can lead to decreased synthesis of insulin receptors and to a decline in glucose tolerance and insulin sensitivity (48). Moreover, an insufficient intake of zinc could promote the incidence of atherosclerotic vascular changes and its consequences for diabetics (e.g., coronary heart disease) (49). As a rule, zinc status is poorer in type 1 and type 2 diabetics compared to non-diabetics. Zinc elimination is increased two- to threefold and zinc absorption is diminished (50). Apart from this, medication administered to lower blood pressure (ACE inhibitors) can increase renal zinc loss in diabetics (51). Since a key enzyme of folic acid metabolism is zinc-dependent, zinc deficiency can also worsen folic acid status. A meta-analysis of several studies showed that a supplementary intake of zinc can bring about a significant lowering of fasting glucose values and a slight reduction in the concentrations of glycosylated hemoglobin (HbA1C) (52).
Chromium supports the activity of insulin and sensitizes the pancreatic beta cells, promoting the expression of insulin. Chromium deficiency can lead to reduced glucose tolerance and disordered glucose utilization (53). Studies showed that supplementation with chromium (III) could bring about an improvement in glucose and/or lipid metabolism, in particular in diabetes sufferers with insufficient chromium intake (54). A meta-analysis of numerous clinical studies with type-2 diabetes patients revealed that supplementary administration of chromium (III) improved HbA1C values and fasting blood sugar, as well as lipid metabolic status (55).