Ginseng and Diabetes

It is alarming how the supplement industry is not really strictly regulated by the FDA, especially when some of the doses of these supplements can be considered very high and can potentially induce pharmacologic effects (for example, multivitamins and minerals that provide way above and beyond the RDA). Perhaps, this is the case because a) there is scarcity of scientific evidence about some supplements, b) the properties of a compound of interest is complicated and c) there is more unknown than known about the bioactive compound/s in a supplement.

Nevertheless, there are some supplements, specifically those used in Traditional Chinese Medicine (TCM) that is promising in terms of diabetes management. This blog will focus on ginseng, which contains bioactives called ginsenosides . A review by Yin et al. (2008) lists the effects of ginseng on animal models and humans with type 2 diabetes. Some of the beneficial effects of ginseng are glucose lowering properties in both obese mice and diabetic humans; lowering of glycated hemoglobin (HbA1c is a biomarker of glucose control by measuring the levels of glucose attached to red blood cells) levels in type 2 diabetics, and prevention of pancreatic beta-cell death. Ginseng also prevented weight gain in mice models of obesity and type 2 diabetic humans.

Interestingly, it has been proposed that ginseng exerts its glucose lowering effects through its anti-inflammatory properties. It is proposed that ginseng inhibits the NFkB, IKK and JNK inflammatory pathways. By inhibition of the inflammatory pathways, insulin signaling (pathway that leads to the uptake of glucose into the cell) can work properly, with the overall effect of lowered blood glucose and increased insulin sensitivity.

As ginseng has both anti-hyperglycemic and anti-obesity properties, it appears to be a very good candidate for an anti-diabetic or diabetic management supplement.

Reference:

Yin J, Zhang H, Y J. Traditional Chinese medicine in treatment of metabolic syndrome. Endocr Metab Immune Disord Drug Targets 2008; 8:99-111.