Re: White rice consumption and risk of type 2 diabetes: meta-analysis and systematic review
Many developed countries see a large increase in their prevalence of obesity and T2D.
Weight reduction programmes aim to reduce unhealthy body fat. Insulin stimulates fat production making weight loss difficult or impossible when insulin is the predominant metabolic hormone.
In pre T2 Diabetes conditions there is glucose intolerance which is often characterised by high circulating insulin levels and insulin resistance. A similar picture exists in the early stages of T2D but as B cell function deteriorates and if insulin resistance is not reduced the bodies coping mechanisms are overstretched and blood glucose levels rise.
Insulin resistance is difficult to measure and methods such as the euglycaemic clamp simply serve to measure resistance to one of it's many functions. Perhaps functions such as stimulating fat production are less resistant and increased fat production ensues.
For these reasons weight loss in T2 diabetes should be facilitated by lowering the bodies glucose led drive to make Insulin. This is largely fuelled by a carbohydrate rich diet and a lack of exercise to use up such energy.
Carbohydrate counting regimes, low GI diets and simple restriction of carbohydrates are sensible ways of reducing the glycaemic load on the body and controlling Insulin production and glycaemic control without the need for continuingly complex regimes of hypoglycaemic agents. Metformin, glitazones, exercise and weight loss are already known to reduce progression of IGT to diabetes - and all will lower endogenous insulin production. A recent study also suggested that diabetes can be cured by significant calorie restriction and weight loss.
The specific use of lowering of dietary carbohydrate to help to control diabetes is seldom advocated to patients by dietitians and clinicians alike. Yet there is sound physiological reasons why doing so would lower insulin production and reduce the harmful effects that too much circulating insulin can cause.
Biochemists and endocrinologists agree with this physiology yet no one seems to put it into practical use in a clinical setting. It is time that there was a sensible discussion and further research on this important topic. As Gary Taubes eloquently puts it in his well researched novel , "the diet delusion" - the low fat diet remains the ingrained panacea for weight loss.
It is a leap of faith but could a carbohydrate rich diet - in association with a susceptible genetic background - actually "cause" T2D? Certainly epidemiology would suggest that in some populations the prevalence of T2D has risen dramatically as the industrial revolution and similar non physiological forces have made the consumption of carbohydrate (and fat) by the population increase. Food for thought?
Competing interests: No competing interests