Ben Bikman characterises insulin effects as all being related to causing cells to store energy, one way or another.
He also rails against the use of “diabetes” as a medical term. The original form of the disease is Type I, which is a genetic defect that causes the immune system to attack the pancreas and destroy its ability to make insulin. The patient is unable to store energy and therefore starves to death.
The modern “diabetes” is Type II, which is a state of hyperinsulinaemia resulting from too much dietary glucose. In this metabolic milieu, the excess insulin causes the patient to store the dietary glucose as fat, in order to clear it from the bloodstream (since hyperglycaemia can be fatal). This is basic biology, tested with radio-labeled foods. The liver makes triglycerides, packages them into VLDL, and sends them off to the adipose tissue. The processes of gluconeogenesis and ketogenesis are inhibited, since as the body sees things, it is already surfeited with metabolic fuel. The elevated insulin also prevents adipocytes from releasing triglycerides to be metabolised, as documented by Yalow and Bernstein with their radioimmunoassay in the 1960’s. Insulin must drop sufficiently low to allow the shedding of excess stored fat, and the dietary solution is therefore to restrict carbohydrate/glucose intake.
The states of hyperglycaemia and hyperinsulinaemia are inherently damaging to the body, and they have been detailed in many posts in many threads on these forums. Suffice it to say that the modern epidemic of chronic diseases seems to have begun after cheap industrially-refined sugar products flooded the market in the 1860’s. Until then, the early cases of Type II diabetes, first diagnosed in India a millennium ago, were found only in the rich, because only they could afford white flour and refined sugar (making sugar by hand out of beets or cane is a laborious process).
