Sex hormones linked to diabetes

[Eunuchist (imported)]

In view of recent discussions about castration and diabetes, here's an interesting article with an opposing view. It seems that castration actually prevents the development of type 2 diabetes. Possible indications of poor glycemic control and/or insulin resistance observed in some hypogonadal men, do not appear to have any impact on the development of this disease. We have seen previously that diabetes impair testicular function; "low" testosterone (200-500 ng/dl range) in diabetics being merely a symptom (as is impaired immune function and many other functional impairments associated with the disease). And as we see, increased testosterone secretion in subjects with PCOS increases the diabetes risk.

http://www.diabeteshealth.com/read,3,534.html

January 1996

A recent study reported in the September 1995 issue of Diabetes Care by David S.H. Bell, MB, at the University of Alabama, may have answered a question long debated by diabetes researchers. It has been known for some time that long-term diabetes complications rarely occur before puberty. Whether this is a result of the short duration of diabetes before puberty or because pre-puberty diabetes simply does not cause complications has remained a controversial question.

Lending credence to the opinion that chronic complications do not occur before puberty because of a lack of sex steroids are animal studies which show that castration prevents diabetic complications. However, no similar human studies have previously been done.

This study reports a unique situation in which the chronic complications of diabetes did not develop, in spite of poor glycemic control, in agonadal (without ovaries) twins who had never had sex-steroid hormone replacement.

Identical female twins, born in 1960, were examined at age 15 and found to have streak gonads (functionless tissue), no adrenal masses, and normal kidneys. Both had Perrault's syndrome, a nerve deafness associated with ovarian dysgenesis (defective embryonic development) in females. They both refused to take estrogen.

The twins developed type I diabetes at ages 12 and 20. They were started on insulin twice daily, mixed NPH and regular. They have consistently refused to do home glucose monitoring or increase their insulin. Because of this, their A1c readings over the last seven years reached as high as 15.6% (non-diabetic range 5.5-8.5%).

An examination in March of 1994 showed no evidence of retinopathy, neuropathy, or nephropathy.

In addition to sex steroids, levels of serum growth hormone and somatomedin C (the growth hormone made by the liver in response to pituitary growth hormone release) increase at puberty. These hormone levels may be linked to the development of diabetes complications. It has been shown that serum somatomedin C levels are increased in type I patients with rapidly deteriorating retinopathy.

The study supports the theory that type I diabetes before puberty does not significantly contribute to the risk of chronic diabetic complications because the presence of sex steroids is necessary for their development.

Alan Marcus, MD adds, "An interesting note from the New England Journal of Medicine is that an increased level of sex hormones in the body [as is present in polycystic ovary disease] can itself cause an increased risk for macrovascular disease."

And: http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract