Despite the negative news about hormone replacement therapy (HRT) in recent months, new research suggests that HRT may provide a significant benefit in helping some women reduce their risk of diabetes. But even the study researchers say it's still too early to make any recommendations about using HRT as a tool to prevent type 2 diabetes.

According to the American Diabetes Association, diabetes was the sixth leading cause of death in 2007. Ninety-five percent of diabetes is type-2 that develops in older people or at any age in overweight people. Diabetes dramatically increases the risk for heart disease and stroke.

Women who do not take HRT have up to a 30% increased risk of developing type-2 diabetes. Use of estrogen or estrogen plus a progestin/progesterone is associated with a decrease in the risk for type-2 diabetes.

Women in their forties or fifties often complain about a tendency to gain weight, especially when they don’t take hormones. I recall Greta, a 38 year-old menopausal woman with obesity, diabetes, high blood pressure, and sleep apnea. She was only five feet tall and weighed 200 pounds. She told me, “When I was growing up I was skinny and barely weighted 100 pounds soaking wet! I could eat as much as the football players and never gained a pound. In my late 20s, I started having heavy bleeding from fibroids and when I was 28 years old, everything was taken out. No one ever told me I needed estrogen. Within a year of my hysterectomy, I gained 100 pounds and developed severe depression. My husband left me soon after that. A doctor finally gave me oral estrogen when I was 32 and I felt better but couldn’t lose the weight. I was diagnosed with diabetes and high blood pressure when I was 35.” Changing Greta to topical HRT and correcting her sleep apnea started her recovery toward losing weight and improving control of her blood pressure and diabetes. However, it saddens me that she suffered needlessly for ten years before getting help.

Weight gain with a change in body composition favoring central or visceral obesity accompanies menopause. Women lament the fact they start having thickening around their midriff! With loss of estrogen comes an increase in fasting glucose and the development of insulin resistance leading to diabetes in genetically susceptible women. Insulin resistance is a condition where the body becomes “desensitized” to the actions of insulin. Because insulin is a vital hormone, the pancreas responds by making more insulin. This satisfies the need for insulin action but at the expense of higher circulating levels of insulin. High levels of insulin signal fat cells to conserve fat stores and to convert new food into more fat! This is not a signal you want going to your fat cells!

In individuals who are genetically predisposed to diabetes, this relentless drive for more and more insulin production eventually exhausts the pancreas leading to the onset of diabetes. Even if they never develop diabetes, the presence of ongoing insulin resistance is associated with continued weight gain and accelerates the risk of heart disease, cancer and strokes.

In a group of 505 normal weight non-diabetic women, menopause was the determining factor and not age that was associated with insulin resistance. Leptin, a hormone made in fat cells is responsible for regulating appetite and metabolism. Although leptin is a hormone that reduces appetite, obese people tend to have elevated leptin levels and also seem to develop resistance to the effects of leptin.

A prospective study of 44 healthy postmenopausal women randomized to receive either no treatment or topical estradiol 0.05 mg per day combined with a cyclic progestin were followed for one year. Untreated postmenopausal women had an increase in total and percent body fat and increased visceral body fat. Untreated postmenopausal women also showed corresponding increases in serum leptin levels. The women receiving topical estradiol had no increase in leptin and had no increase in body fat.

Excerpt from “Outliving Your Ovaries” © 2012 by Marina Johnson MD. 

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