WHAT ARE THE TOP TEN SUPPLEMENTS TO CONSIDER WHEN CHANGING?
WHY DO I CONSIDER THEM THE BEST CORE SUPPLEMENTS FOR A PALEO LIFESTYLE?
WHAT IS THE MOST IMPORTANT TO LEAST SUPPLEMENT IN A PALEO LIFESTYLE? (more…)
Menopause is the time in a woman’s life when menstruation stops. Menopause is usually a gradual process. The ovaries begin to produce lower amounts of hormones. The reduced amounts of hormones cause menstrual periods to become irregular and eventually to stop completely. This process of irregular menses and fluctuating hormone levels can take several months to 5 years and is often called “perimenopause” or “transition.”
Most women go through menopause between ages 45 and 60. In the U.S. the average age for menstrual periods to stop completely is 51. There may be a genetic link for the age of onset. Smoking lowers the age at which menopause begins.
Menopause can also occur when the ovaries are surgically removed.
Estrogen Treatment ‘Failure’: Hyperexcretion of Estrogen
If your patient doesn’t experience the usual relief of “low estrogen” symptoms when given the same amount of estrogen-including BHRT that works for the large majority of women – and especially if there’s no change with an increased dose – her body may be “hyperexcreting” estrogens into the urine and stool, retaining too little to achieve symptom relief. Estrogen hyperexcretion can be confirmed (or not) with a finding of higher than anticipated estrogens in a 24-hour urine specimen, while serum estrogens remain low normal or low. In most (but all) instances, there is a history of prior Premarin or other nonbioidentical hormone use. (more…)
Two hundred sixteen postmenopausal women (median age, 58 years) with symptomatic vaginal atrophy were randomly assigned to daily intravaginal administration of a suppository containing 3.25, 6.5, or 13 mg of DHEA or placebo at bedtime for 12 weeks. After 2 weeks, all 3 doses of DHEA induced a decrease in the percentage of parabasal cells (indicating histologic improvement in vaginal atrophy), a significant reduction in vaginal pH, and a significant improvement in the most bothersome vaginal symptom (e.g., dryness, irritation/itching, or pain during sexual activity). After 12 weeks, the 6.25 mg dose produced a 46% decrease in the percentage of parabasal cells (p < 0.0001 vs. placebo), a 1.3-unit decrease in vaginal pH (p < 0.0001 vs. placebo), and a 1.5-point decrease (on a 3-point scale) in the severity of the most bothersome vaginal symptom (p = 0.0001 vs. placebo). Comparable improvements were seen with the other DHEA dosages. No endometrial proliferation was observed after 3 months of DHEA treatment.
Comment: The results of this study indicate that intravaginal administration of DHEA improved signs and symptoms of vaginal atrophy in postmenopausal women, without causing endometrial proliferation. Intravaginal DHEA therefore compares favorably with estrogen therapy, which is known to cause endometrial proliferation, a possible precursor to endometrial cancer. Previous studies by this same group of investigators found that intravaginal administration of DHEA caused little or no change in serum concentrations of estrogen and testosterone. In contrast, serum levels of these hormones often increase after oral administration of DHEA, although oral DHEA does not appear to cause endometrial proliferation. Oral DHEA has been found to be an effective alternative to estrogen-replacement therapy in women suffering from vasomotor and psychological symptoms of menopause. The results of the present study suggest that intravaginal DHEA may be the preferred treatment for women whose postmenopausal symptoms are related mainly to vaginal atrophy.
Labrie F et al. Intravaginal dehydroepiandrosterone (Prasterone), a physiological and highly efficient treatment of vaginal atrophy. Menopause. 2009;16:907–922.
Fifty-five men and 58 women (aged 65–75 years) were randomly assigned to receive, in double-blind fashion, 50 mg per day of dehydroepiandrosterone (DHEA) or placebo for one year. Thereafter, all participants received 50 mg per day of DHEA for an additional year. All participants received daily 640 IU of vitamin D and 700 mg of calcium. In women, mean lumbar spine bone mineral density (BMD) increased during the first year by 1.9% (p = 0.0003 compared with baseline) in the DHEA group and by 0.8% in the placebo group (p = 0.03 for the difference in the change between groups). After two years, mean spine BMD increased by a total of 3.6% in the DHEA group. Hip BMD did not change. In men, there were no differences in BMD between DHEA and placebo.
Comment: DHEA is an androgen produced in women primarily by the adrenal glands and to a lesser extent by the ovaries. It is metabolized in part to estrogen and testosterone. In addition, DHEA appears to have physiological actions that are unrelated to its function as a precursor hormone, including stimulation of osteoblasts. The results of the present study indicate that DHEA can increase bone mass in elderly women, although it was not effective in men.
Weiss EP et al. Dehydroepiandrosterone replacement therapy in older adults: 1- and 2-y effects on bone. Am J Clin Nutr. 2009;89:1459–1467.
Forty men (mean age, 56.5 years) with erectile dysfunction were studied. None of the men had well-known causes of erectile dysfunction, such as hypertension, diabetes, or ischemic heart disease. All men achieved a full erection after an erection test with intracavernosal administration of prostaglandin E1. Other inclusion criteria were normal serum levels of testosterone, dihydrotestosterone, and prostate-specific antigen (PSA), and a serum DHEA-sulfate level below 1.5 µmol/L. The men were randomly assigned to receive, in double-blind fashion, 50 mg per day of DHEA or placebo for six months. (more…)