Men & Testosterone
Andropause, the male equivalent of menopause is real, although more subtle than menopause. While estrogen levels in women decline abruptly after menopause, there is a gradual decline in androgens, the male sex hormones, starting in the late 40s to early 50s, along with a rise in SHBG (sex hormone binding globulin)- literally, antibodies to testosterone which limit the amount and effectiveness of this hormone as men age. As with the age-related decline of HGH, the loss of testosterone contributes to the familiar “pot belly”; and declining muscle tone in middle-aged men. The symptoms of the male menopause include a decreased interest in sex, difficulty in having and maintaining an erection, and decreased sexual satisfaction, as well as fatigue, depression, irritability, aches and pains, and muscle loss.
How is testosterone produced:
Androgens
For men with a low level of free testosterone in the blood, testosterone or other hormone replacement therapy (HRT) can be considered. HRT can help men with low testosterone levels increase their libido and sexual arousal. Testosterone replacement also can improve muscle strength and bone mineral density in men and women with low levels of the hormone.
Androgens such as testosterone, also promote an overall decrease in fat and an increase in muscle strength and lean body mass. Testosterone replacement therapy has been shown to lift mood and decrease anxiety. It may enhance orientation and memory and it may also have antidepressant effects.
The testes produce testosterone regulated by a complex chain of signals that begins in the brain. This chain is called the hypothalamic-pituitary-gonadal axis. The hypothalamus secretes gonadotropin-releasing hormone (GnRH) to the pituitary gland in carefully timed pulses (bursts), which triggers the secretion of leutenizing hormone (LH) from the pituitary gland. Leutenizing hormones thus stimulate the Leydig cells of the testes to produce testosterone. Normally, the testes produce 4–7 milligrams (mg) of testosterone daily.
Testosterone production increases rapidly at the onset of puberty and starts to decrease there after. It decreases rapidly after age 40 (to 20% to 70% of peak level by age 70). Approximately 8 million men in the United States experience testosterone deficiency; approximately 700,000 receive treatment.
Signs and Symptoms
Men are generally reluctant or unwilling to acknowledge that the syndrome has crept up on them. The symptoms are not as overwhelming as the dramatic changes women experience and it may not affect all men; however, about 40% of men in the 40s, 50s, and 60s will experience some of the symptoms, including lethargy, depression, irritability, mood swings, and erectile dysfunction.
Testosterone levels begin to decrease for a number of reasons, including (1) the Leydig cells begin to decrease in number and function, (2) a sex hormone binding globulin (SHBG) increase with age, resulting in greater binding of testosterone with less free testosterone. There is a higher relative amount of estradiol with less testosterone being produced.
As men pass 50, they tend to develop an enlarged prostate. As the gland increases in size, it squeezes the urethra, often causing increased urinary frequency, a weaker flow and difficulty beginning urination. The current treatments include finasteride (Proscar) and Saw Palmetto (made from the berries of a plant native to the American Southeast) which reduces the size of the prostate in only four to six weeks and is relatively effective. Zinc is also used to maintain a healthy prostate. In addition to enlarged prostate, other prostate problems include prostatitis, and prostate cancer. It has been stated that men have odds of 100% of experiencing one of these three disorders.
Visceral fat increase has been associated with an increased vascular risk. Body fat in men increases from 18% to 36% between 18 and 85 years of age, with the largest increases in intraabdominal fat. Also, by age 70, an average man has about 26 pounds less lean body mass than at age 25.
Low testosterone can lead to osteoporosis in elderly men. This tends to happen later in men than in women because of the general tendency for men’s bones to be thicker and denser than women’s. In hypogonadal men, bone mineral density tends to increase with testosterone treatment. In men, there may be an increase in circulating estrogen levels; common causes of estrogen increase during mid-life include age-related increases in aromatase activity, alteration in liver function, zinc deficiency, obesity, overuse of alcohol, drug-induced estrogen imbalance and ingestion of estrogen-enhancing food or environmental substances. Also, fatty tissue contains more aromatase activity as compared with lean tissue resulting in more testosterone being converted to estradiol. Vitamin C deficiency is associated with high levels of aromatase activity whereas zinc inhibits aromatase activity.
Low testosterone levels may tend towards depression; the decrease in sexual function may also lead to depression, irritability, and mood swings…this depression further leading to decreased sexual function.
Complications
Testosterone deficiency has been linked to muscle weakness and osteoporosis. In one study, proximal and distal muscle weakness was detected in 68% of men with primary or secondary hypogonadism. Spinal, trabecular, and radial cortical bone density may also be dignificantly reduced in testosterone-deficient men. Thirty percent of men with spinal osteoporosis have long-standing testosterone deficiency, and one-third of men have subnormal bone density that puts them at risk for fracture.
Diagnosis
Serum and blood testing is done to determine the availability of testosterone and levels of leutenizing and gonadotropin-releasing hormones in the body. Men with low testosterone in whom normal or high gonadotropin levels are found typically have primary hypogonadism, which stems from a problem in the testicles. Secondary and tertiary types, caused by problems of the hypothalamus or pituitary gland, often result in low testosterone and low gonadotropin level.