A Testosterone Mystery Solved by Jerry Brainum

 

 

 

Although female menopause, which is characterized by a decline in the primary hormones in women, such as estradiol or estrogen, is an accepted medical fact, the existence of a similar decline in testosterone in men remains controversial. So-called "Low-T" syndrome consists of a number of symptoms, all of which are attributed to a gradual decline in the production of testosterone as men age. These symptoms include decreased sexual function, such as loss of libido or sex drive, and problems with obtaining an erection. Lack of testosterone is also related to adverse body composition changes, such as an increase in body fat, particularly in the abdominal and visceral (deep-lying abdominal) fat depots. Since testosterone plays a major role in maintaining muscle mass, both muscle size and strength decline with the advent of low T levels. Psychological effects include higher rates of depression, lack of motivation, and possible increased risk of Alzheimer's disease. So if all of these bad effects are linked to low T levels, where does the controversy about testosterone replacement therapy (TRT) arise?

Some scientists maintain that age-related declines in hormones such as testosterone, estrogen, and growth hormone occur as a protective mechanism of the body. With age, cellular replication becomes less efficient. On a cellular basis, telomeres, the ends of chromosomes, shorten with each successive cell replication event. When the telomeres are "used up," the cell undergoes rapid senescence or aging and soon dies. The aging process, however, is a bit more complicated. For one, telomeres don't affect the aging of either skeletal muscle or neurons in the brain. But in relation to hormones, most of them promote cellular growth, and without the efficient activity of DNA, which is lessened with aging, cellular mutations could arise. These mutations, in turn, are the cornerstone of cancer. So the theory goes that the body recognizes the ability of hormones such as testosterone and GH to stimulate cell replication and growth, and gradually reduces the ability to synthesize these hormones as a means of protecting against cancer onset. The problem with this theory is that there is no evidence that a lack or even a normal level of these hormones will promote cancer in any way.

In fact, a major reason why many physicians are loath to prescribe testosterone drugs to men who are clinically deficient in the hormone is the fear of stimulating prostate cancer. I will deal with this issue more completely in an upcoming issue of Applied Metabolics but suffice to say now that the fear that testosterone causes prostate cancer (PC) is unfounded. The notion that testosterone causes or promotes PC is based on one patient written up in a 1942 medical journal article. This man had been castrated, so was not producing testosterone. When he was provided testosterone, PC was stimulated. Based on that single case, doctors today still believe that testosterone stimulates PC . . .