All of us guys want to stay young, have terrific muscle builds and think of ourselves as studs. However, the facts don’t support this desire. With aging comes a loss of a lot of male ego along with other items. Thus, the introduction of male “menopause” and the burst of therapies aimed at susceptible male subjects bent on improving their performance.
Glenn Braunstein, MD, MACP, professor of medicine at Cedars-Sinai in Los Angeles explained his opinion on this matter in the ACP Internist publication (April 2014, Vol. 34, No. 4) from the American College of Physicians. Dr. Braunstein described three phases: adrenopause (a decline in dehydroepiandrosterone, DHEA), somatopause (a decline in growth hormone, GH) and andropause (a decline in testosterone).
Dr. Braunstein points out that replacing DHEA has failed to have any positive benefit. As for growth hormone decline, true deficiency in adults is uncommon, “unless there is underlying pituitary condition”. Furthermore, Dr. Braunstein notes that a low GH level does not mean that a person has an abnormal disease state nor “giving growth hormone is going to reverse the aging process”.
The first two stages are “biochemical concepts that have not been tied to any physical or pathophysiological reality”.
However, “andropause is a different story…testosterone typically declines with age. When declining testosterone is combined with signs and symptoms of hypogonadism, men may have a legitimate health concern”, so says Dr. Braunstein.
The key word is “COMBINED”. Studies have varied dramatically as to the prevalence of hypogonadism amongst middle aged males. This has ranged in studies from 39%, 6-12% and in one study 2-3%. Not exactly reassuring as to what to believe!
In order to diagnose hypogonadism and true hypo testosterone levels, it must be unequivocal. Findings should include: “erectile dysfunction, a decrease in muscle mass, loss of bone mass and the development of breast tissue”. Other associated but less easily defined symptoms include fatigue, decreased libido and difficulty concentrating. These latter symptoms, however, clearly can be present for a variety of reasons and not necessarily related to the need for testosterone replacement. Rather ascertaining what other issues might be in play is required.
Measuring of low testosterone is met with its own issues. A single low level is not diagnostic of anything. Many levels will return to normal on retesting months or years later without any intervention. Testing needs to be done in the morning due to diurnal variations. The gold standard test is “gas chromatography tandem mass spectroscopy”. This is often difficult to find in the average laboratory. Dr. Braunstein points out that common laboratory testing can “lack accuracy”. Plus, the normal range varies widely amongst male age groups (300-1,000 ng/dL).
Dr. Braunstein recommends having “3 blood samples at 20 minute intervals between 8 to 10 a.m. and combine equal amounts of the serum into one test tube and measure the testosterone in that”. I wonder how many labs would be able to perform this request?
If the serum testosterone level is found to be low then the workup moves on to truly assess if hypogonadism is present. Recall above that it is the combination of low testosterone and hypogonadism that should guide therapy. Measurements of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) should follow. If these are elevated then primary testicular causes are to explain the low testosterone level. If, on the other hand, LH and FSH are low as well, primary pituitary issue may be present. If present, the next step is to measure prolactin level. If found to be low then the pituitary gland needs further workup including an MRI scan to rule out a pituitary tumor.
Finally, introducing testosterone therapy in aging male population should be done with caution of the patient has significant coronary artery disease and only be instituted for “severe symptoms of androgen deficiency”.
For now, testosterone replacement, like many other issues, remains controversial.