While not as severe as the female menopause, the male version is lengthier, usually lasting 15 to 20 years. About 40% of men in their 40s, 50s and 60s experience some degree of lethargy, depression, increased irritability, mood swings, and difficulty in attaining and sustaining erections that characterize andropause.
The concept of a male andropause has been more controversial than that of the female menopause, with many arguing that it doesn't even exist. Part of the reason for the controversy is that, in contrast to women, men do not have a clear-cut external sign, namely the cessation of menstruation.
A man often begins to experience changes in his body somewhere between the ages of 40 and 55. These bodily changes may be accompanied by changes in attitudes and moods. The aging process alone can not be responsible for this problem as well over 40% of males remain sexually active at 70 years of age and beyond.
Acute andropause in men is relatively uncommon, compared to acute menopause in women, because testicular function declines gradually in most men. There are a number of other causes, however, for acute testicular failure in adult men and these include: viral infections such as mumps, surgical removal of or surgical injury to the testes and male reproductive tract, diseases when the immune system attacks and destroys the testes such as variations of systemic lupus erythematosis, subtle genetic abnormalities which permit normal adult development but lead to premature testicular failure, generalized vascular diseases such as diabetes, chemotherapy, and pituitary tumors (rare).
The second form of this syndrome, while more common, is more insidious since it occurs gradually. It is often confused with male midlife psychological adjustment disorders because it exactly mimics depression in midlife men. Some known contributors to this condition are excessive alcohol consumption, smoking, hypertension, prescription and non-prescription medications, poor diet, lack of exercise, poor circulation, and psychological problems.
Male hormones decline gradually. Testosterone (from the testes), human growth hormone (from the pituitary), and DHEA and androstenedione (from the adrenal gland) levels all begin to drop. For many men this does not occur until their 60s or 70s but there are others where it occurs much earlier. In addition, there are proteins in the blood which bind testosterone into a biologically inactive form – sex hormone binding proteins or globulins. Their levels can rise in response to many conditions including medical disorders and exposure to other hormones such as phytoestrogens (estrogens derived from plant sources such as soy) and environmental estrogen-like compounds (pesticides, hormones used in agribusiness to produce fatter animals, etc.) As an example, there is some data suggesting that men on low fat or vegetarian diets have lower testosterone levels. The overall effect of rising sex hormone binding proteins is that there is less bio-available testosterone.
Typical symptoms include:
This list sounds a little similar to women in menopause because it is the same condition. The relationship between the ovaries, estrogen, the brain, and the pituitary are the same as the relationship between the testes, testosterone, the brain, and the pituitary.
The diagnosis is simple – measuring either free testosterone blood levels or computing the Free Androgen Index (FAI) which is [total testosterone x 100 / sex hormone binding globulin]. There is some controversy as to what level of total blood testosterone in men is normal with low end values ranging from 250-400ng/dl. Free testosterone in men should be well within the range of 300-1100ng/dl with the FAI between 70-100%. At a FAI of less than 50%, symptoms of andropause appear.
Risks of replacement therapy. Though often suggested, there is no evidence in the medical literature that testosterone replacement therapy increases the risk of prostate cancer. Men using synthetic testosterone supplementation should have their serum lipids carefully evaluated and rechecked periodically. Using a natural testosterone is safer than using a synthetic form, but may require the transdermal route of administration.
As a general principle, whenever any hormone is administered, the gland which normally produces it ceases to function and recovery when therapy stops can be variable. Patients with borderline low testosterone levels may be committing themselves to lifelong therapy if they start with testosterone replacement.
Benefits of replacement therapy
There is no doubt that the administration of testosterone to men with true testosterone deficiency will improve their health and sense of well being. The symptoms listed above should disappear. Unfortunately impotence, or the inability to sustain and erection, does not respond well to testosterone therapy except perhaps in men with severe hormone deficiencies. This comprises approximately 8-16% of men presenting themselves to physicians with erectile disorders. There is no evidence that administering testosterone to men with borderline low testosterone levels will improve sexual functioning, although libido may be enhanced.
Lethargy and lack of vitality are early signs that your anti-aging hormones (such as testosterone) are diminishing.
The sensation of weakness, especially muscle weakness, may be due to the loss of muscle mass seen in andropause.
Impotence or erectile dysfunction is one of the most common symptoms of andropause.
For more insight, The Testosterone Syndrome, by Eugene Shippen, M.D. and William Fryer, provides a persuasive argument in favor of hormone modulation in the male andropause.
The April 2004 issue of the journal Urology published the findings of Italian researchers that the amino acid carnitine was more active than testosterone in improving symptoms of aging in men, such as sexual dysfunction and depression, associated with the decline of androgenic hormones.
120 men between the ages of 60 and 74 with symptoms of low testosterone were randomized to receive 160mg orally administered testosterone undecanoate, 2gm propionyl-L-carnitine plus 2gm acetyl-L-carnitine per day, or a placebo for a six month period.
Erectile function, sexual desire, sexual satisfaction and nocturnal penile tumescence increased over the course of the study in the group receiving testosterone as well as in the group receiving carnitine. However, the group receiving carnitine also experienced an increase in orgasm and general sexual well-being. Erectile function and nocturnal penile tumescence were significantly more improved in this group than in those receiving testosterone. While both treatments lowered depression scores, carnitine's effect was greater.
Predictably, treatment with testosterone increased serum total and free testosterone and decreased luteinizing hormone levels, but carnitine's effect on these hormones was not significant. Treatment with carnitine was not associated with an increase in prostate volume as was testosterone treatment.
Fatigue was likewise improved in both groups. As one negative effect, the men taking testosterone developed enlargement of their prostates, which did not occur in the carnitine-treated group. Although both testosterone and carnitine improved symptoms of male aging, there was overall superior benefit to carnitine with no real side-effects.
Administration of tribestan, an extract of Tribulus, leads to increased muscle mass during exercise by activating an enzyme associated with energy metabolism. It has also been reported to increase the body's natural testosterone and luteinizing hormone (LH) levels. With the increase of testosterone it has helped to alleviate some symptoms associated with male menopause.
There is a new appreciation of the effects of changing estrogen metabolism that come with male aging, now identified as andropause. German researchers have clearly documented a dramatic, aging-related accumulation of estrogen in human prostate glands. This work correlated age, estrogen accumulation, and the presence of benign prostatic hypertrophy (BPH). This underscores the role of estrogen as a growth promoting hormone in men as well as women.
Tissue accumulation of estrogen is a unique hallmark of andropause, distinct from estrogen deficiency which characterizes menopause. Recent work shows that estradiol, the active form of estrogen, provokes increases in prostate specific antigen (PSA) production in human prostate tissue. This increase in PSA is as great as that seen with testosterone. Increased PSA production was specifically inhibited by 2-methoxyestradiol, the beneficial estrogen metabolite whose production is promoted by DIM.
Accumulation of estrogen during andropause is amplified by obesity since fat tissue is the site of conversion of both testosterone and DHEA into estrogen. In case control studies, higher levels of circulating estrogen predict the degree of prostate enlargement. More importantly, increased estrogen levels have been repeatedly noted as a risk factor for early atherosclerosis and heart attack. The risks of elevated estrogen in men further correlate to decreased ability to dissolve blood clots. The specific deficiency in men of an active, beneficial metabolism of estrogen leading to 2-methoxy estrogens would explain many, if not all, of these observations.
In studies culturing human vascular endothelial cells, it has been shown that 2-methoxy estradiol is a primary regulator of cell growth and apoptosis. Active and regulated apoptosis may contribute to the prevention of atherosclerotic plaque formation. At the basic level of lipoprotein status, 2-hydroxy and 2-methoxy estrogens are powerful antioxidants. In recent experiments, these metabolites, whose production is promoted by DIM, have been shown to prevent the oxidation of human lipoproteins. Lipoprotein oxidation is now accepted as an early, initiating event in atherosclerosis. While it remains to be demonstrated through intervention studies that DIM supplementation can slow the progression of prostate disease and atherosclerosis, it is clear that DIM supplementation in men can beneficially shift estrogen metabolism.
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