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HORMONE REPLACEMENT HRT Controversies

Similar to menopause, andropause can be treated with a combination of lifestyle, nutritional, botanical, and HRT approaches. The recent backlash against esterified estrogens used in combination with synthetic progesterone (progestin) molecules for treating menopause16 has led to a near-revolution and altered prescribing habits by physicians. Several events (popular media and research evidence) have led to a wave of interest in using bioidentical hormones to achieve hormonal balance. An offshoot of this trend involves the use of hormone replacement in men. Among these are pro-hormones (DHEA, androstenedione, and pregnenolone) and testosterone. Combined with other natural medicines, treatment of andropause symptoms is rather successful but, as will be discussed, is not without controversy.

Testosterone Replacement

The knowledge base surrounding replacement of testosterone and androgens at physiologic levels in men with andropausal symptoms is much newer and less widely accepted in conventional medicine compared to the many accepted allopathic choices available to women. It is true that women, without a doubt, experience greater fluctuations and resultant symptoms because of the cyclical nature of female hormones. This has led in part to the vast "medical-ization'' of both the menses and menopause, wherein a solution to nearly any type of perturbation can be answered with one or more combinations of hormone replacement. Protocols and forms of HRT for men are quite limited by comparison. Medicine has long held that prostate-specific problems, such as hypertrophy and cancer, are solely initiated by testosterone. However, a small body of evidence is accumulating that these problems may not be solely related to this hormone. This evidence indicates that accumulation of estrogen in aging may be the primary factor in the development of prostate disease later in life whereas testosterone and DHT play a secondary role, or act as promoters.17 Another study showed that there were no associations between testosterone, SHBG, or androstenedione concentrations and the incidence of prostatic carcinoma, further refuting the notion that androgens are the sole determinants of future prostate disease.18 What is more, with aging, testosterone levels begin to decline; yet at the same time, prostatic hypertrophy incidence elevates. The standard argument for this is that

Table 2-1. Dosing Table

Treatment

Doses

Hormone replacement

Testosterone replacement

Dehydroepiandrosterone

Chrysin

Zinc

Puncture vine or tribulus

(Tribulus terrestris) Potency wood (Muira puama)

Should be evaluated on an individual therapy basis following extensive testing; typically introduced after all other means have been used Typical starting dose is 5-10 mg, topically 25-50 mg per day 500-750 mg per day 30 mg per daya

Variable; 250-1,500 mg per day; standardized to 30%-45%

steroidal saponins (also known as furostanol) 1-2 mL, extract, 2 times per day aPatients should always supplement with copper when taking extra zinc.

Diagnostic Confounders of Andropause

Diabetes, renal failure, cirrhosis, anemia, or hypothyroidism Depression

Alcohol abuse=poor nutrition leading to decreased albumin levels Abnormal circadian rhythm of testosterone

Medications, such as cimetidine [Tagamet], digoxin [Digitek, Lanoxicaps , Lanoxin ], spironolactone [Aldactone ], or antidepressants Acute stressors, such as surgery, severe burns, or accidents Vigorous athleticism

Other confounders, including hypothalamic-pituitary tumors, Cushing's syndrome, hemochromatosis, Kallmann's syndrome, Klinefelter's syndrome, or Prader-Willi syndrome hypertrophy results from the cumulative effect of testosterone on the prostate gland. However, when focusing on incidence rates during the years of highest testosterone levels (20s, 30s, and 40s), when most of the exposure has occurred, this time period is associated with the lowest risk of prostate disease.19

The transformation (aromatization) of testosterone to estrogen occurs most readily in the fat stores of the body. Therefore, as one ages and gains weight, the aromatase enzyme system is fueled, resulting in elevated levels of estradiol, perhaps promoting prostatic disease. Conversely, as testosterone is metabolized via 5-alpha reductase, it is transformed into DHT, a molecule that androgen-related disease is currently blamed on. When viewing the routes of metabolization of testosterone, we noticed that the two main avenues are via aromatase, leading to estradiol and 5-alpha reductase, leading to DHT. An unproven idea worth considering is the possibility that by blocking the 5-alpha reductase enzyme, one essentially creates a ''backup'' at this point in testosterone metabolism, forcing testosterone to be dismantled via aromatase, possibly leading to greater levels of estradiol and exacerbating the problem. The problem is addressed by attempting to restore a more youthful balance between estrogen and testosterone by decreasing estrogen influence and increasing testosterone influence in the male body. This is referred to as increasing the testosterone-estrogen ratio. This is achieved with testosterone supplementation, often at doses of 5-10 mg per day, and taking steps to reduce estrogen load in the body, such as using phytoestrogens, dietary strategies, exercise, and nutraceutical options. In addition, some physicians may augment this process by prescribing progesterone to men, further blunting estrogen's effect in the body. Prior to, and during, androgen replacement, a prostate examination should be conducted at the outset of therapy, and baseline and prostate-specific antigen levels should be measured, three and six months later and then every six months thereafter, if latent prostate symptoms develop.

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