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From the March 17th, 1999 issue of
Smart Life News [v7n2]. Copyright (c) 1999.
All rights reserved.
Book Review and Smart Life Update:
Testosterone is a vital steroid hormone that plays many critical roles in human health. Despite its importance, testosterone is poorly understood by many health professionals. Although well known for its masculinizing (androgenic) effects, testosterone also serves many diverse functions that are essential to both sexes. Declining testosterone levels play a major role in a broad range of age-associated symptoms and pathologies, including declining sexuality, cardiovascular disease, osteoporosis, and prostate hypertrophy. Hormone replacement therapy with testosterone and/or testosterone precursors is rapidly becoming a standard of anti-aging medicine.
Testosterones many functions and uses are poorly appreciated by both the public and the medical profession alike. This is partly due to our cultural stereotyping of testosterone as as the male hormone, which obscures its anabolic (tissue-building) functions and its role in female health. However, ignorance about testosterone is also due to vestiges of the wartime propaganda campaign against steroid hormones, which were being extensively researched in Germany in the decades prior to World War II. German scientists were the pioneers in researching the roles of steroids in human health and physiology. US health authorities were encouraged to advance negative notions about steroids, which were later entrenched during the Cold War with the Soviet Union. Such prejudices were the basis for such claims as 1) steroids dont work to improve athletic performance, 2) that steroids are exceedingly dangerous, 3) that steroids are regularly abused, and 4) that steroids were cheats in sports competitions. Those steroids that were not banned outright were scheduled to restrict popular and professional access. This legacy remains today. There are well documented medical applications of steroids to many serious conditions like heart disease, osteoporosis and AIDS which remain largely unemployed.
The recent popularity of hormone replacement therapy for women seems to be mitigating this cultural prejudice against steroids. Originally a marketing scheme for anti-fertility estrogen drugs in birth-control pills, hormone therapy has grown to encompass steroid therapy for peri- and post-menopausal symptoms. As the market has matured, significant consumer disenchantment with the pharmaceutical industrys patented-drug options (e.g., Premarin and Provera) has created a demand for natural (unpatentable) hormones. Natural hormone replacement therapy is rapidly becoming a standard of care among alternative practitioners.
This ideological shift from steroid analogs to natural steroids has significantly legitimized popular and professional attitudes towards steroids. This shift has gone far enough that medical seminars on natural hormone replacement therapy regularly discuss testosterone replacement therapy for women (because it helps regulate assertiveness and sexual libido), and sometimes even progesterone replacement therapy for men (because it can counteract age-associated increases in estrogen levels). More on this later. For now, suffice it to say that consumers are more comfortable with the idea of steroid use for health-enhancement purposes.
In the last few years, there have been many books published about testosterone hormone therapy. Two of those books deserve special mention for providing comprehensive, accessible, and scientifically accurate information about testosterone for people interested in hormone replacement therapy.
The first, The Testosterone Syndrome: The Critical Factor for Energy, Health & Sexuality Reversing the Male Menopause, is written by Eugene Shippen, M.D. and William Fryer (ISBN: 0-87131-829-6, $21.95 hardback). The Testosterone Syndrome is a well written book with many valuable insights into testosterone replacement therapy and makes good use of Dr. Shippens extensive clinical experience with testosterone. It is an outstanding effort, evenly mixing 1) simple explanations of concepts, 2) readily understandable presentation of scientific studies, and 3) client anecdotes that illustrate the human dimension of the information being presented. Although the book is specifically about testosterone, there is mention of parallel issues, like 1) the involvement of insulin and homocysteine in heart disease, and 2) the ability of deprenyl to increase testosterone levels in men. I especially appreciated the emphasis given to the antagonistic role that that estrogen plays in aggravating testosterone deficiency. This book is an ideal choice for readers with little or no technical background in medicine or biology.
The second book, Maximize Your Vitality and Potency for Men Over 40, is written by Jonathan V. Wright, M.D. and Lane Lenard, Ph.D. (ISBN: 0-9627418-1-7, $14.95 paperback). It also provides an outstanding summary of testosterones many uses and benefits, with a couple of differences. First, Wright and Lenard are much more detailed in their discussion of the medical/scientific issues behind testosterone. Second, they do not use anecdotal stories to illustrate the information they are presenting. These differences may be a liability for readers unfamiliar with hormones and nutrition, but they were a plus for me.
As an example: Maximize your Vitality and Potency has an excellent section on circadian (daily) and sub-circadian (less-than-daily) testosterone rhythms, a subject neglected by Shippen and Fryer. This information is then used to critique the relative merrits of 1) testosterone-ester depot injections (a medically popular but decidedly unphysiologic method of testosterone administration), 2) testosterone patches (a better method, but one that still swamps out sub-circadian hormone fluctuations), 3) transdermal testosterone creams and lotions (which can be applied to support circadian and subcircadian rhythms), and 4) sublingual testosterone products (a convenient method which also can support sub-circadian rhythms).
Because Wright and Lenard are dealing with male vitality and not just testosterone, they cover such related subjects as 1) Viagra (GMP enhancement), 2) arginine (NO enhancement), 3) yohimbine (
Perhaps one of the most significant and controversial issues is the role of testosterone in prostate health. Orthodox Western medical authorities regard testosterone as a significant risk factor for prostate hypertrophy (enlargement) and prostate cancer. This belief is so entrenched that hormone blockade and/or estrogen therapy are considered a standard of care for prostate therapy. Shippen and Fryer, and Wright and Lenard, take a completely different view that testosterone is actually protective.
They base this view on several key findings. One long-term study of 50 men found no association between testosterone levels and the subsequent development of prostate hypertrophy or cancer [Carter et al., 1995]. Other studies have failed to find any connection between testosterone levels and prostate specific antigen (PSA) levels, the most-common currently utilized clinical test for tracking prostate cancer risk.
If testosterone is not the culprit, then what about testosterones downstream metabolites estradiol and dihydrotestosterone (DHT)? Might they be the risk factor?
It is not that difficult to understand how researchers could mistake testosterones role in the health of the prostate. First, there is the conceptual fallacy: if estrogen is the female hormone and causes female sex-organ problems (e.g., endometriosis, breast and ovarian cancer, fibrocystic breast disease, etc.), then shouldnt testosterone (the male hormone) cause the male equivalent (prostate hypertrophy, testicular and prostate cancer, etc.)? With such a preconception, scientists and clinicians might easily attribute effects to testosterone that were actually caused by the biological influence of estradiol and/or DHT metabolites of testosterone. Until recently, the means to inhibit the conversion of testosterone to both estradiol and DHT were not safe enough for humans to scientifically separate the influences of these hormones from each other. Despite such limitations, there is clear evidence that estrogen is the prostate risk factor we should be monitoring.
Two notable studies have looked at the relationship of estrogen levels to prostate enlargement. A Japanese study found that prostate size was directly correlated with estrogen (and inversely correlated with testosterone!) [Suzuki et al. 1995]. A concurrent American study found that men with severe prostate hypertrophy had elevated estrogen levels compared to men without prostate hypertrophy [Gann et al. 1995]. Furthermore, low levels of testosterone aggravated the risk of high estrogen levels.
Although dihydrotestosterone (DHT) may also be correlated with prostate
hypertrophy, the relationship appears not to be linear. Excessive DHT may
be a risk, but abnormally low levels also may be a risk (DHT levels fall
as prostate cancer worsens). This may be another indication of the virtue
of moderation. Moderation of enzyme inhibition may explain why saw palmeto
berry (serenoa repens) may be more effective at reducing the
clinical symptoms of prostate hypertrophy than finasteride (Proscar).
Saw palmeto is much milder than finasteride at inhibiting 5
There is good evidence that steroid deficiencies play a role in heart disease. Despite many well designed clinical research studies documenting a broad range of cardiovascular benefits from testosterone, steroids are virtually ignored by US cardiologists. In the 1940s, testosterone was successful in treating 91 out of 100 angina patients [Lesser, 1946]. Although the testosterone took 1-2 months to have its beneficial effects on angina, as opposed to mere minutes for nitroglycerine, testosterone lasted for months after discontinuation of therapy.
Thirty years later, a well designed study (randomized, double-blind, placebo controlled) of post-exercise electrocardiograms confirmed that testosterone had powerful therapeutic benefits in cardiovascular disease [Jaffe, 1977]. ST segment depression (an early EKG marker of angina) decreased 30% after 1 month and 50% after 2 months.
A decade later, a large epidemiological study of 2500 men in Wales established that men with heart disease had significantly lower testosterone levels (and higher insulin levels and lower HDL) [Lichtenstein et al., 1987].
More recently, a study of 55 consecutive male coronary angioplasty patients (none of whom had had strokes or heart attacks) demonstrated an inverse relationship between testosterone and coronary artery occlusion [Phillips et al., 1994]. Patients with the highest occlusion (the greatest arterial blockage) had the lowest free testosterone levels and vice versa.
Testosterone also appears to positively affect several factors which are considered risk factors for heart disease. It decreases obesity and raises lean body mass, it normalizes blood clotting, and it shifts the HDL/LDL-cholesterol ratio towards HDL (the good cholesterol).
The decline of DHEA and testosterone is a central feature of the aging process in men. The characteristic shift in hormone dominance from steroids with anabolic and androgenic steroids to estrogens provides a clear rationale for the specific nature of many symptoms and conditions associated with aging. Techniques for correcting both andropause and estrogen dominance are readily available. Natural hormone replacement therapy with testosterone is a potentially valuable option that should be considered for many age-associated conditions, including many neurological and cognitive syndromes.
The Testosterone Syndrome and Maximize Your Vitality and Potency do an outstanding job of covering the much neglected topic of testosterone therapy. These books are sufficiently well referenced to the primary scientific and medical literature to provide a credible educational resource for practitioners unfamiliar with natural hormone replacement therapy. Both books would make a worthy addition to any smart-drug or longevity library.
Carter HB et al. Longitudinal evaluation of serum androgen levels in men with and without prostate cancer. The Prostate 27: 25-31, 1995.
Gann PH et al. A prospective study of plasma hormone levels, nonhormonal factors, and development of benign prostatic hyperplasia. The Prostate 26: 40-9, 1995.
Jaffe M. Effect of testosterone cypionate on postexercise ST segment depression. Br Heart J 39: 1217-22, 1977.
Lesser M. Testosterone propionate therapy in one hundred cases of angina pectoris. J Clin Endocrinol 6: 549-57, 1946.
Lichtenstein MJ et al. Sex hormones, insulin, lipids, and prevalent ischemic heart disease. Am J Epidemiol 126(4): 647-57, 1987.
Phillips GB, Pinkernell BH and Jing TY. The association of hypotestosteronemia with coronary artery disease in men. Atheroscler Thromb 14: 701-6, 1994.
Shippen E and Fryer W, The Testosterone Syndrome: The Critical Factor for Energy, Health & Sexuality Reversing the Male Menopause. M Evans and Company, New York, 1998 (ISBN: 0-87131-829-6).
Suzuki K et al. Endocrine environment of benign prostatic hyperplasia: prostate size and volume are correlated with serum estrogen concentration. Scand J Urol Nephrol 29: 65-8, 1995.
Wright JV and Lenard L. Maximize Your Vitality and Potency for Men Over 40. Smart Publications, Petaluma, California, 1999 (ISBN: 0-9627418-1-7).