With all the ballyhoo in the US congress about anabolic steroid use in sports (to the point where athletic performance in the pro sports will decline to pre 1968 levels - boring), the line between anabolic steroid drugs and natural testosterone has been blurred to the point of not being recognizable. So, let’s point out the facts and put some distance between the growth drugs and testosterone. Let’s also take a serious look at the good that testosterone replacement can do in both men and women to improve their overall health without the danger of creating other problems such as cancer (as the estradiol docs prescribe so freely often does).

Androgens, or male hormones have two main functions #1 to be androgenic or to produce libido, sexual ability, grow the penis and testicles, make sperm, increase mental drive and sexual desire. The #2 function is to be anabolic; to build bone, build muscle. Natural Testosterone has both the androgenic and anabolic functions. Anabolic steroids are a synthetic androgen having almost no androgenic ability while only having anabolic ability. This is the reason why bodybuilders on the “juice” may look all buff and sexy but their sexual equipment doesn't work. They have swapped growing biceps for a shrinking penis, not a good trade off!

The second thing wrong with anabolic steroids is that they are patented synthetics. You can’t patent nature and so the drug companies in order to make the biggest profit possible will vary the structure of the anabolic drug so that it does not resemble testosterone and so can be patented. There are two drawbacks here: those differences will surely produce side effects. Matter of fact most all of the side effects listed for natural testosterone in the PDR are actually those for the anabolic drugs. Like they have with natural progesterone vs the synthetic drug progestine, the drug firms want to lower the legal liability for the side effects of their drugs by making the claim that natural hormones have the same side effects - a definite and bold faced lie, demonstrating Hegel's point that if you tell a big enough lie folks will believe you. (BTY, don't tell me Hitler invented the Big Lie, he got it and a few other things from the philosopher Hegel).

The second drawback is that all synthetic testosterone and anabolic drugs are methylated so that when taken orally, that process prevents their being washed out of the blood by the liver the first time they go through. But the methylization stuff is very heavy on the liver and a source of producing liver cancer. So, in this instance the hormone gets the blame for the cancer when in actuality it is the methyl group the liver has to separate from the hormone to metabolize it, that produces the disease!

Now, let’s touch on one of the major side effects of anabolic steroid use - higher estrogen levels! Body builders, pro wrestlers, football linemen, distance cyclists, track and field athletes are well known anabolic steroid users. But by far the most serious anabolic junkies are the muscle heads and fake wrestlers. With these over the top steroid users, they use what amounts to some 5 times the therapeutic dosage of the drugs. For example, of the old stand by anabolic, Dianabol, the standard medical dosage for the drug in burn, kidney failure, orthopedic injury or muscle wasting patient was 4 tablets of 5 mg each a day. Champion bodybuilders I’ve met in the 60’s and 70’s were using 12 to 25 tablets a day! Excessive, you bet! They took this much androgen without having available the stuff to keep it from turning into estrogen! So they made tons and tons of estrogen! And they suffered the side effects of having too much estrogen: water weight gain, breast development in men (gynocomasty), depression and moodiness, fat gain from the waist to knees.

Now that bodybuilders are cycling from one drug to another and even stacking them (taking several drugs together) to have an even greater effect, they are using estrogen based drugs like Clomid to supposedly increase Luteinizing Hormone production during cycling. LH brings the signal from the pituitary for the testicles to make more testosterone. Any gal who’s used Clomid as fertility therapy will tell you about “Clomid Hell”, the deep depression and mood swings caused by the drug. It is these drugs that are responsible for the aggressive behavior seen by anabolic steroid users, and I believe the chemical trigger for the recent murder suicide of a well known pro wrestler.

Natural testosterone has no such depressive effects, as many MD parrot, and no hyper aggressive or hyper sexual effects leading to rape as many femiNAZI’s assert! The research abstracts below tell the story.

This is research your MD likely won’t know exists. Docs are afraid of testosterone because "Higher Powers", from politicians to the feminists, have long blamed testosterone for a myriad of things from aggressive behavior to degenerative diseases. All those assertions are wrong; those folks have a few hidden agendas:

• Governments: They like docile subjects over assertive citizens and lowering testosterone levels in general and testosterone's lack of availability makes for an easier to control population. Estrogen dominant subjects may be bitchy but the bitchy don't overthrow governments, they look to others (i.e. governments, doctors etc.) to solve their problems!
• Medicine: The use of testosterone would negate the need for expensive life long therapy using heart, circulation or anti depression drugs. The drug companies and the hospitals would lose billions. The medical business is here to stay in business and any lofty ideals folks may have of docs and drug companies being here to better the lot of mankind are dead head fairy tales.
• Feminists: They have blamed testosterone for all the ill’s of mankind since the 70’s. Many a piece of absolute garbage junk science was created by the man hater crowd to show how much better the world would be being dominated by estrogen over testosterone. While their numbers dwindle, the extreme femiNAZI’s still hold great sway and influence these Politically Correct days, especially in the halls of academia where a straight man would not dare to hold his head up high and assert “I am Man hear me roar”.... Yea I know, this song sounded just as stupid when women sang it in the 70’s! (Don’t worry gals, to be fair I get to beat up on stupid men later in this article)!

Like all the other advances in medicine, conventional docs have to be brought into new information kicking and screaming!

Studies and comments:

It’s the estrogen stupid! Testosterone not shown to cause enlarged prostates:

[Endocrine environment of benign prostatic hyperplasia--relationships of sex steroid hormone levels with age and the size of the prostate].
[Article in Japanese]
Suzuki K, Inaba S, Takeuchi H, Takezawa Y, Fukabori Y, Suzuki T, Imai K, Yamanaka H, Honma S
Division of Urology, Shakai Hoken Mishima Hospital.
Nippon Hinyokika Gakkai Zasshi 1992 May;83(5):664-71

To determine the influence of endocrine factors on benign prostatic hyperplasia (BHP), the levels of three sex steroid hormones i.e., total testosterone (Total-T), free testosterone (Free-T) and estradiol (E2), were measured in serum of healthy 154 men. Their ages ranged from 18 to 91 years old. In 59 men, prostatic size was estimated by digital examination and was subdivided into three groups: smaller than or equal to walnut size, small hen's egg size and equal to or larger than hen's egg size. Firstly, relationships of sex hormone levels with age were studied. There was a slight decrease in Total-T over 60 years old, a significant decrease in Free-T, and no change in E2 with age. Thus, E2/Total-T and E2/Free-T ratio increased significantly after middle-age. Secondly, relationships of hormone levels with prostatic size were studied. In the larger prostate group, a significantly lower level of Total-T and significantly higher level of E2 were detected. But there was no difference in Free-T. Thus, the prostatic size was correlated positively with E2 level, E2/Total-T and E2/Free-T ratio. These suggest that the endocrine environment tended to be estrogens-dominant with age, in particular, after middle-age, and that patients with large prostates have more estrogens-dominant environments. We conclude that estrogens are key hormones for the induction and the development of BPH.

Testosterone and making sick hearts healthy:

Therapeutic effects of an androgenic preparation on myocardial ischemia and cardiac function in 62 elderly male coronary heart disease patients.
Wu SZ, Weng XZ
Department of Internal Medicine, Beijing Red Cross Chao Yang Hospital.
Chin Med J (Engl) 1993 Jun;106(6):415-8

The elevated estradiol/testosterone (E2/T) ratio had been proved to be a risk factor for coronary heart disease (CHD) in elderly men. We conducted a randomized placebo controlled crossover study on the effects of a new androgenic preparation "Andriol" in 62 elderly men with CHD over a period of 2.5 months. The results showed significant differences between Andriol- and placebo-treated groups at the end of this period: in the former, serum T level was elevated significantly (P < 0.001), E2 level was unchanged (P > 0.05), E2/T ratio was reduced (P < 0.05), angina pectoris (AP) was relieved (total effective rate, 77.4%), and myocardial ischemia in ECG and Holter recordings were improved (total effective rate, respectively 68.8% and 75%). Doppler echocardiography showed that 12 parameters of cardiac function were unchanged in both groups. No obvious side effect was found in those who took Andriol.

The pharmacokinetics of intravenous testosterone in elderly men with coronary artery disease.

White CM, Ferraro-Borgida MJ, Moyna NM, McGill CC, Ahlberg AW, Thompson PD, Chow MS, Heller GV
University of Connecticut School of Pharmacy, Hartford, USA.
J Clin Pharmacol 1998 Sep;38(9):792-7

Intracoronary testosterone injections have recently been shown to possess coronary vasodilating effects. The same may be true for intravenous testosterone, but the pharmacokinetic and hemodynamic aspects need exploration before pharmacologic studies can begin. This trial determined the pharmacokinetic and hemodynamic properties of 300 microg of testosterone given intravenously. Degree of testosterone aromatization to 17-beta estradiol after exogenous administration and overall patient tolerability also were evaluated. Eleven elderly men with coronary artery disease participated in the study and were given 300 microg of testosterone intravenously over 10 minutes. Serum blood concentrations of testosterone and 17-beta estradiol were measured at baseline and then periodically. Testosterone serum concentrations were stripped and fit to a two-compartment model for all patients. The volume of distribution (Vdarea) was 80.36 +/- 24.51 L, and the elimination half-life was 55.93 +/- 23.06 minutes. No hemodynamic differences or side effects were noted. The serum concentrations of 17-beta estradiol were significantly increased from baseline beginning 5 minutes after infusion to the end of the study (180 minutes after infusion).

Why low teststosterone and high estrogen produce blood clots and heart disease:

The association of hyperestrogenemia with coronary thrombosis in men.
Phillips GB, Pinkernell BH, Jing TY
Department of Medicine, Columbia University College of Physicians and Surgeons, St. Luke's-Roosevelt Hospital Center, New York, NY, USA.
Arterioscler Thromb Vasc Biol 1996 Nov;16(11):1383-7

Both hyperestrogenemia and hypotestosteronemia have been reported in association with myocardial infarction (MI) in men. It was previously observed that the serum testosterone concentration correlated negatively with the degree of coronary artery disease (CAD) in men who had never had a known MI. The present study investigated the relationship of sex hormone levels to the thrombotic component of MI by comparing these levels in 18 men who had had an MI (ie, thrombosis) and 50 men with no history of MI (ie, no thrombosis) whose degree of CAD was in the same range. The mean degree of CAD, age, and body mass index in these two groups was not significantly different. The mean serum estradiol level in the men who had had an MI (38.5 +/- 8.8 pg/mL) was higher (P = .002) than the level in the men who had not had an MI (31.9 +/- 7.1 pg/mL). The mean levels of testosterone, free testosterone, sex hormone-binding globulin, insulin, dehydroepiandrosterone sulfate, cholesterol, HDI, cholesterol, and systolic and diastolic blood pressure did not differ significantly. Estradiol was the only variable measured that showed a significant relationship to MI (P < .003 by multivariate logistic regression). These findings suggest that hyperestrogenemia may be related to the thrombosis of MI.

Let’s beat a dead horse some more: extra evidence on high estrogen and low testosterone in vascular and heart disease:

Evidence for hyperestrogenemia as the link between diabetes mellitus and myocardial infarction.

Phillips GB
Am J Med 1984 Jun;76(6):1041-8

The previous findings of hyperestrogenemia in men with myocardial infarction and of a correlation between the ratio of serum estradiol to testosterone and the glucose-insulin-lipid defect have led to the hypothesis that hyperestrogenemia may be responsible for the increased incidence of atherosclerosis and its complications in patients with diabetes. The hypothesis predicts that the mean serum level of estradiol and the ratio of serum estradiol to testosterone are elevated in patients with diabetes. To test this hypothesis, the serum levels of estradiol and testosterone were measured in 21 nonobese men with diabetes and in 19 apparently healthy men of similar age and weight. A higher mean serum estradiol level (p less than 0.001) and estradiol-to-testosterone ratio (p less than 0.005) were observed in the patients with diabetes, whereas the mean serum testosterone level was not significantly different. The findings are consistent with the hypothesis.

Abnormalities in sex hormones are a risk factor for premature manifestation of coronary artery disease in South African Indian men.

Sewdarsen M, Vythilingum S, Jialal I, Desai RK, Becker P
Department of Medicine, R.K. Khan Hospital, Durban, South Africa.
Atherosclerosis 1990 Aug;83(2-3):111-7

The relation between sex hormone levels and myocardial infarction was studied in a case-control study among 117 Indian men with myocardial infarction aged 30-60 years and in 107 healthy Indian male controls. The patients and controls were further divided into subsets defined by age in decades. In the total patient population, testosterone concentration was significantly lower than in the controls (P less than 0.01), whilst oestradiol (P less than 0.0005) and the oestradiol to testosterone ratio (P less than 0.0005) were significantly higher. Multivariate stepwise logistic regression analyses demonstrated that free testosterone index, the free oestradiol index, and the oestradiol to testosterone ratio were significantly associated with myocardial infarction, and that this association was independent of age, body mass index, smoking and serum lipids. Further analyses according to age subsets revealed that compared to respective control groups, patients in the 4th decade had both significant hypotestosteronaemia and hyperoestrogenaemia, whereas in patients of the 5th decade significant differences in total and in the calculated free oestradiol index were noted, and in the 6th decade a significant difference was detected only in the free oestradiol index. Hence, we conclude that aberrations in endogenous sex hormones are significantly associated with myocardial infarction, and that this association appears to be strongest in young men and diminishes with age, suggesting that these disturbances in sex hormones may be associated with premature manifestation of coronary artery disease.

Relationship between serum sex hormones and glucose, insulin and lipid abnormalities in men with myocardial infarction.

Phillips GB
Proc Natl Acad Sci U S A 1977 Apr;74(4):1729-33

Fifteen patients who had had a myocardial infarction before the age of 43 were compared with thirteen age-matched normal subjects. Twelve of the patients and three of the controls had a delayed glucose and insulin peak in the glucose and insulin areas than normal curves. When the measurements of the four patients with the largest areas under the glucose tolerance curve were separated, significant correlations were observed in the remaining patients and controls. The ratio in serum of the concentrations of estradiol-17beta to testosterone (E/T) correlated with serum glucose area (r equals + 0.69, P is less than 0.001), insulin area (r equals + 0.80, P is less than 0.001), and the ratio of insulin area to glucose area (I/G) (r equals + 0.64, P is less than 0.005) in the glucose tolerance test. Serum cholesterol concentration correlated with E/T, insulin area, and I/G, and serum triglyceride concentration correlated with glucose area, I/G, and serum cholesterol concentration. The hypothesis is presented (i) that in men who have had a myocardial infarction, an abnormality in glucose tolerance and insulin response and elevation in serum cholesterol and triglyceride concentrations are all part of the same defect (glucose-insulin-lipid defect), (ii) that this glucose-insulin-lipid defect when glucose intolerance is present is the "mild diabetes" commonly associated with myocardial infarction but is based on a mechanism different from that of classical diabetes, (iii) that this glucose-insulin-lipid defect is secondary to an elevation in E/T, and (iv) that an alteration in the sex hormone milieu is the major predisposing factor for myocardial infarction.

Relationship between sex hormones, myocardial infarction, and occlusive coronary disease.

Luria MH, Johnson MW, Pego R, Seuc CA, Manubens SJ, Wieland MR, Wieland RG
Arch Intern Med 1982 Jan;142(1):42-4

An alteration in sex hormones has been considered a risk factor for myocardial infarction. In this study, estradiol (E2) and testosterone (T) levels were evaluated in healthy firefighters, patients with myocardial infarction acutely and during their convalescence, patients with no evidence of occlusive coronary artery disease on arteriography, and patients with chronic angina pectoris in whom there was at least one vessel that indicated 50% occlusive coronary artery disease. Although T levels were similar in all groups, E2 levels were substantially higher in patients with myocardial infarction and in patients with chronic angina pectoris. These results support the hypothesis that elevated estrogen levels may be a risk factor for myocardial infarction and coronary artery disease, possibly by promoting clotting or coronary spasm.

Estradiol, testosterone, apolipoproteins, lipoprotein cholesterol, and lipolytic enzymes in men with premature myocardial infarction and angiographically assessed coronary occlusion.

Mendoza SG, Zerpa A, Carrasco H, Colmenares O, Rangel A, Gartside PS, Kashyap ML
Artery 1983;12(1):1-23

A series of thirty-three Venezuelan men with premature myocardial infarction (mean age (M +/- SEM) 45 +/- 1.5 yrs) and with greater than 50% occlusion of at least 2 coronary arteries, and 19 weight matched control men (age 44 +/- 2 yrs) with normal coronary arteries on coronary angiography were studied. The percentages of significantly abnormal (greater than +/- 2 S.D. of controls) serum or plasma concentrations of various measurements (in decreasing order) were: estradiol (33%), total apolipoprotein (apo)B (24%), estradiol/testosterone ratio (21%), low density lipoprotein (LDL) apo B (19%), apo AI (17%), apo AI/total plasma apo B ratio (17%), total cholesterol (17%), and LDL-cholesterol (LDL-C) (11%). In addition, a multivariate discriminant function analysis showed that only estradiol, apo AI, LDL-C, estradiol/testosterone ratio and total cholesterol were statistically significant independent markers of myocardial infarction with occlusive coronary disease in these patients. Both serum estradiol and estradiol/testosterone ratio correlated positively with plasma apo B and LDL apo B, and inversely with apo AI; serum testosterone correlated inversely with plasma apo B (p less than 0.05). The data suggest that circulating sex hormones (estrogens, testosterone) are not only independent markers of coronary disease but may be pathogenetically linked to apo B and apo AI metabolism.

The association of hypotestosteronemia with coronary artery disease in men.

Phillips GB, Pinkernell BH, Jing TY
Department of Medicine, Columbia University College of Physicians and Surgeons, St. Luke's-Roosevelt Hospital Center, New York, NY.
Arterioscler Thromb 1994 May;14(5):701-6

Hyperestrogenemia and hypotestosteronemia have been observed in association with myocardial infarction (MI) and its risk factors. To determine whether these abnormalities may be prospective for MI, estradiol and testosterone, as well as risk factors for MI, were measured in 55 men undergoing angiography who had not previously had an MI. Testosterone (r = -.36, P = .008) and free testosterone (r = -.49, P < .001) correlated negatively with the degree of coronary artery disease after controlling for age and body mass index. When the patient group was successively reduced to a final study group of 34 men by excluding the patients with other major disorders, the testosterone and free testosterone correlations persisted (r = -.43, P < .02 and r = -.62, P < .001, respectively). Neither estradiol nor the risk factors, except for high-density lipoprotein cholesterol, correlated with the degree of coronary artery disease in the final group. Testosterone correlated negatively with the risk factors fibrinogen, plasminogen activator inhibitor-1, and insulin and positively with high-density lipoprotein cholesterol. The correlations found in this study between testosterone and the degree of coronary artery disease and between testosterone and other risk factors for MI raise the possibility that in men hypotestosteronemia may be a risk factor for coronary atherosclerosis.

Increasing oxygen to the heart via testosterone:

Effect of acute testosterone on myocardial ischemia in men with coronary artery disease.

Webb CM, Adamson DL, de Zeigler D, Collins P
Cardiac Medicine, National Heart & Lung Institute, Imperial College School of Medicine, and Royal Brompton Hospital, London, United Kingdom.
Am J Cardiol 1999 Feb 1;83(3):437-9, A9

The effect of acute testosterone administration on exercise-induced myocardial ischemia was assessed in 14 men with coronary artery disease and low plasma testosterone concentrations in a study of randomized, double-blind, crossover design. Testosterone increased time to 1-mm ST-segment depression compared with placebo by 66 (15 to 117) seconds (p = 0.016), suggesting a beneficial effect of testosterone on myocardial ischemia in these patients.

Acute anti-ischemic effect of testosterone in men with coronary artery disease.

Rosano GM, Leonardo F, Pagnotta P, Pelliccia F, Panina G, Cerquetani E, della Monica PL, Bonfigli B, Volpe M, Chierchia SL
Department of Cardiology, Istituto H. San Raffaele, Roma and Milano, Italy.
rosanog@roma.hsr.it
Circulation 1999 Apr 6;99(13):1666-70

BACKGROUND: The role of testosterone on the development of coronary artery disease in men is controversial. The evidence that men have a greater incidence of coronary artery disease than women of a similar age suggests a possible causal role of testosterone. Conversely, recent studies have shown that the hormone improves endothelium-dependent relaxation of coronary arteries in men. Accordingly, the aim of the present study was to evaluate the effect of acute administration of testosterone on exercise-induced myocardial ischemia in men.
METHODS AND RESULTS: After withdrawal of antianginal therapy, 14 men (mean age, 58+/-4 years) with coronary artery disease underwent 3 exercise tests according to the modified Bruce protocol on 3 different days (baseline and either testosterone or placebo given in a random order). The exercise tests were performed 30 minutes after administration of testosterone (2.5 mg IV in 5 minutes) or placebo. All patients showed at least 1-mm ST-segment depression during the baseline exercise test and after placebo, whereas only 10 patients had a positive exercise test after testosterone. Chest pain during exercise was reported by 12 patients during baseline and placebo exercise tests and by 8 patients after testosterone. Compared with placebo, testosterone increased time to 1-mm ST-segment depression (579+/-204 versus 471+/-210 seconds; P<0. 01) and total exercise time (631+/-180 versus 541+/-204 seconds; P<0. 01). Testosterone significantly increased heart rate at the onset of 1-mm ST-segment depression (135+/-12 versus 123+/-14 bpm; P<0.01) and at peak exercise (140+/-12 versus 132+/-12 bpm; P<0.01) and the rate-pressure product at the onset of 1-mm ST-segment depression (24 213+/-3750 versus 21 619+/-3542 mm Hgxbpm; P<0.05) and at peak exercise (26 746+/-3109 versus 22 527+/-5443 mm Hgxbpm; P<0.05).
CONCLUSIONS: Short-term administration of testosterone induces a beneficial effect on exercise-induced myocardial ischemia in men with coronary artery disease. This effect may be related to a direct coronary-relaxing effect.

Low Testosterone levels and depression:

Testosterone, gonadotropin, and cortisol secretion in male patients with major depression.
Schweiger U, Deuschle M, Weber B, Korner A, Lammers CH, Schmider J, Gotthardt U, Heuser I
Max-Planck-Institute of Psychiatry, Clinical Institute, Munich, Germany.
schweiger.u@psychiatry.mu-Luebeck.de
Psychosom Med 1999 May-Jun;61(3):292-6

OBJECTIVE: Previous studies of sex hormone concentrations in depression yielded inconsistent results. However, the activation of the hypothalamic-pituitary-adrenal system seen in depression may negatively affect gonadal function at every level of regulation. The objective of this study was to explore whether major depressive episodes are indeed associated with an alteration of gonadal function. METHODS: Testosterone, pulsatile LH secretion, FSH, and cortisol were assessed using frequent sampling during a 24-hour period in 15 male inpatients with major depression of moderate to high severity and in 22 healthy comparison subjects (age range 22-85 years).

RESULTS: An analysis of covariance model showed that after adjustment for age only, daytime testosterone (p < .01), nighttime testosterone (p < .05), and 24-hour mean testosterone secretion (p < .01) were significantly lower in the depressed male inpatients. There was also a trend for a decreased LH pulse frequency in the depressed patients (p < .08).

CONCLUSIONS: Gonadal function may be disturbed in men with a depressive episode of moderate to high severity.

Steroid hormones, memory and mood in a healthy elderly population.

Carlson LE, Sherwin BB
Department of Psychology, McGill University, Montreal, Canada.
lindac@ego.psych.mcgill.ca
Psychoneuroendocrinology 1998 Aug;23(6):583-603

Men (n = 31), women estrogen-users (n = 14), and women estrogen non-users (n = 41), whose average age was 72.1 +/- 5.6 years, were tested with a battery of psychological tests measuring verbal memory, visual memory, concentration and attention, language fluency and semantic memory, and mood. Plasma levels of testosterone (T), estradiol (E2), cortisol (CRT) and dehydroepiandrosterone-sulfate (DHEAS) were assessed by radioimmunoassay. The ratio of DHEAS to CRT was calculated to determine it's relationship to memory functioning. The men had higher T and DHEAS levels than both groups of women. Women estrogen-users had higher E2 levels than both men and estrogen non-users and the men had higher E2 levels and a higher DHEAS/CRT ratio than the (female) estrogen non-users. There were no group differences in CRT levels. Men and estrogen-users had higher total (p < .01) and forward (p < .001) digit span scores compared with non-users. Women estrogen-users also had higher backward digit span scores than non-users (p < .05), while both groups of women performed better than men on category retrieval (p < .01). The implications of these findings with respect to hormonal influences on memory in elderly men and women are discussed.

Testosterone and depression in aging men.

Seidman SN, Walsh BT
Department of Psychiatry, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA.
Am J Geriatr Psychiatry 1999 Winter;7(1):18-33

In men, testosterone secretion affects neurobehavioral functions such as sexual arousal, aggression, emotional tone, and cognition. Beginning at approximately age 50, men secrete progressively lower amounts of testosterone; about 20% of men over age 60 have lower-than-normal levels. The psychiatric sequelae are poorly understood, yet there is evidence of an association with depressive symptoms. The authors reviewed 1) the physiology of the hypothalamic-pituitary-gonadal axis and its changes with age in men; and 2) the evidence linking testosterone level and major depression in men. Data on this relationship are derived from two types of studies: observational studies comparing testosterone levels and secretory patterns in depressed and non-depressed men, and treatment studies using exogenous androgens for male depression. The data suggest that some depressed older men may have state-dependent low testosterone levels and that some depressed men may improve with androgen treatment.

Bioavailable testosterone and depressed mood in older men: the Rancho Bernardo Study.

Barrett-Connor E, Von Muhlen DG, Kritz-Silverstein D
Department of Family and Preventive Medicine, School of Medicine, University of California, San Diego, La Jolla 92093-0607, USA.
J Clin Endocrinol Metab 1999 Feb;84(2):573-7

A cross-sectional population-based study examined the association between endogenous sex hormones and depressed mood in community-dwelling older men. Participants included 856 men, ages 50-89 yr, who attended a clinic visit between 1984-87. Total and bioavailable testosterone, total and bioavailable estradiol, and dihydrotestosterone levels were measured by radioimmunoassay in an endocrinology research laboratory. Depressed mood was assessed with the Beck Depression Inventory (BDI). Levels of bioavailable testosterone and bioavailable estradiol decreased with age, but total testosterone, dihydrotestosterone, and total estradiol did not. BDI scores increased with age. Low bioavailable testosterone levels and high BDI scores were associated with weight loss and lack of physical activity, but not with cigarette smoking or alcohol intake. By linear regression or quartile analysis the BDI score was significantly and inversely associated with bioavailable testosterone (both Ps = 0.007), independent of age, weight change, and physical activity; similar associations were seen for dihydrotestosterone (P = 0.048 and P = 0.09, respectively). Bioavailable testosterone levels were 17% lower for the 25 men with categorically defined depression than levels observed in all other men (P = 0.01). Neither total nor bioavailable estradiol was associated with depressed mood. These results suggest that testosterone treatment might improve depressed mood in older men who have low levels of bioavailable testosterone. A clinical trial is necessary to test this hypothesis.

Testosterone therapy for human immunodeficiency virus-positive men with and without hypogonadism.

Rabkin JG; Wagner GJ; Rabkin R
New York State Psychiatric Institute and Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York 10032, USA.
jgr1@columbia.edu
J Clin Psychopharmacol (UNITED STATES) Feb 1999, 19 (1) p19-27

This study was designed to evaluate the safety and effectiveness of testosterone therapy for clinical symptoms of hypogonadism (low libido, low mood, low energy, loss of appetite/weight) in human immunodeficiency virus-positive men with CD4 cell counts less than 400 cells/mm3 and deficient or low normal serum testosterone levels. The trial consisted of 8 weeks of open treatment with 400 mg of intramuscular testosterone cypionate biweekly. Responders were maintained at this dosage for another 4 weeks and then were randomized in a double-blind, placebo-controlled, 6-week discontinuation trial. Of the 112 men who completed at least 8 weeks of treatment, 102 (91%) were rated as responders on a global assessment of sexual desire/function. Of the 34 study completers with major depressive disorder and/or dysthymia, 79% reported significant improvement in mood at week 8. Average weight change was a gain of 3.7 pounds, with 45% gaining more than 5 pounds. Eighty-four men entered and 77 completed the double-blind phase; of these, 78% of completers randomized to testosterone and 13% randomized to placebo maintained their response. No significant medical or immunologic adverse effects were identified. Testosterone therapy was well tolerated and effective in ameliorating symptoms of clinical hypogonadism, and equally so for men with and without testosterone deficiency. For patients with major depression and/or dysthymia, improvement was equal to that achieved with standard antidepressants.

Editors Note: The long and the short of it is that we need high testosterone to keep from being depressed. Period.

Why we need to work at keeping testosterone from becomeing estrogen:

The effect of testosterone aromatization on high-density lipoprotein cholesterol level and postheparin lipolytic activity.

Zmuda JM, Fahrenbach MC, Younkin BT, Bausserman LL, Terry RB, Catlin DH, Thompson PD
Department of Medicine, Miriam Hospital, Providence, RI.
Metabolism 1993 Apr;42(4):446-50

Stanozolol, an oral 17 alpha-alkylated androgen, increases hepatic triglyceride lipase activity (HTGLA) and decreases high-density lipoprotein cholesterol (HDL-C) levels, whereas intramuscular testosterone has comparatively little effect. In the present study, we tested the hypothesis that aromatization of androgen to estrogen blunts the lipid and lipase effects of exogenous testosterone. Fourteen male weightlifters received testosterone enanthate (200 mg/wk intramuscularly), the aromatase inhibitor testolactone (250 mg four times per day), or both drugs together in a randomized cross-over design. Serum testosterone level increased during all three drug treatments, whereas estradiol level increased only with testosterone alone (+47%, P < .05), demonstrating that testolactone effectively inhibited testosterone aromatization. Testosterone decreased HDL-C(-16%, P < .05), HDL2-C(-23%, NS), and apoprotein (apo) A-I (-12%, P < .05) levels, effects that were consistently but not significantly greater with simultaneous testosterone and testolactone administration (HDL-C, -20%; HDL2-C, -30%; apo A-I, -15%; P < .05 for all). In contrast, both testosterone regimens decreased HDL3-C levels by 13% (P < .05 for both). HTGLA increased 21% during testosterone treatment and 38% during combined testosterone and testolactone treatment (P < .01 for both). Lipoprotein lipase activity (LPLA) increased only during combined testosterone and testolactone treatment (+31%, P < .01), suggesting that estrogen production may counteract the effects of testosterone on LPLA. Testolactone alone had little effect on any lipid, lipoprotein, apoprotein, or lipase concentration.

Editors Note:

In the natural health world we can use the Chinese herb formula Myomin as the aromatase inhibitor. Myomin is also an estrogen blocker helping keep estrogen form having an effect on the body and excreting estrogen out faster.

Testosterone and aromatase inhibition to increase sperm production:

[Therapeutic efficacy of testolactone (aromatase inhibitor) to oligozoospermia with high estradiol/testosterone ratio].

[Article in Japanese]
Itoh N, Kumamoto Y, Maruta H, Tsukamoto T, Takagi Y, Mikuma N, Nanbu A, Tachiki H
Department of Urology, Sapporo Medical College.
Nippon Hinyokika Gakkai Zasshi 1991 Feb;82(2):204-9

To our knowledge, the action of estradiol which is produced from testosterone by aromatase on human spermatogenesis has not been fully clarified. In oligozoospermia, with high values of E2/T ratio, it is considered that the role of estradiol is suppressive to spermatogenesis. In this study, alteration of spermatogenesis was evaluated when serum estradiol levels were decreased by suppression of aromatase activity. Nine male infertile patients were treated with testolactone (Teslac: 1.0 g/day, for 3 months), one of the aromatase inhibitors. Four of them had an increase in sperm count (more than 10 x 10(6)/ml relative to base line). In endocrinological findings, serum estradiol levels and E2/free T ratio were significantly decreased after treatment. Serum free testosterone levels were significantly increased in all cases, presumably from decreased sex hormone binding globulin (SHBG) levels. These findings suggested the effectiveness of the administrated aromatase inhibitor. In particular four patients whose sperm counts were improved after testolactone treatment had high values of basal serum estradiol levels and E2/free T ratio before treatment, and these values were normalized after treatment. In conclusion we suggest that an aromatase inhibitor may be effective to male infertile patients with high serum estradiol levels.

Low testosterone high estrogen in liver disease:

Conversion of androgens to estrogens in cirrhosis of the liver.

Gordon GG, Olivo J, Rafil F, Southren AL
J Clin Endocrinol Metab 1975 Jun;40(6):1018-26

The contribution, by peripheral conversion, of androstenedione and testosterone to the circulating estrogens was determined in men with cirrhosis of the liver. The conversion ratio of androstenedione to estrone, estradiol and testosterone and the conversion ratio of testosterone to estrone (but not estradiol) and androstenedione were significantly increased. The plasma concentrations of androstenedione and testosterone were increased and decreased respectively; the mean plasma concentration of androstenedione being similar to that found in normal women. The metabolic clearance rate of androstenedione was not altered in cirrhosis although the metabolic clearance rate of testosterone was decreased. The production rate of androstenedione was elevated while that of testosterone was reduced. The instantaneous contribution of plasma androstenedione to estrone and estradiol was increased in cirrhosis as was the contribution of testosterone to estrone (but not to estradiol). Thus the increased estradiol levels in cirrhosis result, in large part, from increased peripheral conversion from the androgens. The percent contribution of plasma testosterone to plasma androstenedione was decreased although the absolute amount derived by conversion was normal. The percent contribution of plasma androstenedione to plasma testosterone was increased sevenfold in cirrhosis. The fraction of the daily androstenedione production derived from the plasma testosterone pool was not significantly altered. However, a significant fraction of the daily production rate of testosterone was derived from androstenedione. Thus, 15% of the circulating testosterone is not secreted but is derived by peripheral conversion from androstenedione. Normal levels of gonadotropins were found in cirrhosis.

Conversion of androgens to estrogens in idiopathic hemochromatosis: comparison with alcoholic liver cirrhosis.

Kley HK, Niederau C, Stremmel W, Lax R, Strohmeyer G, Kruskemper HL
J Clin Endocrinol Metab 1985 Jul;61(1):1-6

Hypogonadism is common in patients with some liver diseases, such as idiopathic hemochromatosis (IHC) and alcoholic cirrhosis (AC). However, gynecomastia, a typical feature in AC, does not occur in IHC. To determine the hormonal basis for this difference, the following parameters were determined in patients with IHC and AC as well as in normal men: plasma concentrations of androgens and estrogens, metabolic clearance and production rates of androstenedione and testosterone, and the contribution of peripheral conversion of androstenedione and testosterone to the circulating estrogens. Severe impotence in both patients with IHC and those with AC was associated with more than 50% reduction in plasma testosterone. The reduction was due to 63% and 70% decreases in testosterone production in IHC and AC, respectively. The MCRs were less affected in IHC and AC (19% and 37% reductions, respectively). In IHC, the fall in testosterone concentrations was accompanied by decreased production and plasma concentrations of androstenedione, a precursor for estrogen synthesis. In contrast, production and plasma concentrations of androstenedione were significantly increased in AC. Patients with IHC had estradiol und estrone levels similar to those in normal men (mean +/- SD, 16.2 +/- 4.6 vs. 20.3 +/- 3.7 pg/ml; P = NS), whereas in AC, estradiol and estrone were significantly elevated (38.0 +/- 5.3 and 68.5 +/- 17.2 pg/ml, respectively). In IHC, sex hormone-binding globulin levels were in the same range as in the normal men, whereas sex hormone-binding globulin was increased in AC. In IHC, the instantaneous contribution of plasma androstenedione to estrone and estradiol was normal, whereas that of plasma testosterone to plasma estrogens was decreased by about 50%. In contrast, in AC, the instantaneous contribution of plasma androstenedione to estrogens was greatly enhanced, and that of testosterone was in the normal range. Since the MCRs of androgens and the conversion ratios of androgens to estrogens indicate normal peripheral metabolism of sex hormones in IHC, decreased androgen formation implies decreased testicular synthesis. This was confirmed by a significantly decreased LH level in IHC (5.5 +/- 1.9 vs. 10.5 +/- 3.1 mU/ml in normal men), indicating pituitary failure. In AC, however, increased LH (20.0 +/- 2.7 mU/ml) may be indicative of primary testicular failure. These results confirm clinical features of hypogonadism and normal estrogenic activity in patients with IHC.

Editors Note:

Now this study begs the question: if the testosterone levels had been higher would the disease state have set in? The study mainly should serve as a warning to all those macho guys who drink excessively and think they can go womanize. The liver disease they are bringing on via the alcohol will shrink their testicles into dried peanuts with a little limp noodle in front to match and a set of breasts to boot. (Hypogonadism with gynocomasty). These are common symptoms in men with serious liver disease.

I’m going to get on my sopabox here: A daily beer, a glass of wine or two and an occasional shot of hard alcohol is okay. What we are talking of here is the abuse of alcohol, mostly by those bad boys who’ve never grown up and never faced their manly responsibilities! You superanurated teenagers who are still hanging out with your “buddies” at 40+ know who I mean! All the one night stands don’t speak well of your sexual prowess, they scream of the fact that you can’t satisfy a woman enough for her to come back for more! Gee, I guess you do need to drink to forget your lack of not just responsiblity but also sexual ability! Nuff Said.

No hyper sexual behavior or increased aggressiveness from high testosterone levels:

The effects of exogenous testosterone on sexuality and mood of normal men.

Anderson RA, Bancroft J, Wu FC
Medical Research Council Reproductive Biology Unit, Centre for Reproductive Biology, Edinburgh, Scotland.
J Clin Endocrinol Metab 1992 Dec;75(6):1503-7

The effects of supraphysiological levels of testosterone, used for male contraception, on sexual behavior and mood were studied in a single-blind, placebo-controlled manner in a group of 31 normal men. After 4 weeks of baseline observations, the men were randomized into two groups: one group received 200 mg testosterone enanthate (TE) weekly by im injection for 8 weeks (Testosterone Only group), the other received placebo injections once weekly for the first 4 weeks followed by TE 200 mg weekly for the following 4 weeks (Placebo/Testosterone group). The testosterone administration increased trough plasma testosterone levels by 80%, compatible with peak testosterone levels 400-500% above baseline. Various aspects of sexuality were assessed using sexuality experience scales (SES) questionnaires at the end of each 4-week period while sexual activity and mood states were recorded by daily dairies and self-rating scales. In both groups there was a significant increase in scores in the Psychosexual Stimulation Scale of the SES (i.e. SES 2) following testosterone administration, but not with placebo. There were no changes in SES 3, which measures aspects of sexual interaction with the partner. In both groups there were no changes in frequency of sexual intercourse, masturbation, or penile erection on waking nor in any of the moods reported. The Placebo/Testosterone group showed an increase in self-reported interest in sex during testosterone treatment but not with placebo. The SES 2 results suggest that sexual awareness and arousability can be increased by supraphysiological levels of testosterone. However, these changes are not reflected in modifications of overt sexual behavior, which in eugonadal men may be more determined by sexual relationship factors. This contrasts with hypogonadal men, in whom testosterone replacement clearly stimulates sexual behavior. There was no evidence to suggest an alteration in any of the mood states studied, in particular those associated with increased aggression. We conclude that supraphysiological levels of testosterone maintained for up to 2 months can promote some aspects of sexual arousability without stimulating sexual activity in eugonadal men within stable heterosexual relationships. Raising testosterone does not increase self-reported ratings of aggressive feelings.

Back to Why Estrogen is the cause of enlarges prostate and not testosterone:

[Physiopathological aspects of the treatment of benign prostatic hypertrophy. Role of prostatic stroma and estrogens].

[Article in French]
Sole-Balcells F
Instituto de Urologia, Nefrologia y Andrologia, Fundacion Puigvert Escuela de Post-Graduados, Universidad Autonoma de Barcelona, Espagne.
J Urol (Paris) 1993;99(6):303-6

The hypothesis of the etiopathogenesis of Benign Prostatic Hypertrophy (BPH) on the basis of stroma-epithelium interaction is presented. The fetal prostate has its origin in the urogenital sinus depending on the dehydrotestosterone stimulating the stromal cells having androgenic receptors. This stroma hyperplasia is considered to be the initial factor in the BPH formation. The inequality in growth factors is also relevant for its formation. Stimulating factors, especially the epidermal growth factor (EGF) prevail on involution factors. The stromal cell has estrogenic receptors. The estrogens from the testosterone aromatization are the first stimulus on the prostatic stroma on the transitional and periurethral area stimulating the glandular epithelium causing BPH. The knowledge of BPH etiopathogenesis will make its rational medical treatment possible, and eventually slow or stop its growth when therapy in its early evolutive stages is prescribed.

Editors note:

What these guys are saying is that during the period of infant development in the womb there is a time when the same structures can become either a penis or a vagina and clitoris, another structure can become either a uterus or a prostate. What it grows into depends on the hormone signal. Around androgens it becomes a prostate, around estrogens a uterus. These hormone receptors are kept for life. When we age and have a high estrogen to testosterone ratio the hormone receptors in the prostate take up the estrogen and the swelling is from the thing trying to grow into a uterus. Eeek!

Estrogen receptor-beta: implications for the prostate gland.

Chang WY, Prins GS
Department of Urology, University of Illinois College of Medicine, Chicago 60612, USA.
Prostate 1999 July 1;40(2):115-24

Estrogens can have profound effects on prostate growth and differentiation. These effects were thought to be mediated by the classical estrogen receptor; however, the discovery of a second estrogen receptor has redefined the estrogen signaling pathway and may have broad implications on estrogen-responsive tissues, including the prostate. The new estrogen receptor, named estrogen receptor-beta (ERbeta), is preferentially expressed in the prostate and maintains some characteristics that are different from ERalpha. Establishing the distribution and function of ERbeta in the various estrogen-responsive tissues is critical