The Testosterone Way to A Healthy Heart, Liver, Circulation, Fertility and Mood!

[Guest guest]

The Testosterone Way to A Healthy Heart, Liver, Circulation, Fertility and

Mood! Or: Testosterone Research Congress and the Feminists Won’t Tell You

About.

By: William Wong ND, PhD, Member WOrld Sports Medicine Hall of Fame.

_http://www.drwong.us/CurrentHealthArticle2.htm_

(http://www.drwong.us/CurrentHealthArticle2.htm)

 

 

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 draw a distance line 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 handily so 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 traded a 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 they

are making ever so slightly so that it does not fully 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 liability for the side effects of their

drugs by making like the natural hormones have the same side effects - a

definite

and bold faced lie, demonstrating Heagels point that if you tell a big

enough lie folks will believe you.

 

The second drawback is that all synthetic 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 Lutinizing

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 Hellâ€, 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. Medicine: the use of testosterone would

negate the need for expensive live 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 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 an absolute piece of 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

roarâ€.... I

know this is 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 evidense 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_

(rosanog) 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_

(schweiger.u) 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_

(lindac)

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.

 

 

97. 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_ (jgr1)

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.

 

(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 eh 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

testostero

ne 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.

 

 

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

developement in the womb there is a time when the same structrues can become

either a penis or a vagina and clitorus, 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 estgrogen to

testosterone ratio the hormone erceptors 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 Jul 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 to defining its pharmacological and physiological impact.

Differential expression of ERbeta may facilitate development of tissue-specific

estrogen agonists and antagonists, a goal in the treatment of diseases in

estrogen-sensitive tissues such as breast cancer. This article reviews the

current

knowledge on ERbeta and its potential impact on the prostate.

 

 

 

Okay, do we get the message?! Testosterone, though much maligned is a

vitally needed hormone not only for anti aging, sexual function and fertility

but

also for its positive effects on mood, heart health, vascular health, liver

health, bone density, muscle density and fighting diabetes. Natural

testosterone, either from pigs, cows or whittled down from mexican yam or soy

(yes this

is one instance where somthing good can come from soy), is nearly side effect

free and a Godsend to high level wellness.

 

 

 

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