Male Hormones Products

Androgens - More than Just a Guy Thing

Testosterone is well known for its effect on male sexual expression.  However, it is also cited as affecting Mood, Metabolism, Weight, Cognitive Function, Bone Density, and fertility in both men and women.

Mitochondria use testosterone for Kreb's cycle to occur and energy to be produced.  The Krebs cycle is a series of enzymatic reactions in aerobic organisms that lead to the production of high-energy phosphate compounds. Testosterone enhances aerobic metabolism. This has the result of improving muscle tone, burning fat, and improving energy.  Indirectly, it is suggested this increase in testosterone also effects mood.

Key Word Click

Hypogonadism

SHBG

Free Testosterone

Bound Testosterone

Luteinizing Hormone

Aromatase

Sexual Function

Spermatogenesis


1.  What is the normal testosterone level?

2.  How does the body know to produce testosterone

3.  Testosterone & Andropause in men & women

4.  Dangers of testosterone replacement therapy & synthetic supplementation

5.  How does testosterone affect mood

6.  How does testosterone affect fertility



1. What is the normal testosterone level?

As a man ages, the Leydig cells that secrete testosterone begin to wear away. Because of this, between the ages of 40 and 70, the average man loses nearly 60% of the testosterone inside of his body! Other lifestyle factors, such as overtraining, stress and alcohol, can also hasten the deterioration of Leydig cells, and cause testosterone levels to drastically decline.

Although there's growing awareness of the vital role testosterone plays in health, the vast majority of men still don't recognize the key symptoms of testosterone deficiency. These include: depression, fatigue, low sex drive, irritability, and loss of facial/body hair, thinning and wrinkling of skin, weight gain, and weakening of the bone and muscle tissue. In some cases, there may also be a gradual decrease in the size of the sex organ. Eventually, imbalances of testosterone can set the stage for the development of even more serious diseases.

Normal testosterone level should be as follows:

Serum Levels

Lab Reference Range

Optimal Range

Total Testosterone

200-825 ng/dl

600-750 ng/dl

Free Testosterone

35-195 pg/ml

140-175 pg/ml

Saliva Levels

Lab Reference Range

Optimal Range

Bioavailable Testosterone

30-130 pg/ml

75-100 pg/ml

2. How Does the Body know to Produce Testosterone?

The hypothalamus is the part of the brain which regulates homeostasis in the body.  These are all the non-cognitive functions of the body such as breathing, production of hormones, alkaline balance, body temperature, etc.  It receives input from a variety of factors regarding the circulation of steroidal hormones.  If too much is in the blood, it will not give the signal to produce more testosterone or it may even signal production of estrogen.  The hypothalamus doesn’t respond only to current hormone levels, but also to the past history of hormone levels. (See below the dangers of Testosterone supplementation).    

The hypothalamus releases a hormone that tells the pituitary to initiate the Thyroid in production of  luteinizing hormone (LH) releasing hormone, also called GnRH (gonadotropin releasing hormone.)  The pituitary uses the amount of LHRH as one of its signals in deciding how much LH it should produce. Proper response depends on having sufficient receptors for LHRH. These receptors must be activated for LH to be produced. (Find out how Synthetic Testosterone Negatively impacts this process).  The pituitary also uses sex hormone levels, both current and the past history, in deciding how much LH to produce. Some aspects of the pituitary’s behavior are peculiar. So both very low and high levels of estrogen can inhibit LH production.  LH produced by the pituitary then stimulates the testicles to produce testosterone. Here, the amount of LH is the main factor, and high levels of sex hormones do not seem to cause inhibition at this level.  (Tongkat Ali works by staving off factors in the body that would tell the pituitary to decrease natural production of LH.  It works at this level of testosterone production.)

LH synthesizes into progesterone, a pre-cursor to testosterone.  It does not lead to Estrogen because it does not bind to the receptors that would release aromatase, necessary for Estrogen aromatization.   (Click here for LJ100® info)

Back to Top


3. Testosterone & Andropause

Andropause occurs in both men and women.  Because it is directly linked to the body's use of testosterone its symptoms are lower energy, weight gain, depression, grumpiness, decreased libido, in ability to perform sexually, and poor bone formation.  

In Men:

If a man were to live to be 90 years old, he could potentially have as little of 10% of the testosterone in his blood that he had when he was 20.  This decline is sometimes medically referred to as adult onset hypogonadism.  In younger males, it is simply hypogonadism.

The process that occurs during aging is not a straight forward decline in testosterone levels.  For men, simultaneous with lower testosterone production is an increase in Sex Hormone Binding Globulin (SHBG).  Produced in the liver, SHBG makes testosterone inactive by binding it to fat cells.  When testosterone is bound, it becomes Bound Testosterone (BT) and unable for bioactivity or use in the body.  Free Testosterone (FT) is the type of testosterone that is available for bioactivity.  

The decline is less dramatic than Menopause in women, because it is not the result of the decline of an organ's function.  Regardless of whether overall testosterone levels decline, an increase in BT over FT is often associated with Andropause symptoms.  

Studies have clearly shown that increased testosterone levels has a beneficial effect overall health, weight, libido, and energy in men.  In particular, BT is noted as promotionally causal of prostate cancer.  Herbs which unbind BT can be beneficial to maintaining overall prostate health.

In Women:

Like estrogen, women also produce testosterone in the Ovaries.  It is for this reason that scientists now believe that some of the symptoms of Menopause are actually related to Andropause in women.  For example, improper testosterone levels have very specific results on weight gain, mood and libido disorders in women.  Moreover, studies have shown that women on HRT (which is primarily Estrogen based) who supplement with TRT (Testosterone Replacement Therapy) will often see improvements in these three areas.

Remember however, that a woman generally needs only 1/10th the testosterone a man does.  Too much testosterone can cause a host of negative side effects.  This is the danger underlying TRT for women and the rational behind why many choose to use less evasive herbal methods to improve Andropause conditions.  


4. What are the dangers of Testosterone Replacement Therapy (TRT) or Synthetic Testosterone?

There are a number of problems with Testosterone Replacement Therapy.  For one, as with most drugs, high levels of TRT can be toxic.  For this reason anyone on TRT, should be regularly consulting a physician.

Secondly, taking TRT or anabolic hormones ignores the processes of the body and how they regulate hormone levels.  As mentioned on the hormone main page, hormones both are the result of and maintain the Nervous System. The hypothalamus takes input from a variety of sources to determine whether to produce more testosterone.  Moreover, this part of the brain is trying to create homeostasis or balance in the body.  It concludes "high levels" in relation to the functioning and balance of other inputs.  

Synthetic supplementation often ignores this facet and raises only testosterone levels.  If the hypothalamus senses too much testosterone, it will react as if the body is out of homeostasis.  A few of the things it can do is send a message to the pituitary gland  to cut off all production of gonadotropins.  This is definitely worst case for men.  

Remember the Hypothalamus creates testosterone indirectly via production of progesterone stimulated by LHRH.  In other words, you're not just ending testosterone production, but also DHEA and all the Androgens.  This is what is happening in the nightmares you hear where athletes take steroids and loose use of their sexual organs or exhibit decrease in size of gonads and loss of fertility.  Though they may continue with bulk, because the synthetic testosterone is powering muscle development, they loose all the necessary precursor hormones.

Another way the hypothalamus can seek homeostasis is by telling the body to produce more Estrogen.  Moreover, it can do this in two ways.  First, it can directly instruct the pituitary gland to tell the thyroid to make more estrogen.  Also, it can increase the production of aromatase in the body thereby transforming or aromatizing the supplemented testosterone into estrogen.  This process is frustrated even further by the fact that SHBG has a greater affinity for testosterone binding over estrogen.  This condition is medically called gynecomasticia or more commonly boy breasts. 


5. How does testosterone effect mood?

It is unclear how testosterone effects mood.  However, studies have shown that depression in middle aged men is directly correlated to and can be improved by increasing lower testosterone levels.  Generally, it is thought to either directly or indirectly impact overall mood functioning.   

In the indirect camp, some theorize that the overall increase in metabolism produced by testosterone indirectly affects mood.  A person feels more energized, so they feel better.  Similar to a "runner's high", the some scientists go even further and suggest that marginal improvements in FT levels improves overall homeostasis of endorphin levels.

The direct camp looks for correlations between a variety of androgens and mood.  DHEA, Testosterone, Pregnonlene and Estrogen are all found in the brain in various levels.  As these levels adjust, they can directly affect a number of mood related proteins and hormones.  DHEA and Pregnonlene both affect dopomine and seretonin in the brain which is responsible for happy or euphoric feelings.  Balance of Androgens and Estrogens affect the amount of Nitric Oxide (NO) production. NO is seen to have anti-depressive affects.  It is moreover a blood stimulant and directly responsible for improving circulation to the genitals.  It is no wonder that improving testosterone levels has a direct impact on improving sexual function.


6.   How does Testosterone Improve Fertility?

Infertility in Men is most commonly the result of either poor sperm formation or poor motility.  In cases where a mechanical difficulty (blocked tubes, etc) exists, Testosterone will not be helpful.  

Male Factor Infertility involves a number of hormones in the androgen family.  LH is directly responsible for stimulating testosterone production and spermatogenesis (production of sperm) in men  Adequate testosterone levels also have a metabolic effect that both can act on the sperm to improve motility and improve the rate of spermatogenesis. It is also cited as beneficial and necessary to the production of healthy sperm.  This may be a result of the affect of testosterone on Antioxidant production.

Adequate Testosterone levels assist in the physical process of copulation.  It's correlation to Nitric Oxide activity in the body will assist in improved arousal and erection. 



Dehydroepiandrosterone (pronounced dee-hi-dro-epp-ee-ann-dro-stehr-own), or DHEA as it is more often called, is a steroid hormone. It is the most abundant steroid in the bloodstream and is present at even higher levels in brain tissue. As a pre-cursor to testosterone, it is not surprising that DHEA also fall with age in men and women. 

Quick Link:

Cancer   AntiOxidants  Anti-Aging  

Immune System  Glucose Metabolism

Brain Functioning


DHEA is produced in the adrenal glands and can become either testosterone or estrogen.  For this reason, stimulation of production of this hormone can be affective for women in Menopause.  Its role as a precursor hormone is less understood and the source of much current scientific work.  It is difficult for searchers to separate the effects of DHEA from those of the primary sex steroids into which it is metabolized. The apparent lack of any direct hormone action for DHEA has prompted the suggestion that it may serve the role of a “buffering hormone” which would alter the state-dependency of other steroid hormones. Still, supplementing DHEA has been shown to have anti-aging, anti-obesity and anti-cancer influences. In addition, it is known to stabilize nerve-cell growth and is being tested in Alzheimer’s patients.


DHEA and Cancer

Early reports from England [Bulbrook, 1962, 1971] suggested that DHEA was abnormally low in women who developed breast cancer, even as much as nine years prior to the onset or diagnosis of the disease. Dr. Arthur Schwartz of Temple University found that supplemental DHEA significantly protected cell cultures from the toxicity of carcinogens.

While the mechanics are still not completely understood, numerous studies exist attesting to a correlation of DHEA and this type of anti-cancerous property.  Some suspect it is the effect of DHEA on immune antioxidants.  DHEA is known to improve lipid antioxidant functioning when Vitamin E levels are low.


DHEA & the Immune System

DHEA has been reported to counteract the thymic involution [shrinking of the thymus gland] and immuno-suppression caused by corticosteroids. This affects the ability of immune surveillance and antigen presentation.  Studies suggest these cells may be a site of DHEA. 

In test-tube studies, DHEA is not shown to have any direct anti-viral activity.  It is therefore believed that it is the interaction of DHEA with other amino acids, proteins, and hormones that affects this response in living organisms.


DHEA and Aging

In animal studies, DHEA has shown to extend rodent life spans up to 50%. The animals not only lives longer, they looked younger. The graying, course-haired controls could easily be distinguished from the sleek, black-haired, DHEA-treated animals.  Similar findings are seen human studies. 

DHEA and Glucose Metabolism

Investigators have shown that DHEA inhibits glucose-6-phosphate dehydrogenase (G6PDH), an enzyme that breaks down glucose. G6PDH is shown to turn glucose into fat by changing anabolic activity into catabolic energy metabolism.

DHEA also enlarges the liver and improves its catalase activity resulting in improvement of the antioxidant enzymes and proliferation of the peroxisomes (cellular organelles which help to eliminate toxins) produced in this organ.  

Glucose Metabolism affects appetite and weight gain.  Since G6PDH is inhibited the body’s ability to synthesize fat from carbohydrates means that sources of fat become more important. This has a direct impact on appetite. In studies done to assess DHEA benefits in animals, it was found that those treated with improved DHEA levels consistently weighed less than control animals, even when their appetites dictated a food increase.  In other words, increases in appetite, when indulged, did not negate the anti-obesity property of DHEA.




Enhancing Brain Function

DHEA is even more concentrated in the brain than in the bloodstream. Many neurologically degenerative patients such as those with Alzheimer's Disease show very low DHEA levels in the brain. Early research in this field by Dr. Eugene Roberts found that DHEA added in small concentrations to cell cultures were found to “increase the number of neurons, their ability to establish contacts, and their differentiation”. He also found that DHEA also enhanced long-term memory in mice undergoing avoidance training. It is suggested that a similar function exists in the human brain.

References

Barrett-Connor E, Khaw KT and Yen SS. A prospective study of dehydroepiandrosterone sulfate, mortality, and cardiovascular disease. New England Journal of Medicine 315(24): 1519-24, 11 December 1986.

Bulbrook RD, Hayward JL and Spicer CC. Abnormal excretion of urinary steroids by women with early breast cancer. Lancet 2: 1238-40, 1962.

Bulbrook RD, Hayward JL and Spicer CC. Relation between urinary androgen and corticoid excretion and subsequent breast cancer. Lancet 2: 395-98, 1971.

Chen TT, et al. Prevention of obesity in Avy/a mice by dehydroepiandrosterone. Lipids 12: 409-13, 1977.

Cleary MP and Fisk JF. Anti-obesity effect of two different levels of dehydroepiandrosterone in lean and obese middle-aged female Zucker rats. International Journal of Obesity 10(3): 193-204, 1986.

Coleman DL, Leiter EH and Applezweig N. Therapeutic effects of dehydroepiandrosterone metabolites in diabetes mutant mice (C57BL/KsJ-db/db). Endocrinology 115: 239-43, 1984.

Coleman DL, Leiter EH and Schweizer RW. Therapeutic effects of dehydroepiandrosterone (DHEA) in diabetic mice. Diabetes 31: 830-33, 1982.

Coleman DL, Schweizer RW and Leiter EH. Effect of genetic background on the therapeutic effects of dehydroepiandrosterone (DHEA) in diabetes-obesity mutants and in aged normal mice. Diabetes 33: 26-32, 1984.

de Peretti E and Forest MG. Pattern of plasma dehydroepiandrosterone sulfate levels in humans from birth to adulthood: Evidence for testicular production. J Clin Endocrinol Metab 47: 572-77, 1978.

Kahn, Carol. Beyond the Double Helix: DNA and the Quest for Longevity, Times Books, 1985, page 143. A thorough and highly readable “inside” account of DHEA research.

Loria RM, Regelson W and Padgett DA. Immune response facilitation and resistance to virus and bacterial infections with dehydroepiandrosterone (DHEA). In: The Biologic Role of Dehydroepiandrosterone (DHEA), Mohammed Kalimi and William Regelson [Eds], page 107-130, Walter de Gruyter, New York, 1990. ISBN 3-11-012243-X.

Loria RM and Padgett DA. Androstenediol regulates systemic resistance against lethal Infections in mice. Annals of NY Academy of Sciences 685: 293-95, 1993.

Nyce JW, Magee PN, Hard GC and Schwartz AG. Inhibition of 1,2-dimethylhydrazine-induced colon tumorigenesis in Balb/c mice by dehydroepiandrosterone. Carcinogenesis 5: 57-62, 1984.

Orentreich N, Brind JL, Rizer RL and Vogelman JH. Age changes and sex differences in serum dehydroepiandrosterone sulfate concentrations throughout adulthood. J Clin Endocrinol Metab 59: 551-55, 1984.

Pashko LL and Schwartz AG. Effect of food restriction, dehydroepiandrosterone, or obesity on the binding of 3H-7,12-dimethylbenz(alpha)anthracene to mouse skin DNA. J Gerontology 38: 8-12, 1983.

Schwartz AG. Inhibition of spontaneous breast cancer formation in female C3H(Avy/a) mice by long-term treatment with dehydroepiandrosterone. Cancer Research 39: 1129-32, 1979.

Schwartz AG, Hard GC, Pashko LL, Abou-Gharbia M and Swern D. Dehydroepiandrosterone: An antiobesity and anti-carcinogenic agent. Nutrition and Cancer 3: 46-53, 1981.

Schwartz AG, Nyce JW and Tannen RH. Inhibition of tumorigenesis and autoimmune development in mice by dehydroepiandrosterone. Mod Aging Res 6: 177-84, 1984.

Schwartz AG, Fairman DK and Pashko LL. The Biological Significance of Dehydroepiandrosterone. In: The Biologic Role of Dehydroepiandrosterone (DHEA), Mohammed Kalimi and William Regelson [Eds], Walter de Gruyter, New York, 1990.

Yen TT, Allan JA, Pearson DV, Acton JM and Greenberg MM. Prevention of obesity in Avy/a mice by dehydroepiandrosterone. Lipids 12: 409-13, 1977.