It seems that adequate testosterone levels are an important influence on sexual symptoms in the aging male and also influence the response of men to PDE-5 inhibitors, the first line treatment for erectile dysfunction in men. Many would now suggest screening for testosterone deficiency in all men presenting with erectile dysfunction (Gore and Rajfer 2004; Shabsigh 2005). This would seem appropriate because, in addition to benefits on sexual function, identification and treatment of hypogonadal men with testosterone could improve other symptoms of hypogonadism and protect against other conditions such as osteoporosis.
As you can see, the entire workout is only 20 minutes. Twenty minutes! That really is a beautiful thing. And within those 20 minutes, 75 percent of that time is warming up, recovering or cooling down. You're really only working out intensely for four minutes. It's hard to believe if you have never done this that you can actually get that much benefit from four minutes of exercise. That's all it is.

But when a premenopausal woman’s testosterone levels are too high, it can lead to polycystic ovary syndrome (PCOS), a condition that increases the risk of irregular or absent menstrual cycles, infertility, excess hair growth, skin problems, and miscarriage. High levels of testosterone in women, whether caused by PCOS or by another condition, can cause serious health conditions such as insulin resistance, diabetes, high cholesterol, high blood pressure, and heart disease. (12)
You can search every supplement on the market, and you can try reading “how to be good at sex” books (there’s about a million of them); You can even try those strange penis exercises (please do not waste your time). Or you can take a daily supplement that is designed and developed to do one thing: transform your penis and sex life so the next time a girl is talking about some guy who “could not stop making me orgasm,” that guy is you!

Testosterone is used as a medication for the treatment of males with too little or no natural testosterone production, certain forms of breast cancer,[10] and gender dysphoria in transgender men. This is known as hormone replacement therapy (HRT) or testosterone replacement therapy (TRT), which maintains serum testosterone levels in the normal range. Decline of testosterone production with age has led to interest in androgen replacement therapy.[105] It is unclear if the use of testosterone for low levels due to aging is beneficial or harmful.[106]

A large number of trials have demonstrated a positive effect of testosterone treatment on bone mineral density (Katznelson et al 1996; Behre et al 1997; Leifke et al 1998; Snyder et al 2000; Zacharin et al 2003; Wang, Cunningham et al 2004; Aminorroaya et al 2005; Benito et al 2005) and bone architecture (Benito et al 2005). These effects are often more impressive in longer trials, which have shown that adequate replacement will lead to near normal bone density but that the full effects may take two years or more (Snyder et al 2000; Wang, Cunningham et al 2004; Aminorroaya et al 2005). Three randomized placebo-controlled trials of testosterone treatment in aging males have been conducted (Snyder et al 1999; Kenny et al 2001; Amory et al 2004). One of these studies concerned men with a mean age of 71 years with two serum testosterone levels less than 12.1nmol/l. After 36 months of intramuscular testosterone treatment or placebo, there were significant increases in vertebral and hip bone mineral density. In this study, there was also a significant decrease in the bone resorption marker urinary deoxypyridinoline with testosterone treatment (Amory et al 2004). The second study contained men with low bioavailable testosterone levels and an average age of 76 years. Testosterone treatment in the form of transdermal patches was given for 1 year. During this trial there was a significant preservation of hip bone mineral density with testosterone treatment but testosterone had no effect on bone mineral density at other sites including the vertebrae. There were no significant alterations in bone turnover markers during testosterone treatment (Kenny et al 2001). The remaining study contained men of average age 73 years. Men were eligible for the study if their serum total testosterone levels were less than 16.5 nmol/L, meaning that the study contained men who would usually be considered eugonadal. The beneficial effects of testosterone on bone density were confined to the men who had lower serum testosterone levels at baseline and were seen only in the vertebrae. There were no significant changes in bone turnover markers. Testosterone in the trial was given via scrotal patches for a 36 month duration (Snyder et al 1999). A recent meta-analysis of the effects on bone density of testosterone treatment in men included data from these studies and two other randomized controlled trials. The findings were that testosterone produces a significant increase of 2.7% in the bone mineral density at the lumber spine but no overall change at the hip (Isidori et al 2005). These results from randomized controlled trials in aging men show much smaller benefits of testosterone treatment on bone density than have been seen in other trials. This could be due to the trials including patients who are not hypogonadal and being too short to allow for the maximal effects of testosterone. The meta-analysis also assessed the data concerning changes of bone formation and resorption markers during testosterone treatment. There was a significant decrease in bone resorption markers but no change in markers of bone formation suggesting that reduction of bone resorption may be the primary mode of action of testosterone in improving bone density (Isidori et al 2005).

No one will argue with the well-established fact that the dramatic lows of testosterone as seen in castration or other significant primary testicular disturbances such as those induced by chemotherapy, radiation therapy, congenital problems, or as seen in secondary testicular insufficiency (eg, large compressive pituitary or hypothalamic tumors) produce dramatic signs and symptoms of testosterone deficiency that require testosterone replacement therapy. Less clear, or at least more controversial, is the necessity of treating the gentler reduction of testosterone seen in the aging process.

Intracoronary artery infusion of testosterone causes significant coronary artery dilatation and not constriction as previously thought (Webb et al 1999). When degree of coronary obstruction is assessed by angiography, there is a direct relationship between degree of coronary artery narrowing and reduced testosterone levels (Phillips et al 1994). Men with low testosterone levels have been observed to have: premature atherosclerosis, increased visceral adipose tissue, hyperinsulinemia, and other risk factors for myocardial infarction (Phillips 2005). Insulin resistance has been shown to be associated with a decrease in Leydig cell secretion of testosterone (Pitteloud et al 2005). Muller and colleagues suggest that low endogenous total testosterone and SHBG levels increase the risk of metabolic syndrome in aging and aged men. They demonstrated that low levels of testosterone are related to lower insulin sensitivity and higher fasting insulin levels (Muller et al 2005). These authors speculate that testosterone might play a protective role in the development of metabolic syndrome, insulin resistance, diabetes mellitus and cardiovascular disease in aging men.

The normal development of the prostate gland is dependent on the action of testosterone via the androgen receptor, and abnormal biosynthesis of the hormone or inactivating mutations of the androgen receptor are associated with a rudimentary prostate gland. Testosterone also requires conversion to dihydrotestosterone in the prostate gland for full activity. In view of this link between testosterone and prostate development, it is important to consider the impact that testosterone replacement may have on the prevalence and morbidity associated with benign prostatic hypertrophy (BPH) and prostate cancer, which are the common conditions related to pathological growth of the prostate gland.
Dr. Anthony’s Notes: I use Maca often in cycles throughout the year. I typically buy the raw Maca powder, which has a VERY “dirt-like” earthy taste. Beware if you are a bit squeamish on tastes! How To Take Maca: 1500-3000mg of Maca powder is a typical dosage take daily alongside food. From personal experience, I've found that it’s best to buy the Maca powder as a standalone supplement and throw it into a blended protein shake to mask the taste.
Testosterone functions within the brain. There are several lines of evidence for this: there are androgen receptors within the brain; testosterone is converted to both dihydrotestosterone (DHT) and estradiol by the actions of 5-α-reductase and aromatase respectively in the brain; steroid hormones promote neuronal cell growth and survival (Azad et al 2003). Testosterone enhances cerebral perfusion in hypogonadal men and that perfusion takes place specifically in Brodman areas 8 and 24, regions of the brain that are concerned with: strategic planning, higher motor action, cognitive behaviors, emotional behavior, generalized emotional reaction, wakefulness and memory (Greenlee 2000; Azad et al 2003). Studies of cognition demonstrate that older men with higher levels of free testosterone index (a surrogate measure of bioavailable testosterone) have better scores in tests of: visual memory, verbal memory, visuospatial functions and visuomotor scanning. Hypogonadal men have lower scores in tests of memory, visuospatial function, with a faster decline in visual memory (Moffat et al 2002). In a very small, short term placebo-controlled study hypogonadal men with Alzheimer’s Disease (AD) treated with testosterone demonstrated a modest improvement in a cognition assessment score in AD (Tan and Pu 2003).

If you're a man who's experiencing symptoms such as decreased sex drive, erectile dysfunction, depressed mood, and difficulties with concentration and memory, and you think low testosterone may be to blame, you can have your levels tested. Since testosterone levels fluctuate throughout the day, you'll probably need more than a blood test to get a true picture of your levels.
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Let’s do a quick review of what I shared in the introduction to this series. August of last year was a tough month for me, primarily because of a huge and grueling project we were in the midst of here on the site. I was stressed out and my sleeping, healthy eating habits, and workout regimen all suffered. At the end of the month I got my testosterone levels tested and found that my total T was 383 ng/dL and my free T was 7.2 pg/mL – close to the average for an 85-100-year-old man.
Instead of turning to some drug that can only ameliorate symptoms and cause additional complications, I recommend using a natural saw palmetto supplement. Dr. Moerck says that there are about 100 clinical studies on the benefits of saw palmetto, one of them being a contributed to decreased prostate cancer risk. When choosing a saw palmetto supplement, you should be wary of the brand, as there are those that use an inactive form of the plant.
Testosterone is a steroid from the androstane class containing a keto and hydroxyl groups at the three and seventeen positions respectively. It is biosynthesized in several steps from cholesterol and is converted in the liver to inactive metabolites.[5] It exerts its action through binding to and activation of the androgen receptor.[5] In humans and most other vertebrates, testosterone is secreted primarily by the testicles of males and, to a lesser extent, the ovaries of females. On average, in adult males, levels of testosterone are about 7 to 8 times as great as in adult females.[6] As the metabolism of testosterone in males is more pronounced, the daily production is about 20 times greater in men.[7][8] Females are also more sensitive to the hormone.[9]
The largest amounts of testosterone (>95%) are produced by the testes in men,[2] while the adrenal glands account for most of the remainder. Testosterone is also synthesized in far smaller total quantities in women by the adrenal glands, thecal cells of the ovaries, and, during pregnancy, by the placenta.[126] In the testes, testosterone is produced by the Leydig cells.[127] The male generative glands also contain Sertoli cells, which require testosterone for spermatogenesis. Like most hormones, testosterone is supplied to target tissues in the blood where much of it is transported bound to a specific plasma protein, sex hormone-binding globulin (SHBG).
Testosterone belongs to a class of male hormones called androgens, which are sometimes called steroids or anabolic steroids. In men, testosterone is produced mainly in the testes, with a small amount made in the adrenal glands. The brain's hypothalamus and pituitary gland control testosterone production. The hypothalamus instructs the pituitary gland on how much testosterone to produce, and the pituitary gland passes the message on to the testes. These communications happen through chemicals and hormones in the bloodstream.

You can search every supplement on the market, and you can try reading “how to be good at sex” books (there’s about a million of them); You can even try those strange penis exercises (please do not waste your time). Or you can take a daily supplement that is designed and developed to do one thing: transform your penis and sex life so the next time a girl is talking about some guy who “could not stop making me orgasm,” that guy is you!
Testosterone makes a contribution to nitric oxide formation. Nitric oxide, released from penile nerves stimulates guanylate cyclase which catalyzes the transformation of guanosine-5-triphosphate into 3′,5′-cyclic, guanosine monophosphate (cyclic GMP). Gyclic GMP causes vasodilatation and hence erection formation (Morelli et al 2005). The breakdown of cyclic GMP to GMP is mediated by the enzyme, phosphodiesterase type-5, the inhibitors of which (eg, sildenafil citrate) enhance erection formation and maintanence (Carson and Lue 2005).
There are studies that show Soy consumption in humans leads to lower sperm count, but unfortunately they did not look at testosterone levels in the study (40). This (41) particular study compared the estrogen production of men drinking soy protein to those drinking whey. After two weeks they found the estradiol levels were equal, however soy drinkers had LOWER Testosterone levels and HIGHER cortisol levels (both bad).
Dobs and colleagues found that men with an increased body mass index had both reduced testosterone and reduced high density lipoprotein (HDL) levels. Treatment with testosterone increased the levels of HDL (Dobs et al 2001). Rising levels of HDL are not a consistent finding with TRT. More often, however, one finds reduced total cholesterol, low density lipoprotein (LDL) cholesterol and triglyceride levels with TRT (Zgliczynski et al 1996; Whitsel et al 2001).
Michael T. Murray, ND, is widely regarded as one of the leading authorities on natural medicine. He is the author of many books, including the classic Encyclopedia of Nutritional Supplements. His latest book is What the Drug Companies Won’t Tell You and Your Doctor Doesn’t Know. Visit him online at   Article Courtesy of Better Nutrition  
Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T.[114] The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
Sharma, R., Oni, O. A., Gupta, K., Chen, G., Sharma, M., Dawn, B., … & Barua, R. S. (2015, August 6). Normalization of testosterone level is associated with reduced incidence of myocardial infarction. European Heart Journal, 36(40), 2706-2715. Retrieved from