There are valid concerns about the safety of long-term treatment with testosterone particularly with respect to the cardiovascular system and the potential for stimulating prostate cancer development. There are no convincing hard data, however, to support these concerns. If anything, the data strongly suggest that adequate testosterone availability is cardioprotective and coronary risk factors such as diabetes, obesity and the metabolic syndrome are associated with reduced testosterone levels. It is certainly appropriate to avoid giving testosterone to men with prostate or breast cancer but it is not appropriate to accuse testosterone of inducing the development of de novo prostate cancers since evidence for this accusation is lacking (Wang et al 2004; Feneley and Carruthers 2006).
Growth of spermatogenic tissue in testicles, male fertility, penis or clitoris enlargement, increased libido and frequency of erection or clitoral engorgement occurs. Growth of jaw, brow, chin, and nose and remodeling of facial bone contours, in conjunction with human growth hormone occurs.[21] Completion of bone maturation and termination of growth. This occurs indirectly via estradiol metabolites and hence more gradually in men than women. Increased muscle strength and mass, shoulders become broader and rib cage expands, deepening of voice, growth of the Adam's apple. Enlargement of sebaceous glands. This might cause acne, subcutaneous fat in face decreases. Pubic hair extends to thighs and up toward umbilicus, development of facial hair (sideburns, beard, moustache), loss of scalp hair (androgenetic alopecia), increase in chest hair, periareolar hair, perianal hair, leg hair, armpit hair.
Intramuscular testosterone injections were first used around fifty years ago. Commercially available preparations contain testosterone esters in an oily vehicle. Esterification is designed to retard the release of testosterone from the depot site into the blood because the half life of unmodified testosterone would be very short. For many years intramuscular preparations were the most commonly used testosterone therapy and this is still the case in some centers. Pain can occur at injection sites, but the injections are generally well tolerated and free of major side effects. Until recently, the available intramuscular injections were designed for use at a frequency of between weekly and once every four weeks. These preparations are the cheapest mode of testosterone treatment available, but often cause supraphysiological testosterone levels in the days immediately following injection and/or low trough levels prior to the next injection during which time the symptoms of hypogonadism may return (Nieschlag et al 1976). More recently, a commercial preparation of testosterone undecanoate for intramuscular injection has become available. This has a much longer half life and produces testosterone levels in the physiological range throughout each treatment cycle (Schubert et al 2004). The usual dose frequency is once every three months. This is much more convenient for patients but does not allow prompt cessation of treatment if a contraindication to testosterone develops. The most common example of this would be prostate cancer and it has therefore been suggested that shorter acting testosterone preparations should preferably used for treating older patients (Nieschlag et al 2005). Similar considerations apply to the use of subcutaneous implants which take the form of cylindrical pellets injected under the skin of the abdominal wall and steadily release testosterone to provide physiological testosterone levels for up to six months. Problems also include pellet extrusion and infection (Handelsman et al 1997).
When females have a higher baseline level of testosterone, they have higher increases in sexual arousal levels but smaller increases in testosterone, indicating a ceiling effect on testosterone levels in females. Sexual thoughts also change the level of testosterone but not level of cortisol in the female body, and hormonal contraceptives may affect the variation in testosterone response to sexual thoughts.[51]
Experts have also found that fertile men have a lot of D-aspartic acid. D-aspartic acid is a complex amino acid linked with virility not found commonly. Oysters not only hold a good dose of D-aspartic acid but also has N-methyl-D-aspartate. N-methyl-D-aspartate sparks the production of sex hormones. Eating daily oysters has shown to be raising testosterone levels a lot in as little as six weeks.
Up Regulation – Many herbs available in natural test boosters function as testosterone up regulators or promoters. These function by use of specific natural compounds inside the herb, which once inside the body can naturally signal your DNA to express greater testosterone production. There is a variety of herbs that do this, and by signaling different ‘zones’ in your DNA. In addition, some many work better than others for different people due to variation in the genetic code between different people.
This content is strictly the opinion of Dr. Josh Axe and is for informational and educational purposes only. It is not intended to provide medical advice or to take the place of medical advice or treatment from a personal physician. All readers/viewers of this content are advised to consult their doctors or qualified health professionals regarding specific health questions. Neither Dr. Axe nor the publisher of this content takes responsibility for possible health consequences of any person or persons reading or following the information in this educational content. All viewers of this content, especially those taking prescription or over-the-counter medications, should consult their physicians before beginning any nutrition, supplement or lifestyle program.

There is also solid research indicating that if you take astaxanthin in combination with saw palmetto, you may experience significant synergistic benefits. A 2009 study published in the Journal of the International Society of Sports Nutrition found that an optimal dose of saw palmetto and astaxanthin decreased both DHT and estrogen while simultaneously increasing testosterone.6 Also, in order to block the synthesis of excess estrogen (estradiol) from testosterone there are excellent foods and plant extracts that may help to block the enzyme known as aromatase which is responsible producing estrogen. Some of these include white button mushrooms, grape seed extract and nettles.7


One long-term study observed that those who slept only four hours per night had borderline deficient levels. Other long-term studies support this. One study calculated that for every additional hour of sleep you get, testosterone levels rise 15% higher, on average. Although some people seem to do fine with less sleep, research suggests around 7–10 hours of sleep per night is best for long-term health and your testosterone.
Another recent development is the production of adhesive tablets which are applied twice daily to the buccal mucosa on the gum above the incisor teeth. The tablets gradually release testosterone into the systemic venous circulation and steady state physiological concentrations are achieved in most patients within two days (Ross et al 2004). Some patients do not like the feeling of the tablet in the mouth or find that there is an abnormal taste in the mouth, but local adverse effects are usually mild and transient (Wang, Swerdloff et al 2004).

Your body’s circadian rhythm essentially resets itself every night and releases chemicals like cortisol, which contribute to the overall hormone balance that can prevent low T-levels. I have even heard one endocrinologist claim that one hour of sleep between 10 p.m. and 2 a.m. has the same healing effects on your body as two hours of sleep before or after this timeslot!

Both testosterone and 5α-DHT are metabolized mainly in the liver.[1][151] Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively.[1] An additional 40% of testosterone is metabolized in equal proportions into the 17-ketosteroids androsterone and etiocholanolone via the combined actions of 5α- and 5β-reductases, 3α-hydroxysteroid dehydrogenase, and 17β-HSD, in that order.[1][151][152] Androsterone and etiocholanolone are then glucuronidated and to a lesser extent sulfated similarly to testosterone.[1][151] The conjugates of testosterone and its hepatic metabolites are released from the liver into circulation and excreted in the urine and bile.[1][151][152] Only a small fraction (2%) of testosterone is excreted unchanged in the urine.[151]
The regular intake of testosterone boosters is known for the high level of safety comparing to the hormone injections and the use of illegal steroids. But still to protect yourself against any possible adverse reactions, you should remember that the supplementation can’t be continuous. The breaks from time to time are required. Such an approach to the use of boosters is healthy and best-working if you aspire to enhance own hormone production without any harm.
When you're under a lot of stress, your body releases high levels of the stress hormone cortisol. This hormone actually blocks the effects of testosterone,6 presumably because, from a biological standpoint, testosterone-associated behaviors (mating, competing, aggression) may have lowered your chances of survival in an emergency (hence, the "fight or flight" response is dominant, courtesy of cortisol).

Now, you may not accept it when you hear people saying that saturated fats and cholesterol are good for you. But these elements are crucial for testosterone production. Without cholesterol, the Leydig cells inside the testes cannot synthesize the testosterone hormone. Leydig cells absorb the cholesterol from our blood and release T. Eggs quickly become the #1 source to meet these needs. It is so because they are cheap, easy to find and you can use them in many ways while cooking.
As blood levels of testosterone increase, this feeds back to suppress the production of gonadotrophin-releasing hormone from the hypothalamus which, in turn, suppresses production of luteinising hormone by the pituitary gland. Levels of testosterone begin to fall as a result, so negative feedback decreases and the hypothalamus resumes secretion of gonadotrophin-releasing hormone. 
"By expanding the boundaries of this disease to common symptoms in aging males, such as fatigue and reduced libido, drug companies seek to increase their markets and boost their sales," wrote Barbara Mintzes, an assistant professor at the University of British Columbia School of Public Health, and Agnes Vitry, a senior research fellow at the University of South Australia, in a 2012 article in the Medical Journal of Australia .
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.
Although some men believe that taking testosterone medications may help them feel younger and more vigorous as they age, few rigorous studies have examined testosterone therapy in men who have healthy testosterone levels. And some small studies have revealed mixed results. For example, in one study healthy men who took testosterone medications increased muscle mass but didn't gain strength.
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