Millions of American men use a prescription testosterone gel or injection to restore normal levels of the manly hormone. The ongoing pharmaceutical marketing blitz promises that treating "low T" this way can make men feel more alert, energetic, mentally sharp, and sexually functional. However, legitimate safety concerns linger. For example, some older men on testosterone could face higher cardiac risks.

“We need carbs, fats, and proteins to have optimal T levels,” says Howse. A healthy amount of carbs, for example, keeps cortisol levels low (more on why this is important to come). Meanwhile, dietary fats produce cholesterol, which our body can later convert into testosterone. And, finally, protein supports body composition by enhancing muscle repair and growth and increasing satiety.
Testosterone was first used as a clinical drug as early as 1937, but with little understanding of its mechanisms. The hormone is now widely prescribed to men whose bodies naturally produce low levels. But the levels at which testosterone deficiency become medically relevant still aren’t well understood. Normal testosterone production varies widely in men, so it’s difficult to know what levels have medical significance. The hormone’s mechanisms of action are also unclear.

“Our hypothesis was that testosterone would be good for the coronary arteries because we thought that by repleting testosterone to healthy levels there would be an improvement in the cholesterol panel and atherosclerosis burden. But what we found was the opposite, that atherosclerosis actually progresses faster under the influence of testosterone.”
“Poor lifestyle can mimic the symptoms of low testosterone and can actually cause low testosterone as well,” says Hodzovic. “The main culprits include lack of sleep, excessive stress, too little or too much exercise and too little or too much body fat. Getting healthy and active and eating a balanced nutritious diet along with enough sleep are the most important things to do.
if you’re a physician, you’re the real one who’s playing doctor. Stop prescribing low T treatment and let your patients go to a real doctor and not continue suffering. A simple picture of how hormones are created and their pathways will make you understand that E follows T, when we increase T, E2 will follow which negates all the positive effects of treatment. Without understanding this, you better leave the patient alone.
The biggest problem with supplementing your testosterone levels is it can shut off your own natural production and it can also permanently lower your sperm count. Taking testosterone boosters may also leave you open to some of the other unwanted side effects, like acne, male pattern baldness, mood swings and aggressive behaviour. To give yourself the best possible chance of avoiding these side effects, you need to see an expert before going for boosters.

Autopsy studies have found histological prostate cancer to be very common, with one series showing a prevalence of greater than fifty percent in men over age sixty (Holund 1980). The majority of histological cancers go undetected so that the clinical incidence of the disease is much lower, but it is still the most prevalent non-skin cancer in men (Jemal et al 2003). Prostate cancer is also unusual in comparison to other adult cancers in that the majority of those with the disease will die of other causes. Treatment of prostate cancer with androgen deprivation is known to be successful and is widely practiced, indicating an important role for testosterone in modifying the behavior of prostate cancer. In view of this, testosterone treatment is absolutely contraindicated in any case of known or suspected prostate cancer. The question of whether testosterone treatment could cause new cases of prostate cancer, or more likely cause progression of undiagnosed histological prostate cancer that would otherwise have remained occult, is an important consideration when treating ageing males with testosterone.
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There is a polymorphic CAG repeat sequence in the androgen receptor gene, which codes for a variable number of glutamine amino acids in the part of the receptor affecting gene transcription. A receptor with a short CAG sequence produces greater activity when androgens attach, and men with shorter CAG polymorphisms exhibit androgenic traits, such as preserved bone density (Zitzmann et al 2001) and prostate growth during testosterone treatment (Zitzmann et al 2003). Indirect evidence of the importance of androgens in the development of prostate cancer is provided by case control study findings of a shorter, more active CAG repeat sequence in the androgen receptor gene of patients with prostate cancer compared with controls (Hsing et al 2000, 2002).
Keep in mind that you can use virtually any type of equipment you want for this – an elliptical machine, a treadmill, swimming, even sprinting outdoors (although you will need to do this very carefully to avoid injury) -- as long as you're pushing yourself as hard as you can for 30 seconds. But do be sure to stretch properly and start slowly to avoid injury. Start with two or three repetitions and work your way up, don't expect to do all eight repetitions the first time you try this, especially if you are out of shape.

Since then, multiple studies have found no link between high testosterone levels and increasing your chances of developing prostate cancer. However — and this is a BIG however — if you already have prostate cancer, increased levels of testosterone may exacerbate the problem. It’s best to wait until after you treat your prostate cancer before you begin any T-boosting regimens. Tread carefully and talk with your doctor.
Some of them can benefit dieters or competitive athletes. These individuals often experience significant decreases in their testosterone levels as a result of the restrictive or stressful exercise or diet regimen. It is worth mentioning that many of them can actually benefit healthy and hyper-active individuals (for example, professional weight lifters), but we can’t know that for sure because there aren’t enough studies to back up this claim.
The unsexy truth is that increasing T naturally simply comes down to making some long-term changes in your diet and lifestyle. As you’ll see, what I did to increase T largely boils down to eating better, exercising smarter, and getting more sleep. That’s pretty much it. But as with most things in life, the devil is in the details, so I’ll share with you exactly what I did and provide research that explains why the things I did helped boost my testosterone.
In addition, the gel forms of testosterone, applied under your arm or on your upper arm and shoulder, can be transferred to others if you don’t wash the area after applying it. Children exposed to the hormone have experienced enlargement of the penis or clitoris, growth of pubic hair, increased libido, and aggressive behavior. Women can experience acne and the growth of body hair and, if they are pregnant or breastfeeding, can transfer the hormone to their babies.

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At the National Population and Family Development Board in Malaysia, men between the ages of 31 and 52 were given two capsules of the herb (E. longifolia) in Andro400 every day for three weeks. They reported erections were stronger and, in some cases, lasted longer. Overall, they felt more virile. Their levels of testosterone doubled within three weeks.5
Based on my research, I guess fenugreek is kind of a crapshoot, a toss-up, a gamble, a coin toss, a roulette spin of sorts, you get the idea.  There are a lot of conflicting reports on whether it increases or decreases testosterone levels, but it seems like the libido-improvement is consistent.  The vast majority of men report positive effects from fenugreek so go ahead and give it a shot.
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).
The use of anabolic steroids (manufactured androgenic hormones) shuts down the release of luteinising hormone and follicle stimulating hormone secretion from the pituitary gland, which in turn decreases the amount of testosterone and sperm produced within the testes. In men, prolonged exposure to anabolic steroids results in infertility, a decreased sex drive, shrinking of the testes and breast development. Liver damage may result from its prolonged attempts to detoxify the anabolic steroids. Behavioural changes (such as increased irritability) may also be observed. Undesirable reactions also occur in women who take anabolic steroids regularly, as a high concentration of testosterone, either natural or manufactured, can cause masculinisation (virilisation) of women.
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