More can be learned from a large, randomized, placebo-controlled trial of finasteride treatment in 18,800 men aged 55 or more. Finasteride is a 5α-reductase inhibitor which acts to prevent the metabolism of testosterone to dihydrotestosterone (DHT) – the most active androgen in the prostate. The trial showed a greater overall incidence of prostate cancer in the control group, but men treated with finasteride were more likely to have high grade tumors (Thompson et al 2003), suggesting that reduced androgen exposure of the prostate may delay the presentation of prostate cancer and/or promote advanced disease in some other way.
More can be learned from a large, randomized, placebo-controlled trial of finasteride treatment in 18,800 men aged 55 or more. Finasteride is a 5α-reductase inhibitor which acts to prevent the metabolism of testosterone to dihydrotestosterone (DHT) – the most active androgen in the prostate. The trial showed a greater overall incidence of prostate cancer in the control group, but men treated with finasteride were more likely to have high grade tumors (Thompson et al 2003), suggesting that reduced androgen exposure of the prostate may delay the presentation of prostate cancer and/or promote advanced disease in some other way.
Some boys even develop enlarged testicles and penis, armpit or pubic hair, as well as facial hair as early as age nine! Early puberty is not something to be taken lightly because it can significantly influence physical and psychological health, including an increased risk of hormone-related cancers. Precocious sexual development may also lead to emotional and behavioral issues, such as:

And remember, saturated fats work best (along with monounsaturated fats – olive oil, almonds, avocados etc.). In fact higher intakes of polyunsaturated fats (canola oil, sunflower oil, soybean oil, safflower oil, margarine etc.) are linked to LOWER testosterone levels (14 & 15). I explore the dangers of PUFA's in a lot more detail in this article - PUFA's: The Worst Thing For Your Health That You Eat Everyday.
Do low levels of testosterone produce symptoms in middle-aged men? Absolutely. In fact, the classic symptoms were first recognized more than 70 years ago when two American physicians, Carl Heller, MD, and Gordon Myers, MD, showed the effectiveness of testosterone treatment for symptoms of fatigue, depression, irritability, low sex drive, erectile dysfunction, night sweats, and hot flashes in men. Over the years, subsequent studies have found that some—but not all—men with low, age-adjusted testosterone levels exhibit symptoms consistent with andropause. All experience improvement with testosterone therapy.

Testosterone retains nitrogen and is an essential ingredient in the development and maintenance of muscle mass (Sinha-Hikim et al 2006). With a diminution in testosterone, muscle mass diminishes as does strength. Weakness and fatigue result. A number of studies have demonstrated the ability of testosterone to restore lean body mass (muscle) in hypogonadal men, while at the same time causing a reduction in fat mass (Wang et al 2004). Treatment of hypogonadal men with testosterone results in improvement in overall physical performance as well as strength as assessed by, eg, hand grip power (Page 2005). Because of decreased muscle strength and impaired balance, older hypogonadal men are susceptible to falling and since they may already be osteopenic or osteoporotic as a consequence of hypogonadism, they are at increased risk for fracture as a result of the fall (Szulc et al 2003). Men with low levels of testosterone as in androgen deprivation therapy for prostate cancer, have a significant decrease in lean body mass and hemoglobin, while at the same time they experience an increase in weight, body fat and body mass index (Smith et al 2002). Treatment of frail hypogonadal men with testosterone, therefore, can result in changes in muscle gene expression, increased muscle mass, improvements in strength, power and endurance and improved physical function.
There have been case reports of development of prostate cancer in patients during treatment with testosterone, including one case series of twenty patients (Gaylis et al 2005). It is not known whether this reflects an increase in incidence, as prostate cancer is very common and because the monitoring for cancer in patients treated with testosterone is greater. Randomized controlled trials of testosterone treatment have found a low incidence of prostate cancer and they do not provide evidence of a link between testosterone treatment and the development of prostate cancer (Rhoden and Morgentaler 2004). More large scale clinical trials of longer durations of testosterone replacement are required to confirm that testosterone treatment does not cause prostate cancer. Overall, it is not known whether testosterone treatment of aging males with hypogonadism increases the risk of prostate cancer, but monitoring for the condition is clearly vital. This should take the form of PSA blood test and rectal examination every three months for the first year of treatment and yearly thereafter (Nieschlag et al 2005). Age adjusted PSA reference ranges should be used to identify men who require further assessment. The concept of PSA velocity is also important and refers to the rate of increase in PSA per year. Patients with abnormal rectal examination suggestive of prostate cancer, PSA above the age specific reference range or a PSA velocity greater than 0.75 ng/ml/yr should be referred to a urologist for consideration of prostate biopsy.
Trials of testosterone treatment in men with type 2 diabetes have also taken place. A recent randomized controlled crossover trial assessed the effects of intramuscular testosterone replacement to achieve levels within the physiological range, compared with placebo injections in 24 men with diabetes, hypogonadism and a mean age of 64 years (Kapoor et al 2006). Ten of these men were insulin treated. Testosterone treatment led to a significant reduction in glycated hemoglobin (HbA1C) and fasting glucose compared to placebo. Testosterone also produced a significant reduction in insulin resistance, measured by the homeostatic model assessment (HOMA), in the fourteen non-insulin treated patients. It is not possible to measure insulin resistance in patients treated with insulin but five out of ten of these patients had a reduction of insulin dose during the study. Other significant changes during testosterone treatment in this trial were reduced total cholesterol, waist circumference and waist-hip ratio. Similarly, a placebo-controlled but non-blinded trial in 24 men with visceral obesity, diabetes, hypogonadism and mean age 57 years found that three months of oral testosterone treatment led to significant reductions in HbA1C, fasting glucose, post-prandial glucose, weight, fat mass and waist-hip ratio (Boyanov et al 2003). In contrast, an uncontrolled study of 150 mg intramuscular testosterone given to 10 patients, average age 64 years, with diabetes and hypogonadism found no significant change in diabetes control, fasting glucose or insulin levels (Corrales et al 2004). Another uncontrolled study showed no beneficial effect of testosterone treatment on insulin resistance, measured by HOMA and ‘minimal model’ of area under acute insulin response curves, in 11 patients with type 2 diabetes aged between 33 and 73 years (Lee et al 2005). Body mass index was within the normal range in this population and there was no change in waist-hip ratio or weight during testosterone treatment. Baseline testosterone levels were in the low-normal range and patients received a relatively small dose of 100 mg intramuscular testosterone every three weeks. A good increase in testosterone levels during the trial is described but it is not stated at which time during the three week cycle the testosterone levels were tested, so the lack of response could reflect an insufficient overall testosterone dose in the trial period.
The reason I started the experiment at that point is because I know a lot of guys who live my last-August lifestyle all the time, and I wanted to see what would happen to an “average” guy who turned things around. At the same time, there was no “normal” time in my life which would have been better for me to start the experiment. My stress level and diet fluctuates throughout the year anyway, so at any point, factors in my current lifestyle would have influenced the results. I wanted to begin at “ground zero.”
We kept it simple, and followed the premise of testosterone boosters: testosterone affects muscle gain, weight loss, and libido, so by increasing the amount of testosterone in the body, we can improve on each of those goals. This meant that we looked for ingredients proven to increase testosterone levels, not ingredients that might increase libido or help build muscle mass independently of testosterone (like having a healthy diet and feeling good about yourself). In addition, we dove deep into the specific ingredient lists of our finalists and cross-checked them against WebMD and the National Institutes of Health (NIH) database to make sure that they did not contain ingredients known to be harmful.

Withania Somnifera is another name for Ashwagandha which is an ancient herb used as a medicine. It is an adaptogen because it helps the body to handle anxiety and stress. It improves T levels along with increasing sperm production. Other than improvement in sexual performance it also helps in fat loss, strength, and stamina. It reduces the stress by reducing the output of the cortisol hormone, which acts antagonist to testosterone. This reduction helps to body to trigger the testosterone production.
“This study establishes testosterone levels at which various physiological functions start to become impaired, which may help provide a rationale for determining which men should be treated with testosterone supplements,” Finkelstein says. “But the biggest surprise was that some of the symptoms routinely attributed to testosterone deficiency are actually partially or almost exclusively caused by the decline in estrogens that is an inseparable result of lower testosterone levels.”
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).
For people who are worried about low or high testosterone, a doctor may perform a blood test to measure the amount of the hormone in the patient's blood. When doctors find low-T, they may prescribe testosterone therapy, in which the patient takes an artificial version of the hormone. This is available in the following forms: a gel to be applied to the upper arms, shoulders or abdomen daily; a skin patch put on the body or scrotum twice a day; a solution applied to the armpit; injections every two or three weeks; a patch put on the gums twice a day; or implants that last four to six months.

Before assessing the evidence of testosterone’s action in the aging male it is important to note certain methodological considerations which are common to the interpretation of any clinical trial of testosterone replacement. Many interventional trials of the effects of testosterone on human health and disease have been conducted. There is considerable heterogenicity in terms of study design and these differences have a potential to significantly affect the results seen in various studies. Gonadal status at baseline and the testosterone level produced by testosterone treatment in the study are of particular importance because the effects of altering testosterone from subphysiological to physiological levels may be different from those of altering physiological levels to supraphysiological. Another important factor is the length of treatment. Randomised controlled trials of testosterone have ranged from one to thirty-six months in duration (Isidori et al 2005) although some uncontrolled studies have lasted up to 42 months. Many effects of testosterone are thought to fully develop in the first few months of treatment but effects on bone, for example, have been shown to continue over two years or more (Snyder et al 2000; Wang, Cunningham et al 2004).
‘Testosterone boosting’ products  - found online, or in health food or body-building shops, these products claim to boost testosterone levels if you buy them. The majority of these products will not have the effect you want and are not worth spending money on. Any of these products that do have a real effect may have a form of prescription medication in which is both dangerous and illegal.
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.
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