Zinc is involved in virtually every aspect of male reproduction, including testosterone metabolism. Several studies support the use of zinc for treating low sperm counts, especially when accompanied by low testosterone levels. In these studies, zinc has shown an ability to raise both sperm counts and testosterone levels. Many men may be suffering from low testosterone simply because of a zinc deficiency. Taking 30–45 mg of zinc per day is recommended; balance with 2–3 mg of copper for best results.
Epidemiological studies have also assessed links between serum testosterone and non-coronary atherosclerosis. A study of over 1000 people aged 55 years and over found an inverse correlation between serum total and bioavailable testosterone and the amount of aortic atherosclerosis in men, as assessed by radiological methods (Hak et al 2002). Increased intima-media thickness (IMT) is an early sign of atherosclerosis and has also been shown to predict cardiovascular mortality (Murakami et al 2005). Cross-sectional studies have found that testosterone levels are negatively correlated with carotid IMT in independently living men aged 74–93 years (van den Beld et al 2003), diabetic men (Fukui et al 2003) and young obese men (De Pergola et al 2003). A 4-year follow up study of the latter population showed that free testosterone was also inversely correlated with the rate of increase of IMT (Muller et al 2004).
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).
Finally, we looked at the proprietary blends of our remaining boosters, and dug into their ingredient lists. Supplements frequently include ingredients known for their “folk-lore” value; they’re believed to work, even when there isn’t any scientific background to prove it. Though we didn’t ding points if an ingredient wasn’t proven to be good (just so long as it wasn’t proven to be bad), we didn’t want to include any ingredient with evidence of causing harm.
Levels of testosterone naturally decrease with age, but exactly what level constitutes "low T," or hypogonadism, is controversial, Harvard Medical School said. Testosterone levels vary wildly, and can even differ depending on the time of day they're measured (levels tend to be lower in the evenings). The National Institutes of Health includes the following as possible symptoms of low testosterone:
Thus, alcohol metabolism destroys the essential coenzyme required for T synthesis. Alcohol also contributes to the release of special endorphins which inhibit hormone production. In addition, drinking too much alcohol leads to the elevation of estrogen levels in men because of the conversion of testosterone in estrogen. It means that T levels come down with a run.
Take in no less than 25 to 30 percent of your calories from fat. Taking in very low levels of fat inhibits the body's ability to product testosterone naturally. In fact, increasing your intake of healthy monounsaturated and polyunsaturated fats has a direct effect on how much testosterone your body makes, according to Anderson. Testosterone-boosting fats include olive oil, egg yolks, peanut butter, avocados and nuts and seeds.
While researchers in Brisbane, Australia, found that while Testofen (“a standardized [fenugreek] extract and mineral formulation”) significantly improved the sexual arousal, orgasm, and the general quality of life of participants, it did not remarkably increase testosterone above normal levels. Participants who took Testofen were more satisfied with their energy, well-being, and muscle strength than those who took the placebo.
Carbs play a big part in determining your Testosterone levels. Let's start with what to avoid. First, research shows that a large serving of sugar (75g of glucose), decreased Testosterone levels by as much as 25%! (25 & 26). I know this is a pretty extreme dosage, but you may want to avoid massive servings of sugar! Also, men who have Metabolic syndrome have lower Testosterone levels (27). Metabolic syndrome is often brought about by chronic high blood sugar which leads to insulin resistance.
I highly recommend using a great essential amino acid mix post-exercise in order to boost testosterone. These essential amino acids and especially the concentrated branched chain amino acids leucine, isoleucine and valine stimulate muscle protein synthesis. Getting these amino acids in the post-workout window dramatically boosts testosterone production (14). I like using our Amino Strong and will often recommend a scoop pre-workout and post-workout for the best muscle building, testosterone boosting benefits.
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“I'm having great results. Everybody is seeing a difference. People say, “You look good! Did you lose weight? What are you taking?” I'm 59, and I'm bringing my belt down a couple different notches. I couldn't break 180 lbs for nothing, no matter what I tried. Now it's 175 lbs. and she's going from there. I was just doing it for the belly -- no matter what I just couldn't get rid of the belly (until now). And I'm not as tired as I used to be.“
Regardless of the method of testosterone treatment chosen, patients will require regular monitoring during the first year of treatment in order to monitor clinical response to testosterone, testosterone levels and adverse effects, including prostate cancer (see Table 2). It is recommended that patients should be reviewed at least every three months during this time. Once treatment has been established, less frequent review is appropriate but the care of the patient should be the responsibility of an appropriately trained specialist with sufficient experience of managing patients treated with testosterone.
"A lot of the symptoms are mirrored by other medical problems," Hedges says. "And for a long time, we were not attributing them to low testosterone, but to diabetes, depression, high blood pressure, and coronary artery disease. But awareness and appreciation of low testosterone has risen. We recognize now that low testosterone may be at the root of problems."