Because of inconclusive or conflicting results of testosterone treatment studies reported in the literature, Rabkin and colleagues (2004) undertook a comparison study among testosterone, the anti-depressant, fluoxetine, and placebo in eugonadal HIV positive men. They found that neither fluoxetine nor testosterone were different from placebo in reducing depression, but that testosterone did have a statistically significant effect in reducing fatigue. It is note-worthy that fatigue was reduced with testosterone treatment even though virtually all the men in the study had testosterone levels within the reference range.

Zinc plays a variety of roles in regulating the functions of enzymes and chemicals as well as your immune system. Zinc is also a potent antioxidant and can reduce the frequency of illnesses. Studies show that zinc may actually increase testosterone production. Large doses of zinc have actually been found to inhibit aromatase, thus reducing estrogen levels and increasing the effects of testosterone.


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The mechanism of age related decreases in serum testosterone levels has also been the subject of investigation. Metabolic clearance declines with age but this effect is less pronounced than a reduction in testosterone production, so the overall effect is to reduce serum testosterone levels. Gonadotrophin levels rise during aging (Feldman et al 2002) and testicular secretory responses to recombinant human chorionic gonadotrophin (hCG) are reduced (Mulligan et al 1999, 2001). This implies that the reduced production may be caused by primary testicular failure but in fact these changes are not adequate to fully explain the fall in testosterone levels. There are changes in the lutenising hormone (LH) production which consist of decreased LH pulse frequency and amplitude, (Veldhuis et al 1992; Pincus et al 1997) although pituitary production of LH in response to pharmacological stimulation with exogenous GnRH analogues is preserved (Mulligan et al 1999). It therefore seems likely that there are changes in endogenous production of GnRH which underlie the changes in LH secretion and have a role in the age related decline in testosterone. Thus the decreases in testosterone levels with aging seem to reflect changes at all levels of the hypothalamic-pituitary-testicular axis. With advancing age there is also a reduction in androgen receptor concentration in some target tissues and this may contribute to the clinical syndrome of LOH (Ono et al 1988; Gallon et al 1989).
A number of epidemiological studies have found that bone mineral density in the aging male population is positively associated with endogenous androgen levels (Murphy et al 1993; Ongphiphadhanakul et al 1995; Rucker et al 2004). Testosterone levels in young men have been shown to correlate with bone size, indicating a role in determination of peak bone mass and protection from future osteoporosis (Lorentzon et al 2005). Male hypogonadism has been shown to be a risk factor for hip fracture (Jackson et al 1992) and a recent study showed a high prevalence of hypogonadism in a group of male patients with average age 75 years presenting with minimal trauma fractures compared to stroke victims who acted as controls (Leifke et al 2005). Estrogen is a well known determinant of bone density in women and some investigators have found serum estrogen to be a strong determinant of male bone density (Khosla et al 1998; Khosla et al 2001). Serum estrogen was also found to correlate better than testosterone with peak bone mass (Khosla et al 2001) but this is in contradiction of a more recent study showing a negative correlation of estrogen with peak bone size (Lorentzon et al 2005). Men with aromatase deficiency (Carani et al 1997) or defunctioning estrogen receptor mutations (Smith et al 1994) have been found to have abnormally low bone density despite normal or high testosterone levels which further emphasizes the important influence of estrogen on male bone density.
However, along with bone healthy and density, vitamin D may also ensure proper testosterone production in men. Studies suggest a correlation between low testosterone levels and vitamin D deficiencies. Other research suggests that men supplementing with vitamin D experienced a statistically significant increase in testosterone levels. Studies found that simply spending more time in the summer sun increased the subjects’ vitamin D and testosterone levels.
A notable study out of Wayne State University in Indiana found that older men who had a mild zinc deficiency significantly increased their testosterone from 8.3 to 16.0 nmol/L—a 93 percent increase—following six months of zinc supplementation. Researchers of the study concluded that zinc may play an important role in modulating serum testosterone levels in normal healthy men.6
A number of research groups have tried to further define the relationship of testosterone and body composition by artificial alteration of testosterone levels in eugonadal populations. Induction of a hypogonadal state in healthy men (Mauras et al 1998) or men with prostate cancer (Smith et al 2001) using a gonadotrophin-releasing-hormone (GnRH) analogue was shown to produce increases in fat mass and decreased fat free mass. Another experimental approach in healthy men featured suppression of endogenous testosterone production with a GnRH analogue, followed by treatment with different doses of weekly intramuscular testosterone esters for 20 weeks. Initially the experiments involved men aged 18–35 years (Bhasin et al 2001) but subsequently the study was repeated with a similar protocol in men aged 60–75 years (Bhasin et al 2005). The different doses given were shown to produce a range of serum concentrations from subphysiological to supraphysiological (Bhasin et al 2001). A given testosterone dose produced higher serum concentrations of testosterone in the older age group (Bhasin et al 2005). Subphysiological dosing of testosterone produced a gain in fat mass and loss of fat free mass during the study. There were sequential decreases in fat mass and increases in fat free mass with each increase of testosterone dose. These changes in body composition were seen in physiological and supraphysiological treatment doses. The trend was similar in younger versus older men but the gain of fat mass at the lowest testosterone dose was less prominent in older patients (Bhasin et al 2001; Bhasin et al 2005). With regard to muscle function, the investigators showed dose dependent increases in leg strength and power with testosterone treatment in young and older men but there was no improvement in fatigability (Storer et al 2003; Bhasin et al 2005).
Why bother with such common micronutrients? Because it's not uncommon for athletes to suffer from zinc and magnesium deficiencies, partly due to inadequate replenishing of levels after intense bouts of exercise. Deficiencies in these key minerals can lead to a poor anabolic hormone profile, impaired immune function, and increased cortisol, ultimately leading to decreases in strength and performance.[6]
This evidence, together with the beneficial effects of testosterone replacement on central obesity and diabetes, raises the question whether testosterone treatment could be beneficial in preventing or treating atherosclerosis. No trial of sufficient size or duration has investigated the effect of testosterone replacement in primary or secondary prevention cardiovascular disease. The absence of such data leads us to examine the relationship of testosterone to other cardiovascular risk factors, such as adverse lipid parameters, blood pressure, endothelial dysfunction, coagulation factors, inflammatory markers and cytokines. This analysis can supply evidence of the likely effects of testosterone on overall cardiovascular risk. This has limitations, however, including the potential for diverging effects of testosterone on the various factors involved and the resultant impossibility of accurately predicting the relative impact of such changes.
Testosterone is necessary for normal sperm development. It activates genes in Sertoli cells, which promote differentiation of spermatogonia. It regulates acute HPA (hypothalamic–pituitary–adrenal axis) response under dominance challenge.[22] Androgen including testosterone enhances muscle growth. Testosterone also regulates the population of thromboxane A2 receptors on megakaryocytes and platelets and hence platelet aggregation in humans.[23][24]
High intensity exercise is crucial to boost testosterone (13).  Exercises should be explosive in nature and maximize the resistant overload on the muscles.  Large muscle group compound lifts such as squats, deadlifts & burpees are some of the best testosterone boosting exercises.  The training session should be short (5-30 mins) and have very little rest periods between sets.
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.
The chemical synthesis of testosterone from cholesterol was achieved in August that year by Butenandt and Hanisch.[183] Only a week later, the Ciba group in Zurich, Leopold Ruzicka (1887–1976) and A. Wettstein, published their synthesis of testosterone.[184] These independent partial syntheses of testosterone from a cholesterol base earned both Butenandt and Ruzicka the joint 1939 Nobel Prize in Chemistry.[182][185] Testosterone was identified as 17β-hydroxyandrost-4-en-3-one (C19H28O2), a solid polycyclic alcohol with a hydroxyl group at the 17th carbon atom. This also made it obvious that additional modifications on the synthesized testosterone could be made, i.e., esterification and alkylation.
A study out of the University of Mary Hardin-Baylor in Belton, Texas, examined the effects of fenugreek supplementation on strength and body composition in resistance-trained men. Researchers found that while both the placebo and fenugreek groups significantly increased their strength during the first four weeks, only the fenugreek group saw significant increases in strength after eight weeks of training and supplementation.[5]
If a man's testosterone looks below the normal range, there is a good chance he could end up on hormone supplements—often indefinitely. "There is a bit of a testosterone trap," Dr. Pallais says. "Men get started on testosterone replacement and they feel better, but then it's hard to come off of it. On treatment, the body stops making testosterone. Men can often feel a big difference when they stop therapy because their body's testosterone production has not yet recovered."
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