The hypogonadal-obesity-adipocytokine cycle hypothesis. Adipose tissue contains the enzyme aromatase which metabolises testosterone to oestrogen. This results in reduced testosterone levels, which increase the action of lipoprotein lipase and increase fat mass, thus increasing aromatisation of testosterone and completing the cycle. Visceral fat also promotes lower testosterone levels by reducing pituitary LH pulse amplitude via leptin and/or other factors. In vitro studies have shown that leptin also inhibits testosterone production directly at the testes. Visceral adiposity could also provide the link between testosterone and insulin resistance (Jones 2007).
Testosterone has two major effects on bones: (a) through conversion to estradiol by way of the enzyme, aromatase, testosterone inhibits osteoclastic activity and hence bone resorption; and (b) through conversion to DHT via 5-α-reductase, it stimulates osteoblastic activity and so enhances the laying down of bone (Tivesten et al 2004; Davey and Morris 2005). Hypogonadal men are at risk for the development of osteopenia or osteoporosis and hence for subsequent fracture (Fink et al 2006). About one-third of all osteoporotic hip fractures occur in men and the risk of any osteoporotic fracture in men over 50 is as high as 25 percent (Seeman 1997; Adler 2006). Although treatment with testosterone in hypogonadal men increases bone mineral density (Katznelson et al 1996), it has not yet been established that this results in a reduction in fracture rate.
A 46 XY fetus is destined to become a male because the Y chromosome carries testicular determining gene which initiates transformation of the undifferentiated gonad into testes (Töhönen 2003). The testes subsequently produce both Mullerian Inhibiting Factor (to induce degeneration of the Mullerian system, the internal female ductal apparatus) and testosterone (to stimulate growth and development of the Wolffian system – epididymus, vas deferens, seminal vesicle and, after conversion to dihydrotestosterone (DHT) by the enzyme 5-α-reducase, the prostate gland). DHT is also the primary androgen to cause androgenization of the external genitalia.
Male sex characteristics greatly depend on testosterone synthesis in your body. If you keep the levels of this hormone normal, you will prevent sexual potency issues. Accordingly, the elevation of testosterone levels helps combat the impairment of erectile function. The levels of this hormone also affect male fertility. If these levels grow, fertility improves. Aging has a negative impact on testosterone secretion. Such hormonal imbalance is inevitable and permanent. But it’s still possible to positively change the situation and stimulate hormone production by using the high-quality testosterone boosters.
A sedentary lifestyle is another scourge for modern civilization. And this is a serious danger for men. After all, if physical activity is minimal, the testosterone levels will decrease steadily. And in this situation, strength training exercises are a proven method for raising testosterone. Thus, sports exercises always helped raise the levels of male sex hormone. As a result, the testosterone levels elevate after every workout.
In many of the studies we found, those who saw the most improvement in health, testosterone, or muscle gain were those with existing nutrient or vitamin deficiencies. This means that some gains may be due more to dietary changes and generally restoring nutrient and vitamin levels than any one magic ingredient, but also that making sure your diet includes healthy amounts of nutrients should be your first step.
Testosterone levels generally peak during adolescence and early adulthood. As you get older, your testosterone level gradually declines — typically about 1 percent a year after age 30 or 40. It is important to determine in older men if a low testosterone level is simply due to the decline of normal aging or if it is due to a disease (hypogonadism).