When your testosterone levels go up, so does your libido. Unfortunately, the inverse is not true — your libido levels can go up without your testosterone levels also going up. And that’s how most supposed T-boosters “work”: they make you feel ornery, leading you to think that your T levels are appreciably higher, when they actually aren’t. In rare cases, supplementation will result in a 20% testosterone increase. This kind of improvement may sound impressive, but is irrelevant for practical purposes.

Testosterone is significantly correlated with aggression and competitive behaviour and is directly facilitated by the latter. There are two theories on the role of testosterone in aggression and competition.[77] The first one is the challenge hypothesis which states that testosterone would increase during puberty thus facilitating reproductive and competitive behaviour which would include aggression.[77] Thus it is the challenge of competition among males of the species that facilitates aggression and violence.[77] Studies conducted have found direct correlation between testosterone and dominance especially among the most violent criminals in prison who had the highest testosterone levels.[77] The same research also found fathers (those outside competitive environments) had the lowest testosterone levels compared to other males.[77]

Puberty occurs when there is an “awakening” of the hypothalamic-pituitary axis. The hypothalamus increases its secretion of gonadotropin releasing hormone (GnRH) which in turn stimulates the release of luteinizing hormone (LH) and follicle stimulating hormone (FSH). This leads to a significant increase in the production of testicular testosterone and the induction of the well-known secondary sex characteristics associated with puberty: growth spurt, increased libido, increased erectile function, acne, increased body hair, increased muscle mass, deepening of the voice, spermatogenesis, gynecomastia (usually transient).
When you're under a lot of stress, your body releases high levels of the stress hormone cortisol. This hormone actually blocks the effects of testosterone,6 presumably because, from a biological standpoint, testosterone-associated behaviors (mating, competing, aggression) may have lowered your chances of survival in an emergency (hence, the "fight or flight" response is dominant, courtesy of cortisol).
Male hypogonadism becomes more common with increasing age and is currently an under-treated condition. The diagnosis of hypogonadism in the aging male requires a combination of symptoms and low serum testosterone levels. The currently available testosterone preparations can produce consistent physiological testosterone levels and provide for patient preference.
Testosterone is considered to be the "male hormone" that's produced in men by the testes. Although women's ovaries produce some testosterone, the hormone is produced in much higher concentrations in men and it is responsible for many of the secondary sex characteristics seen in men such as a deeper voice and hair on the chest, in addition to contributing to a healthy libido, building muscle mass, and maintaining energy levels.

Brassaiopsis glomerulata is a tree indigenous to Vietnam. While the plant has traditionally been used to remedy back pain and rheumatism, studies show that Brassaiopsis also contains a few compounds that inhibit aromatase. As mentioned above, aromatase is an enzyme that can turn androgens, particularly testosterone, into estrogen. Too much aromatase can significantly reduce testosterone levels while increasing estrogen, causing an imbalance in your body’s chemistry. By inhibiting aromatase, the compounds in Brassaiopsis can effectively boost testosterone levels and prevent them from turning into estrogen.

The aim of treatment for hypogonadism is to normalize serum testosterone levels and abolish symptoms or pathological states that are due to low testosterone levels. The exact target testosterone level is a matter of debate, but current recommendations advocate levels in the mid-lower normal adult range (Nieschlag et al 2005). Truly physiological testosterone replacement would require replication of the diurnal rhythm of serum testosterone levels, but there is no current evidence that this is beneficial (Nieschlag et al 2005).
I will never forget when we went to the locker room and showed me his poses for his upcoming contest. His lats were wider, his chest was thicker, his thighs had deeper cuts, and he had amazing striation in all three heads of his delts. He told me that he gained 12 pounds of pure muscle and lost 1 pound of body fat according to his doctor at the Cleveland clinic. I have never seen such drastic change in anyone in such a short time without steroids or prohormones.
The prevalence of biochemical testosterone deficiency increases with age. This is partly due to decreasing testosterone levels associated with illness or debility but there is also convincing epidemiological data to show that serum free and total testosterone levels also fall with normal aging (Harman et al 2001; Feldman et al 2002). The symptoms of aging include tiredness, lack of energy, reduced strength, frailty, loss of libido, decreased sexual performance depression and mood change. Men with hypogonadism experience similar symptoms. This raises the question of whether some symptoms of aging could be due to relative androgen deficiency. On the other hand, similarities between normal aging and the symptoms of mild androgen deficiency make the clinical diagnosis of hypogonadism in aging men more challenging.
Scientists in Italy found that subjects who consumed roughly 3 grams of D-AA for 12 days observed a 42 percent increase in testosterone levels.[12] The researchers also noted that the D-AA group still had 22 percent more testosterone than the placebo group three days after they stopped supplementing. Conversely, a more recent article published in Nutrition Research found no increase in testosterone levels in resistance-trained males after supplementing with 3 grams of D-AA for 28 days.[13]

As already indicated previously, testosterone levels, particularly bioavailable testosterone, fall with advancing age. This decline in testosterone availability may start to occur early in the forth decade but it usually becomes clinically manifest in the 50s and 60s. Although there is continuing debate about the best way to diagnose hypogonadism in the aging male, there appears to be a general consensus that symptomatic men with reduced levels of testosterone should be given a trial of testosterone therapy if there is no contraindication to do so (Bain et al 2007).
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).
Cardiovascular disease, and its underlying pathological process atherosclerosis, is an important cause of morbidity and mortality in the developed and developing world. Coronary heart disease in particular is the commonest cause of death worldwide (AHA 2002; MacKay and Mensah 2004). As well as increasing with age, this disease is more common in the male versus female population internationally, which has led to interest in the potential role of sex hormones in modulating risk of development of atherosclerosis. Concerns about the potential adverse effects of testosterone treatment on cardiovascular disease have previously contributed to caution in prescribing testosterone to those who have, or who are at risk of, cardiovascular disease. Contrary to fears of the potential adverse effects of testosterone on cardiovascular disease, there are over forty epidemiological studies which have examined the relationship of testosterone levels to the presence or development of coronary heart disease, and none have shown a positive correlation. Many of these studies have found the presence of coronary heart disease to be associated with low testosterone levels (Reviews: Jones, Jones et al 2003; Jones et al 2005).
The researchers found that the dose of testosterone required to produce different effects in the body varied widely. The influence of testosterone and estradiol also differed. As the testosterone gel dose was reduced, the scientists showed, reductions in lean mass, muscle size, and leg-press strength resulted from decreases in testosterone itself. In contrast, increases in body fat were due to the related declines in estradiol. Both testosterone and estradiol levels were associated with libido and erectile function.
Magnesium comes with a strict upper cap. Excess magnesium is hard on your kidneys, and can lead to kidney failure. The NIH recommends that men consume 400-420 mg of magnesium daily, but that they should not exceed 350 mg of supplemental magnesium per day. Because while it’s rare for people to chronically overdose on magnesium through diet (you’d have to eat a lot of almonds and spinach, for example), overdose by supplement is far more common.
Studies have demonstrated reduced testosterone levels in men with heart failure as well as other endocrine changes (Tappler and Katz 1979; Kontoleon et al 2003). Treatment of cardiac failure with chronic mechanical circulatory support normalizes many of these changes, including testosterone levels (Noirhomme et al 1999). More recently, two double-blind randomized controlled trials of testosterone treatment for men with low or low-normal serum testosterone levels and heart failure have shown improvements in exercise capacity and symptoms (Pugh et al 2004; Malkin et al 2006). The mechanism of these benefits is currently unclear, although a study of the acute effects of buccal testosterone given to men with chronic cardiac failure under invasive monitoring showed that testosterone increased cardiac index and reduced systemic vascular resistance (Pugh et al 2003). Testosterone may prove useful in the management of cardiac failure but further research is needed.
Hypogonadism is a disease in which the body is unable to produce normal amounts of testosterone due to a problem with the testicles or with the pituitary gland that controls the testicles. Testosterone replacement therapy can improve the signs and symptoms of low testosterone in these men. Doctors may prescribe testosterone as injections, pellets, patches or gels.