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^ Jump up to: a b Lazaridis I, Charalampopoulos I, Alexaki VI, Avlonitis N, Pediaditakis I, Efstathopoulos P, Calogeropoulou T, Castanas E, Gravanis A (2011). "Neurosteroid dehydroepiandrosterone interacts with nerve growth factor (NGF) receptors, preventing neuronal apoptosis". PLoS Biol. 9 (4): e1001051. doi:10.1371/journal.pbio.1001051. PMC 3082517. PMID 21541365.
Vitamin D is arguably the most important vitamin when it comes to testosterone. A study published in the Journal of Clinical Endocrinology examined the relationship between vitamin D supplementation and testosterone levels in men. The authors found that participants with higher levels of vitamin D had significantly higher levels of free testosterone compared to those with insufficient levels of vitamin D.8 Based on these study results, it appears vitamin D has a strong relationship with testosterone levels.
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).
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Dr. Anthony's Notes: When evaluating the efficacy of a product, it’s tough to balance the currently available human research with thousands of years of anecdotal evidence of efficacy. Tongkat Ali is a perfect example. All of the current studies are on animal models (not humans) – this DOES NOT mean that Tongkat Ali doesn’t work with humans. It simply means more research is needed. Personally, the strong experience of thousands of men (myself included) using this herb can confirm it’s libido enhancing effects. Also, this herb is DAMN BITTER. It makes Maca powder seem like a walk in the park. Hide in a smoothie or you will be sorry haha! How To Take Tongkat Ali: 200-300mg (of a 100:1 extract) 1-2 times per day. If you are using the raw powder (recommended below) that is NOT encapsulated, definitely hide the powder in a fat burning smoothie like the “Fit Father Fat Burning Shake Recipe” we recommend in FF30X. Again, I cannot understand how damn nasty this powder tastes. Beware!
While it would be nice to buy a testosterone pill from the local supplement store and have your testosterone levels go up, such a magic pill does not exist. As you can see from the above rundown, while a few supplements may be somewhat effective if your T levels are already low, none will significantly raise your testosterone above a baseline level. Thus, the basics of keeping your T levels high remain pretty simple:
Also, due to the intake of these synthetic substances, men start behaving in a very excited way, as well as demonstrate high levels of aggression and even violence. So, the men’s behavior may be antisocial. In addition, the men will experience breast enlargement and testicular shrinkage. The other adverse effects include hypertension, tumor growth, heart attacks and strokes, as well as development of liver disorders. It’s obvious that the numerous dangers of steroid use far outweigh a few benefits which they bring.
The hormone also plays a role in sex drive, sperm production, fat distribution, red cell production, and maintenance of muscle strength and mass, according to the Mayo Clinic. For these reasons, testosterone is associated with overall health and well-being in men. One 2008 study published in the journal Frontiers of Hormone Research even linked testosterone to the prevention of osteoporosis in men.

"The Journal of Clinical Endocrinology and Metabolism" published that males who switched from a high-fat diet to a low-fat diet also saw a decrease in their testosterone levels. If you want to put some fat back into your diet without fearing cardiac implications, plant-based saturated fat like coconut is just the ticket. Meat-based fat is also acceptable if kept to less than 10% of your dietary fat intake.

There is a polymorphic CAG repeat sequence in the androgen receptor gene, which codes for a variable number of glutamine amino acids in the part of the receptor affecting gene transcription. A receptor with a short CAG sequence produces greater activity when androgens attach, and men with shorter CAG polymorphisms exhibit androgenic traits, such as preserved bone density (Zitzmann et al 2001) and prostate growth during testosterone treatment (Zitzmann et al 2003). Indirect evidence of the importance of androgens in the development of prostate cancer is provided by case control study findings of a shorter, more active CAG repeat sequence in the androgen receptor gene of patients with prostate cancer compared with controls (Hsing et al 2000, 2002).


Male hypogonadism is a clinical syndrome caused by a lack of androgens or their action. Causes of hypogonadism may reflect abnormalities of the hypothalamus, pituitary, testes or target tissues. Increases in the amount of testosterone converted to estrogen under the action of the enzyme aromatase may also contribute to hypogonadism. Most aspects of the clinical syndrome are unrelated to the location of the cause. A greater factor in the production of a clinical syndrome is the age of onset. The development of hypogonadism with aging is known as late-onset hypogonadism and is characterised by loss of vitality, fatigue, loss of libido, erectile dysfunction, somnolence, depression and poor concentration. Hypogonadal ageing men also gain fat mass and lose bone mass, muscle mass and strength.

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Ashwagandha is sometimes included in testosterone supplements because of the hypothesis that it improves fertility. However, we couldn’t find sufficient evidence to support this claim (at best, one study found that ashwagandha might improve cardiorespiratory endurance). WebMD advocates caution when taking this herb, as it may interact with immunosuppressants, sedative medications, and thyroid hormone medications.
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