There are two keys to incorporating fat in your diet: getting enough fat, and getting the right kinds of it. A study from 1984 (done, no doubt, with Big Brother watching) looked at 30 healthy men who switched from eating 40% fat (much of it saturated) to 25% fat (much of it unsaturated), with more protein and carbs to make up the difference in calories. After 6 weeks, their average serum testosterone, free testosterone, and 4-androstenedione (an important hormone for testosterone synthesis) all dropped significantly [6]. I think getting 40% of your calories from fat is too little – I recommend 50-70% of calories from fat, or even more in some cases.
Conflicting results have been obtained concerning the importance of testosterone in maintaining cardiovascular health.[29][30] Nevertheless, maintaining normal testosterone levels in elderly men has been shown to improve many parameters that are thought to reduce cardiovascular disease risk, such as increased lean body mass, decreased visceral fat mass, decreased total cholesterol, and glycemic control.[31]
Testosterone replacement therapy may improve energy, mood, and bone density, increase muscle mass and weight, and heighten sexual interest in older men who may have deficient levels of testosterone. Testosterone supplementation is not recommended for men who have normal testosterone levels for their age group due to the risk of prostate enlargement and other side effects. Testosterone replacement therapy is available as a cream or gel, topical solution, skin patch, injectable form and pellet form placed under the skin.
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Cosgrove et al reported a higher rate of sexual dysfunction in veterans with posttraumatic stress disorder (PTSD) than in veterans who did not develop this problem. [42] The domains on the International Index of Erectile Function (IIEF) questionnaire that demonstrated the most change included overall sexual satisfaction and erectile function. [43, 44] Men with PTSD should be evaluated and treated if they have sexual dysfunction.
Cross-sectional studies conducted at the time of diagnosis of BPH have failed to show consistent differences in testosterone levels between patients and controls. A prospective study also failed to demonstrate a correlation between testosterone and the development of BPH (Gann et al 1995). Clinical trials have shown that testosterone treatment of hypogonadal men does cause growth of the prostate, but only to the size seen in normal men, and also causes a small increase in prostate specific antigen (PSA) within the normal range (Rhoden and Morgentaler 2005). Despite growth of the prostate a number of studies have failed to detect any adverse effects on symptoms of urinary obstruction or physiological measurements such as flow rates and residual volumes (Snyder et al 1999; Kenny et al 2000, 2001). Despite the lack of evidence linking symptoms of BPH to testosterone treatment, it remains important to monitor for any new or deteriorating problems when commencing patients on testosterone treatment, as the small growth of prostate tissue may adversely affect a certain subset of individuals. 
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