In males, testosterone is synthesized primarily in Leydig cells. The number of Leydig cells in turn is regulated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). In addition, the amount of testosterone produced by existing Leydig cells is under the control of LH, which regulates the expression of 17β-hydroxysteroid dehydrogenase.
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.
Zinc deficiency also negatively affects testosterone levels, according a 2014 article in the Journal of Plant Biochemistry and Physiology. The authors of this review note that zinc supplementation can increase circulating testosterone in some populations. In fact, daily supplementation with typical doses may double testosterone within a few months.
In fact, studies on vegetarian and low-fat diets both show reduced testosterone levels of about 12 percent. Where higher fat diets of at least 40 percent of calories, with a higher intake of saturated fat, show increased testosterone levels. Why? It’s not rocket science. After all, cholesterol makes up the building blocks from which testosterone is formed; without it, the hormone simply can’t synthesize. Organic eggs are one of the best dietary sources. In addition to essential fatty acids, a whole egg is rich in aspartic acid, an amino acid that triggers production of testosterone.
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 . 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.
My preference is to start men on testosterone, for a couple of reasons. First, if a man has successful return of his own erections, it’s like a home run for him. He doesn’t have to take a pill in anticipation of having sex. He can have sex whenever he wants. Second, the benefits of testosterone-replacement therapy often go way beyond erectile dysfunction. That may be what brought the patient into the office originally, but then he comes back saying how much better he feels in general, how much more energetic and motivated he is, how his drives on the golf course seem to be going farther, and how his mood is better.
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.