The largest amounts of testosterone (>95%) are produced by the testes in men,[2] while the adrenal glands account for most of the remainder. Testosterone is also synthesized in far smaller total quantities in women by the adrenal glands, thecal cells of the ovaries, and, during pregnancy, by the placenta.[126] In the testes, testosterone is produced by the Leydig cells.[127] The male generative glands also contain Sertoli cells, which require testosterone for spermatogenesis. Like most hormones, testosterone is supplied to target tissues in the blood where much of it is transported bound to a specific plasma protein, sex hormone-binding globulin (SHBG).
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).
The chemical synthesis of testosterone from cholesterol was achieved in August that year by Butenandt and Hanisch.[183] Only a week later, the Ciba group in Zurich, Leopold Ruzicka (1887–1976) and A. Wettstein, published their synthesis of testosterone.[184] These independent partial syntheses of testosterone from a cholesterol base earned both Butenandt and Ruzicka the joint 1939 Nobel Prize in Chemistry.[182][185] Testosterone was identified as 17β-hydroxyandrost-4-en-3-one (C19H28O2), a solid polycyclic alcohol with a hydroxyl group at the 17th carbon atom. This also made it obvious that additional modifications on the synthesized testosterone could be made, i.e., esterification and alkylation.
At the present time, it is suggested that androgen replacement should take the form of natural testosterone. Some of the effects of testosterone are mediated after conversion to estrogen or dihydrotestosterone by the enzymes aromatase and 5a-reductase enzymes respectively. Other effects occur independently of the traditional action of testosterone via the classical androgen receptor- for example, its action as a vasodilator via a cell membrane action as described previously. It is therefore important that the androgen used to treat hypogonadism is amenable to the action of these metabolizing enzymes and can also mediate the non-androgen receptor actions of testosterone. Use of natural testosterone ensures this and reduces the chance of non-testosterone mediated adverse effects. There are now a number of testosterone preparations which can meet these recommendations and the main factor in deciding between them is patient choice.
In accordance with sperm competition theory, testosterone levels are shown to increase as a response to previously neutral stimuli when conditioned to become sexual in male rats.[40] This reaction engages penile reflexes (such as erection and ejaculation) that aid in sperm competition when more than one male is present in mating encounters, allowing for more production of successful sperm and a higher chance of reproduction.
Japanese Knotweed (a.k.a Hu Zhang or Polygonum cuspidatum) is highlighted by WebMD as needing more evidence to rate its effectiveness in a number of different areas: like treating constipation and liver or heart disease. They also warn that it can interact poorly with medications that are changed and broken down by the liver, and those that slow blood clotting (anticoagulants and antiplatelets).
"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.
Phthalates are found to cause poor testosterone synthesis by disrupting an enzyme required to create the male hormone. Women with high levels of DEHP and DBP (two types of phthalates) in their system during pregnancy were found to have sons that had feminine characteristics Phthalates are found in vinyl flooring, detergents, automotive plastics, soaps and shampoos, deodorants, perfumes, hair sprays, plastic bags and food packaging, among a long list of common products. Aside from phthalates, other chemicals that possess gender-bending traits are:

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.
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