A: Testosterone production declines naturally with age. Low testosterone, or testosterone deficiency (TD), may result from disease or damage to the hypothalamus, pituitary gland, or testicles that inhibits hormone secretion and testosterone production. Treatment involves hormone replacement therapy. The method of delivery is determined by age and duration of deficiency. Oral testosterone, Testred (methyltestosterone), is associated with liver toxicity and liver tumors and so is prescribed sparingly. Transdermal delivery with a testosterone patch is becoming the most common method of treatment for testosterone deficiency in adults. A patch is worn, either on the scrotum or elsewhere on the body, and testosterone is released through the skin at controlled intervals. Patches are typically worn for 12 or 24 hours and can be worn during exercise, bathing, and strenuous activity. Two transdermal patches that are available are Androderm (nonscrotal) and Testoderm (scrotal). The Androderm patch is applied to the abdomen, lower back, thigh, or upper arm and should be applied at the same time every evening between 8 p.m. and midnight. If the patch falls off before noon, replace it with a fresh patch until it is time to reapply a new patch that evening. If the patch falls off after noon, do not replace it until you reapply a new patch that evening. The most common side effects associated with transdermal patch therapy include itching, discomfort, and irritation at the site of application. Some men may experience fluid retention, acne, and temporary abnormal breast development (gynecosmastia). AndroGel and Testim are transdermal gels that are applied once daily to the clean dry skin of the upper arms or abdomen. When used properly, these gels deliver testosterone for 24 hours. The gel must be allowed to dry on the skin before dressing and must be applied at least 6 hours before showering or swimming. Gels cannot be applied to the genitals. AndroGel is available in a metered-dose pump, which allows physicians to adjust the dosage of the medication. Side effects of transdermal gels include adverse reactions at the site of application, acne, headache, and hair loss (alopecia). For more specific information on treatments for low testosterone, consult with your doctor or pharmacist for guidance based on current health condition. Kimberly Hotz, PharmD
Like other steroid hormones, testosterone is derived from cholesterol (see figure).[124] The first step in the biosynthesis involves the oxidative cleavage of the side-chain of cholesterol by cholesterol side-chain cleavage enzyme (P450scc, CYP11A1), a mitochondrial cytochrome P450 oxidase with the loss of six carbon atoms to give pregnenolone. In the next step, two additional carbon atoms are removed by the CYP17A1 (17α-hydroxylase/17,20-lyase) enzyme in the endoplasmic reticulum to yield a variety of C19 steroids.[125] In addition, the 3β-hydroxyl group is oxidized by 3β-hydroxysteroid dehydrogenase to produce androstenedione. In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone.
The same study showed that drinking did, however, lower semen count and quality. And I want to remind you – this is an article  on improving testosterone levels, not general health as there are a lot of studies that show drinking leads to an assortment of health issues. This acute spike in Testosterone could be due to the effect alcohol has on libido, and also the energy influx in the liver?
I know the experiment didn’t simply bring me back to my pre-August levels because of the fact that when I learned that the original test I took can sometimes overestimate your T levels, I took a more accurate test around four months after the start of the experiment (I’ve continued the lifestyle changes made during the experiment) and my total T had gone up again to 826.9 ng/dL.
During the second trimester, androgen level is associated with sex formation.[13] This period affects the femininization or masculinization of the fetus and can be a better predictor of feminine or masculine behaviours such as sex typed behaviour than an adult's own levels. A mother's testosterone level during pregnancy is correlated with her daughter's sex-typical behavior as an adult, and the correlation is even stronger than with the daughter's own adult testosterone level.[14]
Such sort of injuries varies in severity and extent of damage markedly from one person to the other and withdrawal of the drug/supplement coupled with proper medical attention suffice in terms of alleviating the symptoms.[8,12] This was observed in the present case. However, the liver injury observed here may not be confidently linked to product consumption as the subject later reported that the following recovery he consumed two more courses of the booster with no side effects. Tests performed following hospital discharge, and repeated use of the product showed AST and ALT to be slightly high, whereas the rest of the blood parameters tested appeared to be normal. The AST/ALT ratio is considered to be a very important parameter for the evaluation of liver diseases, such as non-alcoholic fatty liver disease,[13] though it is rarely considered alone. Overall, the evidence was inconclusive in the present work in terms of linking the use of a testosterone booster with liver injury. However, even though a single case report cannot establish causality with statistical power.[13] Further research on the usage of a commercial testosterone booster within large populations for a long period is necessary to investigate whether the symptoms shown in the present case were significantly present in other athletes consuming the same commercial product or not. To guarantee an optimal outcome with no severe side effects, further research is warranted to confirm the present findings and determine whether the effects observed in this case report would be statistically significant in larger samples.

The participants were seen every 4 weeks. Blood was taken to measure hormone levels, and questionnaires were given to assess physical function, health status, vitality, and sexual function. Body fat and muscle measurements were also taken at the beginning and end of the 16 weeks. The study was funded in part by NIH’s National Institute on Aging (NIA) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Results appeared in the September 12, 2013, issue of the New England Journal of Medicine.
In addition to conjugation and the 17-ketosteroid pathway, testosterone can also be hydroxylated and oxidized in the liver by cytochrome P450 enzymes, including CYP3A4, CYP3A5, CYP2C9, CYP2C19, and CYP2D6.[155] 6β-Hydroxylation and to a lesser extent 16β-hydroxylation are the major transformations.[155] The 6β-hydroxylation of testosterone is catalyzed mainly by CYP3A4 and to a lesser extent CYP3A5 and is responsible for 75 to 80% of cytochrome P450-mediated testosterone metabolism.[155] In addition to 6β- and 16β-hydroxytestosterone, 1β-, 2α/β-, 11β-, and 15β-hydroxytestosterone are also formed as minor metabolites.[155][156] Certain cytochrome P450 enzymes such as CYP2C9 and CYP2C19 can also oxidize testosterone at the C17 position to form androstenedione.[155]
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