|Animal-based|| Glandular / Live Cell Therapy
Tribulus (Tribulus terrestris)
| ||In patients with below-normal serum testosterone levels, physiological levels were reached after treatment with Tribulus. Amongst patients with normal initial levels, the testosterone level was not significantly changed after treatment.|
A product called Forza-T combines Tribulus, 6-OXO and ZMA to increase testosterone levels.
Nettle (Urtica urens)
| ||A highly concentrated extract from the nettle root provides a unique mechanism for increasing levels of free testosterone. European research has identified constituents of nettle root that bind to SHBG in place of testosterone, thus reducing SHBG's binding of free testosterone. |
As the authors of one study state: "these constituents of nettle root may influence the blood level of free, i.e. active, steroid hormones by displacing them from the SHBG bindings site"
Licorice Root (Glycyrrhiza glabra)
| ||17 healthy males between 22 and 24 years of age consumed 7g/day of licorice tablets containing 7.6% glycyrrhizic acid over a 7-day period. On days 4 and 8, serum testosterone levels were decreased by 25%, with an increase in 17-hydroxyprogesterone and luteinizing hormone, and a slight but not significant reduction in free testosterone. [Exp Clin Endocrinol Diabetes. 2003;111: pp.341-343]|
High Fat Diet
| ||A Swedish study showed that switching from a high-fat to a low-fat diet lowered blood testosterone levels by 10 percent.|
Conventional Drugs / Information
| ||The most commonly used aromatase inhibitor in bodybuilding is aminoglutethimide (Cytadren). This drug also inhibits an enzyme (desmolase) necessary for synthesis of cortisol, but fortunately, aromatase can be inhibited with levels of drug that cause only limited inhibition of desmolase.|
For an average male, a dose of 250mg per day (one tablet) appears optimal. The half-life is 8 hours, so the drug is better taken in divided doses. The best plan seems to be to take half a tablet on arising, and quarter tabs six and twelve hours later. This keeps levels generally fairly constant, but allows a small drop in the hours shortly before arising, which is then compensated for by the higher dose on arising. With this scheme, inhibition of cortisol production is generally too low to be noticed, and generally there is no rebound effect on discontinuance. However it is not a bad idea nonetheless to taper off, first omitting the midday quarter tab dose for a few days, then omitting both quarter tab doses, then reducing the initial dose to one quarter tab, and then ending completely. A week is sufficient for the taper.
Some people suffer a degree of lethargy or sedation from aminoglutethimide, even at this low dose, but most do not. Anastrozole (Arimidex) is a superior aromatase inhibitor which does not have these side effects. It is, however, very expensive. With moderate doses of testosterone it seems that 1mg per day is sufficient, and some have claimed half a tab to be sufficient.
Aromatization is the process of converting testosterone to estrogens. This process increases with age. Aromatase blockers include prescription medication such as Arimidex (anastrozole), Aromasin (exemestane), Femara (letrozole), Nolvadex (tamoxifen), and Faslodex (fulvestrant). Nonprescription items such as Chrysin, Tribulus, DHEA, and Vitamin D can reduce estrogen levels and enhance testosterone levels. If these fail to increase free testosterone and lower excess estradiol, then ask your doctor to prescribe the potent aromatase inhibiting drug Arimidex (anastrozole) in the very low dose of 0.5mg, twice per week. Arimidex reduced estradiol by approximately 70% within 24 hours and by approximately 80% after 14 days of daily use.
| ||In a study published in Biochemical Pharmacology (1999, Vol.58), the specific mechanisms of chrysin's absorption impairment were identified. It was found that the addition of a pepper extract (piperine) significantly enhances the bioavailability of chrysin. Studies have found that when chrysin is combined with piperine, reductions in serum estrogen (estradiol) and increases in total and free testosterone result in 30 days.|
Diindolylmethane DIM / Indole 3 Carbinol IC3
| ||The bulk of evidence indicates that DIM and IC3, though similar, can have differing effects on free testosterone and estrogen levels. Overall, these items may have the opposite effect of what is desired - increased free testosterone and reduced estrogens.|
One contributor concluded:
I have not found any research to support DIM inhibiting Aromatase activity, in fact in may increase Aromatase activity. There is research to support that DIM increases conversion of some estrogen hormones into their estrogen metabolites. This reduction in estrogen hormones down regulates testosterone conversion to DHT, and DHT is an inhibitor of aromatase activity therefore aromatase activity increases. It is important to understand that estrogen also plays a role in total testosterone levels as increased levels of estrogen increases SHBG which binds free testosterone. Also decreased levels of estrogen increases LH and FSH which increases testosterone production and should result in higher free testosterone, but this will not result in higher total levels of testosterone due to decreased SHBG. Also keep in mind that if testosterone production is turned on high, the body may not produce enough DHEA to meet this new found demand.
Taking DIM should result in:
Lower Total Testosterone
Higher LH and FSH
Higher Free Testosterone (Unless Aromatase activity is to high, and is also subject sufficient DHEA production)
Clinical studies using testosterone injections, creams, or patches have often failed to provide a long-lasting, libido-enhancing effect in aging men. This is because testosterone can be converted to estrogen. The estrogen is then taken up by testosterone receptor sites in cells throughout the body. When an estrogen molecule occupies a testosterone receptor site on a cell membrane, it blocks the ability of serum testosterone to induce a healthy hormonal signal. It does not matter how much serum free testosterone is available if excess estrogen is competing for the same cellular receptor sites.
| ||Androstenedione is a metabolite of DHEA and a natural precursor of testosterone. 25 to 50mg of androstenedione taken at bedtime, and perhaps again first thing in the morning, will mimic the body's normal diurnal rhythm of testosterone. |
This same dose may be taken 30 to 60 minutes before exercise to enhance performance, or after completion of exercise to enhance muscle recovery and growth. Serum levels of testosterone start rising about 15 minutes after oral administration and stay elevated for around 3 hours. Blood testosterone levels usually peak in around 1 to 1.5 hours after ingestion. Because the elevated testosterone levels swiftly return to normal baseline levels, there is little risk of negative feedback suppression of your usual testosterone levels.
Test Testosterone Levels
Test / Monitor Hormone levels
| ||The Testosterone Syndrome by Dr. Eugene Shippen and William Fryer. In this inexpensive paperback, they successfully demonstrate that testosterone replacement has made significant improvements in the symptoms of male menopause, and they discuss the role of testosterone in men's overall health.|
| ||Researchers at Stanford�s School of Medicine wanted to see what vitamin D�s active form, calcitriol, would do regarding breast cancer. What they found was that calcitriol reduced aromatase expression in two ways � firstly, by directly suppressing its transcription at the gene level i.e. reducing how much of it is produced by the body. And secondly, by suppressing Cyclooxygenase-2 (COX-2), a pro-inflammatory pathway, and increasing 15-Hydroxyprostaglandin Dehydrogenase (15-PGDH), an anti-inflammatory pathway. |
Combined, this effect reduces the levels of local prostaglandins including Prostaglandin E2 (PGE2), which is a major stimulator of aromatase transcription. They also found that calcitriol downregulates the expression of estrogen receptor alpha (Era) in breast cancer cells, therefore reducing the effects of estrogen signalling at the receptor level. [Krishnan AV, Swami S, Feldman D. Vitamin D and breast cancer: Inhibition of estrogen synthesis and signaling. J Steroid Biochem Mol Biol. 2010 Feb 13.]