Vitamin D3: Vitamin D3 is actually more hormone than it is a vitamin. Vitamin D is taken in by around 10% of our diets and D3 is mostly absorbed from the sun, which can be linked to greater testosterone production. The link between the two is a result from the luteinizing hormone playing its role. Read more about how vitamin D3 effects testosterone — the evidence is staggering.
I’m currently 64 y.o. After close to 10 years of twice-weekly injections of 20 units of testosterone cypionate my PSA gradually increased from 4.4 to more than 16. My urologist has performed 4 biopsies and one prostate MRI over that time, all of them negative. The last was 15 months ago. Early last year, after my fluctuating PSA reached 16, I discontinued the injections for about 6 months. My PSA dropped back to 6.1, and by the end of that time, my testosterone levels were about 240 but my libido seemed almost non-existent. I resumed the injections at a reduced level, 15 units, and 3 months later, the testosterone level was in the 700 range but the PSA was back to 16. My doctor told me to discontinue the injections pending another biopsy when I’m 65 in June.(I can’t afford another one immediately because of a high insurance deductible and previous family medical bills.) I am now gradually reducing the injections to 10 units once weekly, in hopes of limiting the withdrawal. Am I playing with fire or doing the right thing and have you had other patients with similar histories?
The overweight men participated in one German study. The first group of the participants used a placebo for one year. The second group of the participants consumed vitamin D3. All the participants aspired to shed excessive weight. Those men who took this vitamin lost up to 6 kg of unwanted weight. Also, they got the additional bonus; that is, the increase in testosterone production by about 25%.4
If your need is greater though, there are other legal options to consider. DHEA is a precursor steroid hormone that is only available on prescription in the UK, but if taken under close supervision it can have dramatic effects. It must be taken under supervision though because too high a dose can cause mood changes and aggression — roid rage, in other words — as well as all the other unwanted by-products of too much testosterone.
Both testosterone and 5α-DHT are metabolized mainly in the liver. Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively. An additional 40% of testosterone is metabolized in equal proportions into the 17-ketosteroids androsterone and etiocholanolone via the combined actions of 5α- and 5β-reductases, 3α-hydroxysteroid dehydrogenase, and 17β-HSD, in that order. Androsterone and etiocholanolone are then glucuronidated and to a lesser extent sulfated similarly to testosterone. The conjugates of testosterone and its hepatic metabolites are released from the liver into circulation and excreted in the urine and bile. Only a small fraction (2%) of testosterone is excreted unchanged in the urine.
A related issue is the potential use of testosterone as a coronary vasodilator and anti-anginal agent. Testosterone has been shown to act as a vasodilator of coronary arteries at physiological concentrations during angiography (Webb, McNeill et al 1999). Furthermore men given a testosterone injection prior to exercise testing showed improved performance, as assessed by ST changes compared to placebo (Rosano et al 1999; Webb, Adamson et al 1999). Administration of one to three months of testosterone treatment has also been shown to improve symptoms of angina and exercise test performance (Wu and Weng 1993; English et al 2000; Malkin, Pugh, Morris et al 2004). Longer term studies are underway. It is thought that testosterone improves angina due its vasodilatory action, which occurs independently of the androgen receptor, via blockade of L-type calcium channels at the cell membrane of the vascular smooth muscle in an action similar to the dihydropyridine calcium-channel blockers such as nifedipine (Hall et al 2006).
This has become a common practice despite an Institute of Medicine (IOM) report issued in 2003, indicating insufficient evidence of any benefit derived from testosterone hormone therapy to address expected symptoms of male aging.4 These studies, and 2 others (to be presented in a separate EW research brief) come on the heels of research on the efficacy of prescribing testosterone5 that appeared in the NEJM last year.
Finally, we looked at the proprietary blends of our remaining boosters, and dug into their ingredient lists. Supplements frequently include ingredients known for their “folk-lore” value; they’re believed to work, even when there isn’t any scientific background to prove it. Though we didn’t ding points if an ingredient wasn’t proven to be good (just so long as it wasn’t proven to be bad), we didn’t want to include any ingredient with evidence of causing harm.
In 1927, the University of Chicago's Professor of Physiologic Chemistry, Fred C. Koch, established easy access to a large source of bovine testicles — the Chicago stockyards — and recruited students willing to endure the tedious work of extracting their isolates. In that year, Koch and his student, Lemuel McGee, derived 20 mg of a substance from a supply of 40 pounds of bovine testicles that, when administered to castrated roosters, pigs and rats, remasculinized them. The group of Ernst Laqueur at the University of Amsterdam purified testosterone from bovine testicles in a similar manner in 1934, but isolation of the hormone from animal tissues in amounts permitting serious study in humans was not feasible until three European pharmaceutical giants—Schering (Berlin, Germany), Organon (Oss, Netherlands) and Ciba (Basel, Switzerland)—began full-scale steroid research and development programs in the 1930s.
Sprinting has been shown numerous times that it has positive effects on testosterone levels. One 2011 study (ref 84) looked at weightlifters who performed 4x35m sprints twice a week. In contrast to the control group (who continued lifting but did not sprint), it was found that “After the 4-week training program, total testosterone and the total testosterone/cortisol ratio increased significantly in the (sprinters) EXP group”.