Rest In Peace (17/6/1925 - 2/6/2014)
Tuesday, April 22, 2014
Sunday, October 20, 2013
Gamma Oryzanol ("Gamma-O") is a highly lipophilic sterol-like compound extracted from rice bran oil. It is used in various supplements with the belief that it increases testosterone by elevating Luteinizing Hormone (LH).
Evidence that it increases Testosterone or LH
In 1997, a placebo-controlled study was performed that examined gamma oryzanol supplementation in resistance trained men (1). The treatment group received 500 mg of gamma oryzanol for 9 weeks. Tested variables were 1 repetition max's of bench press and squat, as well as vertical jump power. No differences were seen between groups (placebo vs. gamma oryzanol). They also tested various laboratory parameters including testosterone, estrogen, cortisol, and cholesterol ratios. Again, no differences between groups were seen.
Is Lipophilicity a Problem?
Could lack of absorption be the reason why Gamma Oryzanol failed to effect testosterone and muscular strength in men? One of the most recent companies to market this product claims this is indeed the case. As a highly lipophilic compound, Gamma Oryzanol would need to be properly emulsified for gastrointestional absorption. A 1991 study found <5% absorption of phytosterols similar to gamma oryzanol when fed to rats by mouth (2). In order to circumvent the absorption problem, they then administered gamma oryzanol to rats through IV (intravenous) or subq (subcutaneous) and examined its effects on Luteinizing Hormone, and Growth Hormone (GH). Unexpectedly, they found that Gamma Oryzanol actually decreased LH, and GH. Interestingly, it also decreased the release of various catecholamines, including dopamine. The authors concluded:
"Although it hasn't been directly measured, this metabolic milieu...may actually reduce testosterone production."
- Gamma Oryzanol does not increase testosterone, or increase muscular strength in humans
- In rats, IV or subq administration actually decrease testosterone and growth hormone
- Its lack of absorption is probably a good thing
Friday, September 27, 2013
Sulbutiamine is a synthetic thiamine derivative designed to overcome thiamine’s inherently poor bioavailability. It was designed in the 70’s in Japan in response to widespread thiamine deficiency. Later studies revealed that it had a significant effect on treating asthenia, a type of centrally mediated fatigue.
Sulbutiamine is a lipid soluble analogue of thiamine which has been demonstrated to increase thiamine levels in tissue. Unfortunately, very little human pharmacokinetic data exists. Studies published from Servier, the French manufacturer of sulbutiamine, indicate that peak plasma levels of sulbutiamine...
Wednesday, August 14, 2013
Galantamine is by far my favorite nootropic. Not only is it a mild acetylcholinesterase inhibitor, it also positively modulates the alpha 7 nicotinine acetylcholine receptor. The end effect is a global increase in acetylcholine levels and the facilitation of the activation of the particular type of receptor intimately involved in learning and memory.
The strength of AchE inhibition is directly proportional to the reciprocal increase in the amount of acetylcholinesterase present. In other words, the stronger you inhibit the enzyme, the more the body produces to counteract its absence. This has been quantified in studies examining this effect with galantamine in comparison to donepezil, which saw much greater AchE enzyme elevation with donepezil. This isn't surprising since donepezil is roughly 40-300 times more potent at inhibiting this enzyme . In the context of Alzheimer's disease, or other forms of dementia, this fact is relatively unimportant since the user will continue to supplement with the AchE inhibitor until death. Conversely, for a healthy individual using an AchE inhibitor for a relatively shorter amount of time, this may result in fairly significant rebound once supplementation ceases. This effect would be considerably more muted when supplementing with galantamine, especially since nootropic effects can be seen with doses much smaller then what is required to inhibit AchE.