So with these 8 results in hand, what do I think? Roughly, I was right 5 of the days and wrong 3 of them. If not for the sleep effect on #4, which is - in a way - cheating (one hopes to detect modafinil due to good effects), the ratio would be 5:4 which is awfully close to a coin-flip. Indeed, a scoring rule ranks my performance at almost identical to a coin flip: -5.49 vs -5.5420. (The bright side is that I didn’t do worse than a coin flip: I was at least calibrated.)
Take the synthetic nootropic piracetam, for example. Since piracetam has been shown to improve cell membrane function and cause a host of neuroprotective effects, when combined with other cell membrane stabilizing supplements such as choline and DHA, the brain cells on piracetam can better signal and relay messages to each other for a longer period of time, which improves cognition and brain activity and decreases risk of a crash. So one example of an intelligent “stack” is piracetam taken with choline and DHA.

By the way, since I’ll throw around the term a few more times in this article, I should probably clarify what an adaptogen actually is. The actual name adaptogen gives some hint as to what these fascinating compounds do: they help you to adapt, specifically by stimulating a physiological adaptive response to some mild, hormesis-like stressor. A process known as general adaptation syndrome (GAS) was first described by the 20th-century physician and organic chemist Hans Selye, who defined GAS as the body’s response to the demands placed upon it. When these demands are excessive and consistent, it can result in the common deleterious symptoms now associated with long-term exposure to chronic stress. GAS is comprised of an alarm stage (characterized by a burst of energy), a resistance stage (characterized by resistance or adaptation to the stressor), and – in the case of excessive and chronic stress – an exhaustion stage (characterized by energy depletion). Adaptogens are plant-derived compounds capable of modulating these phases of GAS by either downregulating stress reactions in the alarm phase or inhibiting the onset of the exhaustion phase, thus providing some degree of protection against damage from stress.
The benefit of sequential analysis here is being able to stop early, conserving pills, and letting me test another dosage: if I see another pattern of initial benefits followed by decline, I can then try cutting the dose by taking one pill every 3 days; or, if there is a benefit and no decline, then I can try tweaking the dose up a bit (maybe 3 days out of 5?). Since I don’t have a good idea what dose I want and the optimal dose seems like it could be valuable (and the wrong dose harmful!), I can’t afford to spend a lot of time on a single definitive experiment.
In this large population-based cohort, we saw consistent robust associations between cola consumption and low BMD in women. The consistency of pattern across cola types and after adjustment for potential confounding variables, including calcium intake, supports the likelihood that this is not due to displacement of milk or other healthy beverages in the diet. The major differences between cola and other carbonated beverages are caffeine, phosphoric acid, and cola extract. Although caffeine likely contributes to lower BMD, the result also observed for decaffeinated cola, the lack of difference in total caffeine intake across cola intake groups, and the lack of attenuation after adjustment for caffeine content suggest that caffeine does not explain these results. A deleterious effect of phosphoric acid has been proposed (26). Cola beverages contain phosphoric acid, whereas other carbonated soft drinks (with some exceptions) do not.

When many of us think of memory enhancers, we think of ginkgo biloba, the herb that now generates more than $240 million in sales a year worldwide. The October 22-29, 1997 issue of the Journal of the American Medical Association reported that Alzheimer's patients who took 120 mg of ginkgo showed small improvements in tests designed to measure mental performance.

Systematic reviews and meta-analyses of clinical human research using low doses of certain central nervous system stimulants found enhanced cognition in healthy people.[21][22][23] In particular, the classes of stimulants that demonstrate cognition-enhancing effects in humans act as direct agonists or indirect agonists of dopamine receptor D1, adrenoceptor A2, or both types of receptor in the prefrontal cortex.[21][22][24][25] Relatively high doses of stimulants cause cognitive deficits.[24][25]

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