Dr. Lisa Mosconi, PhD, INHC, is the associate director of the Alzheimer's Prevention Clinic at Weill Cornell Medical College (WCMC)/NewYork-Presbyterian Hospital, where she was recruited as an associate professor of Neuroscience in Neurology. She also is an adjunct faculty member in the Department of Psychiatry at NYU School of Medicine, in the Department of Nutrition at NYU Steinhardt School of Nutrition and Public Health, and in the Departments of Neurology and Nuclear Medicine at the University of Florence (Italy). Formerly, Dr. Mosconi founded and was the director of the Nutrition & Brain Fitness Lab at New York University School of Medicine (NYU), and an assistant professor in the NYU Department of Psychiatry, where she served as the director of the Family History of Alzheimer's disease research program. Dr. Mosconi holds a dual PhD degree in Neuroscience and Nuclear Medicine from the University of Florence, Italy, and is a board certified integrative nutritionist and holistic healthcare practitioner. She is well known for her research on the early detection of Alzheimer's disease and is passionately interested in the mitigation and prevention of memory loss through lifestyle modifications including diet, nutrition, and physical and intellectual fitness.
This research is in contrast to the other substances I like, such as piracetam or fish oil. I knew about withdrawal of course, but it was not so bad when I was drinking only tea. And the side-effects like jitteriness are worse on caffeine without tea; I chalk this up to the lack of theanine. (My later experiences with theanine seems to confirm this.) These negative effects mean that caffeine doesn’t satisfy the strictest definition of nootropic (having no negative effects), but is merely a cognitive enhancer (with both benefits & costs). One might wonder why I use caffeine anyway if I am so concerned with mental ability.
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This looks interesting: the Noopept effect is positive for all the dose levels, but it looks like a U-curve - low at 10mg, high at 15mg, lower at 20mg, and even lower at 30mg 48mg and 60mg aren’t estimated because they are hit by the missingness problem: the magnesium citrate variable is unavailable for the days the higher doses were taken on, and so their days are omitted and those levels of the factor are not estimated. One way to fix this is to drop magnesium from the model entirely, at the cost of fitting the data much more poorly and losing a lot of R2:
Jump up ^ Sattler, Sebastian; Mehlkop, Guido; Graeff, Peter; Sauer, Carsten (February 1, 2014). "Evaluating the drivers of and obstacles to the willingness to use cognitive enhancement drugs: the influence of drug characteristics, social environment, and personal characteristics". Substance Abuse Treatment, Prevention, and Policy. BioMed Central Ltd. p. 8. doi:10.1186/1747-597X-9-8. ISSN 1747-597X. Retrieved April 5, 2014.
Cytisine is not known as a stimulant and I’m not addicted to nicotine, so why give it a try? Nicotine is one of the more effective stimulants available, and it’s odd how few nicotine analogues or nicotinic agonists there are available; nicotine has a few flaws like short half-life and increasing blood pressure, so I would be interested in a replacement. The nicotine metabolite cotinine, in the human studies available, looks intriguing and potentially better, but I have been unable to find a source for it. One of the few relevant drugs which I can obtain is cytisine, from Ceretropic, at 2x1.5mg doses. There are not many anecdotal reports on cytisine, but at least a few suggest somewhat comparable effects with nicotine, so I gave it a try.
In the study, which evaluated the eating habits and mental ability of more than 950 older adults for an average of five years, those adults who ate a serving of leafy green veggies once or twice a day experienced slower mental deterioration than those who ate no vegetables, even when factors like age, education and family history of dementia were factored in.
On 15 March 2014, I disabled light sensor: the complete absence of subjective effects since the first sessions made me wonder if the LED device was even turning on - a little bit of ambient light seems to disable it thanks to the light sensor. So I stuffed the sensor full of putty, verified it was now always-on with the cellphone camera, and began again; this time it seemed to warm up much faster, making me wonder if all the previous sessions’ sense of warmth was simply heat from my hand holding the LEDs
I tried taking whole pills at 1 and 3 AM. I felt kind of bushed at 9 AM after all the reading, and the 50 minute nap didn’t help much - I was sleep only around 10 minutes and spent most of it thinking or meditation. Just as well the 3D driver is still broken; I doubt the scores would be reasonable. Began to perk up again past 10 AM, then felt more bushed at 1 PM, and so on throughout the day; kind of gave up and began watching & finishing anime (Amagami and Voices of a Distant Star) for the rest of the day with occasional reading breaks (eg. to start James C. Scotts Seeing Like A State, which is as described so far). As expected from the low quality of the day, the recovery sleep was bigger than before: a full 10 hours rather than 9:40; the next day, I slept a normal 8:50, and the following day ~8:20 (woken up early); 10:20 (slept in); 8:44; 8:18 (▁▇▁▁). It will be interesting to see whether my excess sleep remains in the hour range for ’good modafinil nights and two hours for bad modafinil nights.
As you may or may not know, curcumin has become a darling of the nutrition world in the last several years, thanks to a flurry of research that indicates the turmeric derivative can do everything from support the brain to reduce painful body-wide inflammation to even support positive mood. You can learn more about the research behind curcumin here:
"In an era of confusion about what we should eat, Brain Food is a shining light. This is the straight story about 'neuro-nutrition' firmly rooted in research by a neuroscientist who has a deep understanding of how food affects our cognitive health. Dr. Mosconi gives us advice we can easily implement into our lives and a story about the science behind it that is both delightful and accessible. A must read!"
Systematic reviews and meta-analyses of clinical human research using low doses of certain central nervous system stimulants found enhanced cognition in healthy people. 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. Relatively high doses of stimulants cause cognitive deficits.