Choline is a nootropic: it enhances your ability to pay attention and learn efficiently, probably because you use a lot of acetylcholine during mentally-demanding tasks, and choline helps you synthesize enough to work harder and go longer. Choline also links to decreased brain inflammation in a dose-dependent manner — the more choline you eat, the less inflamed your brain tends to be.
Dr Hart explained how communication between the gut and the brain is controlled via our immune system, our endocrine system (hormones) and our central nervous system, which are all under the influence of the bacteria in our gut. The types and amount of these bacteria, known as our gut microbiome, can be directly impacted by factors such as diet, stress, pollution and medications (2) and the composition of the microbiome is also understood to affect one’s susceptibility to food sensitivities and intolerances (3).
As a general class, nootropics are not usually addiction-forming. Two of the strongest hallmarks of addiction-forming drugs is that they cause users to develop dependency and experience withdrawal when the drug use is eliminated or reduced. While there are some reports of nootropic users experiencing brain fog after use is discontinued, these side effects are not considered to be akin to withdrawal effects of addiction-forming drugs.
My worry about the MP variable is that, plausible or not, it does seem relatively weak against manipulation; other variables I could look at, like arbtt window-tracking of how I spend my computer time, # or size of edits to my files, or spaced repetition performance, would be harder to manipulate. If it’s all due to MP, then if I remove the MP and LLLT variables, and summarize all the other variables with factor analysis into 2 or 3 variables, then I should see no increases in them when I put LLLT back in and look for a correlation between the factors & LLLT with a multivariate regression.
She speaks from professional and personal experience. When she first moved to the United States from Italy at age 24 she was struck by how shifting from the Mediterranean-style diet she grew up on to a standard American diet negatively impacted her physical health and work performance. The experience led her to more closely study nutrition and the link between diet and brain health. In this excerpt from a longer interview, she discusses the brain foods you should be eating.
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(In particular, I don’t think it’s because there’s a sudden new surge of drugs. FDA drug approval has been decreasing over the past few decades, so this is unlikely a priori. More specifically, many of the major or hot drugs go back a long time. Bacopa goes back millennia, melatonin I don’t even know, piracetam was the ’60s, modafinil was ’70s or ’80s, ALCAR was ’80s AFAIK, Noopept & coluracetam were ’90s, and so on.)
We all wish success came in a pill form. That was the premise of the hour and half Adderall commercial/ thriller film ‘Limitless’ starring Bradley Cooper. In the film he popped a transparent round pill and instantly his brain power skyrocketed- anything became possible. Most of us wished that pill existed- and now it does. Donepezil is a drug that is used to treat Alzheimers, but it’s effects on normal people make Adderall and Vyvanse look like a cup of coffee.
Caffeine dose dependently decreased the 1,25(OH)(2)D(3) induced VDR expression and at concentrations of 1 and 10mM, VDR expression was decreased by about 50-70%, respectively. In addition, the 1,25(OH)(2)D(3) induced alkaline phosphatase activity was also reduced at similar doses thus affecting the osteoblastic function. The basal ALP activity was not affected with increasing doses of caffeine. Overall, our results suggest that caffeine affects 1,25(OH)(2)D(3) stimulated VDR protein expression and 1,25(OH)(2)D(3) mediated actions in human osteoblast cells.
However, as a result of the efficacy of this type of stacking, the supplement world is saturated with brain-boosting blends, and it can be difficult to cut through the confusion and figure out what really works and what could be a waste of time and money, or downright dangerous. The fact is, when creating your own stack, you must carefully think about your specific needs and goals. For example, if you want to reduce anxiety and depression, but don’t necessarily care to enhance your cognitive performance or get through a day of work in a sleep-deprived state, you could just stick to a single nootropic that increases dopamine levels, such as Mucuna pruriens or tryptophan. Or if you wanted to reduce anxiety and depression while simultaneously improving your memory because you’re studying for a school or work exam, you could add Bacopa monnieri to the mucuna or tryptophan. Then, let’s say you want long-term cognitive performance to the mix that lasts an entire day: in this case, you’d add a racetam, and to avoid an end of day crash, a touch of choline or DHA. It’s a bit like cooking in the kitchen, isn’t it?
The main concern with pharmaceutical drugs is adverse effects, which also apply to nootropics with undefined effects. Long-term safety evidence is typically unavailable for nootropics. Racetams — piracetam and other compounds that are structurally related to piracetam — have few serious adverse effects and low toxicity, but there is little evidence that they enhance cognition in people having no cognitive impairments.