Conversely, you have to consider that the long term effects of Modafinil haven’t been studies very well. It significantly upsets sleep cycles, and 50% of Modafinil users report a number of short term side effects, such as mild to severe headaches, insomnia, nausea, anxiety, nervousness, hypertension, decreased appetite, and weight loss. PET scans show it affects the same areas of the brain that are stimulated by substance abuse.
Like caffeine, nicotine tolerates rapidly and addiction can develop, after which the apparent performance boosts may only represent a return to baseline after withdrawal; so nicotine as a stimulant should be used judiciously, perhaps roughly as frequent as modafinil. Another problem is that nicotine has a half-life of merely 1-2 hours, making regular dosing a requirement. There is also some elevated heart-rate/blood-pressure often associated with nicotine, which may be a concern. (Possible alternatives to nicotine include cytisine, 2’-methylnicotine, GTS-21, galantamine, Varenicline, WAY-317,538, EVP-6124, and Wellbutrin, but none have emerged as clearly superior.)
Mercury exposure is among several other heavy metals, such as lead, aluminium and cadmium, that have been implicated in the aetiology of ADHD. Childhood exposure to mercury is predominantly through the consumption of seafood, dental amalgams and vaccines containing thimerosal. The reason why mercury can be so problematic, as well as other metals, is that it is capable of breaching the blood brain barrier. This is the brain’s ‘high fortress’, an intelligent gateway system that filters through molecules that are needed in the brain such as cells, nutrients and signalling molecules, and filters out pathogens and toxins.
The low-carb & high-fat diet (includes keto-diet) are not good for you because the brain needs glucose for fuel. It can burn fat. But, the brain’s preferred energy source is glucose. The key is to provide the brain with glucose without raising glucose/serum blood level. You do that by avoiding sugar and eating complex carbohydrates (fresh produce) that convert into glucose.
The body has its own inherent detoxification pathways that are responsible for packaging and removing heavy metals safely from the system. For example, glutathione is known as the body’s ‘master antioxidant’ and aside from playing an important role in preventing free radicals from causing damage to the body’s cells, it also helps to bind to heavy metals and remove them from the body. Research shows that glutathione levels are lower than normal in those on the autism spectrum, so enhancing levels through the diet may be an effective way to prevent the accumulation of heavy metals. Consuming sulfur-rich foods such as broccoli, cabbage, onions, garlic, kale and cauliflower can boost glutathione levels, as well as milk thistle, which has unique flavonoids that also support glutathione production.
I noticed what may have been an effect on my dual n-back scores; the difference is not large (▃▆▃▃▂▂▂▂▄▅▂▄▂▃▅▃▄ vs ▃▄▂▂▃▅▂▂▄▁▄▃▅▂▃▂▄▂▁▇▃▂▂▄▄▃▃▂▃▂▂▂▃▄▄▃▆▄▄▂▃▄▃▁▂▂▂▃▂▄▂▁▁▂▄▁▃▂▄) and appears mostly in the averages - Toomim’s quick two-sample t-test gave p=0.23, although a another analysis gives p=0.138112. One issue with this before-after quasi-experiment is that one would expect my scores to slowly rise over time and hence a fish oil after would yield a score increase - the 3.2 point difference could be attributable to that, placebo effect, or random variation etc. But an accidentally noticed effect (d=0.28) is a promising start. An experiment may be worth doing given that fish oil does cost a fair bit each year: randomized blocks permitting an fish-oil-then-placebo comparison would take care of the first issue, and then blinding (olive oil capsules versus fish oil capsules?) would take care of the placebo worry.
Evidence in support of the neuroprotective effects of flavonoids has increased significantly in recent years, although to date much of this evidence has emerged from animal rather than human studies. Nonetheless, with a view to making recommendations for future good practice, we review 15 existing human dietary intervention studies that have examined the effects of particular types of flavonoid on cognitive performance. The studies employed a total of 55 different cognitive tests covering a broad range of cognitive domains. Most studies incorporated at least one measure of executive function/working memory, with nine reporting significant improvements in performance as a function of flavonoid supplementation compared to a control group. However, some domains were overlooked completely (e.g. implicit memory, prospective memory), and for the most part there was little consistency in terms of the particular cognitive tests used making across study comparisons difficult. Furthermore, there was some confusion concerning what aspects of cognitive function particular tests were actually measuring. Overall, while initial results are encouraging, future studies need to pay careful attention when selecting cognitive measures, especially in terms of ensuring that tasks are actually sensitive enough to detect treatment effects.
The use of cognition-enhancing drugs by healthy individuals in the absence of a medical indication spans numerous controversial issues, including the ethics and fairness of their use, concerns over adverse effects, and the diversion of prescription drugs for nonmedical uses, among others. Nonetheless, the international sales of cognition-enhancing supplements exceeded US$1 billion in 2015 when global demand for these compounds grew.