I have elsewhere remarked on the apparent lack of benefit to taking multivitamins and the possible harm; so one might well wonder about a specific vitamin like vitamin D. However, a multivitamin is not vitamin D, so it’s no surprise that they might do different things. If a multivitamin had no vitamin D in it, or if it had vitamin D in different doses, or if it had substances which interacted with vitamin D (such as calcium), or if it had substances which had negative effects which outweigh the positive (such as vitamin A?), we could well expect differing results. In this case, all of those are true to varying extents. Some multivitamins I’ve had contained no vitamin D. The last multivitamin I was taking both contains vitamins used in the negative trials and also some calcium; the listed vitamin D dosage was a trivial ~400IU, while I take >10x as much now (5000IU).
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.
But there’s a surprising lack of skepticism in the room. That’s because this is a weekly meetup of amateur biohackers. In fact, positivity is one of their ground rules. Members share experiences with ketogenic diets, biofeedback apps, sensory-deprivation tanks, and, lately, a class of smart drugs known as “nootropics.” Their primary obsession is brain enhancement.
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.
Reason: More than 50 percent of your brain is comprised of DHA! Among a big group of elderly Americans, those with the highest blood levels of DHA were about half as apt to develop dementia and 39% as apt to develop Alzheimer’s as those with lower blood levels of DHA over a nine-year period. The top 25% of those with the highest blood DHA got about 180 mg DHA a day or three servings of fish a week, researchers said. In this study, the other major fatty acid in fish oil. EPA had no effect.
Breathing carefully, I clutched the Costco special edition family size 1.5-liter glass bottle of vodka and carefully extracted 10 milliliters with a miniature glass pipette, which I then transferred into a small amber glass bottle. Then, with my nine-year-old son’s tiny set of school scissors, I snipped exactly 1/10 of LSD from the blotter square I’d ordered from a psychedelic research chemical supplier website the week prior, with a cloaked browser, of course, so the feds didn’t come knocking at my door. I dropped the LSD into the bottle, gave it a thirty-second shake, then placed the bottle in the pantry, next to my protein powder and creatine. I smiled. Within 24 hours, I’d be ready to sample my first homemade, volumetric “microdose” of a drug reported to increase lateral thinking patterns, improve creativity, massively boost productivity and much, much more.
Eliminating foggy-headedness seems to be the goal of many users of neuroenhancers. But can today's drugs actually accomplish this? I recently posed this question to Chatterjee's colleague Martha Farah, who is a psychologist at Penn and the director of its Center for Cognitive Neuroscience. She is deeply fascinated by, and mildly critical of, neuroenhancers, but basically in favour - with the important caveat that we need to know much more about how these drugs work. While Farah does not take neuroenhancers, she had just finished a paper in which she reviewed the evidence on prescription stimulants as neuroenhancers from 40 laboratory studies involving healthy subjects. Most of the studies looked at one of three types of cognition: learning, working memory, and cognitive control. A typical learning test asks subjects to memorise a list of paired words; an hour, a few days, or a week later, they are presented with the first words in the pairs and asked to come up with the second. Neuroenhancers did improve retention, especially where subjects had been asked to remember information for several days or longer.
I have a needle phobia, so injections are right out; but from the images I have found, it looks like testosterone enanthate gels using DMSO resemble other gels like Vaseline. This suggests an easy experimental procedure: spoon an appropriate dose of testosterone gel into one opaque jar, spoon some Vaseline gel into another, and pick one randomly to apply while not looking. If one gel evaporates but the other doesn’t, or they have some other difference in behavior, the procedure can be expanded to something like and then half an hour later, take a shower to remove all visible traces of the gel. Testosterone itself has a fairly short half-life of 2-4 hours, but the gel or effects might linger. (Injections apparently operate on a time-scale of weeks; I’m not clear on whether this is because the oil takes that long to be absorbed by surrounding materials or something else.) Experimental design will depend on the specifics of the obtained substance. As a controlled substance (Schedule III in the US), supplies will be hard to obtain; I may have to resort to the Silk Road.
Ngo has experimented with piracetam himself (“The first time I tried it, I thought, ‘Wow, this is pretty strong for a supplement.’ I had a little bit of reflux, heartburn, but in general it was a cognitive enhancer. . . . I found it helpful”) and the neurotransmitter DMEA (“You have an idea, it helps you finish the thought. It’s for when people have difficulty finishing that last connection in the brain”).
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.
Because modafinil works in a manner similar to methylphenidate, it also bears similar risks. The improper dosage or abuse of modafinil may lead to the disrupted development of executive controls like decision-making and working memory. Modafinil’s effects may also depend upon the IQ of the taker. Two university studies determined that in a test of sustained attention, modafinil only improved cognition in the group with “lower” IQs. Although safer than other stimulants due to its milder effect on neurotransmitter levels, there are still risks associated with any kind of drug that affects dopaminergic neurotransmission, mostly because this can lead to addiction and, similar to a pornography user who needs increasingly fringe porn to achieve the same effect, can produce a resistance or lowered sensitivity to dopamine.
Even party drugs are going to work: Biohackers are taking recreational drugs like LSD, psilocybin mushrooms, and mescaline in microdoses—about a tenth of what constitutes a typical dose—with the goal of becoming more focused and creative. Many who’ve tried it report positive results, but real research on the practice—and its safety—is a long way off. “Whether microdosing with LSD improves creativity and cognition remains to be determined in an objective experiment using double-blind, placebo-controlled methodology,” Sahakian says.
The real culprit at the heart of the problem may be impossible to regulate – the human desire to have a supercharged brain. For now, this wish is still largely relegated to the domain of fiction. Researchers point out that increasing the power of certain parts of the brain, such as areas responsible for learning and focus, would likely deprive other parts of the brain that are needed to live. Despite the appeal of a super-brain, a better goal is still to maintain a balanced brain and lifestyle.
If I stop tonight and do nothing Monday (and I sleep the normal eight hours and do not pay any penalty), then that’ll be 4 out of 5 days on modafinil, each saving 3 or 4 hours. Each day took one pill which cost me $1.20, but each pill saved let’s call it 3.5 hours; if I value my time at minimum wage, or 7.25/hr (federal minimum wage), then that 3.5 hours is worth $25.37, which is much more than $1.20, ~21x more.
As with any thesis, there are exceptions to this general practice. For example, theanine for dogs is sold under the brand Anxitane is sold at almost a dollar a pill, and apparently a month’s supply costs $50+ vs $13 for human-branded theanine; on the other hand, this thesis predicts downgrading if the market priced pet versions higher than human versions, and that Reddit poster appears to be doing just that with her dog.↩
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.