As Sulbutiamine crosses the blood-brain barrier very easily, it has a positive effect on the cholinergic and the glutamatergic receptors that are responsible for essential activities impacting memory, concentration, and mood. The compound is also fat-soluble, which means it circulates rapidly and widely throughout the body and the brain, ensuring positive results. Thus, patients with schizophrenia and Parkinson’s disease will find the drug to be very effective.
In a broad sense, this is enhancement; in a stricter one, it’s optimisation. “I think people think about smart drugs the way they think about steroids in athletics,” Arnsten says, “but it’s not a proper analogy, because with steroids you’re creating more muscle. With smart drugs, all you’re doing is taking the brain that you have and putting it in its optimal chemical state. You’re not taking Homer Simpson and making him into Einstein.”
I largely ignored this since the discussions were of sub-RDA doses, and my experience has usually been that RDAs are a poor benchmark and frequently far too low (consider the RDA for vitamin D). This time, I checked the actual RDA - and was immediately shocked and sure I was looking at a bad reference: there was no way the RDA for potassium was seriously 3700-4700mg or 4-5 grams daily, was there? Just as an American, that implied that I was getting less than half my RDA. (How would I get 4g of potassium in the first place? Eat a dozen bananas a day⸮) I am not a vegetarian, nor is my diet that fantastic: I figured I was getting some potassium from the ~2 fresh tomatoes I was eating daily, but otherwise my diet was not rich in potassium sources. I have no blood tests demonstrating deficiency, but given the figures, I cannot see how I could not be deficient.
Results: Women with high caffeine intakes had significantly higher rates of bone loss at the spine than did those with low intakes (−1.90 ± 0.97% compared with 1.19 ± 1.08%; P = 0.038). When the data were analyzed according to VDR genotype and caffeine intake, women with the tt genotype had significantly (P = 0.054) higher rates of bone loss at the spine (−8.14 ± 2.62%) than did women with the TT genotype (−0.34 ± 1.42%) when their caffeine intake was >300 mg/d…In 1994, Morrison et al (22) first reported an association between vitamin D receptor gene (VDR) polymorphism and BMD of the spine and hip in adults. After this initial report, the relation between VDR polymorphism and BMD, bone turnover, and bone loss has been extensively evaluated. The results of some studies support an association between VDR polymorphism and BMD (23-,25), whereas other studies showed no evidence for this association (26,27)…At baseline, no significant differences existed in serum parathyroid hormone, serum 25-hydroxyvitamin D, serum osteocalcin, and urinary N-telopeptide between the low- and high-caffeine groups (Table 1⇑). In the longitudinal study, the percentage of change in serum parathyroid hormone concentrations was significantly lower in the high-caffeine group than in the low-caffeine group (Table 2⇑). However, no significant differences existed in the percentage of change in serum 25-hydroxyvitamin D
Articles and information on this website may only be copied, reprinted, or redistributed with written permission (but please ask, we like to give written permission!) The purpose of this Blog is to encourage the free exchange of ideas. The entire contents of this website is based upon the opinions of Dave Asprey, unless otherwise noted. Individual articles are based upon the opinions of the respective authors, who may retain copyright as marked. The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the personal research and experience of Dave Asprey and the community. We will attempt to keep all objectionable messages off this site; however, it is impossible to review all messages immediately. All messages expressed on The Bulletproof Forum or the Blog, including comments posted to Blog entries, represent the views of the author exclusively and we are not responsible for the content of any message.
My predictions were substantially better than random chance7, so my default belief - that Adderall does affect me and (mostly) for the better - is borne out. I usually sleep very well and 3 separate incidents of horrible sleep in a few weeks seems rather unlikely (though I didn’t keep track of dates carefully enough to link the Zeo data with the Adderall data). Between the price and the sleep disturbances, I don’t think Adderall is personally worthwhile.
Proteus Digital Health (Redwood City, Calif.) offers an FDA-approved microchip—an ingestible pill that tracks medication-taking behavior and how the body is responding to medicine. Through the company’s Digital Health Feedback System, the sensor monitors blood flow, body temperature and other vital signs for people with heart problems, schizophrenia or Alzheimer’s disease.
In addition, the cognitive enhancing effects of stimulant drugs often depend on baseline performance. So whilst stimulants enhance performance in people with low baseline cognitive abilities, they often impair performance in those who are already at optimum. Indeed, in a study by Randall et al., modafinil only enhanced cognitive performance in subjects with a lower (although still above-average) IQ.
Interesting. On days ranked 2 (below-average mood/productivity), nicotine seems to have boosted scores; on days ranked 3, nicotine hurts scores; there aren’t enough 4’s to tell, but even ’5 days seem to see a boost from nicotine, which is not predicted by the theory. But I don’t think much of a conclusion can be drawn: not enough data to make out any simple relationship. Some modeling suggests no relationship in this data either (although also no difference in standard deviations, leading me to wonder if I screwed up the data recording - not all of the DNB scores seem to match the input data in the previous analysis). So although the 2 days in the graph are striking, the theory may not be right.
Adrafinil is a prodrug for Modafinil, which means it can be metabolized into Modafinil to give you a similar effect. And you can buy it legally just about anywhere. But there are a few downsides. Patel explains that you have to take a lot more to achieve a similar effect as Modafinil, wait longer for it to kick in (45-60 minutes), there are more potential side effects, and there aren’t any other benefits to taking it.
Drugs and catastrophe are seemingly never far apart, whether in laboratories, real life or Limitless. Downsides are all but unavoidable: if a drug enhances one particular cognitive function, the price may be paid by other functions. To enhance one dimension of cognition, you’ll need to appropriate resources that would otherwise be available for others.
The general cost of fish oil made me interested in possible substitutes. Seth Roberts uses exclusively flaxseed oil or flaxseed meal, and this seems to work well for him with subjective effects (eg. noticing his Chinese brands seemed to not work, possibly because they were unrefrigerated and slightly rancid). It’s been studied much less than fish oil, but omega acids are confusing enough in general (is there a right ratio? McCluskey’s roundup gives the impression claims about ratios may have been overstated) that I’m not convinced ALA is a much inferior replacement for fish oil’s mixes of EPA & DHA.
Clearly, the hype surrounding drugs like modafinil and methylphenidate is unfounded. These drugs are beneficial in treating cognitive dysfunction in patients with Alzheimer's, ADHD or schizophrenia, but it's unlikely that today's enhancers offer significant cognitive benefits to healthy users. In fact, taking a smart pill is probably no more effective than exercising or getting a good night's sleep.
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.
First half at 6 AM; second half at noon. Wrote a short essay I’d been putting off and napped for 1:40 from 9 AM to 10:40. This approach seems to work a little better as far as the aboulia goes. (I also bother to smell my urine this time around - there’s a definite off smell to it.) Nights: 10:02; 8:50; 10:40; 7:38 (2 bad nights of nasal infections); 8:28; 8:20; 8:43 (▆▃█▁▂▂▃).
As already mentioned, AMPs and MPH are classified by the U.S. Food and Drug Administration (FDA) as Schedule II substances, which means that buying or selling them is a felony offense. This raises the question of how the drugs are obtained by students for nonmedical use. Several studies addressed this question and yielded reasonably consistent answers.
Those who have taken them swear they do work – though not in the way you might think. Back in 2015, a review of the evidence found that their impact on intelligence is “modest”. But most people don’t take them to improve their mental abilities. Instead, they take them to improve their mental energy and motivation to work. (Both drugs also come with serious risks and side effects – more on those later).
The peculiar tired-sharp feeling was there as usual, and the DNB scores continue to suggest this is not an illusion, as they remain in the same 30-50% band as my normal performance. I did not notice the previous aboulia feeling; instead, around noon, I was filled with a nervous energy and a disturbingly rapid pulse which meditation & deep breathing did little to help with, and which didn’t go away for an hour or so. Fortunately, this was primarily at church, so while I felt irritable, I didn’t actually interact with anyone or snap at them, and was able to keep a lid on it. I have no idea what that was about. I wondered if it might’ve been a serotonin storm since amphetamines are some of the drugs that can trigger storms but the Adderall had been at 10:50 AM the previous day, or >25 hours (the half-lives of the ingredients being around 13 hours). An hour or two previously I had taken my usual caffeine-piracetam pill with my morning tea - could that have interacted with the armodafinil and the residual Adderall? Or was it caffeine+modafinil? Speculation, perhaps. A house-mate was ill for a few hours the previous day, so maybe the truth is as prosaic as me catching whatever he had.
For 2 weeks, upon awakening I took close-up photographs of my right eye. Then I ordered two jars of Life-Extension Sea-Iodine (60x1mg) (1mg being an apparently safe dose), and when it arrived on 10 September 2012, I stopped the photography and began taking 1 iodine pill every other day. I noticed no ill effects (or benefits) after a few weeks and upped the dose to 1 pill daily. After the first jar of 60 pills was used up, I switched to the second jar, and began photography as before for 2 weeks. The photographs were uploaded, cropped by hand in Gimp, and shrunk to more reasonable dimensions; both sets are available in a Zip file.
Another interpretation of the mixed results in the literature is that, in some cases at least, individual differences in response to stimulants have led to null results when some participants in the sample are in fact enhanced and others are not. This possibility is not inconsistent with the previously mentioned ones; both could be at work. Evidence has already been reviewed that ability level, personality, and COMT genotype modulate the effect of stimulants, although most studies in the literature have not broken their samples down along these dimensions. There may well be other as-yet-unexamined individual characteristics that determine drug response. The equivocal nature of the current literature may reflect a mixture of substantial cognitive-enhancement effects for some individuals, diluted by null effects or even counteracted by impairment in others.
I can only talk from experience here, but I can remember being a teenager and just being a straight-up dick to any recruiters that came to my school. And I came from a military family. I'd ask douche-bag questions, I'd crack jokes like so... don't ask, don't tell only applies to everyone BUT the Navy, right? I never once considered enlisting because some 18 or 19 year old dickhead on hometown recruiting was hanging out in the cafeteria or hallways of my high school.Weirdly enough, however, what kinda put me over the line and made me enlist was the location of the recruiters' office. In the city I was living in at the time, the Armed Forces Recruitment Center was next door to an all-ages punk venue that I went to nearly every weekend. I spent many Saturday nights standing in a parking lot after a show, all bruised and bloody from a pit, smoking a joint, and staring at the windows of the closed recruiters' office. Propaganda posters of guys in full-battle-rattle obscured by a freshly scrawled Anarchy symbol or a collage of band stickers over the glass.I think trying to recruit kids from school has a child-molester-vibe to it. At least it did for me. But the recruiters defiantly being right next to a bunch of drunk and high punks, that somehow made it seem more like a truly bad-ass option. Like, sure, I'll totally join. After all, these guys don't run from the horde of skins and pins that descend every weekend like everyone else, they must be bad-ass.
^ 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. 9 (1): 8. doi:10.1186/1747-597X-9-8. ISSN 1747-597X. PMC 3928621. PMID 24484640.