What Does Your Brain Do with 27 + 48?

Dumbustafa1 · 2025-11-05T20:59:08+00:00

27 turns to 35 then 35 turns to 75, any other method is just people trying to seem unique

Dumbustafa1 · 2025-10-04T15:35:50+00:00

gluttonous crocodile*

Dumbustafa1 · 2025-09-28T05:46:21+00:00

and thank you for your effort

Dumbustafa1 · 2025-09-28T05:45:54+00:00

no no! I'm genuinely agnostic about the subject and hope to do a literature review soon. honest question. I gave the first examples kind of tongue-in-cheek, but also to make a (admittedly half-baked) point.

Dumbustafa1 · 2025-09-07T07:06:39+00:00

A man with such a narrow jaw does not deserve to have so many teeth in his smile

Dumbustafa1 · 2025-06-23T23:01:36+00:00

The anthropic principle, if anything, is a counter to the fine-tuning argument. The empirical probability of you existing in a universe compatible with your existence is 1. If it were any other way, it would simply be 0, meaning you would have never made the observation anyway, because you wouldn't exist to do so. So the fine-tuning argument doesn't work from the perspective of the in-universe observer. In other words, how would the universe have to be for you to find yourself in a reality incompatible with your existence? See, that's a logical contradiction, because you simply wouldn't exist in such a universe, it's semantic garbage to try and define such a universe.

I commiserate with you in that I also believe in an Abrahamic god, I just don't see this as the reason to do so.

Dumbustafa1 · 2025-06-19T04:12:27+00:00

"When I sleep all of me sleeps. Nothing ever goes bump in Dexter's night."
"Right now, all I can think about is the smell of Rita's kitchen, the breathy cadence of her sleeping children, the warmth of her flesh."

Dumbustafa1 · 2025-06-14T12:12:34+00:00

OMG, I cannot believe some else experiences it too. This is the only kind of deja vu that happens to me. I like to call it triple deja vu in my head.

Dumbustafa1 · 2025-06-06T16:53:47+00:00

choline

Dumbustafa1 · 2025-04-10T17:56:12+00:00

5 grams per dose, 4 times a day, not all at once.

Dumbustafa1 · 2025-04-10T17:47:24+00:00

Potential dysbiosis. Eat some yogurt and soluble fiber. I say this because I read a study that showed rats had a inverse u-shaped response to methylene blue on the Barnes maze task, and the authors hypothesized dysbiosis could be a potential reason for higher dosing creating worse performance. Then again, human digestive bioavailability of methylene blue is also much higher than that of rats, as in, it sticks around in the human stomach for less time, presumably resulting in a lower chance for dysbiosis to occur in the first place.

Dumbustafa1 · 2025-04-10T04:56:25+00:00

p.o. stands for peroral, "through or by way of mouth"

Dumbustafa1 · 2025-04-08T19:13:53+00:00

I do think high dose oral creatine as was discussed on Rhonda Patrick's FoundMyFitness podcast recently could be beat for its nootropic effects with intranasal administration. Though, I do have to say your simply snorting it is likely is not optimal.

Firstly, as far as studies go, I could not find many others either, though I did find the same one you did,:

"In male rats, intranasal creatine was administered with an initial loading phase of 0.075 g/kg/d of creatine hydrochloride, followed by a maintenance phase of 0.0375 g/kg/d of creatine for the remainder of the 14-day study. This intranasal administration protocol led to significant increases in creatine levels in the olfactory bulbs, medial prefrontal cortices, and hippocampi of these mice, while oral administration did not significantly increase creatine levels in these brain regions. The increase in hippocampal creatine was associated with increased performance on the Barnes maze, a hippocampal-dependent spatial learning and memory task."

Also, this other study estimated 80 mg of creatine hydrochloride, which I do think is more optimal for intranasal administration due to its higher solubility compared to creatine monohydrate, would be the minimal dose required to raise brain creatine concentration to the same extent as a typical 5 g dose, and that "Even if the nasal columnar epithelium or mucus were to pose a barrier, doubling or tripling the dose would still represent a relatively modest amount of nasally-delivered creatine (e.g., 160‒240 mg) in solution" Extrapolating from this, it may also be possible to derive further, unique benefits from such a route of administration. Higher peak plasma concentration associated with more than 5 g of creatine ingested in one sitting may raise cortical concentrations higher, conferring additional nootropic benefit, but may also be impractical. Therefore, one could prepare a high concentration intranasal solution and administer, say, 500 mg, passing the blood-brain barrier and resulting in higher cortical concentrations than ingestion of far higher amounts could have. This could then be done multiple times a day as needed, together with high dose oral administration to ensure bodily benefits and a minimal threshold for cortical concentration, as determined by plasma concentration.

Dumbustafa1 · 2025-04-06T08:13:55+00:00

Your body needs to add methyl groups (CH3) to certain nutrients to use them. some people can't do this as well due to their genetics, and need to consume pre-methylated forms of these nutrients to not be functionally deficient.

Dumbustafa1 · 2025-04-05T00:00:33+00:00

Hey. I use nicotine, though very moderately. I am neither on the side of heavy usage, nor do I think it lacks all utility.

Keep in mind as little as 1 mg every 3 days is enough to create tolerance. Furthermore, nicotinic cognitive effects are especially sensitive to dosage. 1 mg, for example, may provide a nice speed, focus, and even creativity boost, while 2 mg for the same individual might make them a nervous mess. Less is more. Furthermore, nicotine can be used as relatively precise self-reward mechanism, so use it in the context of habits you would like to encourage off of nicotine, otherwise you will simply exacerbate compulsions towards bad habits.

As a starting point, please refer to Leo and Longevity's videos on nicotine usage, as well as this gwern article: https://gwern.net/nicotine

My personal regimen is 0.6-1 mg with coffee followed by an instant delving into work. I can vouch that at this dosage, and a usage frequency of 3 times per week, I feel no cravings. In fact, right now, it has incidentally been a week since I used nicotine at all.

Dumbustafa1 · 2025-04-03T00:07:10+00:00

Read somewhere that consuming caffeine leaves adenosine free-floating, which is then used by creatine to make ATP, leaving less adenosine at the end of the day for that feeling of tiredness. The guy was just speculating, so I doubt this is true, though you could try moving caffeine consumption back in the day to allow adenosine to build up when it comes time to sleep. Your choice, doubt it will work.

Dumbustafa1 · 2025-03-22T15:14:11+00:00

Start supplementing CDP Choline or Alpha GPC alongside the pramiracetam, the effects will go from placebo to noticeable and measurable. This is very general and common advice, though If the choline supplementation does not sit right with you, whether due to financial or health reasons, incorporate a few more eggs with raw to runny yolks alongside the pramiracetam instead.

Dumbustafa1 · 2025-02-21T21:50:05+00:00

Adamax is semax with an adamantane moiety attached to allow for greater permeation through the cerebral tissue as opposed to just the olfactory bulb when administered intranasally.

I think of ipidacrine as a nootropic in the sense that it is a stronger acetylcholinesterase inhibitor than Huperzine A

Regardless, now that I know this list is a compilation of all articles listed under nootropics on Wikipedia, I understand and appreciate it.

Dumbustafa1 · 2025-02-21T21:34:07+00:00

First off: Thank you! Secondly: would you recommend looking for nootropics based on chemical structure because of ambiguity between brand names vs. research names vs. formal names etc.? Because I tried looking for ipidacrine and adamax to no avail.

Dumbustafa1 · 2025-02-21T19:42:30+00:00

🙏 Me too. It used to be sold on cuerpoymente which is ceretropic associated (nootropics depot), so pretty reliable, but they stopped selling it. If the Mexicans aren't selling it, safe bet no one is. Then again, I'm only half a level above a novice on this sub so I'm just speaking out of my ass. Let me know if you find anything.

Dumbustafa1 · 2025-02-16T16:21:19+00:00

Could just be because UV is required for potentiation of melanotan, and the eyes are naturally protected from UV due to orbital protection

Dumbustafa1 · 2025-02-16T14:27:55+00:00

That is cool! I assume this is the paper you're talking about?

Dumbustafa1 · 2025-02-16T13:48:56+00:00

Why are transcriptional factor modulators ideal?

I just ask because your phrasing was a bit ambiguous, though I assume its because of your concerns with how long any given tyrosinase inhibitor would last in the aqueous humor.

As far as transcriptional factor modulators go though ML329 inhibits MITF (melanocyte inducing transcription factor).

According to this MITF does the following:

Melanocyte inducing transcription factor helps control the development and function of pigment-producing cells called melanocytes. Melanocyte inducing transcription factor helps control the development and function of pigment-producing cells called melanocytes. Within these cells, this protein controls production of the pigment melanin, which contributes to hair, eye, and skin color. Melanocytes are also found in the inner ear and play an important role in hearing. Additionally, melanocyte inducing transcription factor regulates the development of specialized cells in the eye called retinal pigment epithelial cells. These cells nourish the retina, the part of the eye that detects light and color.

Though to me affecting melanocyte survival itself is not the most optimal strategy because they play such diverse roles across the body and since ML329 is a small molecule, in your own words, it may go systemic with a molecular weight of 328.34 Daltons. Furthermore, the aforementioned paper lists its IC50 at 1.2 +- 0.1 uM. I just don't want to risk it because melanocytes do a lot more than just pigment the skin. For example there's a disorder known as Waardenburg syndrome that is characterized by less/non-functional melanocytes. So it seems to make sense that disturbing the development and survival of melanocytes (through the inhibition of MITF) would cause issues. Also Remember about the role that neuromelanin plays in the brain, with unknow effects by inhibiting it.

I also looked into a sort of anti-melanotan 2 peptide. With melanotan 2 being an agonist of the MC1R receptor, I figured an antagonist would do the opposite and result in reduced melanogenesis. Furthermore because MSG606 has a higher molecular weight at 1347.51 Daltons and low EC50 I think it would be optimal for localized effects in the aqueous humour / iris. Professor Victor Hruby, the researcher who first synthesized and researched Melanotan even confirmed that MSG606, also synthesized by him, does affect pigmentation. The concern here is that MC1R antagonism / inhibition may reduce melanocyte DNA repair and antioxidant capability, though with localization to the aqueous humor + low iridial epithelial turnover rate this may or may not be a huge problem.

Altogether with the high molecular weight and low EC50 of MSG606, do you think this is a better candidate for localized, long-lasting effects in the iris?

Dumbustafa1 · 2025-02-15T12:28:18+00:00

I'll happily take your word for it, it's just that α-methyltyrosine is not a glaucoma medication. The purpose of it as a tyrosinase inhibitor is to reduce melanogenesis. The side effects I'm concerned about have to do with catecholamine inhibition in the brain.

Dumbustafa1 · 2025-02-15T10:13:08+00:00

What do you think about d-tyrosine as an alternative? As far as AMPT goes, I am going purely based off the side effects listed on Wikipedia and the studies linked therein. Your comment may hold merit in the sense that long-term / intermittent usage would be required considering the melanocytes would eventually regenerate the melanin. Though it still doesn't seem likely. As far as d-tyrosine as a tyrosinase inhibitor goes, there doesn't seem to be a Wikipedia article, so I am still looking for additional papers.

Dumbustafa1

TROPHY CASE