I read that it enhanced the utilization of choline in the brain, which somehow has varying effects in addition to making colors more vivid.

Here is someone's supposed anecdote of it turning up colors, permanently...? Rare but interesting effect

>I purchased some Coluracetam in early January 2025, then took 15mg sublingual. The first time I took it, I had richer color perception (similar to what HDR looks like contrasted with a non-HDR image), higher optical resolution (like a 720p video vs. a 1440p video), better short-term memory, focus, and a brightened mood. It was a lovely experience for about 4 hours until it wore off.

>Then I tried it again a few days later, and I had the same results. I tried it one last time before going to the gym, wherein I did heavy exercise and cardio with it coursing through my system. The next day, I noticed that ONLY the richer color perception remained, and it has never gone away since. It is now October and I still have that effect. I think waiting 9 months before proclaiming the effect as "permanent" should be a long enough wait, right?

Truly one of the more interesting racetams.

While this sub has always touted fundamental brain health tenets such as exercise, nutrition, and sleep, there are still many on the sub who chase after a limitless pill.

Limitlessness: a dangerous idea

The current state of nootropics requires that you take on an important idea:

There is no limitless pill, and it's dangerous to think there ever will be one.

Yes, there is an ideal "you", an ideal nootropic theory, but it won't just be one supplement or noot, but the results of years of testing and trailing and reflection, in which most who try will fail.

Believing one thing will cure you is sadly laughable and not realistic.

It's even sadder when you see people asking about overhyped things that feature drastic mechanisms with zero human data.

This is not to say that nootropics will never be able to increase the finite 'area under the curve' in the same way exercise, nutrition, and sleep do. In fact, there are already some nootropics that appear to do this (various noots in the last few years, racetams, use of caffeine in short cycles, etc). However, the extent to which these nootropics increase the area under the curve is mild, not extraordinary, when used at dosages where long-term debt is not accumulated.

Area under the curve mentality

I think the area under the curve idea is somewhat represented by steroids usage, of which effects have been documented throughout entire lifetimes. While steroid use may allow a higher net amount of testosterone x time throughout one's lifetime, it drastically radicalizes the area under the curve from a steadily declining baseline to a huge mountain followed by a plummet to the trough.

T levels during steroid usage refer to the T equivalent of a steroid, even if androgenic/anabolic ratios differ between synthetic steroids and testosterone. Conceptual graph, magnitude is not based on data.

Of course, in some ways, hormones are far more drastic and complex in the balancing act than most nootropics, but the idea is still present, especially for noots that mechanistically push and pull, instead of optimizing and remodeling.

Is it possible to truly hack your way out of debt? Sure, but it's not likely you'll test, trial, and nail every intricacy. Most people cannot trial their life like a carefully planned out study.

This concept doesn't only apply to the long-term effects of nootropics, steroids, or any biologically active substance. With nootropics like caffeine, this effect is observable after a single week due to resistance (and subsequent baseline drop after discontinuing).

To add to the complexity, some people, due to their genetics, see far less accumulation to their debt. Some people are almost allergic, hyper-sensitive to things, like those who just can't take caffeine. Or the rare reactions from supplements the vast majority don't experience.

Debt

For caffeine to not come with a 'debt', one must cycle its usage. Even then, a 'caffeine debt' should be expected.

The real value of such nootropics is in their ability to modulate the shape of your finite area under the curve. This is useful in making your peaks come when you need them (work, social time, etc), and conversely, your troughs to do the same (sleep, relaxation, etc). With most things, you should always expect to repay a debt, even if it might not happen to a great extent (like with caffeine cycling).

Failure to repay your debt can result in dependence at best, and permanent neurological damage at worst (think MDMA without 5HTP recovery). A mild example of this is noopept, which can cause short-term (but easily reversible) memory deficit with chronic use.

Nootropics that are nearly debt free do exist, but their effects are far more narrow for who they benefit, and the change is not obvious or immediate.

Nootropics don't change your brain, they tell your brain how to change itself

Remember that these compounds merely stimulate pre-existing pathways (like how noopept seems to activate pathways that would activate during hypoxia). They do not contain the necessary energy to make these changes occur on their own, and thus will not significantly increase your area under the curve. Even if some might appear to on the surface, it is best to approach this in a pessimistic way. Never assume a compound is increasing your area under the curve. Over time, neural adaptations and efficiencies do come out,

How can I increase my area under the curve?

Increasing your area under the curve comes back down to the basic triad of health: sleep, exercise, and nutrition. Relationships, fulfillment, and self-esteem are all also capable of elevating your area under the curve but are difficult to achieve without the basic triad of health.

In fact, a lot of nootropics, especially older ones, are really just things that aid in achieving this basic triad of health. Choline is a dietary component, theanine helps sleep, and creatine aids in exercise (although it might have some direct nootropic effects). New innovations in recent years in nootropic research may eventually challenge this idea of debt always occuring, but alas, these fundamentals of socialness, sleep, exercise, nutrition, what you spend time on, should not be lumped in with nootropics, which operate best under a healthy base.

Without the triad nailed down, you will have little area under the curve to shift around and your debts will be enormous. Maximize your baseline, then try to manipulate its curves with nootropics.

Note: This is a repost, check out og post here

https://preview.redd.it/z5tixdkf4q1h1.png?width=808&format=png&auto=webp&s=a9576ed41c33b595ff22fde102af4be90f4562a4

The neurotransmitter Acetylcholine (ACh) plays a leading role in alertness, focus, memory and mood. ACh also contributes to neuroplasticity that supports long-term potentiation needed to form long-term memory. And for a healthy, optimized brain.

If you use any of the racetam-family of nootropics in your stack, you likely should add a choline supplement. Because the racetams all affect choline and/or acetylcholine use in your brain in some way.

https://maze.conductscience.com/nootropic-racetam-effects-on-behavior-and-cognition/

• Piracetam weak positive allosteric modulator of AMPA receptors; indirectly influences cholinergic function.
• Aniracetam rapidly metabolized; primarily modulates AMPA and glutamate transmission with downstream effects on dopamine and serotonin.
• Oxiracetam may prevent decreases in brain acetylcholine from damage, and also protects against induced memory loss.
• Phenylpiracetam poorly characterized mechanism with DRI psychostimulant properties
• Coluracetam is thought to influence high-affinity choline uptake (HACU), the transport system that pulls choline into neurons for ACh synthesis
• Pramiracetam may also affect HACU, limited evidence.
• Nefiracetam potentiates presynaptic nicotinic ACh receptors in the hippocampus.

Profound effects of combining choline and piracetam on memory enhancement and cholinergic function in aged rats (1981)

Taking choline with racetams can be achieved with any of the choline supplements. There are several types of choline available for supplemental use:

• CDP-Choline (Citicoline) is a popular and efficient stack with racetams and supports phospholipid synthesis
• Alpha-GPC has been documented to keep levels of choline steadier than CDP-choline
• Choline Bitartrate is the least expensive salt form of choline with a lower bioavailability.
• Choline Citrate is a honorable mention, with some preferring the citrate for energy in the brain.

Choline is often the center of a great nootropic stack. Because without adequate levels of choline in your brain, the rest of your stack is unlikely to work very well.

Choline is neither a vitamin or mineral.  It is a water-soluble “nutrient” related to the B-Vitamin group. Choline was recognized as an “essential” nutrient by the US Institute of Medicine in 1998.[i]  “Essential” because your body cannot make enough choline on its own. You need to get it from food, or a supplement.

Not using a choline supplement while taking racetams is only one of the ways to you can deplete your brain of acetylcholine. Racetam-headaches happen because your brain needs it to function. (Credit goes to Nootropicsexpert)

About choline and racetams, re: recent threads. (Old post)

https://preview.redd.it/vezk96wj2q1h1.png?width=601&format=png&auto=webp&s=a85e1ba05d5d899b205c22762c6cc944545643eb

>Animal studies are always preliminary. They are only a safe avenue to research potential treatments for humans. Thousands of compounds or stacks of compounds have shown great promise in animal studies, only to fail in human trials. There is a general trend in the nootropics community of placing too much emphasis on animal studies, not because they aren't valuable (they are), but because they often fail to translate to humans. And more importantly: because researchers theorize about neurochemical mechanisms based on animal research, and nootropics enthusiasts then take it as gospel and start devising stacks based on this theory, before it has ever borne out results in humans. That is putting the cart before the horse: as much as possible, the emphasis should be on which studies have shown things to work in humans, before one goes about theorizing about mechanisms.

>The other problem is that people seem to be unable to grasp the difference between nootropics for people with age- or disease-related mental decline and healthy, young adults (the demographic most commonly found on nootropics forums). What works for those with pre-existing mental decline may be correcting deficiencies caused by illness, but that doesn't necessarily mean that those without such deficiencies can see benefits from the same remedies.

>The emphasis on cholinergic mechanisms with regards to racetams is intimately related with the growing evidence of cholinergic decline as an important factor in age- and disease-related cognitive decline. Healthy young volunteers will have well-functioning cholinergic systems, and it is not a given that these systems will become even more efficient in healthy volunteers. Studies in young, healthy humans for nootropics as a whole are lacking.

>Now, for the animal studies. This rat study found that in a simple animal test, post-session intraperitonal administration of 2000mg/kg piracetam showed improvement against controls. 50mg/kg choline + 50mg/kg piracetam also showed statistically significant improvement, at doses which were inactive alone. But the improvement seen with 2000mg/kg piracetam was inhibited by coadministering choline. The takeaways from that study must be that there is some kind of synergistic relationship between piracetam and choline, but that there is a delicate balance. 1:1 was the ratio that worked in that study.

>In the study linked by OP of the previous post, also an animal study mind, a 1:1 ratio was again seen to show "retention scores several times better than those given piracetam alone." Note, however, that these were aged rats. There is much evidence suggesting that acetylcholine neurotransmission declines with age. In young adults, choline from normal diet may be enough, as they have yet to experience age-related decline in that department.

>However. Here is another rat study that examined a variety of combinations of piracetam and choline, as well as the drugs alone. This study failed to replicate the findings above. In fact, at some dosages, combinations of choline and piracetam produced significantly inferior acquisition to controls or separate administrations of piracetam or choline.

>Research on the choline + racetam combination in humans is very limited, and at the moment inconclusive. The contrast between the astonishing results seen in some animal trials and the modest to ineffective results seen in the very few humans who have been scientifically treated and observed on this combination is striking. More research is needed, of course, but what little evidence exists must be taken into account and given a good deal of weight, since we are humans, not rats, mice or animals in laboratory cages.

>Piracetam Plus Lecithin Trials in Senile Dementia of the Alzheimer Type:

>Eleven patients with a diagnosis of senile dementia of the Alzheimer's type (SDAT) participated in a six-month double-blind, placebo controlled crossover study (three months drug, three months placebo). Active medication consisted of 35 g lecithin/day + 4.8 g piracetam/day. (Note that there was no comparison to piracetam alone, only to placebo.) 8 out of the 11 patients displayed varying degrees of improvement (mainly in memory performance) during the active phase. The three nonresponders were those with the mildest symptoms, in particular, little to no aphasia. 'One previous open-design study of piracetam also suggested that this drug has a greater therapeutic effect in more severely demented patients.'

>Important to note, then: those with the most advanced disease received benefits. Those with more moderate disease progression did not. This, again, points to the idea that choline supplementation with racetams may be beneficial to those with advanced-stage dementia, but not for healthy young adults. Not that there are any trials in healthy young adults.

>Piracetam combined with lecithin in the treatment of Alzheimer's disease, however, found no benefit whatsoever to either piracetam or piracetam + lecithin.

>Racetams cannot be treated as equal. What holds for one might not hold for another, despite their structural similarities. There is little human data on the effects the combination of choline supplementation and piracetam have on cognitive function, but what little exists is inconclusive. The rave results from the animal studies have not been replicated. This can also be seen in numerous studies and meta-reviews which show that piracetam and piracetam-like compounds do not have nearly as strong cognitive enhancing effects in humans as in animal research. Research in healthy individuals is lacking, but this is not a point in favor of the choline hypothesis given the inconclusive or weak results in the Alzheimer's research.

>The choline angle exists in the literature because of the known connection between cholinergic malfunction and dementia or related cognitive diseases. Healthy people lack these malfunctions, and there is no good evidence I'm aware of, barring anecdotal reports—some of which are positive, some of which are negative—that there is any need or benefit to coadministering acethylcholine precursors and racetams. Furthermore, all racetams are not alike. They do not all interact with all the different neurotransmitter systems in the same way. The glutamatergic side of things must not be ignored. Racetams are AMPAkines, at least some of them.

>One could argue that perhaps choline could be a preventative measure, that it might not just restore existing malfunction but nip it in the bud. Perhaps. But that is another matter, and I don't think there are any prospective studies on this subject to support the idea. Such a prospective study could perhaps show whether supplementing choline at an early age could prevent future cognitive decline—but no such study exists at the moment. And also, that is a different matter from the idea that it synergizes or is necessary to get anything out of racetams. Racetams as a whole are not well-documented as nootropics in healthy volunteers, anyway.

>Perhaps certain choline sources are neuroprotective—but are there any human studies on that? Prospective studies? Well, again, that is a different matter from saying you need choline with phenylpiracetam.

>With a healthy diet and a relatively healthy, young body, you are probably just fine without choline. At least as an adjunct to racetams. This meme needs to die. It's not backed by solid research. Sure, there is some research, but the research has been misinterpreted or hypotheses have been extrapolated from them by hobbyists, and those hypotheses have not been confirmed in humans.

choline!

https://preview.redd.it/go7py0uiid1h1.png?width=683&format=png&auto=webp&s=bad41d5fad525213f597959e41f306ba1e5a8e23

(FYI Paracetamol is the same thing as Acetaminophen)

https://teams.semel.ucla.edu/sites/default/files/publications/July%202010%20-%20Tylenol%20reduces%20social%20pain.pdf

https://academic.oup.com/scan/article/11/9/1345/2224135

https://www.frontiersin.org/journals/psychology/articles/10.3389/fpsyg.2019.00538/full

So I stumbled across this a while ago and it kind of stuck with me.

We all know paracetamol for headaches and sore muscles, but apparently it also takes the edge off emotional pain, like the sting of rejection or feeling left out. There’s actually a study from 2010 where people took 1000mg a day for three weeks, and they consistently reported less social pain than the placebo group. Brain scans backed it up too, showing lower activity in the exact same regions that light up during physical pain.

Which is already pretty wild, but it gets weirder.

Another follow-up study literally called it an “empathy killer.” People who had taken paracetamol were measurably less bothered when reading about someone else going through something painful. Not dramatically less, but enough to show up consistently in the data. And it’s not just negative emotions either. Another study found it also dulls your ability to share in someone else’s happiness.

So, it’s less of a painkiller and more of a general emotional volume dial, turned down a notch.

The explanation has to do with the brain regions involved. Physical and emotional pain share a lot of the same neural circuitry, so it makes sense that something affecting one would bleed into the other.

Anyway, just something I found interesting. Feels a bit strange knowing that a drug most people take without a second thought has this side effect that basically nobody talks about.​​​​​​​​​​​​​​​​ (repost link)

>Specifically, we administered 1,000 mg acetaminophen or a placebo and measured effects on different measures of positive empathy while participants read scenarios about the uplifting experiences of other people. Results showed that acetaminophen reduced personal pleasure and other-directed empathic feelings in response to these scenarios. In contrast, effects on perceived positivity of the described experiences or perceived pleasure in scenario protagonists were not significant. These findings suggest that (1) acetaminophen reduces affective reactivity to other people’s positive experiences and (2) the experience of physical pain and positive empathy may have a more similar neurochemical basis than previously assumed. Because the experience of positive empathy is related to prosocial behavior, our findings also raise questions about the societal impact of excessive acetaminophen consumption.

https://preview.redd.it/nz8s2efr381h1.png?width=586&format=png&auto=webp&s=c6b075a0632eb6677c32b2230983bf2e11c5c0db

Mr. Happy Stack was an old but original nootropic stack from Mr.Happy

Caveats: This is a research topic. Substances discussed in this thread are being used in human clinical trials for bipolar disorder, alzheimer's disease and some other ailments. While these trials and >12 months of user-feedback from these forums have been largely successful, this protocol is not yet within the realms of well-trodden medical circles. Proceed at your own risk, preferably after reading the entire thread.

Uridine promotes cellular growth and DNA repair. By virtue of this, it can accelerate the effects of a folate (Vitamin B9) deficiency.

Folate deficiency can lead to DNA transcription errors, strand breakage and carcinogenesis. Conversely, too much folate can also cause the same issues.

Obtaining the RDA for B group vitamins from food or supplements should be part of any normal daily regimen, but if you are going to take uridine, it is a suggested requirement to take a multi-B vitamin with it, regardless of your diet.

For the first 2 weeks:

• 150-250mg (Uridine) UMP, orally, twice per day
• A good multi vitamin, that includes RDA of B-group Vitamins and a broad range of trace minerals, including magnesium
• 500IU of mixed vitamin E
• A large dose of fish oil with >700mg DHA + >300mg EPA (or 3000mg ALA / flaxseed oil, if you are vegetarian)

After 2 weeks:

• Slowly introduce choline - start with 50mg of eg.alpha-GPC or CDP-choline and ramp it up to around 300mg.
• If you experience depressive symptoms from choline, discontinue choline and consider ALCAR as an alternative.

Finding the optimal dose of uridine for you:

• Too little uridine and you likely won't see the benefits for a long time
• Too much uridine and you'll likely feel emotionally dull / overly focused.

Sublingual or Oral?: Sublingual doses are predicted to be around 7x-10x the equivalent oral dose. If you are troubleshooting brainfog, you may benefit from these higher doses. People primarily looking for a mood lift would be advised to start with an oral dose first and make adjustments from there.

Differences between UMP and TAU: Uridine-5'-Monophosphate (UMP) is water soluble and can be taken sublingually, if higher doses are desired. Triacetyluridine (TAU) is fat soluble, but 4x-7x stronger, orally, than UMP. From user reports, UMP appears to be more effective / better value, overall. UMP is available in bulk powder. TAU is available in capsule form, which is convenient for travelling.

Who SHOULDN'T take uridine: Over-methylators. If you do not respond well to Vitamin B, or SAMe, you are unlikely to enjoy any benefits from uridine supplementation.

 

Edit: I'll also explain the why's. This can also all be found in Mr. Happy's first post.

• Uridine is the main part of the stack, it has many benefits such as dopamine modulation, neurogenesis, synaptogenesis, etc.
• Uridine is more effective with DHA ^(1)
• Uridine is more effective with Choline ^(2)
• Uridine can make folate (B9) and B12 deficiencies worse, so you need to take them ^(3)

References:

Benefits reported for -
Uplifting and stabilising mood
Stress
OCD
Anxiety
Modulating / normalising dopamine release
http://www.ncbi.nlm....pubmed/15705349
Antidepressant-like effects of uridine and omega-3 fatty acids are potentiated by combined treatment in rats.

http://cat.inist.fr/...cpsidt=17035532
Dietary uridine-5'-monophosphate supplementation increases potassium-evoked dopamine release and promotes neurite outgrowth in aged rats

http://ebm.rsmjourna...4/1/49.abstract
Chronic uridine modulates the stimulant-induced release of dopamine

http://wurtmanlab.mi...ic/pdf/1034.pdf
Restorative effects of uridine plus docosahexaenoaic in in a rat model of Parkinson' disease

http://www.ncbi.nlm....ubmed/20504471/
Effects of chronic treatment with uridine on striatal dopamine release and dopamine related behaviours in the absence or the presence of chronic treatment with haloperidol.

http://cds.ismrm.org...iles/001482.pdf
Brain 31P-MRS at 4.0 Tesla: Effects of Triacetyluridine (TAU) in the treatment of mood disorders

http://www.sciencedi...09130579500169W
Uridine reduces rotation induced by l-Dopa and methamphetamine in 6-OHDA-treated rats

http://www.ncbi.nlm....pubmed/26188642

Short-term supplementation of acute long-chain omega-3 polyunsaturated fatty acids may alter depression status and decrease symptomology among young adults with depression: A preliminary randomized and placebo controlled trial.

Cellular growth / health and replication
Mitochondrial efficiency
http://www.ncbi.nlm....ubmed/15654852/
Secretion of ATP from Schwann cells in response to uridine triphosphate.

http://www.ncbi.nlm....pubmed/17538545
Uridine supplementation in HIV lipoatrophy: pilot trial on safety and effect on mitochondrial indices

Sleep / sleeping patterns
http://www.ncbi.nlm....pubmed/11322706
Uridine receptor: discovery and its involvement in sleep mechanism.

Learning and memory
General cognitive decline
Synaptogenesis
Neurogenesis
Myelation
Increasing free phosphatidylcholine
Increasing receptor densities
Improving lipid membrane health
http://www.fasebj.or...1/3938.abstract
Dietary uridine enhances the improvement in learning and memory produced by administering DHA to gerbils

http://www.sciencedi...074742703000248
Combined uridine and choline administration improves cognitive deficits in spontaneously hypertensive rats

http://www.ncbi.nlm....pubmed/17950710
Oral supplementation with docosahexaenoic acid and uridine-5'-monophosphate increases dendritic spine density in adult gerbil hippocampus.

http://www.ncbi.nlm....pubmed/18631994
Oral administration of circulating precursors for membrane phosphatides can promote the synthesis of new brain synapses.

http://www.ncbi.nlm....pubmed/17349923
Phosphatidylserine and phosphatidylcholine-containing liposomes inhibit amyloid beta and interferon-gamma-induced microglial activation.

http://www.ncbi.nlm....34/?tool=pubmed
Dietary supplementation with uridine-5′-monophosphate (UMP), a membrane phosphatide precursor, increases acetylcholine level and release in striatum of aged rat

http://www.ncbi.nlm....pubmed/19262950
Synapse formation is enhanced by oral administration of uridine and DHA, the circulating precursors of brain phosphatides.

http://www.dementiat...eimers-disease/
Nutritional intervention helps in mild Alzheimer’s disease

http://m.pnas.org/co...4/21/11601.full
Developmental disorder associated with increased cellular nucleotidase activity

http://content.karge...roduktNr=224107
Giving Uridine and/or Docosahexaenoic Acid Orally to Rat Dams during Gestation and Nursing Increases Synaptic Elements in Brains of Weanling Pups

http://www.bbc.co.uk...health-16344228
Alzheimer's: Diet 'can stop brain shrinking'

Bowel flora and fauna
http://ajcn.nutritio.../87/6/1785.full
Dietary nucleotides and fecal microbiota in formula-fed infants: a randomized controlled trial

Anemia
http://www.moreirajr...id_materia=3707
Efficacy and tolerability of a combination of uridine, cytidine, and vitamin B12 in anemia. A double-blind, comparative study versus nucleotide monotherapy

Cardiovascular health
Neural bloodflow
Antiviral properties
Type-2,3 diabetes (Alzheimers' disease being discussed elsewhere as T3D)
Halting a 5FU chemotherapy overdose and increasing selectivity of 5FU.
NMDA antagonist
AMPA agonist

https://preview.redd.it/01g1y40ogl0h1.png?width=750&format=png&auto=webp&s=56df09be46a8120a1ae321367708ddc2de02c1f7

https://preview.redd.it/e5qlrxfogl0h1.png?width=681&format=png&auto=webp&s=f11a13d4b4eef09aacdafed4b9d73bd50191e29e

IC50 (Lower is stronger)

Found in: https://www.authorea.com/users/997876/articles/1358174-comprehensive-in-vitro-profiling-of-traditional-and-emerging-stimulants-at-monoamine-transporters-and-the-5ht2a-receptor?commit=8f2542181955379c30bfda5a4d552af63a958a16

The original 1996 paper implied the inhibitory properties were secondary to CAE action; however, this is challenged by a 2025 assay study. PPAP still has no human studies nor any half-life data, not even half-life data in rats.

**CLARIFICATION:**The CAE has never been independently verified, but the original researcher who studied PPAP tied it to his theory on CAE and a theory of "natural death." Knoll, the name of the researcher, focused so much on CAE for PPAP that he downplayed PPAP's DAT inhibition. This 2025 study, which was done on human neurotransmitter inhibitors with both functional uptake inhibition testing and DAT ligand binding testing, was also head-to-head with street and medical stimulants, showing how strong PPAP is and how it could make sense that PPAP's effects mirror the feeling of similar stimulants. Knoll, the original researcher, was quoted as saying PPAP's uptake inhibition was by interference, as if to suggest it was a secondary property that was unrelated to the DRI action. He then claimed CAE must have been primary, as he compared PPAP to desmethylimipramine in a behavioral test, ignoring the idea that DMI has far weaker DRI activity versus PPAP. The CAE theory is just a theory, just obviously outshined by the major DRI activity confirmed in this 2025 paper. CAE has never had any identified receptor, channel, or protein that causes its effect, with the idea being that it stimulated neuron release in an impulse-dependent way. It's very likely he was seeing TAAR1 action that is seen in selegiline, which was his proof of concept drug for his CAE theory.

This should not be possible.

Studies show that 100% of men have microplastics in their semen. I am the first human ever to show a complete reduction to zero.

This may be a world-first breakthrough in fertility research.

I had 165 microplastic particles in my semen just 18 months ago. Now, I have zero.

Five published studies have measured microplastics in human semen. Two found them in 100% of men. The other three found then in 44 to 76% of men tested, but those used methods that miss the smallest particles and the clear ones. Corrected for that, the real rate is likely 100%. Almost every man alive has plastic in his semen right now. The same applies to testicular tissue, testing 100% positive for microplastics.

Microplastics hurt sperm.

Human studies show the impact of various types of plastic, associated chemicals, and other toxins on male fertility:

+ 60% fewer normal shaped sperm (from PFAS)
+ 5x higher odds of low sperm count (from PTFE)
+ 10% lower sperm concentration (from PTFE)
+ 15% lower swimming ability (from PTFE)
+ 41% lower swimming ability (from PET)
+ 12% lower sperm swimming ability (from BPA)
+ 3x higher odds of low sperm count (from Phthalates)
+ 2x higher odds of poor swimming (from Phthalates)

The effects compound: each extra type of plastic drops sperm swimming ability by about 21%.

This matters even if you’re NOT trying to get pregnant.

Sperm count is one of the cleanest biomarkers of overall health we have. And microplastics don't stop at the testes.

The same particles are showing up everywhere we look. Studies show 4.5x higher rate of heart attack, stroke, and death in people with microplastics in their arterial plaque vs. those without. Microplastics were also found in 100% of human placentas tested.

100% of post-mortem human brains tested positive for microplastics. Brain concentrations rose ~50% between 2016 and 2024, and now sit at roughly 11x the levels found in the liver or kidney.

Where do these come from?
+ PTFE, commonly in non-stick pans
+ PET, water bottles
+ Phthalates, makes plastic soft and bendy
+ BPA, can linings
+ PFAS, stain-resistant fabrics & food packaging

Inside the body, plastic causes a kind of cellular rust. It triggers inflammation in the testicles, kills the cells that make sperm and drops testosterone. It's been confirmed across 39 animal and cell studies, then in human data.

MY PROTOCOL:

Note, what I did is n=1, not a controlled trial, I cannot prove cause.

1. Sauna (dry). My toxin blood panel confirms sauna clears plastic related chemicals: BPA, phthalates, PFAS, flame retardants, pesticides. The plastic particles themselves are too big to sweat out directly. Heat may activate other clearance routes: bile flow through the liver, the cell's internal cleanup system, and the gut barrier. Humans have almost no enzymes that can break plastic apart, so the body has to physically push it out.

2. Reverse osmosis water filter. Drinking water is likely a major source of microplastic getting into your body. A reverse osmosis filter pushes water through a very tight membrane and strains the particles out. I filter everything I drink.

3. Trying to rid my environment of the big plastic items: cutting boards, cups, plates, food storage containers, non-stick pans, cling wrap, tea bags, water bottles, kitchen utensils, kettles, and synthetic clothing. Note, as hard as I try, I'm always finding new plastic things in my life. This can be all-consuming thing so try to just knock out the big ones.

I did all three interventions at the same time. I cannot say which one did the most work. What I can say is this: going from 165 to zero in 18 months is possible.

Results:
Nov 2024: 165 particles/mL
Jul 2025: 20 particles/mL
Apr 2026: 0 particles/mL

The 18 month window also captures roughly 7 full spermatogenesis cycles.

https://preview.redd.it/q4zrbys6mk0h1.jpg?width=1294&format=pjpg&auto=webp&s=53574f46b15d6e5847ac71b306484fec0154825d

Background info: Iam a computer science and maths student in my early 20s, I am a male 185cm, 88kg. I am into lifting, which is my 2nd priority after University, I struggle with attention and motivation to study, I relied mostly on discipline, which I realized after experiencing some of the dopaminergic compounds in my list. I value problem solving ability, memory and clear mindedness. I also struggle with quite severe depressive episodes which reveal themselves in the form of apathy and emotional numbness.

>NOTE: This is an old repost, original post from 4 years ago here, reposting for discussion purposes

My testing varies a bit, generally I don't ever test my response to two things at the time, always one at the time. I try to keep exogenous variables like sleep, diet, excercise, stress etc. as constant as possible.I have taken Zn,Mg, O3, Creatine and D3 forever, I introduced them one at the time and then established these as my "baseline" maybe together with caffeine.

All of what I describe is solely my personal opinion, let me know what you think.

S-Tier

(these compound are great, because they work and do not need to be cycled and don't have any drawbacks to me)

- Creatine Monohydrate, I take 10g a day, reduces my brain fog quite significantly also improves my mood

- Zink, I take 25mg in the morning on an empty stomach, also reduces my brainfog in the morning

- Magnesium Glycinate, I take 300mg in the evening, makes me fall asleep in 10min compared to 30min and improves my sleep quality

- Omega 3, mostly for the EPA content, I take 3g of EPA content, improves my mood significantly

- Vitamin D3, I take 5000 IU's daily improves my mood greatly, especially in winter, where I struggle with depression the most.

- L-Tyrosine, I take 10g daily pre workout, since my workouts are very mentally draining I always felt incapable of doing any work after, taking the Tyrosine in that dose greatly reduced my perceived mental exertion, thus making me able to sill work after my workouts.

EDIT: I only take the 10g twice in 8 days on my heaviest training days. 3g is the normal dose. This is something a few very highly regarded pl coaches do with their clients and I wanted to try it out and haven't seen any negatives from it.

- Noopept, I take 10-30mg a day sublingual on weekdays, makes me seek social interactions. I don't have any social anxiety, I just dont want to talk to people especially on bad days, Noopept makes me a lot more social and also more focused and engaged while talking to people/ while doing work. this was a game changer for me.

- Alpha-GPC, I take 150-300mg, makes me incredibly sharp, and very resistant to distractions.

- Huperzine-A, I take 200qg, prolonges and increases the effects of the cholinergics, like AGPC, Noopept and the racetams, also nicotine

A-Tier

(these compound also work great for me, but I experience side effects or need to cycly on and off)

- Phenylpiracetam, I take 100mg sublingual on week days, gives me great energy and motivation, but I feel a tolerance build-up when I take it straight through, 5 days on 2 days off works well, sometimes I take more breaks when I feel fine, taking it sublingual improved the benefits greatly for me, my favorite racetam.

- Mucuna Pruriens(20% Dopa), I take 100mg of Dopa content with ECGC, in the morning, on weekdays, helps me greatly with focus, motivation and mood, but I need a break from it or it will stop working. Crashes on the weekends is manageable tho.

- Nicotine Gum (2mg, but split into .5mg doses), I only take nicotine during exam week, to really boost my cognition, I have never smoked or taken any form of nicotine prior and low doses work incredibly well for me, a feeling of being "locked in", but supresses ocno-ihibitor acitvity, which is why I stay away from it other than special occasions.

- Caffeine, I take between 100-300mg per day, I love caffeine, gives me a great mood boost and energy, only in A-Tier because of resistance build-up.

EDIT: Everytime I take caffeine I also take the equivalent amount of l-theanine with it, but never l-theanine on its own.

- Bacopa monnieri, I take 300mg of extract, works well, improves my memory.

- Ginkgo biloba, I take 120mg, with every time I take AGPC, improves the cholinergics effects.

B-Tier

- CDP-Choline, doesn't really do anything for me, only noticed a difference when my diet was low in choline, APGC works way better for me.

- Uridine Monophosphate, for me this is a worse form of Huperzine.

- Piracetam, first racetam I ever took, worse than noopept or phenylpiracetam for me tho. So I dont take it anymore

C-Tier

- Oxi-, Prami-, Aniracetam, all significantly worse than normal Piracetam for me.

D-Tier

- Ashwagandha (KSM-66), makes it really hard to get out of bed in the morning and gives me borderline insomnia for the first 2 or 3 days of taking it, also blunts my emotions, again this is counter productive to me, since I already struggle with feeling numb.

- NAC, also blunts my emotions, therefore I don't take it.

- 5-HTP, helps greatly with sleep, but the reported side effects scare me, so I have only taken it twice in my life.

Most importantly: Lifestyle habits: (If they are not into place, the supps won't help you either)

- Wake up at the same time, go to bed roughly at the same time, pay attention to sleep cycles.

- See sunlight in the morning.

- Fast as long as possible for mental clarity, delay ingestion of carbs for as long as possible.

- Clean diet, no processed food

- Enough good fats (1g per kg of bodyweight)

- Exercise

- at least 6.5 and no more than 7.5 hours of sleep.

- Journaling, for goals and "to stay on the path", accountability

- Also, if you want to enjoy studying, limit the sources you derive your dopamine, so social media, video games, etc. And try to get excited about your field of study, whether through career prospects, new and exciting research or developments.

Share your thoughts in the comments below, thanks for reading