Nootropic Stack Progress

A hefty stack you got going there. Be careful though and make a full stop if you experience discomforts in the chest region. This has happened to me in the past.

Current stack

500mg niacinamide
D vitamin 2000IU
P5P 50mg
Pyridoxine 25mg
Folate 400mcg
Zink 25mg
Pumpkin oil 1000mg
Fish oil 1 table spoon
Cat’s claw 1000mg
Andrographis 400mg extract
Lithium 1mg every 2nd day
Iron 14mg every 2nd day
B1 100mg every 4th day
B2 100mg every 4th day
B5 500mg every 4th day

Magnesium 200mg
Melatonin 1mg
Tryptophan 260mg
Zyprexa 7.5mg

My stack is massive maybe too much. I came off the antidepressants at the start of my last stack. Today it hit me like a train, overstimulated and a little anxious. I also feel like Beta-Alanine or something in my morning stack is quite sedating as well. Focus was good when I could pull myself to do things.

Phosphatidylserine is a MOA-B so I think it and the Saffron was interacting with NALT, DL-Phenylalanine, and Bupropion. Which was something I wasn’t prepared for. The wash out of the Phenylalanine is pretty quick though and the anexity wore off rapidly.

Someone close to me in my life actually said they didn’t like how I was behaving because I was being a bit soft and gentle, and yeah the Bupropion makes me more intellectually aggressive and assertive so I think people have come to expect that from me, to be a bit more lazer.

I think I might remove the Bupropion because I feel I can make do without it in a stack this large.

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I want to share something which I feel is a really important idea that I wish I could pin to the top of this thread

Related to this video

Follow on in this paper

and the function of dopamine.

This basically says that organisms act as structure systems to maintain a state of aliveness by minimising surprise. Taking a path of least resistance by minimising danger and increasing survival. Suprise happens as a result of a prediction error between the internal representation of the world and expectations of what is happening. Schizophrenia can then be seen as a problem of predicting what is happening. Dopamine aberrant/hyperfunction changes affect entire brain pathways that create prediction errors and the flow-on effect being you change your internal state to match the number of surprising prediction errors you see. Medication, dopamine antagonists then act in a way that minimises prediction errors. Basically, they modulate neurotransmission acting as dampeners and tranquilisers to remove errors. Which is also how antidepressants work for depression.

Basically that antipsychotics act in an analogous way to for prediction errors as SSRIs do for depression by acting as numbing agents to fine-tune the number of prediction errors into a lower symptom range.

How antidepressants work

The key learning is that more anything that modulates neurotransmission to remove errors will fix the issue. Namely, anything which has dampening or tranquilising effects. This is how NDMA agents, TAAR1 Agonists, CBD ect work even though they work via different pathways. As long as you modulated neurotransmission to remove prediction errors then you’re going to treat symptoms regardless of if you change dopamine. This is also kind of self-evident if you think about it because antipsychotics aren’t anti-schizophrenics since they only treat symptoms and not cure the disorder. Further, the whole dopamine hypothesis is built around the idea that it’s dopamine which is the issue when it’s really not it’s just that aberrant dopamine is encoding prediction errors and that modulating smooths some of these errors.

The key learning is that anything that modulates neurotransmission to remove errors will fix the issue. Particularly stuff which has dampening or tranquilising effects. Not the entire picture since this doesn’t hold true for GABA, Anti-convulsants, SSRIs for positive symptoms, but the brain isn’t that simple. Basically, the idea is simply the reformulation of the dopamine hypothesis in Bayesian brain terms where medication works by treating the symptom of prediction errors. Not an entirely wild idea but regardless this has important implications as the proposed mechanism for the above stack which works via other mechanisms than dopamine alone.

Secondly, I learnt that ipseity disturbance explains schizophrenia prodrome.

These involve the person feeling as if they lack an identity, as if they are not really existing, that the sense of their experiences being their own (the “mine-ness” of their experiential world) is failing or diminishing, as if their inner experiences are no longer private, and that they don’t really understand the world. These experiences lead to the person engaging in hyper-reflectivity , or abnormally prolonged and intense self-reflection, to attempt to gain a grasp on these experiences, but such intense reflection may further exacerbate the self-disorders. Self-disorders tend to be chronic, becoming incorporated into the person’s way of being and affecting “how” they experience the world and not necessarily “what” they experience. This instability of the minimal self may provoke the onset of psychosis.


NAC 700mg
Lion’s mane 500mg
Beta-Alanine ~1000mg
NALT & DL-Phenylalanine ~133/333mg
Phosphatidylserine 100mg
Curcumin 500mg (Every 3rd day)
Chondroitin & Glucosamine 600/750mg
Hyaluronic acid 100mg
MSM ~2g
Collegen 10g
Tadalafil ~2.5mg
Vitamin D 1000iu
Ubiquinol & PQQ100mg/10mg
Zinc 50mg (Every 2nd day)
P-5-P 100mg (Every 4th day)
Vitamin K2 90mcg
Vitamin C 1000mg
Selenium 200mcg & Vitamin E 20mg (Every 4th day)
Creatine 7g
Astragalus extract 50mg

NAC 700mg
L-theanine 200mg
Beta-Alanine 1000mg
ALA 500mg (3 on 4 off)
Vitamin C 1000mg


Latuda 10mg
NAC 700mg
Melatonin 500mcg
Magnesium ~600mg
GABA ~700mg
Guanfacine ~0.5mg
Lithium 1mg (Every 2nd day)
Vitamin C 1000mg
Taurine 700mg
Fish Oil 5g
CBD 25mg +

Sometimes? Caffeine 16mg/Strong tea

Garlic 1200mg
Acetyl-L-carnitine 500mg

Too many changes at once thus I have pulled out the saffron, sulforaphane & Bupropion.

Changes from the last stack
Latuda is down from 15 to 10mg
Sabroxy removed
Buprioprion removed
CBD oil 25mg added
Guanfacine was added at 1mg, now reduced to ~0.5mg
Phosphatidylserine added
Gaba added
NAC reduced from 2400 to 2100
Beta-alanine split dosages
Vitamin C increased from 1000 to 3000 and split dosages
Lithium increased from every 3rd to every 2nd day
Ubiquinol & PQQ100mg increased from alternating days to every day
ALA changed from alternating days to 3 on 4 off
Vitamin D 1000iu increased from every second day to every day
Curcumin reduced to from every day to every 3rd day
Creatine increased

Sleep is poor, mood and symptoms are good

Things I still need to figure out which are supposed to work.
Increase L-theanine

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Hope your sleep improves. Some things can have a paradoxal effect though. GABA only works for me if I take it every 3-4 days, if I take it every day it hinders sleep. I have actually seen other people write similar things, maybe at webmd userreviews. For me personally Taurine keeps me awake too. Also ashwaganda keeps me awake.

Relying too much on theory can give problems. I learned this the hard way.

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Good point.

I will think about the gaba, you have to take Beta-Alanine at a different time to Taurine because the are antagonist in their uptake. Zinc and Magnesium also. Beta-Alanine also depletes Taurine levels overtime. Beta-Alanine requires multidaily dosing and is ineffective because saturated of carnosine takes forever. They both work at gaba but I am just assuming that taking 700mg Taurine at night is favourable then taking ~1g+ of Beta-Alanine. Taurine is commonly used in OTC sleep formulations so I thought I would just move with the crowd on that one but no idea if I have it the right way around.

The disadvantage of so many moving parts and having such a large stack is that it takes a lot longer to pin down the site effects of things. Testing one thing at time is always the way to go but if I pull everything out at this point and test one thing at a time I will either get depressed or experience positive symptoms. Realising that, I’m not taking a very scientific approach at all but it is loosely evidence based and hence I’m forced to rely on piecing together user reports of side effect and the theory a lot more then anything else including subjective effects. I mainly just note overall activation levels and positive symptoms.

To be honest I don’t really know what my stack does but the totality of it’s effects are that it definitely works for me. Also targeting that many different pathways it much have some small effect over placebo. But I will admit that I do enjoy experimenting with my medication :astonished: However that also helps me stay in a positive way with it mentally as I feel like I keep making progress with it and the helps with my adherence. Medication, placebo or not the progress is real and that’s what really matters.

It could be that you are building tolerance to the gaba and then what you not isn’t a paradoxical effect but just it’s lack of efficacy with rebound symptoms as you build tolerance. Still if that happens then in anycase if 3/4 works you’re going to be saving yourself some money which isn’t necessarily a bad reason to lower your dosing schedule. I figure that with a few things I take which are in doses above RDI. I feel that most drugs/medications/supplements will give you a hyperbolic dose response curve but that if you take a smaller dose then your getting a smaller effect size which isn’t picked up by the research literature. Having a stack this large you don’t want to take more stuff if you can avoid it at all and I assume the small benefits add up which is again more of a personal opinion then it is evidenced based. Not a complete asinine line of reasoning though.

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If you get by on such a low dose of latuda maybe you could get by at a low dose of something more effective for sleep. 10mg latuda is equvialent to 25-50mg seroquel which would probably serve you much better sleepwise. I have tried this dose before and didn’t find it sedating except at night when I needed it.

I am going to try transition to 50mg seroquel in 1-3 months. I’m just aiming at rebuilding my physical constitution before experimenting. My doctor actually approved of me trying this med and dose alone. I have heard stories of others getting by on such a low dose. I am sensitive to drugs and have virtually no symptoms for a long time so it might just work. I have been taking 5mg zyprexa for a long time which also is a good argument. But zyprexa is a heavy drug even at low doses. I am stuggling with lack of emotions and almost non existent libido. Naturally I want to get away from that if I can.

The generic zyprexa I was taking has been a disaster. I have had serious insomnia for almost 9 years. At the pharmacy and even doctors say it’s the same as original medicine so it took me a real long time to try out the original med again. It was a move of desperation. I heard many stories online about others who struggled with insomnia on zyprexa so I thought it was just the way it was, but guess what. 3 months on original zyprexa and the best sleep I had for 9 years. I guess I was lucky to find out.

Makes sense actually, good description, thank you.

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Yes. I normally recommend to other who are experiencing sleep issue to whilst still having positives simply to increase antipsychotics. Zyprexa and quetiapine a both good options for PRN and heavily sedating effective as sleep medication. Quetiapine hits histamine strongly but because of sequential binding and it’s affinity for histamine receptions you only get appreciably dopamine blockage at high dosages. Therefore quetiapine is grossly sedating for the amount of dopamine blockade it creates. Making it a good adjunctive for sleep and also one of the best of the antipsychotics as a sleep aid but not one as an antipsychotic. I have also heard of many people getting by on 25-50mg quetiapine. This is mainly since general practitioners aren’t pdocs so they don’t know antipsychotics well meaning that of the stuff they know about and can pick out of a hat they have experience using quetiapine and know it’s side effect profile and therefore feel comfortable prescribing. Also people who see general practitioners are lower symptoms. The drug also has generic options. Not necessarily the best choice for people who are psychotic.

If you are tapering then the dosage ranges you can get quetiapine in are much better then many other medications so it make tapering easier in that regard. Also because it is sedating you can use it for sleep, many advantages being on quetiapine during a taper. However since I’m already tapering I don’t want to add a second antipsychotics and if I started taking it I have to restart my baseline again balancing 2 antipsychotics which would take months. If I could go back to the start of my taper I would reconsider swapping to quetiapine but yeah now I down to 10mg I feel I’m beyond that stage in terms of how far it would set me back to spend the time trying to figure out quetiapine when I know the ins and outs of latuda well enough. I also don’t feel like histamine sedation is the best pathway for sleep but combine as a sleep medication/antipsychotics it is the best. Without access to a sleep stack then undoubtedly this would be a good pathway and I could see quetiapine being used as a good tapering medication. However I don’t know if my individual response to quetiapine would be any good. So I can’t swap to it and I want to be taking less APs if anything. Never the less a very relevant and informed suggestion and also not a bad approach. You could basically scrap everything which you use in a sleep stack and replace it with small dose of quetiapine.

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