Eliminating Vs Blocking Serotonin

[Wolf]

Recently I cut out a few of the anti serotonin measures I've taken and unfortunately it caused the rebound from hell.
I've ridden it out for a few days and I'm curious about the elimination vs blocking of serotonin from the body and brain. Are there permanent means of making sure serotonin doesn't come to be in large amounts? P chlorophenylalanine? Tryptophan restriction isn't logical for me given its ubiquity and the extra cost of avoiding it(college student). My fear is that in some form or another serotonin may just be floating around bound up in some way or another and waiting to make me sick again. Or the suspected serotonin secreting growth in my abdomen will get me one day.
I'm pretty happy with the high dht, dopamine, and productivity occurring, but I would hate to randomly fall ill due to some lurking variable.
I would say the same of histamine or estrogen, but the mast cells in my body have definitely stabilized and allergens don't affect me. On the estrogen side some of my fatty growths on my arms have shrunk significantly.
I am aware that in the absence of available serotonin the receptors will likely become more sensitive and that may also be causing the adverse reaction. If that is so and suffering a day or two every so often is necessary to metabolize whatever is floating around then so be it.
Sent from phone. Apologies for typos

 

[Terma]

Some of the serotonin-lowering measures backfire on people with health issues, because at the Trp conversion level where you can't limit Trp intake, diverting Trp away from serotonin only sends it down the Kyn pathway. Kyn crosses the BBB and wreaks havoc in the brain if it's not converted to Kyn acid or B3 before, conversions which can be impaired, and in my opinion in the brain I'd much rather have some serotonin or just Trp to avoid excess Kyn and its metabolites there.

Cortisol sends Trp down the Kyn pathway while Estrogen (more weakly, iirc) diverts it from Kyn into serotonin (one reason why I think Cortisol is worse unless you're bordering on serotonin syndrome from drugs).

There probably isn't a perfect substitute for Trp restriction, unless you can stop its absorption in the gut (if you don't mind some looser stools from extra serotonin local to gut, which also ends up triggering the immune system in a different way... you can't win). So the simplest working patch is probably far-downstream 5-HT receptor antagonists, which is just trial and error. Unfortunately your finances aren't great so you probably can't fill this prescription either. You could say f uck it and play around with nicotinic acid and niacinamide, or eliminating them if you already take (remember lean meats are already high and grains are fortified), but it's a crapshoot.

 

[Wolf]

What would theoretically fit the bill ideally insofar as 5HT receptor antagonists go?
I tend towards the high end of niacinamide intake as it has helped tremendously.

 

[Terma]

Never found one to change my life, but metergoline is go-to still available for experimenting imo (there are 3-4 different dosing strategies to try with it so it's versatile albeit a little unpredictable - certainly cyproheptadine is more predictable but it's so broad-spectrum it's entirely useless to me). Since you bring it up - niacinamide weakish benzo-like effects - to me modulating GABA-A/-B was ten times more bang for buck on several health problems than chasing serotonin, while niacinamide is suboptimal there. I mean, how has it helped [and in what dose]? I tend to assume people like the benzo-like effect.

 

[Terma]

You might not want to hear any of this, but serotonin isn't the worst thing for studying and sitting through lectures. The predominant 5-HT1 (post-synaptic) receptors have as a main effect increasing "patience", which I don't have to explain the value to you. Meanwhile, even in stressed state, 5-HT2a receptors have a pro-nootropic effect. [Imo] the worst of the "damage" done comes from the fact they both increase cortisol, but even that can feel good acutely.

Meanwhile, it's quite likely that taking high enough niacinamide can increase serotonin, misleading since the predominant mental effect is probably the GABA/benzo-like one (maybe even histamine? I didn't follow that part).

Personally I target dopamine and GABA first, and serotonin becomes more about blocking specific receptors like 5-HT3/7/2c/etc. This is far from the metabolic perspective, but (disclaimer:) I stopped caring.

 

[Wolf]

Niacinamide amplifies the androgenic effects of dhea/preg/prog and lets me assimilate more. Its kinda hard to explain. Any form of interaction with my environment is more easily recalled and I can automatically react to stimuli. The bottleneck ends up being glycine and salt intake for whatever reason.
I target dopamine above all else and then everything kinda goes from there. I'm not in any way dying, ill, or in any type of physical distress. If there's a way to improve my performance then I may as well take it before the guy next to me in class ends up taking my future job.

 

[Elephanto]

The chemicals that antagonize serotonin receptors are really crutches and shouldn't be used for more than a few weeks as per Peat's advice. It does cause serotonin receptors sensitization.

One of the safest ways that doesn't cause rebounds is chelating Iron, since tryptophan hydroxylase is promoted by Iron. Modifying systemic Amino Acids ratios is another, being high in Lysine, Tyrosine, Phenylalanine is going to lead to long-term Serotonin reduction. While you can reduce Tryptophan by taking BCAA+Tyrosine. There's also the fact that most of Serotonin is produced in the gut, avoiding gut irritants and fixing intestinal integrity (Zinc is potent at this, Glutamine usually but maybe not as safe) will lead to reduced Serotonin. Avoiding darkness and wearing blue-blocking glasses when starring at screens, eating enough salt, controlled breathing and bag breathing as CO2 opposes Serotonin (blocks platelets from releasing it), using natural calcium receptor antagonists as EMFs promote Serotonin through it (Magnesium, Selenium, Zinc), avoiding Alcohol and Cannabis, fixing kidney damage which is correlated with prolactin which inhibits dopamine (Thiamine, Niacinamide, Zinc, Potassium, Calcium, lower Phosphate intake and proper hydratation), reducing ejaculation frequency which triggers prolactin, restoring Pregnenolone levels. Those are strategies with broader systemic effects than taking things that temporarily inhibit Serotonin or increase Dopamine.

You might not want to hear any of this, but serotonin isn't the worst thing for studying and sitting through lectures.

This honestly matches my experience, society/authoritarianism is built around expecting you to be high Serotonin : passive and not impulsively desiring to express your unrestricted mind. Waiting is the worst thing I experience, I just want to go back in a space of freedom.

Except the studying part. Learning can be a source of dopamine. I usually prefer to learn from books than from attending class, making the logical deductions myself (teaching yourself in a way) always led to better test results than trying to memorize what someone said without questioning it.

 

[Terma]

Niacinamide amplifies the androgenic effects of dhea/preg/prog and lets me assimilate more. Its kinda hard to explain. Any form of interaction with my environment is more easily recalled and I can automatically react to stimuli.

That's part of GABA(-A) effects. It helps filter out noise information from the environment in the hippocampus and can improve reactions that way (ofc these things are dependent on the part of the brain, and can hamper things in another one or if overdone which is easily done). The DHEA and Preg are (unless sulfated) nootropic through NMDA agonism but this may need some GABA regulation (and glycine has input in both). I think those aren't a bad combo at all, if the B3 dose is reasonable. Except I wouldn't take progesterone during the day (if you do). Ofc it's possible the B3 helps metabolism and steroid conversions but it's a question of which do you honestly think is most likely producing your effects (ignoring the androgenic part here).

I gotta stop here for the week, but I mean, essentially you want nootropics - or avoiding anti-nootropics - to compete academically, working through metabolism or otherwise? This forum has mixed advice; if you do improve metabolism that certainly helps, even androgens a bit, but stuff like antihistamines, anticholinergics, NMDA antagonists, and too many inhibitory substances can easily work against this goal, so tread carefully. Serotonin is mostly negative to neutral overall depending on receptors and context (with some positive effects in more stressful situations), while Kyn metabolites in the brain are exclusively anti-nootropic/productive (except end-product B3).

 

[Waynish]

Which anti-serotonin measure? Isn't this critical information for advice in this case? Not sure why'd you want someone giving you advice on it without this critical information - unless they have the key to understand the correct mechanisms behind it all... And that's a pretty big ask! If we are adapting to a chemical we are taking, then there are ways to increase or decrease that level of adaptation. Nothing should be assumed to be neutral.

 

[Wolf]

The chemicals that antagonize serotonin receptors are really crutches and shouldn't be used for more than a few weeks as per Peat's advice. It does cause serotonin receptors sensitization.

One of the safest ways that doesn't cause rebounds is chelating Iron, since tryptophan hydroxylase is promoted by Iron. Modifying systemic Amino Acids ratios is another, being high in Lysine, Tyrosine, Phenylalanine is going to lead to long-term Serotonin reduction. While you can reduce Tryptophan by taking BCAA+Tyrosine. There's also the fact that most of Serotonin is produced in the gut, avoiding gut irritants and fixing intestinal integrity (Zinc is potent at this, Glutamine usually but maybe not as safe) will lead to reduced Serotonin. Avoiding darkness and wearing blue-blocking glasses when starring at screens, eating enough salt, controlled breathing and bag breathing as CO2 opposes Serotonin (blocks platelets from releasing it), using natural calcium receptor antagonists as EMFs promote Serotonin through it (Magnesium, Selenium, Zinc), avoiding Alcohol and Cannabis, fixing kidney damage which is correlated with prolactin which inhibits dopamine (Thiamine, Niacinamide, Zinc, Potassium, Calcium, lower Phosphate intake and proper hydratation), reducing ejaculation frequency which triggers prolactin, restoring Pregnenolone levels. Those are strategies with broader systemic effects than taking things that temporarily inhibit Serotonin or increase Dopamine.


This honestly matches my experience, society/authoritarianism is built around expecting you to be high Serotonin : passive and not impulsively desiring to express your unrestricted mind. Waiting is the worst thing I experience, I just want to go back in a space of freedom.

Except the studying part. Learning can be a source of dopamine. I usually prefer to learn from books than from attending class, making the logical deductions myself (teaching yourself in a way) always led to better test results than trying to memorize what someone said without questioning it.

What are your personal recommendations for iron chelators? Bleed myself? /Joke

 

[Wolf]

That's part of GABA(-A) effects. It helps filter out noise information from the environment in the hippocampus and can improve reactions that way (ofc these things are dependent on the part of the brain, and can hamper things in another one or if overdone which is easily done). The DHEA and Preg are (unless sulfated) nootropic through NMDA agonism but this may need some GABA regulation (and glycine has input in both). I think those aren't a bad combo at all, if the B3 dose is reasonable. Except I wouldn't take progesterone during the day (if you do). Ofc it's possible the B3 helps metabolism and steroid conversions but it's a question of which do you honestly think is most likely producing your effects (ignoring the androgenic part here).

I gotta stop here for the week, but I mean, essentially you want nootropics - or avoiding anti-nootropics - to compete academically, working through metabolism or otherwise? This forum has mixed advice; if you do improve metabolism that certainly helps, even androgens a bit, but stuff like antihistamines, anticholinergics, NMDA antagonists, and too many inhibitory substances can easily work against this goal, so tread carefully. Serotonin is mostly negative to neutral overall depending on receptors and context (with some positive effects in more stressful situations), while Kyn metabolites in the brain are exclusively anti-nootropic/productive (except end-product B3).

The progesterone:dhea+Preg ratio is highly favorable to dhea/preg. That took a bit of trial and error, but its perfect for me now. Transdermal scrotal application for the dht.
I want to compete academically while keeping my health intact. No sense in being top of my class and throwing up blood in between classes.

 

[Elephanto]

What are your personal recommendations for iron chelators? Bleed myself? /Joke

Well yeah, with the assistance of a registered professional (blood donation). I can only do it every 3 months where I live so I've been using 2 tsps of grounded coriander seeds daily, and sometimes cranberry juice or IP6. Some member here had a significant reduction in Iron levels with the coriander seeds powder :
Cilantro Works! Finally Reduced My Ferritin, Serum Iron And Transferrin Saturation!
I don't test for Iron levels but when I've been eating red meat a lot my skin tone becomes grey-ish (I was also tested pretty high in Iron a few years ago, I probably accumulate it easily) and generally look unhealthy, after a few days of taking these or giving blood it becomes more lively and I lose the grey/green tone.

 

[Wolf]

Well yeah, with the assistance of a registered professional (blood donation). I can only do it every 3 months where I live so I've been using 2 tsps of grounded coriander seeds daily, and sometimes cranberry juice or IP6. Some member here had a significant reduction in Iron levels with the coriander seeds powder :
Cilantro Works! Finally Reduced My Ferritin, Serum Iron And Transferrin Saturation!
I don't test for Iron levels but when I've been eating red meat a lot my skin tone becomes grey-ish (I was also tested pretty high in Iron a few years ago, I probably accumulate it easily) and generally look unhealthy, after a few days of taking these or giving blood it becomes more lively and I lose the grey/green tone.

Using a lancet and a vaccuum based chinese fire cup helped remove globs of black blood from old injuries once upon a time when I did lots of martial arts.

 

[Wolf]

As a side note: I get much better results from riboflavin than r5p, little results from r5p, and amazing results from r5p plus riboflavin. My thoughts are that Ma0-A gets upregulated and things bottleneck at aldehyde dehydrogenase. Likely it may make sense down the line to either inhibit tryptophan hydroxylase or provide precursors to aldehyde dehydrogenase.
EDIT
Cardenosine fits the bill.
"The main effect of Metadoxine, observed across many human and animal studies, is to accelerate alcohol metabolism (by speeding up BOTH alcohol dehydrogenase and aldehyde dehydrogenase) and reduce the negative effects of acetaldehyde on the entire organism. While initially it was thought that increase of activity in the alcohol metabolizing enzymes was the main mechanism of action for Metadoxine, more recent studies discovered that the chemical also prevents the depletion of ATP that alcohol consumption induces. This prevention of ATP depletion is likely at least as important for the observed benefits of Metadoxine, as speeding up the activity of the alcohol-metabolizing enzymes."
Cardenosine - Liquid Product For R&D
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Parasites screw it up too. Vit A.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3757314/pdf/pim0035-0229.pdf
"In this study, we show, for the first time, that the number of macrophages and DCs expressing ALDH enzymes (the enzymes important in retinoic acid production) is significantly decreased locally in the gut during an ongoing T. muris infection, both in a chronic model of infection and at early stages of an acute infection. This is in line with previous work that has described a decreased RALDH2 expression and activity in CD103+DCs from MLNs in colitic mice compared with steady-state controls (16). Our study extends this work, however, in that we find that the reduction in ALDH+ gut macrophages and DCs, triggered by inflammation, is absent at later stages of an acute infection. Indeed, percentages of ALDH+ gut macrophages and DCs are significantly higher than na€ıve levels at day 42 p.i. when the parasite has been expelled and the inflammation is resolving"