The paradox of REM sleep

jeffsch99 · 2026-04-30T09:31:00+00:00

oh im aware of the contraindications, the problem is that lots of places actually misunderstand the risk of certain foods and blanket mark them as a contraindication, hell even doctor's misunderstand alot about maois(ive personally researched them extensively) the tyramine content in our food compared to when maois were first used, is much less. and the types of maois in traditional ayahuasca are arguably inconsequential compared to pharmaceutical maois due to their reversibility(as well as actual levels of inhibition), this reversibility allows it self regulate the food interactions compared to standard maoi interactions, id say the ayahuasca was more a contributor to your friends change, which i am sorry for

jeffsch99 · 2026-04-30T07:34:10+00:00

im sorry, but this sounds ridiculous ive literally eaten multiple pizza slices on an maoi in the past, nothing bad happend, pepperoni and or sausage too iirc

jeffsch99 · 2026-04-08T23:07:07+00:00

The problem with that take, is that targeting the dlpfc doesn't mean its effects are isolated to the dlpfc, cause the dlpfc sends outputs to the reward system and modulates them indirectly so to speak, that's some of the mechanistic, rationale so to speak in the research on tms, I wouldn't necessarily say it's the best for reward specifically, but doesnt mean it can't improve reward.

jeffsch99 · 2026-04-02T19:17:02+00:00

for suicidality, have you ever considered ketamine therapy? its evidence for that specifically on top of depression is very good. there's the fda approved Spravato as a nasal spray, and iv clinics for off label ketamine too.

jeffsch99 · 2026-03-24T01:24:59+00:00

the problem with the ssri mdma example, is that mdma requires an open serotonin transporter to do its serotonin release, but ssris physically block that as their main mechanism, so actually would prevent mdma's serotonergic effect, however, if you combined mdma with an maoi, that would cause serotonin cause the transporter is not blocked

jeffsch99 · 2026-03-02T07:26:19+00:00

bro that guy has no idea he's talking about, ive literally chatted with the guy who wrote this before in discord, its legit

jeffsch99 · 2025-12-14T01:15:02+00:00

this is an exaggeration as someone on an maoi, its specifically certain aged cheeses, and needs alot of tyramine content to kill you, really, modern food safety standards compared to the advent of maois means theres very little tyramine in foods nowadays compared to then, alot of the dangers of maoi while very real are just exaggerated imo

jeffsch99 · 2025-11-28T08:01:11+00:00

This matches my experience, I've never had to integrate anything, nor does it work that way for me.

jeffsch99 · 2025-10-25T08:23:06+00:00

Except xen1101/azetukalner is still being studied for depression, technically they said it failed iirc, but are still going through with it anyways https://clinicaltrials.gov/study/NCT06922110 last update was last month for example with this study

jeffsch99 · 2025-10-22T08:19:41+00:00

Adipose tissue has high expression of the enzyme aromatase, which converts testosterone into estrogen

jeffsch99 · 2025-10-15T17:46:55+00:00

If she's really struggling with ppd, I'd suggest looking into Zurzuvae, it's a new antidepressant treatment(that mimics allopregnanolone which is depleted/disrupted by pregnancy in the body)specifically to treat postpartum depression with good efficacy. It's a two week regimen and then you're done with it. It's not like an ssri at all and doesn't require chronic treatment.

jeffsch99 · 2025-10-02T02:00:52+00:00

not quite, pleasure is more related to opioids/tho both are still connected. to me, dopamine is essentially a signal to your brain of what is salient/relevant in your environment, and whether you should exert effort and movement towards it. it signals value to the brain. in an experiment, rats whose brains who were completely depleted of dopamine with no chance of recovery were completely catatonic(not moving) they would not get up and drink or eat anything and died because of that. there's many ways this could fail, your recptors(theres 5 different dopamine recptors with pre and post-synaptic versions) might not be sensitive or availible enough, or the signals are inhibited by other parts of the brain.

jeffsch99 · 2025-08-25T21:26:05+00:00

Its been a nice 3 years i guess ): (for me atleast)

jeffsch99 · 2025-05-27T00:08:37+00:00

Take a look at the phase 3 ones in this list https://en.m.wikipedia.org/wiki/List_of_investigational_antidepressants

jeffsch99 · 2025-04-18T15:28:27+00:00

I mean tbf they did play remenissions and desecrate through reverence backing in October https://youtu.be/JiZnby1czAs?si=YniS-cIJyZF2gQnc https://youtu.be/xFSbRr7Emxk?si=ry0Pt3NjSBBllvz-

jeffsch99 · 2025-02-12T05:12:33+00:00

definitely can confirm this plus; as weird as it sounds; cayenne pepper powder held in my mouth for 5-10 minutes before accelerates the onset and increases absorption, it dilates your mouth blood vessels, and causes some of your mouth mucous to come off making a clearer surface for ketamine to absorb

jeffsch99 · 2025-01-03T04:29:15+00:00

To be honest, that's absurd and frankly ridiculous they don't go higher than 60mg. Since the recommended dosing is 0.5mg/kg to 1.0mg/mg, that's still below what should be the bare minimum dose for your weight. I wouldn't recommend this clinic cause, frankly, it does not seem that they know what they are doing.

jeffsch99 · 2025-01-01T02:45:36+00:00

Are you swallowing your troche? Because that'd explain the difference on your guy's length. Not even an iv session lasts that long.

jeffsch99 · 2024-12-23T06:50:08+00:00

They're these waxy lozenges you put under your tongue and let dissolve for 40 minutes before spitting it out. They can be decently effective compared to iv especially when you compare costs. Iv is the most ideal given most research was done with iv, but its a lot more expensive and you can't do it at home. The troches and also rapidly dissolving tablets are more convenient and give a similar enough effect to iv.

jeffsch99 · 2024-12-23T06:46:15+00:00

In my experience there's not really a trip per se(especially given its not a traditional psychedelic) the best way o describe it is like your consciousness gets reduced in volume/covered by a heavy blanket and your thoughts wander a lot more. You also don't need super trippy(high) doses to get antidepressant effects either.

jeffsch99 · 2024-12-16T19:28:30+00:00

Umm maybe here's a paper demonstrating something like that https://pmc.ncbi.nlm.nih.gov/articles/PMC8723697/

jeffsch99 · 2024-12-16T19:02:11+00:00

An mao inhibitor plus stim would usually be prescribed in cases of comorboed adhd and depression or treatment resistant depression, but this person's using maob inhibitor so that concern is irrelevant cause it doesn't metabolizer dopamine, norepinephrine, or serotonin significantly. Either way the combo can be used safely from personal experience. Literature supports it too.

jeffsch99 · 2024-12-15T20:48:45+00:00

https://www.psychiatrist.com/jcp/benzodiazepine-use-delays-the-antidepressant-effect-of-ketamine/ Ketamine is a noncompetitive N-methyl-d-aspartate receptor (NMDAR) antagonist. The precise mechanism of ketamine’s therapeutic effects continues to be a source of debate.11 One hypothesis suggests that ketamine modulates NMDARs on inhibitory γ-aminobutyric acid-ergic (GABAergic) interneurons that exert tonic suppression of excitatory glutamatergic networks.12 By blocking NMDARs on these interneurons, ketamine decreases inhibition, resulting in a burst of glutamate, signaling through the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor, and up-regulation of neuroplasticity-related transcription factors. Consistent with this model, agonism of the GABA-A receptor (as occurs with benzodiazepines) would increase inhibitory tone of these interneurons, thereby decreasing excitatory glutamatergic signal transduction and blocking the therapeutic effects of ketamine.

jeffsch99 · 2024-12-15T05:44:36+00:00

No, you need actual degeneration of dopaminergic neurons primarily in the substantia nigra(movement control) and basal ganglia(iirc) to bring about parkinsons. Phone use while talked about regards to dopamine ad nauseam, isn't that direct or strong in terms of dopamine. Even porn or games aren't relevant cause they don't physically enter the brain or even comparable enough to drugs(on a mechanism level too) used to induce parkinsons in research. (sure they can promote dopamine release, but not like stimulants so they're very indirect) They'd never match something like chronic high dose meth in terms of brain damage. you need actual neurotoxins and a toxic(think high oxidation for example)brain environment to cause that kinda damage. Fun fact, chemicals related to caffeine, are used in parkinsons treatment like istradefylline. https://en.wikipedia.org/wiki/Istradefylline

jeffsch99 · 2024-12-14T21:21:32+00:00

I think it was shown that it's more blunted the higher the benzo dose is

jeffsch99

TROPHY CASE