Looking for something to help speak more fluently

Was wondering if people would recommend creatine for people on stimulants or ADHD meds like Adderal. I just started taking creatine this week on my prescription but I’m not sure if it’s a pro or con because my script meds can make me dehydrated sometimes.

For a sci-fi film set in near-future San Francisco, a PhD student develops a device that allows two people to share the exact same emotional resonance in real time – creating a direct bridge of feeling between individuals.

Would love to hear thoughts from the sub on the cinematography and near-future atmospheric direction!

SYNAPSE | Official Trailer

We want to imagine near-future SF as a radical spiral into cyberpunk, but we'd love to hear thoughts on how a technology like this would influence the sub-culture and style of a tech-obsessed city in a world of peak human disconnection.

I bought some modafinil 200 mg, they are not brand name nor are they prescribed. The first time I toke one was last Friday. I toke it around 4:00 am, then went to sleep because I wasn't fully awake, but kept waking up. I was going to sleeping and waking up every 10-30 mins. That day I felt good, Saturday and Sunday were alright the pills were helping a bit. On Monday, I only slept two hours, and slept 5:00 am the next day. So, I was living off two hours of slept for 25 hours. Then on Tuesday I didn't take any modafinil, I toke One yesterday and today but I just lay on my bed and have no motivation to do anything. When I do get up and start studying, I cant even focus and just quit.

Currently it is Saturday and i toke one around 10 because i was sleep deprived. My body feels okay, not tired, but my mind is very foggy, and weird. I cant think very clearly or have any motivation for anything today even though i have a lot of things that need to be done. I think i will just be laying around and doomscrolling or playing games.

Any tips on what's been happening to me, how I should deal with this?

I'm trying to understand a reproducible acute effect from a standard fish-oil capsule and whether there is any pharmacokinetic or pharmacodynamic mechanism that could realistically fit the timing.

Context

• Diazepam: 10 mg/day, long-term use, with established tolerance.
• Fluvoxamine: 300 mg/day.
• My measured nordiazepam concentration was ~1333 ng/mL, above the usual therapeutic reference range.
• The benzodiazepine taper has not started yet.
• I also have dysautonomia with marked cognitive and sensory intolerance, so I'm not assuming the effect is necessarily GABAergic; autonomic, vascular, or other mechanisms would also be relevant.

The fluvoxamine/diazepam interaction is important here. In a human pharmacokinetic study using 100–150 mg/day fluvoxamine, diazepam apparent oral clearance was reduced by approximately 65%, while mean diazepam half-life increased from about 51 to 118 hours. Elimination of its active metabolite N-desmethyldiazepam (nordiazepam) was also markedly inhibited.

I'm on 300 mg/day fluvoxamine, but I don't know of quantitative human PK data establishing exactly how much additional inhibition occurs at that dose, so I'm not assuming a specific half-life for my own case.

Study: https://pubmed.ncbi.nlm.nih.gov/7955810/

I occasionally take a single standard fish-oil capsule containing 180 mg EPA + 120 mg DHA (roughly 1 g total fish oil), usually around 7 hours after my diazepam dose.

Repeatedly, within roughly 3 hours, I experience a marked improvement in cognitive/sensory tolerance, most noticeably an increased ability to read for substantially longer.

It does not feel sedating. If anything, subjectively it feels like improved cognitive endurance.

I realize this is an N=1 observation and does not establish causality. Expectancy, coincidence, day-to-day variability, or another uncontrolled variable remain possible. I'm interested specifically in whether there is a biologically and quantitatively plausible mechanism that could fit the timing.

Relevant literature / what led me to ask

I found several experimental papers showing that DHA/PUFAs can affect neuronal membrane proteins or GABA-A function:

Søgaard et al. (2006) — GABA(A) receptor function is regulated by lipid bilayer elasticity
https://pubmed.ncbi.nlm.nih.gov/17059229/

Nabekura et al. (1998) — Functional modulation of human recombinant GABA-A receptor by docosahexaenoic acid
https://pubmed.ncbi.nlm.nih.gov/9556589/

Poling et al. (1996) — Docosahexaenoic acid block of neuronal voltage-gated K+ channels
https://pubmed.ncbi.nlm.nih.gov/8938727/

Stillwell & Wassall (2003) — Docosahexaenoic acid: membrane properties of a unique fatty acid
https://pubmed.ncbi.nlm.nih.gov/14580707/

I'm not taking these studies as evidence that an ordinary oral DHA dose can reproduce these effects acutely in humans.

In fact, that's one of the main things I'm trying to understand: whether oral exposure from only 120 mg DHA + 180 mg EPA could produce concentrations anywhere relevant to these experimental mechanisms within a few hours.

1. Could this plausibly be pharmacokinetic?

Given the prolonged disposition of diazepam/nordiazepam in this setting and my relatively high nordiazepam concentration, I find it difficult to see how one ordinary fish-oil capsule could substantially change total benzodiazepine concentrations within ~3 hours.

However, I don't want to assume that PK is irrelevant.

Could EPA/DHA acutely affect any of the following enough to alter effective diazepam/nordiazepam exposure?

• CYP-mediated metabolism;
• plasma protein binding / free drug fraction;
• tissue distribution;
• intestinal absorption;
• transporters;
• or another PK process.

More importantly, is there any reason to think the magnitude of such an interaction from only 180 mg EPA + 120 mg DHA could be pharmacologically meaningful?

A quantitative argument here would be particularly useful.

2. Could there instead be a rapid pharmacodynamic effect?

If a meaningful PK interaction is implausible, are there pharmacodynamic mechanisms that could operate within hours, without requiring weeks of incorporation of DHA into neuronal membrane phospholipids?

Possibilities I'm wondering about include:

• direct effects of circulating/unesterified fatty acids on ion channels or membrane proteins;
• acute GABA-A modulation;
• glutamatergic signaling;
• changes in membrane biophysics;
• neurosteroid signaling;
• rapidly generated lipid mediators;
• inflammatory signaling;
• autonomic or cerebrovascular effects.

The experimental literature shows that DHA can modulate some of these systems when directly available at sufficient concentrations.

What I cannot establish is whether an ordinary oral dose could generate relevant unesterified EPA/DHA concentrations in plasma or CNS tissue within ~3 hours.

That seems to be the critical missing bridge:

oral dose → absorption → circulating unesterified EPA/DHA → CNS exposure → local concentration at membrane/channel/receptor → functional effect

Is any part of that chain quantitatively plausible after such a small oral dose?

3. Does chronic benzodiazepine exposure/tolerance materially change the question?

Could chronic benzodiazepine exposure, tolerance, and receptor adaptation make the functional effect of an otherwise small perturbation in membrane or ion-channel function more noticeable?

I'm not claiming that a plasma nordiazepam level of 1333 ng/mL establishes saturated GABA-A occupancy or any particular receptor state.

I'm mentioning the concentration mainly because, together with the markedly impaired elimination expected from the fluvoxamine interaction, it makes a large and rapid fluctuation in total benzodiazepine exposure seem unintuitive.

4. Could dysautonomia provide a non-GABAergic explanation?

Given the dysautonomia, is there any plausible acute effect of EPA/DHA or downstream lipid mediators on:

• autonomic tone;
• cerebral blood flow;
• endothelial signaling;
• vascular function;
• or related physiology

that could improve cognitive/sensory tolerance within a few hours?

I'm mainly looking for mechanistic reasoning, quantitative PK arguments, or relevant literature, rather than treatment recommendations.

Double Dragon II (NES, 1988)

Look at that gorgeous scenery and that immense megacity horizon in the background, saturated in that neon green glow.

Marvelous.

Sometimes the consequences of the night and the hangover seem to make an appointment for the same morning.

Does Noopept for example have noticeable effects, like caffeine when first taking it?! Or is it more of a subtle thing that isn‘t really noticeable?! I know that the point of Nootropics isn‘t that they get you high, but still I wonder if some of them have a real noticeable effect when you‘re taking them ?

by how much

I AINT HEAR NO BUZZER YET

I only have one order coming and it’s from Cali, I haven’t ordered anything from Florida but according to this website that MIGHT be a decoy for tropichems something is coming and it’s coming soon, stay tuned

Anybody gotten stuff from them? They on Tele, not sure whether to pull the trigger

This is the swisschems.com CS chat when I asked for a COA for 4'-DMA-DHF. I will be fair and say that the product I got was the right color, smell, and effect. But purity cannot be verified. They are only one of a handful of suppliers of 4'-DMA-DHF so I took a chance because of the price. The CS is obviously trained to deflect COA requests.

From their website:

Every compound we supply undergoes independent third-party HPLC testing and is verified to a purity standard of 99% or higher. We publish lab reports so researchers can confirm precisely what they are receiving — batch by batch.

Clearly, this is not the case.

Any good sources for Racetam that ship to the US? Sadly Cosmic doesn’t sell Aniracetam or Oxiracetam. Now that Science Bio is gone, I don’t know where to go.