I just reread and it makes me wonder: how do you not get nauseous on 2cb??? It's the main reason for mine to need some dust off, as that nausea is rather intense and spoiling it partially...
low dose and empty stomach, not had any nausea so far at all.
Damn bro I train exactly th same Blood n Guts style , one set to oblivion till can’t no more , I almost passed out the other day doing squats that way. And doing techniques to push past failure rest n pause etc. Blood n Guts is the most effective program I’ve tried also doggcrap is very good program ill do like a hybrid of both.
the improvement shows how many days or weeks abstinence is required before positive effects, setback shows impact that each usage has, breakeven shows how long I must wait until there is a NET positive effect of using a drug, frequency is my planned max usage interval with a Break meaning I'm not going to use it.
Only thing I would change is reduce your frequency of MDMA and Mephedrone use, once a month MDMA use + once a week 4-MMC use will bite you in the ass sooner than laterLots to update...
I've come to a few conclusions after a lot more research
1. My GABA system is fucked I need to take a break from it (think this might be the cause of my sexual dysfunction anorgasmia)
2. Alcohol is very bad for me in multiple ways
3. Nootropics can help me repair my GABA system & improve sexual function
4. Exercise is important for me
5. I might be using due to undiagnosed ADHD as a way to quieten my over active brain - on a waiting list for a diagnosis
My new plan....
Exercise more (walking, running, dumbbells) > stop taking GABA drugs > start taking a Nootripics stack > rotate other drugs while decreasing their usage > use Cannabis more to plug the gap
More excel.....
Nootropics stack (+ vitamin D3)
yeah good shout and I'm aware, right now I'm more like MDMA once every 3-4 months, and I go through phases of Mephedrone.
Summary Table (Qualitative Breakeven Impact)| Substance | Impact on GABA Recovery | Impact on Anorgasmia Recovery | Breakeven Impact (Qualitative) |
|---|---|---|---|
| DMT | Very Low | Very Low | Very Low |
| Psilocybin / Psilocin | Very Low | Very Low | Very Low |
| 2C‑B | Very Low | Very Low–Low | Very Low |
| Ketamine | Low | Low–Moderate | Low |
| Cannabis (THC) | Low–Moderate | Low–Moderate | Low–Moderate |
| Alcohol | Low–Moderate | Low–Moderate | Low–Moderate |
| Pregabalin | Moderate | Moderate | Moderate |
| Xanax (Alprazolam) | Moderate | Moderate | Moderate |
| Diazepam | Moderate | Moderate | Moderate |
| Cocaine | Low–Moderate (indirect) | High | High |
| Amphetamine | Low–Moderate (indirect) | High | High |
| Mephedrone | Moderate (indirect) | High | High |
| MDMA | Low–Moderate (indirect) | Very High | Very High |
| Soma (Carisoprodol) | High | High | High |
| Meprobamate | High | Very High | Very High |
| Phenibut | Very High | Very High | Very High |
| GBL | Very High | Very High | Very High |
Your breakeven point stabilizes.
2. How long it takes for the system to “forget” the heavier drug A) The brain forgets the acute effects first B) Then it forgets the receptor-level disruption C) Finally, it forgets the pattern of switching 3. The simplest way to picture it A) GABA‑B receptors recover much more slowly B) GABA‑B drugs suppress dopamine more deeply The simplest way to understand it A) MDMA causes a “serotonin dip” that overlaps with GABA recovery B) MDMA amplifies sexual‑function disruption C) MDMA destabilizes sleep and stress hormones D) MDMA’s emotional “afterglow” can mask the disruption A) Psychedelics don’t suppress GABA systems B) Psychedelics cause a short, mild serotonin “after‑dip” C) Psychedelics don’t create dopamine debt D) Psychedelics can indirectly improve emotional stability 1. It creates a “double dip” in dopamine and serotonin 2. It destabilizes the emotional curve 3. It amplifies the “reward deficit” created by GABA drugs 4. Sexual‑function breakeven is especially sensitive 1. Ketamine doesn’t suppress GABA receptors 2. It doesn’t deplete dopamine or serotonin 3. It has a short “after‑effect window” 4. It can temporarily reduce emotional stress
Side‑by‑Side Summary: Mephedrone vs Ketamine| Feature | Mephedrone | Ketamine |
|---|---|---|
| Primary action | Dopamine + serotonin releaser | NMDA antagonist |
| After‑effects | Dopamine/serotonin dip | Mild dissociation, short-lived |
| Emotional stability | Volatile | Neutral/calm |
| Interaction with GABA recovery | Destabilizes | Minimal |
| Effect on sexual breakeven | Stretches significantly | Barely affects |
| Effect on GABA breakeven | Indirectly stretches | Minimal |
| Overall impact on breakeven | High | Low |
The simplest way to picture it
In regards to your anorgasmia Im curious how often you microdose or when you used psychedelics last?more AI research, thought i'd share in case anyone interested
my conclusion is to back off all drugs, shift to taking cannabis, with occasional 2C-B and ketamine use, and potentially after a GABA break i will add back in pregabalin.
i'm going to investigate 1. microdosing mushrooms in more detail, 2. microdosing ketamine (I usually just do a few bumps rather than khole, but still concerned about using it too frequently), 3. strains of cannabis to try to get the right high 4. using more CBD
Exercise is going well, I'm sleeping like a baby as a result!
for info my sexual function issue is mainly Anorgasmia, but there are similar parallels for other sexual function issues - if anyone has any questions on something specific pm me, i'm happy to help/take a look at things.
Occasional Use — Impact on GABA Recovery & Anorgasmia Recovery
Impact scale
- Very Low = minimal disturbance
- Low = small, short-lived disturbance
- Moderate = noticeable disturbance
- High = strong disturbance
- Very High = deepest, longest-lasting disturbance
Substance Impact on GABA Recovery Impact on Anorgasmia Recovery Breakeven Impact (Qualitative) DMT Very Low Very Low Very Low Psilocybin / Psilocin Very Low Very Low Very Low 2C‑B Very Low Very Low–Low Very Low Ketamine Low Low–Moderate Low Cannabis (THC) Low–Moderate Low–Moderate Low–Moderate Alcohol Low–Moderate Low–Moderate Low–Moderate Pregabalin Moderate Moderate Moderate Xanax (Alprazolam) Moderate Moderate Moderate Diazepam Moderate Moderate Moderate Cocaine Low–Moderate (indirect) High High Amphetamine Low–Moderate (indirect) High High Mephedrone Moderate (indirect) High High MDMA Low–Moderate (indirect) Very High Very High Soma (Carisoprodol) High High High Meprobamate High Very High Very High Phenibut Very High Very High Very High GBL Very High Very High Very High
1. How the breakeven point changes when you stop switching
When you stop rotating between GABA drugs (GBL, Phenibut, benzos, Soma, Pregabalin, Alcohol), something important happens:
Switching between different GABA drugs creates a kind of “noise” in the system:
When you stop switching, the system finally gets a consistent signal.
- different receptor types are being pushed and pulled
- different half‑lives overlap
- different rebound patterns collide
- the nervous system can’t predict what’s coming next
What this does to the breakeven point:
✔ It stops drifting upward
When you mix drugs, the breakeven point tends to stretch longer and longer because the system keeps getting hit in different ways. Stopping the switching removes that upward pressure.
✔ It gradually shrinks toward the breakeven point of the drug you’re actually using
If you settle on a “lighter” GABA drug (like alcohol or pregabalin), the breakeven point slowly moves toward that drug’s typical pattern.
✔ It becomes predictable again
Instead of the breakeven point being pulled in different directions by different substances, it becomes a single, stable curve.
✔ Recovery becomes smoother
The nervous system prefers consistency. Stopping the switching allows:
…to follow a more stable trajectory.
- receptor regulation
- neurotransmitter balance
- hormonal rhythms
- sleep architecture
This is conceptual, not numerical.
The nervous system “forgets” a heavier GABA drug in layers, not instantly.
Here’s how the forgetting process works:
This is the short‑term fog, sedation, or rebound. It fades relatively quickly once the heavy drug is gone.
Heavier drugs (GBL, Phenibut, Meprobamate, Soma) cause deeper changes in:
These take longer to normalize.
- GABA‑B or GABA‑A receptor sensitivity
- downstream dopamine tone
- stress‑response circuits
During this phase:
- the breakeven point is still influenced by the heavy drug
- even if you’re now using something lighter
- the system behaves as if it’s still “recovering from the big one”
This is the slowest part.
When you’ve been rotating between multiple GABA drugs, the nervous system adapts to unpredictability:
When you stop switching, the system slowly relearns stability.
- tolerance becomes generalized
- rebound becomes more sensitive
- recovery becomes less efficient
This is when the breakeven point:
- stops being inflated
- stops being erratic
- settles into a predictable curve again
Stopping switching = the breakeven point stops stretching and starts shrinking.
Forgetting the heavy drug = the breakeven point slowly moves away from the heavy drug’s influence and toward the baseline of whatever you’re doing now (or toward full recovery if you’re abstinent).
Detail on each class
The short version: GABA‑B drugs push deeper, slower‑recovering systems than GABA‑A drugs do.
Here’s what that means in practice.
GABA‑A receptors (benzos, alcohol, Soma, meprobamate) adjust quickly:
GABA‑B receptors (GBL, Phenibut) adjust slowly:
- fast tolerance
- fast rebound
- fast partial recovery
This means:
- slow tolerance
- slow receptor normalization
- slow downstream dopamine recovery
- slow stress‑system stabilization
→ A single GABA‑B hit stretches the breakeven point far more
The system stays “tilted” longer.
GABA‑B activation strongly inhibits dopamine release in:
- the reward system
- the motivation system
- sexual‑arousal circuits
How dopamine‑acting drugs (MDMA, cocaine, amphetamine) interact with this model
Here’s a clear, grounded explanation of how dopamine‑acting drugs (MDMA, cocaine, amphetamine) interact with the breakeven‑point model you’ve been exploring — meaning how they influence the nervous system’s ability to return to baseline after stress from GABA‑acting substances.
I’ll keep this conceptual, neuroscience‑based, and safe.Even though MDMA, cocaine, and amphetamine don’t act on GABA receptors directly, they interfere with the same downstream systems that GABA drugs disrupt. This creates a kind of “cross‑talk” that affects recovery.
Let’s break it down.
1. They hit the same reward and motivation circuits that GABA drugs suppress
GABA drugs (especially GABA‑B ones like GBL/Phenibut) suppress dopamine release.
Dopamine‑acting drugs do the opposite:
After the high, all three cause a dopamine crash.
- Cocaine blocks dopamine reuptake → dopamine spikes
- Amphetamine forces dopamine release → dopamine floods
- MDMA releases serotonin + dopamine → emotional and sensory surge
Why this matters:
Your breakeven point is partly about how long it takes dopamine systems to stabilize again.
When you combine:
…you create large swings in dopamine tone.
- GABA drugs (dopamine‑suppressing)
- stimulant/entactogen drugs (dopamine‑flooding)
Result:
The breakeven point becomes longer and less predictable.
2. They create “dopamine debt” that overlaps with GABA recovery
After the peak, dopamine‑acting drugs leave behind:
These are the same systems GABA drugs also influence.
- low dopamine
- low motivation
- emotional flatness
- reduced libido
- impaired reward sensitivity
So the effects stack, even if the drugs are used on different days.
Result:
The nervous system has to recover from two kinds of dopamine disruption at once.
This stretches the breakeven point further.
3. They amplify sexual‑function disruption
Sexual function depends heavily on:
MDMA, cocaine, and amphetamine all disrupt these systems.
- dopamine (desire)
- serotonin (sensitivity)
- prolactin (post‑orgasm inhibition)
- stress hormones
- sleep quality
When combined with GABA drugs:
- libido drops more sharply
- arousal becomes more inconsistent
- recovery takes longer
- emotional connection feels blunted
Result:
Sexual‑function breakeven points stretch more than GABA breakeven points.
This is why sexual recovery often lags behind GABA recovery.
4. They destabilize the recovery curve
Think of the nervous system like a balance scale:
When you mix these forces:
- GABA drugs push it down (sedation, suppression)
- Stimulants push it up (activation, dopamine flooding)
- MDMA pushes it sideways (serotonin surge → depletion)
- the system can’t find equilibrium
- recovery becomes nonlinear
- breakeven points become “wobbly”
- emotional stability becomes harder to regain
Result:
The breakeven curve becomes unstable, not just longer.
5. They interfere with sleep — which is the foundation of recovery
All three dopamine‑acting drugs disrupt sleep architecture:
GABA drugs also disrupt sleep, but in a different way.
- REM suppression
- rebound REM
- circadian rhythm disruption
- stress‑hormone elevation
When both categories are involved:
- sleep becomes fragmented
- hormonal rhythms destabilize
- emotional regulation weakens
- recovery slows down
Result:
Breakeven points stretch because the system can’t repair itself efficiently.
GABA drugs push the system down.
(sedation, suppression, rebound)
Dopamine‑acting drugs push the system up.
(stimulation, flooding, depletion)
Together, they create instability.
The nervous system struggles to find a stable baseline.
This instability stretches breakeven points
— especially for sexual function, motivation, and emotional balance.
If you want, I can also explain:
Just tell me what direction you want to explore.
- How serotonin‑acting drugs (like MDMA or psychedelics) affect the breakeven curve
- Why sexual recovery is more fragile than GABA recovery
- How to visualize the breakeven curve as a “stress‑recovery seesaw”
- How switching vs. abstaining changes the shape of the curve
How serotonin‑acting drugs (like MDMA or psychedelics) affect the breakeven curve
Here’s a clear, grounded explanation of how serotonin‑acting drugs — especially MDMA and classic psychedelics like LSD and psilocybin — interact with the breakeven‑point model you’ve been exploring. I’ll keep everything conceptual and neuroscience‑based, without giving medical or harmful specifics.
To make this intuitive, I’ll break it into two parts:
- How MDMA affects the breakeven curve
- How psychedelics (LSD, psilocybin, DMT, 2C‑B) affect the breakeven curve
MDMA is unique because it hits three systems at once:
This creates a very specific pattern in the breakeven curve.
- Serotonin (massive release → depletion)
- Dopamine (moderate release → drop)
- Oxytocin (bonding, emotional openness)
After MDMA, serotonin temporarily drops below baseline. This affects:
These are the same systems that GABA drugs also influence indirectly.
- mood
- emotional regulation
- sexual sensitivity
- sleep
- stress response
Result:
The breakeven curve becomes longer, especially for sexual function.
Sexual function depends heavily on:
MDMA temporarily disrupts all three.
- dopamine (desire)
- serotonin (sensitivity)
- prolactin (inhibition)
Result:
Even if GABA recovery is going well, MDMA can push sexual breakeven further out than expected.
GABA drugs already affect sleep architecture. MDMA adds:
- REM suppression
- cortisol elevation
- circadian disruption
Result:
Recovery becomes less efficient → breakeven stretches.
People often feel emotionally open or connected for a day or two after MDMA.
But underneath that:
- serotonin is low
- dopamine is low
- prolactin is high
Result:
The breakeven curve feels shorter than it actually is.Psychedelics act primarily on serotonin 5‑HT2A receptors, not GABA or dopamine. This means their interaction with the breakeven curve is very different from MDMA.
Unlike GABA drugs, psychedelics:
- don’t downregulate GABA receptors
- don’t cause rebound anxiety
- don’t depress dopamine tone
- don’t disrupt sleep architecture long‑term
Result:
They barely affect the GABA breakeven curve.
After LSD or psilocybin, serotonin signaling briefly dips as receptors reset.
This can cause:
But it’s usually short‑lived.
- mild emotional flatness
- slight sensitivity changes
- temporary introspective mood
Result:
The sexual‑function breakeven curve is only slightly affected.
Unlike MDMA, cocaine, or amphetamine:
- they don’t flood dopamine
- they don’t deplete dopamine
- they don’t cause reward‑system crashes
Result:
They don’t stretch the breakeven curve through dopamine pathways.
Because they don’t suppress GABA or dopamine, and because they often promote:
…they can sometimes smooth the breakeven curve rather than stretch it.
- introspection
- emotional processing
- stress reduction
(Not because they’re “healing,” but because they don’t interfere with the systems that GABA drugs stress.)Mephedrone is a triple‑action stimulant:
It behaves like a hybrid of MDMA + cocaine, which gives it a very specific recovery profile.
- dopamine releaser
- serotonin releaser
- norepinephrine releaser
After the peak, mephedrone leaves behind:
These are the same downstream systems that GABA drugs also influence indirectly.
- low dopamine (motivation, libido, reward)
- low serotonin (mood, sensitivity, emotional tone)
→ Result:
The breakeven curve stretches, especially for sexual function, because both dopamine and serotonin are involved in arousal and sensitivity.
Mephedrone tends to produce:
This volatility interacts with the GABA recovery curve by making the “baseline” harder to stabilize.
- emotional spikes
- emotional crashes
- irritability
- reward‑system volatility
→ Result:
Breakeven becomes less predictable and tends to drift upward.
GABA drugs suppress dopamine. Mephedrone floods dopamine, then drops it.
The combination creates a larger swing than either drug alone.
→ Result:
The nervous system takes longer to return to equilibrium → breakeven stretches.
Because mephedrone affects:
…it tends to push sexual recovery further out than GABA recovery.
- dopamine (desire)
- serotonin (sensitivity)
- prolactin (inhibition)
→ Result:
Sexual breakeven is more distorted than GABA breakeven.Ketamine is a dissociative NMDA antagonist, not a GABA drug and not a dopamine/serotonin releaser.
Its interaction with the breakeven model is almost the opposite of mephedrone.
Unlike benzos, alcohol, GBL, or phenibut, ketamine:
- doesn’t downregulate GABA‑A
- doesn’t downregulate GABA‑B
- doesn’t create GABA rebound
→ Result:
It barely affects the GABA breakeven curve.
Ketamine can modestly increase dopamine in some circuits, but it doesn’t cause:
- dopamine crashes
- serotonin depletion
- reward‑system burnout
→ Result:
It doesn’t stretch the breakeven curve through dopamine pathways.
Ketamine’s subjective effects fade quickly, and the neurochemical after‑effects are short‑lived.
→ Result:
Breakeven curves remain mostly unchanged.
Because ketamine can produce:
…it sometimes smooths the emotional side of recovery rather than destabilizing it.
- detachment
- reduced rumination
- lower anxiety
(Not because it’s “healing,” but because it doesn’t interfere with the systems that GABA drugs stress.)
Feature Mephedrone Ketamine Primary action Dopamine + serotonin releaser NMDA antagonist After‑effects Dopamine/serotonin dip Mild dissociation, short-lived Emotional stability Volatile Neutral/calm Interaction with GABA recovery Destabilizes Minimal Effect on sexual breakeven Stretches significantly Barely affects Effect on GABA breakeven Indirectly stretches Minimal Overall impact on breakeven High Low
Mephedrone
Creates big dopamine + serotonin swings → destabilizes recovery → stretches breakeven curves, especially sexual.
Ketamine
Barely interacts with GABA or dopamine systems → leaves breakeven curves mostly unchanged.
If you want, I can also compare:
- Mephedrone vs MDMA
- Ketamine vs psychedelics
- Which substances tend to “stack” their effects on breakeven curves
- How stress, sleep, and hormones fit into this model
I've just started using psychedelics again after about 30+ years so there's no real relationship. I've taken 2 microdoses and 1 threshold dose of 2C-B in the last 4 weeks.
I laud your efforts and cant help but see a younger me in your post.I'm a poly drug user and could use some advice on how to minimize dependency and tolerance build up risk. I'm also clearly addicted to being high despite no specific drug dependency, I'm cutting back to address this by reducing dosage to threshold and increasing use of less harmful drugs.
I use something almost daily, mainly as a way to reduce my alcohol problem. I'm trying to keep everything I take at as low a dose as possible with intervals between uses of everything to prevent dependency and tolerance build up. I rotate drug uses as much as possible and try to also rotate drug classes where I can to minimize hitting the same receptor classes too frequently. Low dose cannabis eddibles almost daily, alcohol use significantly cut down to a few units a week with a view to stopping again (had a 3 month break already), currently experimenting with micro/threshold dosing of psychedelics as they carry less risk that the other drugs I'm using.
My drug use plan
Soma use has been too high at about 3-4 times a week, but no noticeable tolerance build up, I still nod out taking 600mg subliminal unless I have some caffeine with it (weird given it's rep for rapid tolerance build up, no issues when I stop using for a week or 2 either).
I love GABA, but scared of benzo dependency, my DOC is Pregab, I've been taking it recreationally weekly for ~10 months, it's an amazing base for lots of different combos and I use that a lot when I binge going through multiple different combos with it in a single day but may fav is with diazepam (it stops the hyperactivity phase) and cannabis , but then also add methedrone/cocaine/alcohol/caffeine/ketamine in the mix through the day depending on mood - NOTE I'm very experienced with these drugs, understand half lifes & dosing well, have carefully titrated doses up when I combo them while keeping trip logs so I can establish safe baselines based on my own body. Please don't start dicking about with these combos unless you know what you are doing & the risks, there's real danger in the mix here with CNS stacking, some of these are additive and some potentiate each other.
I think I've recently reset pregab back to baseline after a tolerance break, and will be cutting down usage going forward to prevent tolerance build up. Plan is to add in psychedelics at threshold level instead as a safer alternative.
I've been binging far too often when life is tough and for fun, have cut back on these sessions and aim to do it no more than once a month or 2 as a big treat.
Target rotation plan - Generally these are all at threshold/low doses unless I'm binging
Right now I'm taking more than this I would like but starting to implement this plan after a months GABA break. Cocaine has to date been an occasional treat once every 3 months or so.
My honest goal with all this is to make this a long term sustainable life style choice, I'm complementing my drug use with nootropics to help reduce drug usage further, but I have no intention to stop taking drugs, I know the risks, I'm taking drugs for fun not to mask any mental issues. I think my alcohol use has been driven by undiagnosed mild ADHD, I'm on a waiting list for diagnosis, but experimenting with ADHD nootropics seems to have a very positive effect at work so far, if I do have ADHD I don't plan on taking meds for it. The move from alcohol is also done for health reasons, drugs are simply less harmful. Have tried amphetamines but don't feel they fit in with my usage needs, I don't find them as much fun recreationally as other drugs.
Don't ever want or plan to start using opiods or meth, have tried and like Kratom very much but using it's not an option sadly given home situation.
I'm exercising more and eating better both of which are helping reduce drug use. Drug use is also help me eat less and coupled with exercise lose weight.
So in summary I'm an informed idiot who's addicted to being high but wants to try and do it in a safe way.
any advice? please give me double barrels!
thanks for the kind & wise words.
the 2+2+2 rule is making me think and deal with things differently, thanks Keif!
This seems to be real quality information. Especially the table.more AI research, thought i'd share in case anyone interested
my conclusion is to back off all drugs, shift to taking cannabis, with occasional 2C-B and ketamine use, and potentially after a GABA break i will add back in pregabalin.
i'm going to investigate 1. microdosing mushrooms in more detail, 2. microdosing ketamine (I usually just do a few bumps rather than khole, but still concerned about using it too frequently), 3. strains of cannabis to try to get the right high 4. using more CBD
Exercise is going well, I'm sleeping like a baby as a result!
for info my sexual function issue is mainly Anorgasmia, but there are similar parallels for other sexual function issues - if anyone has any questions on something specific pm me, i'm happy to help/take a look at things.
Occasional Use — Impact on GABA Recovery & Anorgasmia Recovery
Impact scale
- Very Low = minimal disturbance
- Low = small, short-lived disturbance
- Moderate = noticeable disturbance
- High = strong disturbance
- Very High = deepest, longest-lasting disturbance
Substance Impact on GABA Recovery Impact on Anorgasmia Recovery Breakeven Impact (Qualitative) DMT Very Low Very Low Very Low Psilocybin / Psilocin Very Low Very Low Very Low 2C‑B Very Low Very Low–Low Very Low Ketamine Low Low–Moderate Low Cannabis (THC) Low–Moderate Low–Moderate Low–Moderate Alcohol Low–Moderate Low–Moderate Low–Moderate Pregabalin Moderate Moderate Moderate Xanax (Alprazolam) Moderate Moderate Moderate Diazepam Moderate Moderate Moderate Cocaine Low–Moderate (indirect) High High Amphetamine Low–Moderate (indirect) High High Mephedrone Moderate (indirect) High High MDMA Low–Moderate (indirect) Very High Very High Soma (Carisoprodol) High High High Meprobamate High Very High Very High Phenibut Very High Very High Very High GBL Very High Very High Very High
1. How the breakeven point changes when you stop switching
When you stop rotating between GABA drugs (GBL, Phenibut, benzos, Soma, Pregabalin, Alcohol), something important happens:
Switching between different GABA drugs creates a kind of “noise” in the system:
When you stop switching, the system finally gets a consistent signal.
- different receptor types are being pushed and pulled
- different half‑lives overlap
- different rebound patterns collide
- the nervous system can’t predict what’s coming next
What this does to the breakeven point:
✔ It stops drifting upward
When you mix drugs, the breakeven point tends to stretch longer and longer because the system keeps getting hit in different ways. Stopping the switching removes that upward pressure.
✔ It gradually shrinks toward the breakeven point of the drug you’re actually using
If you settle on a “lighter” GABA drug (like alcohol or pregabalin), the breakeven point slowly moves toward that drug’s typical pattern.
✔ It becomes predictable again
Instead of the breakeven point being pulled in different directions by different substances, it becomes a single, stable curve.
✔ Recovery becomes smoother
The nervous system prefers consistency. Stopping the switching allows:
…to follow a more stable trajectory.
- receptor regulation
- neurotransmitter balance
- hormonal rhythms
- sleep architecture
This is conceptual, not numerical.
The nervous system “forgets” a heavier GABA drug in layers, not instantly.
Here’s how the forgetting process works:
This is the short‑term fog, sedation, or rebound. It fades relatively quickly once the heavy drug is gone.
Heavier drugs (GBL, Phenibut, Meprobamate, Soma) cause deeper changes in:
These take longer to normalize.
- GABA‑B or GABA‑A receptor sensitivity
- downstream dopamine tone
- stress‑response circuits
During this phase:
- the breakeven point is still influenced by the heavy drug
- even if you’re now using something lighter
- the system behaves as if it’s still “recovering from the big one”
This is the slowest part.
When you’ve been rotating between multiple GABA drugs, the nervous system adapts to unpredictability:
When you stop switching, the system slowly relearns stability.
- tolerance becomes generalized
- rebound becomes more sensitive
- recovery becomes less efficient
This is when the breakeven point:
- stops being inflated
- stops being erratic
- settles into a predictable curve again
Stopping switching = the breakeven point stops stretching and starts shrinking.
Forgetting the heavy drug = the breakeven point slowly moves away from the heavy drug’s influence and toward the baseline of whatever you’re doing now (or toward full recovery if you’re abstinent).
Detail on each class
The short version: GABA‑B drugs push deeper, slower‑recovering systems than GABA‑A drugs do.
Here’s what that means in practice.
GABA‑A receptors (benzos, alcohol, Soma, meprobamate) adjust quickly:
GABA‑B receptors (GBL, Phenibut) adjust slowly:
- fast tolerance
- fast rebound
- fast partial recovery
This means:
- slow tolerance
- slow receptor normalization
- slow downstream dopamine recovery
- slow stress‑system stabilization
→ A single GABA‑B hit stretches the breakeven point far more
The system stays “tilted” longer.
GABA‑B activation strongly inhibits dopamine release in:
- the reward system
- the motivation system
- sexual‑arousal circuits
How dopamine‑acting drugs (MDMA, cocaine, amphetamine) interact with this model
Here’s a clear, grounded explanation of how dopamine‑acting drugs (MDMA, cocaine, amphetamine) interact with the breakeven‑point model you’ve been exploring — meaning how they influence the nervous system’s ability to return to baseline after stress from GABA‑acting substances.
I’ll keep this conceptual, neuroscience‑based, and safe.Even though MDMA, cocaine, and amphetamine don’t act on GABA receptors directly, they interfere with the same downstream systems that GABA drugs disrupt. This creates a kind of “cross‑talk” that affects recovery.
Let’s break it down.
1. They hit the same reward and motivation circuits that GABA drugs suppress
GABA drugs (especially GABA‑B ones like GBL/Phenibut) suppress dopamine release.
Dopamine‑acting drugs do the opposite:
After the high, all three cause a dopamine crash.
- Cocaine blocks dopamine reuptake → dopamine spikes
- Amphetamine forces dopamine release → dopamine floods
- MDMA releases serotonin + dopamine → emotional and sensory surge
Why this matters:
Your breakeven point is partly about how long it takes dopamine systems to stabilize again.
When you combine:
…you create large swings in dopamine tone.
- GABA drugs (dopamine‑suppressing)
- stimulant/entactogen drugs (dopamine‑flooding)
Result:
The breakeven point becomes longer and less predictable.
2. They create “dopamine debt” that overlaps with GABA recovery
After the peak, dopamine‑acting drugs leave behind:
These are the same systems GABA drugs also influence.
- low dopamine
- low motivation
- emotional flatness
- reduced libido
- impaired reward sensitivity
So the effects stack, even if the drugs are used on different days.
Result:
The nervous system has to recover from two kinds of dopamine disruption at once.
This stretches the breakeven point further.
3. They amplify sexual‑function disruption
Sexual function depends heavily on:
MDMA, cocaine, and amphetamine all disrupt these systems.
- dopamine (desire)
- serotonin (sensitivity)
- prolactin (post‑orgasm inhibition)
- stress hormones
- sleep quality
When combined with GABA drugs:
- libido drops more sharply
- arousal becomes more inconsistent
- recovery takes longer
- emotional connection feels blunted
Result:
Sexual‑function breakeven points stretch more than GABA breakeven points.
This is why sexual recovery often lags behind GABA recovery.
4. They destabilize the recovery curve
Think of the nervous system like a balance scale:
When you mix these forces:
- GABA drugs push it down (sedation, suppression)
- Stimulants push it up (activation, dopamine flooding)
- MDMA pushes it sideways (serotonin surge → depletion)
- the system can’t find equilibrium
- recovery becomes nonlinear
- breakeven points become “wobbly”
- emotional stability becomes harder to regain
Result:
The breakeven curve becomes unstable, not just longer.
5. They interfere with sleep — which is the foundation of recovery
All three dopamine‑acting drugs disrupt sleep architecture:
GABA drugs also disrupt sleep, but in a different way.
- REM suppression
- rebound REM
- circadian rhythm disruption
- stress‑hormone elevation
When both categories are involved:
- sleep becomes fragmented
- hormonal rhythms destabilize
- emotional regulation weakens
- recovery slows down
Result:
Breakeven points stretch because the system can’t repair itself efficiently.
GABA drugs push the system down.
(sedation, suppression, rebound)
Dopamine‑acting drugs push the system up.
(stimulation, flooding, depletion)
Together, they create instability.
The nervous system struggles to find a stable baseline.
This instability stretches breakeven points
— especially for sexual function, motivation, and emotional balance.
If you want, I can also explain:
Just tell me what direction you want to explore.
- How serotonin‑acting drugs (like MDMA or psychedelics) affect the breakeven curve
- Why sexual recovery is more fragile than GABA recovery
- How to visualize the breakeven curve as a “stress‑recovery seesaw”
- How switching vs. abstaining changes the shape of the curve
How serotonin‑acting drugs (like MDMA or psychedelics) affect the breakeven curve
Here’s a clear, grounded explanation of how serotonin‑acting drugs — especially MDMA and classic psychedelics like LSD and psilocybin — interact with the breakeven‑point model you’ve been exploring. I’ll keep everything conceptual and neuroscience‑based, without giving medical or harmful specifics.
To make this intuitive, I’ll break it into two parts:
- How MDMA affects the breakeven curve
- How psychedelics (LSD, psilocybin, DMT, 2C‑B) affect the breakeven curve
MDMA is unique because it hits three systems at once:
This creates a very specific pattern in the breakeven curve.
- Serotonin (massive release → depletion)
- Dopamine (moderate release → drop)
- Oxytocin (bonding, emotional openness)
After MDMA, serotonin temporarily drops below baseline. This affects:
These are the same systems that GABA drugs also influence indirectly.
- mood
- emotional regulation
- sexual sensitivity
- sleep
- stress response
Result:
The breakeven curve becomes longer, especially for sexual function.
Sexual function depends heavily on:
MDMA temporarily disrupts all three.
- dopamine (desire)
- serotonin (sensitivity)
- prolactin (inhibition)
Result:
Even if GABA recovery is going well, MDMA can push sexual breakeven further out than expected.
GABA drugs already affect sleep architecture. MDMA adds:
- REM suppression
- cortisol elevation
- circadian disruption
Result:
Recovery becomes less efficient → breakeven stretches.
People often feel emotionally open or connected for a day or two after MDMA.
But underneath that:
- serotonin is low
- dopamine is low
- prolactin is high
Result:
The breakeven curve feels shorter than it actually is.Psychedelics act primarily on serotonin 5‑HT2A receptors, not GABA or dopamine. This means their interaction with the breakeven curve is very different from MDMA.
Unlike GABA drugs, psychedelics:
- don’t downregulate GABA receptors
- don’t cause rebound anxiety
- don’t depress dopamine tone
- don’t disrupt sleep architecture long‑term
Result:
They barely affect the GABA breakeven curve.
After LSD or psilocybin, serotonin signaling briefly dips as receptors reset.
This can cause:
But it’s usually short‑lived.
- mild emotional flatness
- slight sensitivity changes
- temporary introspective mood
Result:
The sexual‑function breakeven curve is only slightly affected.
Unlike MDMA, cocaine, or amphetamine:
- they don’t flood dopamine
- they don’t deplete dopamine
- they don’t cause reward‑system crashes
Result:
They don’t stretch the breakeven curve through dopamine pathways.
Because they don’t suppress GABA or dopamine, and because they often promote:
…they can sometimes smooth the breakeven curve rather than stretch it.
- introspection
- emotional processing
- stress reduction
(Not because they’re “healing,” but because they don’t interfere with the systems that GABA drugs stress.)Mephedrone is a triple‑action stimulant:
It behaves like a hybrid of MDMA + cocaine, which gives it a very specific recovery profile.
- dopamine releaser
- serotonin releaser
- norepinephrine releaser
After the peak, mephedrone leaves behind:
These are the same downstream systems that GABA drugs also influence indirectly.
- low dopamine (motivation, libido, reward)
- low serotonin (mood, sensitivity, emotional tone)
→ Result:
The breakeven curve stretches, especially for sexual function, because both dopamine and serotonin are involved in arousal and sensitivity.
Mephedrone tends to produce:
This volatility interacts with the GABA recovery curve by making the “baseline” harder to stabilize.
- emotional spikes
- emotional crashes
- irritability
- reward‑system volatility
→ Result:
Breakeven becomes less predictable and tends to drift upward.
GABA drugs suppress dopamine. Mephedrone floods dopamine, then drops it.
The combination creates a larger swing than either drug alone.
→ Result:
The nervous system takes longer to return to equilibrium → breakeven stretches.
Because mephedrone affects:
…it tends to push sexual recovery further out than GABA recovery.
- dopamine (desire)
- serotonin (sensitivity)
- prolactin (inhibition)
→ Result:
Sexual breakeven is more distorted than GABA breakeven.Ketamine is a dissociative NMDA antagonist, not a GABA drug and not a dopamine/serotonin releaser.
Its interaction with the breakeven model is almost the opposite of mephedrone.
Unlike benzos, alcohol, GBL, or phenibut, ketamine:
- doesn’t downregulate GABA‑A
- doesn’t downregulate GABA‑B
- doesn’t create GABA rebound
→ Result:
It barely affects the GABA breakeven curve.
Ketamine can modestly increase dopamine in some circuits, but it doesn’t cause:
- dopamine crashes
- serotonin depletion
- reward‑system burnout
→ Result:
It doesn’t stretch the breakeven curve through dopamine pathways.
Ketamine’s subjective effects fade quickly, and the neurochemical after‑effects are short‑lived.
→ Result:
Breakeven curves remain mostly unchanged.
Because ketamine can produce:
…it sometimes smooths the emotional side of recovery rather than destabilizing it.
- detachment
- reduced rumination
- lower anxiety
(Not because it’s “healing,” but because it doesn’t interfere with the systems that GABA drugs stress.)
Feature Mephedrone Ketamine Primary action Dopamine + serotonin releaser NMDA antagonist After‑effects Dopamine/serotonin dip Mild dissociation, short-lived Emotional stability Volatile Neutral/calm Interaction with GABA recovery Destabilizes Minimal Effect on sexual breakeven Stretches significantly Barely affects Effect on GABA breakeven Indirectly stretches Minimal Overall impact on breakeven High Low
Mephedrone
Creates big dopamine + serotonin swings → destabilizes recovery → stretches breakeven curves, especially sexual.
Ketamine
Barely interacts with GABA or dopamine systems → leaves breakeven curves mostly unchanged.
If you want, I can also compare:
- Mephedrone vs MDMA
- Ketamine vs psychedelics
- Which substances tend to “stack” their effects on breakeven curves
- How stress, sleep, and hormones fit into this model
Alcohol's a problem for me, i want to give it up entirely, did so for a couple of months before and was much happier
i was surprised it and GBH/GBL are so high up as well, longest to recover yes, not sure it's irreversible damage though, if i remember correctly with time they all go back to baseline, the nootropics help repair the damage faster though.
yeah, that's a good way of putting it, i'm trying to find a much better and simpler baseline
it's a sneaky little fucker of a drug, it's taken me ages to figure it out to be honest.
was doing a 1 gram (occasionally 1.5 grams) almost every other day at my worst, but now every 4-5 days so progress. I maybe should have tapered it to be honest but hadn't even realised there was a dependence, I stupidly thought because my tolerance was only slightly increasing that meant there wasn't really any dependence yet, I suspect I was wrong!
