ADD, Depression, and a Five-Year Trip
I was born with ADD and have struggled with suicidality and depression since around age 14. I also have a long history of drug abuse — and after misusing LSD heavily, I ended up stuck in a five-year HPPD nightmare. I went through phases of depersonalization, bipolarity, dissociation, and psychosis. LSD permanently changed something in my brain.
THC and Psychosis: D2 Was the Key
Ever since that LSD experience, THC makes me instantly psychotic. But I found out something crucial: blocking mesolimbic D2 hyperactivity with Amisulpride stops all of it. Voices, racing thoughts, paranoia, anxiety, even things I thought were just my ADD — all gone. Especially the obsessive overthinking when falling asleep, the way thoughts would keep spinning up... it was all due to elevated D2 activity.
Cannabis-Induced Psychosis
After months of smoking over 100g of very strong weed per month, I snapped. I became paranoid. I heard people on the street talking about me, saw faces in shadows, and became convinced the police were observing me. I heard voices constantly — often my father calling my name, sometimes like a loud radio in my head.
That’s when I went to psychiatry and got prescribed SSRIs for depression and antipsychotics for the voices.
SSRIs Fixed a Pain I Didn't Know Wasn't Normal
To my total disbelief, SSRIs completely cured this constant, agonizing pain in my chest. I’d been living in a state of nociceptive suffering for years and thought it was just normal. A small dose of Sertraline made it vanish. With that, the suicidality was gone in an instant — existence stopped being pure agony. Depression became manageable, and for the first time, I could go to sleep looking forward to the next day.
The Voices Fade — and So Did the Patterns
D2 blockers made the voices go quiet, then disappear. I think my brain had gotten so used to that voice-driven thought pattern that it had become part of me. Over time, it unlearned it.
I quit smoking weed for six months, but relapsed and a few months in, psychosis came back. But this time I was prepared and D2 blockers kept it in check.
Learning to Observe Receptor Effects
That’s when I really understood how mesolimbic D2 hyperactivity shaped many of the experiences I had mistaken for personality traits. So I kept experimenting — safely — and started mapping out what different neurotransmitters did to me.
Serotonin: The Soothing Blanket
High serotonin feels like being gently wrapped in a cloud. That’s why I love psilocin, LSD, and MDMA. But I also noticed that selective 5HT2A (and maybe 2C) hyperactivity can cause a serotonergic type of psychosis. It’s not scary in the same way dopamine psychosis is, but it disconnects your thoughts from reality. They flood in too fast to process — you start lagging behind your own mind. This flow of thoughts induces panic attacks, something which I only observed at excessive 5HT2A activity (~6g of shrooms).
This only happens with LSD and psilocybin — not MDMA or cocaine. So it’s not just serotonin levels — it’s which receptors and how selectively they’re activated.
Note: What surprised me is, that longterm use of SSRIs doesn't result in a loss of its effect when 5HT is being down regulated by homeostasis in response to elevated Serotonin levels. Intuitively I would have thought that the prolonged increase of Serotonin levels cause 5HT to desensitize rendering the Serotonin boost less effective, but it doesn't seem to have a directly observable effect.
Broad Serotonin or Dopamine Increase ≠ Psychosis
When serotonin or dopamine is increased across the board, I don’t get psychosis. It’s when specific pathways or receptors are overstimulated — that’s when things break.
Cocaine, Dopamine, and D3 Hell
Cocaine blocks SERT, DAT, and NET — spiking serotonin, dopamine, and norepinephrine. The serotonin makes it feel warm and soothing. Dopamine makes you want more. At higher doses, D3 hyperactivity kicks in, which I can now distinguish from D2 and D1. It causes intense craving, compulsivity, and drug-seeking behavior.
That’s probably why cocaine is so addictive — and why blocking D3 helps rats stay away from it. In case you're suffering from a Cocaine addiction, D2/D3 or partial D3 agonists like Aripripazole or Cariprazin might help reduce D3 hyperactivity in the mesolimbic system by binding with a higher affinity but lower activation. In addition blocking SERT and NET using SSRIs or SNRIs substantially reduces serotonergic and norepinephrine craving.
I'm not a psychiatrist, so take this with a grain of salt, but a combination of SNRIs (e.g. Milnacipran) and D3 modulators (e.g. Cariprazine) might alleviate typical addiction driven behaviour and reduce amplification of serotonergic/norepinephrinergic craving.
If you're also psychotic due to Dopamine hyperactivity I would try a combination of Amisulprid and Cariprazin as both are pretty selective and don't affect too much of the basal dopaminergic signalling.
Note: Sertralin at maximal dose substantially reduces serotonergic craving, but craving for norepinephrine is still present. Increased D3 activity seems to exacerbate this craving.
MDMA Overdose, HPPD, and Sleep Ruined
Back when I was stuck in HPPD, I took a huge dose of MDMA, and that permanently wrecked my ability to fall asleep. I couldn’t sleep for years. I had to meditate instead of sleeping and stay awake for days until physical exhaustion. Sometimes staying awake for 3–4 days before I could crash.
Eventually I realized that blocking H1 only makes you tired — it doesn’t let your brain shut off. Instead it causes so much tiredness that it physically hurts to stay awake. It's like torture and I'm not the only one. Thankfully I discovered that tricyclic antidepressants like Amitriptylin or atypical ones like Mirtazapine both allow me to fall asleep again.
A friend of mine has the exact same problems of falling asleep and told me he's been at a state of being so tired it hurts inside your brain.
Sleep, Hypocretin, and Mirtazapine
High serotonin, dopamine, or norepinephrine all influence wakefulness. I can't sleep with high levels of NE or Dopamine. Even blocking H1 doesn't help. No matter how I balance them, I can’t fall asleep without Mirtazapine. I think this all comes down to abnormal hypocretin (orexin) activity — the system that acts like a master switch for wakefulness.
Even now, years later, if I don’t take Mirtazapine or if I take stimulants, I can lie in bed for 8–12 hours and stay in a meditative state of light sleep. Sometimes I reach slow wave sleep, but without medication I never reach REM. It’s like a light bulb in my brain is constantly lit and the switch is broken. I'm awake while sleeping, I can hear audiobooks, or wander my mind while being in a state of recovering energy.
What doesn't happen is cleansing of the hormones that make you tired. If you have stayed awake for a few consecutive days, you know that dreading feeling of tiredness that seems to hurt you physically.
Sometimes I can enter a state of meditation where the clean up routine get's started and I can feel how the substance that's causing exhaustion get's removed from my brain. It also seems to clean other substances, as it drastically reduces Cocaine activity. If I spend enough time in this state, I feel rested as if I had a good night of sleep, but I only got there twice and it took me 7 hours of focusing on reaching a state of deep sleep.
What Cocaine Addiction Taught Me
Because of my recent cocaine addiction, I learned how to differentiate the effects of serotonin, dopamine, and norepinephrine:
- Serotonin = warm, soothing comfort
- Dopamine = reward, drive, and craving
- Norepinephrine = focus, clarity, streamlined thought
With my ADD, I found that a small norepinephrine boost erased all my ADHD symptoms. No more chaos, no more cluttered thoughts, much less distraction. Just focus, productivity and thoughts get processed one by one instead of jumping between a hundred simultaneous thoughts.
My Current Theory
Now I only need SNRIs and D2/D3 blockers to completely normalize depression, suicidality, and ADHD. My working theory is:
- People with ADD have abnormally high dopaminergic sensitivity in the mesolimbic system, which makes them more impulsive, prone to addiction, and sensitive to THC-induced psychosis.
- At the same time, they likely have deficient norepinephrine signaling, which is why their thoughts don’t flow straight.
The River Metaphor
You can imagine thoughts like a river:
- Dopamine = increases the flow rate
- Serotonin = warms the water, makes it comfortable
- Norepinephrine = straightens the river, avoids swamps and chaos
🔬 What I Learned (Bullet Point Style, Still Me)
- LSD triggered permanent brain changes — made me THC-sensitive and prone to psychosis
- Mesolimbic D2 hyperactivity causes racing thoughts, anxiety, paranoia, and psychosis — D2 blockers fix it
- SSRIs (Sertraline) removed my lifelong chest pain and suicidality — the pain was never “normal”
- Weed + dopamine sensitivity = paranoid psychosis
- 5HT2A/2C hyperactivity causes thought flooding, serotonergic psychosis (unique from dopaminergic psychosis)
- Broad serotonin or dopamine increase feels good — it’s the selective receptor overdrive that causes issues
- Cocaine’s addiction mainly driven by D3 hyperactivity — leads to compulsive cravings
- Cocaine + amphetamines + D2 blockers = hellish D3 overdrive
- D3 blockade could be the key to breaking cocaine addiction (wish we had more selective D3 antagonists)
- High dopamine, serotonin, norepinephrine all keep you awake
- Only Mirtazapine lets me reach proper sleep — likely due to hypocretin modulation
- ADD symptoms likely caused by low norepinephrine and overreactive dopamine circuits
- Best treatment for me = SNRIs + D2/D3 blockers
- Thoughts flow best when dopamine is low, serotonin on a comforting leven, and norepinephrine keeping them straight
This is what I learned from messing with my own brain. It’s not medical advice — just my own reflections from observing the effects of substances like THC, LSD, psilocybin, cocaine, MDMA, amphetamines, 2C-B, ketamine, D2 blockers, SSRIs, and more.
I barely scratched the surface, but neurobiology is fascinating. I hope I get to learn a lot more about how brain chemistry shapes thoughts, perception, emotion — and how it can be rebalanced.
Final Thoughts
The takeaway is that drug abuse can be very dangerous for your mental health. You're way better off if you just stay away from drugs. Especially if you're prone to addiction or psychosis.
The risk of developing psychosis is substantial and I know multiple people who suffer(ed) from drug induced psychosis. LSD has a high chance to cause psychosis (~7%), but empirically it only causes HPPD or Psychosis when you abuse and take it multiple times a week for a prolonged time.
THC can induce acute psychotic symptoms when you have no tolerance and consume strong cannabis with high THC levels, especially strains with low CBD. THC can trigger chronic psychosis that persists even when you stop taking THC, but this has only happened to me twice when I consumed roughly 100g a month for 3 to 6 months.
THC induced psychosis can reliably be negated by blocking D2 which compensates the projection from the VTA to the NAcc.
Be cautious and responsible when you're messing with substances that affect your brain chemistry. Life's much better without substances and mental illness and psychosis can be a nightmare.