What could have caused these changes in my brain chemistry associated with smoking?

[Bewusst]

Tl;dr at the bottom

I've been a smoker for years and about a year ago, I first noticed a change in how I react to nicotine. These changes have not only persisted to this day, they have also started occuring more frequently and become more intense. When I smoke a cigarette, I often get a euphoric rush with goosebumps all over my body and a more or less intense feeling of pleasure. Sometimes it's rather subtle, other times really intense. I never experienced this before late 2020. It all started when I began consuming sugar free energy drinks and diet soda (aspartame -> phenylalanine -> tyrosine?). I still get these effects without drinking those now, albeit not as strong.

According to various studies, nicotine upregulates tyrosine hydroxylase (tyrosine -> L-DOPA - rate limiting step in dopamine synthesis), activates the mesolimbic dopaminergic system (the reward center), limits dopamine transporter availability, causing a reuptake inhibiton like effect and enhances striatal dopamine release. For some reason, the dopaminergic effects I get from smoking cigarettes have become noticeably amplified. On the other hand, I can't even go a few hours without a smoke now without getting nicotine cravings/withdrawal symptoms comprised of massive brain fog, blurred vision, trouble concentrating, irritability and a weird sense of derealization. My brain doesn't function without it anymore. Could these changes be related to adaptive responses to my botox use/iatrogenic botulism somehow? Perhaps nAChR upregulation, modulation of voltage-gated ion channels, axonal sprouting, activation of the IGF-1 signaling pathway? Either way, gonna light one up now

Tl;dr: Smoker for years. A year ago, I started getting a dopamine rush with goosebumps and a strong sense of pleasure/euphoria when smoking. This reaction still occurs a year later and has become more frequent and intense over time. Can't go a few hours without smoking. Nicotine has many effects on the dopaminergic system. Trying to identify the biochemical mechanisms underlying these changes in my brain chemistry

@Seth Walsh @Cope @DrTony @quakociaptockh @tincelw

 

[Wallenberg]

Stop smoking. It's an unhealthy, low-class trait.

 

[JosephGarrot123]

What addiction does to a mf. It's over for your lifespan

 

[Bewusst]

Stop smoking. It's an unhealthy, low-class trait.

What addiction does to a mf. It's over for your lifespan

 

[Wallenberg]

Smoking is white/ethnic trash cope.

 

[Deleted member 756]

Smoking is white/ethnic trash cope.

Ethnic bad boys smoke

 

[Bewusst]

Smoking is white/ethnic trash cope.

Muh stereotypes. Keep trying to fit in, you self esteem-less sheep. Character #404

 

[lutte]

What addiction does to a mf. It's over for your lifespan

Addiction is cope and nicotine isn't bad but smoking is bad because of other things in cigs. OP should switch to snus

 

[Pythagoras]

Move to Weed. at least you get something out of it.



nvm I read the thread

 

[Pythagoras]

Addiction is cope

It's literally a disease that can pass in genes.

 

[Bewusst]

Addiction is cope and nicotine isn't bad but smoking is bad because of other things in cigs. OP should switch to snus

Ik. Anything on topic?

 

[Wallenberg]

Addiction is cope and nicotine isn't bad but smoking is bad because of other things in cigs. OP should switch to snus

Snus is bad too. Better to not use snus.

 

[Bewusst]

Snus is bad too. Better to not use snus.

I tried dipping tobacco a few years ago. It was horrible

 

[lutte]

It's literally a disease that can pass in genes.

I'm not so sure tbh

 

[lutte]

Ik. Anything on topic?

wdym?

Snus is bad too. Better to not use snus.

it's alright. but I don't use it myself it's too expensive

 

[Wallenberg]

wdym?


it's alright. but I don't use it myself it's too expensive

Snus is unhealthy, it causes mouth cancer. Probably not as bad as cigs but still unhealthy.

 

[Bewusst]

wdym?

Anything related to the topic?

 

[lutte]

Snus is unhealthy, it causes mouth cancer. Probably not as bad as cigs but still unhealthy.

Are you sure or is that hearsay? Afaik there's no conclusive evidence of that. The swedish government would love that to be true though they've been trying to pin snus for something for a long time

 

[n0rthface]

Smoking is healthy, it refreshes the lungs.

 

[Seth Walsh]

Tl;dr at the bottom

I've been a smoker for years and about a year ago, I first noticed a change in how I react to nicotine. These changes have not only persisted to this day, they have also started occuring more frequently and become more intense. When I smoke a cigarette, I often get a euphoric rush with goosebumps all over my body and a more or less intense feeling of pleasure. Sometimes it's rather subtle, other times really intense. I never experienced this before late 2020. It all started when I began consuming sugar free energy drinks and diet soda (aspartame -> phenylalanine -> tyrosine?). I still get these effects without drinking those now, albeit not as strong.

According to various studies, nicotine upregulates tyrosine hydroxylase (tyrosine -> L-DOPA - rate limiting step in dopamine synthesis), activates the mesolimbic dopaminergic system (the reward center), limits dopamine transporter availability, causing a reuptake inhibiton like effect and enhances striatal dopamine release. For some reason, the dopaminergic effects I get from smoking cigarettes have become noticeably amplified. On the other hand, I can't even go a few hours without a smoke now without getting nicotine cravings/withdrawal symptoms comprised of massive brain fog, blurred vision, trouble concentrating, irritability and a weird sense of derealization. My brain doesn't function without it anymore. Could these changes be related to adaptive responses to my botox use/iatrogenic botulism somehow? Perhaps nAChR upregulation, modulation of voltage-gated ion channels, axonal sprouting, activation of the IGF-1 signaling pathway? Either way, gonna light one up now

Tl;dr: Smoker for years. A year ago, I started getting a dopamine rush with goosebumps and a strong sense of pleasure/euphoria when smoking. This reaction still occurs a year later and has become more frequent and intense over time. Can't go a few hours without smoking. Nicotine has many effects on the dopaminergic system. Trying to identify the biochemical mechanisms underlying these changes in my brain chemistry

@Seth Walsh @Cope @DrTony @quakociaptockh @tincelw

Didn't read through this fully coz I'm in a rush atm btw how does DAT inhibition consequently cause a striatal release of dopamine? That shouldn't happen naturally.

 

[Deleted member 4301]

The answer is simple - you find a foid late at night, rape her, then mutilate her

 

[Seth Walsh]

Tl;dr at the bottom

I've been a smoker for years and about a year ago, I first noticed a change in how I react to nicotine. These changes have not only persisted to this day, they have also started occuring more frequently and become more intense. When I smoke a cigarette, I often get a euphoric rush with goosebumps all over my body and a more or less intense feeling of pleasure. Sometimes it's rather subtle, other times really intense. I never experienced this before late 2020. It all started when I began consuming sugar free energy drinks and diet soda (aspartame -> phenylalanine -> tyrosine?). I still get these effects without drinking those now, albeit not as strong.

According to various studies, nicotine upregulates tyrosine hydroxylase (tyrosine -> L-DOPA - rate limiting step in dopamine synthesis), activates the mesolimbic dopaminergic system (the reward center), limits dopamine transporter availability, causing a reuptake inhibiton like effect and enhances striatal dopamine release. For some reason, the dopaminergic effects I get from smoking cigarettes have become noticeably amplified. On the other hand, I can't even go a few hours without a smoke now without getting nicotine cravings/withdrawal symptoms comprised of massive brain fog, blurred vision, trouble concentrating, irritability and a weird sense of derealization. My brain doesn't function without it anymore. Could these changes be related to adaptive responses to my botox use/iatrogenic botulism somehow? Perhaps nAChR upregulation, modulation of voltage-gated ion channels, axonal sprouting, activation of the IGF-1 signaling pathway? Either way, gonna light one up now

Tl;dr: Smoker for years. A year ago, I started getting a dopamine rush with goosebumps and a strong sense of pleasure/euphoria when smoking. This reaction still occurs a year later and has become more frequent and intense over time. Can't go a few hours without smoking. Nicotine has many effects on the dopaminergic system. Trying to identify the biochemical mechanisms underlying these changes in my brain chemistry

@Seth Walsh @Cope @DrTony @quakociaptockh @tincelw

Well nicotine is addictive. I don't think smoking cigs is causing an addiction through the dopamine network because even if you are increasing dopamine synthesis and slowing down the clearance of the dopamine from the neurons (all through nicotine?); the DAT blocking aspect shouldn't be the cause of newly formed addictive behaviour.

Concerta/ritalin are less dangerous than the amphetamines since amphetamines not only block DAT but they activate TAAR1 directly causing a striatal release of dopamine. But most DAT inhibitors don't target TAAR1 like adderall and meth... I'm pretty sure cocaine doesn't even target it (could be wrong).

The opioid network is more involved with addiction, and I think nicotine's mechanism of addiction is not dopamine related. I don't know exactly what's the underlying MOA of nicotine addiction but it does cause adaptations to opioid receptors...

 

[Seth Walsh]

Well nicotine is addictive. I don't think smoking cigs is causing an addiction through the dopamine network because even if you are increasing dopamine synthesis and slowing down the clearance of the dopamine from the neurons (all through nicotine?); the DAT blocking aspect shouldn't be the cause of newly formed addictive behaviour.

Concerta/ritalin are less dangerous than the amphetamines since amphetamines not only block DAT but they activate TAAR1 directly causing a striatal release of dopamine. But most DAT inhibitors don't target TAAR1 like adderall and meth... I'm pretty sure cocaine doesn't even target it (could be wrong).

The opioid network is more involved with addiction, and I think nicotine's mechanism of addiction is not dopamine related. I don't know exactly what's the underlying MOA of nicotine addiction but it does cause adaptations to opioid receptors...

I'd assume this is why cocaine and methyphenidate "withdrawals" aren't really full fledged compared to other drugs like gabaergics and opioids (and even other dopaminergics like amphetamines). Sure there's a crash but there's less of a physical dependence/withdrawal type addiction associated with pure DAT blocking dopaminergics compared to multifaceted dopaminergic drugs which cause an increase in transmission in multiple ways.

@TsarTsar444 even posted a few weeks ago that he NEVER gets withdrawals from methylphenidate but feels a huge crash. I was on methylphenidate for years and had no withdrawals going cold turkey off the highest prescribed dose. I guess it's because once homeostatis is reached again after the dopamine gets reuptaken by the neurons (and this is probably when you feel the "crash"), but no dysfunction is caused with TAAR1 which is essentially the modulator of the dopaminergic system. When the TAAR1 receptor is activated non stop it's going to downregulate in its own attempt to self regulate during the heightened period of activation, and after cessation it's going to take time to upregulate which will cause a withdrawal period. On the other hand, trapping dopamine in the synaptic cleft through DAT inhibition isn't going to cause any receptor to downregulate.

 

[Bewusst]

Didn't read through this fully coz I'm in a rush atm btw how does DAT inhibition consequently cause a striatal release of dopamine? That shouldn't happen naturally.

I didn't say that. Those are separate effects mediated through different mechanisms and not necessarily related to one another

 

[TsarTsar444]

I'd assume this is why cocaine and methyphenidate "withdrawals" aren't really full fledged compared to other drugs like gabaergics and opioids (and even other dopaminergics like amphetamines). Sure there's a crash but there's less of a physical dependence/withdrawal type addiction associated with pure DAT blocking dopaminergics compared to multifaceted dopaminergic drugs which cause an increase in transmission in multiple ways.

@TsarTsar444 even posted a few weeks ago that he NEVER gets withdrawals from methylphenidate but feels a huge crash. I was on methylphenidate for years and had no withdrawals going cold turkey off the highest prescribed dose. I guess it's because once homeostatis is reached again after the dopamine gets reuptaken by the neurons (and this is probably when you feel the "crash"), but no dysfunction is caused with TAAR1 which is essentially the modulator of the dopaminergic system. When the TAAR1 receptor is activated non stop it's going to downregulate in its own attempt to self regulate during the heightened period of activation, and after cessation it's going to take time to upregulate which will cause a withdrawal period. On the other hand, trapping dopamine in the synaptic cleft through DAT inhibition isn't going to cause any receptor to downregulate.

Hey bro, im going to start Concerta this week again, some questions:

1. Im going to take 2 × 36mg tablets daily, cause i need 72mg and currently my pharmacy only has 54mg. Does it work like a normals 72mg tablet righr?

2. How does tolerance work with Concerta (reuptake inhibitors) vs Amphetamines? Does the functionality effects from concerta get worse over time and fast in your experience or is it always effective?

Yes you know i used concerta quite the bit, but i wasn't seriously studying with it, amphetamines mog it hard imo for what they do, the motivation drive from amphetamine is insane, concerta just makes me slowed down, calm, and robotic.

But anyway im going to try again because im eating chicken and eggs daily, and other healthy food, started doing cardio and going to the gym, so in theory it should function much more effectively now given that chicken meat is packed with b6 vitamin

 

[Seth Walsh]

limits dopamine transporter availability, causing a reuptake inhibiton like effect and enhances striatal dopamine release

I might've misread or misunderstood

 

[Seth Walsh]

Hey bro, im going to start Concerta this week again, some questions:

1. Im going to take 2 × 36mg tablets daily, cause i need 72mg and currently my pharmacy only has 54mg. Does it work like a normals 72mg tablet righr?

2. How does tolerance work with Concerta (reuptake inhibitors) vs Amphetamines? Does the functionality effects from concerta get worse over time and fast in your experience or is it always effective?

Yes you know i used concerta quite the bit, but i wasn't seriously studying with it, amphetamines mog it hard imo for what they do, the motivation drive from amphetamine is insane, concerta just makes me slowed down, calm, and robotic.

But anyway im going to try again because im eating chicken and eggs daily, and other healthy food, started doing cardio and going to the gym, so in theory it should function much more effectively now given that chicken meat is packed with b6 vitamin

If you can keep your natural dopamine synthesis high with something like bromantane then 18mg will feel like 90mg... Feeling calm with concerta is probably a sign that you're using too high a dose and stopped producing enough new dopamine because your brain feels there's enough in the synaptic cleft. You'll feel that overwhelming drive with increased dopamine synthesis + DAT blocking, and you don't need a huge dose of concerta to get that drive.

Yeah when I first went on concerta it had that "intense drive" feeling for only a short while but that quickly changed to the slowed down / calm robotic feeling, probably because I was just using too high of a dose of a DAT blocker but wasn't producing a fraction of the dopamine that I should've been naturally (maybe dopamine synthesis got slowed due to the prolonged period of having no dopamine being reuptaken into the neurons? idk..

 

[Bewusst]

Well nicotine is addictive. I don't think smoking cigs is causing an addiction through the dopamine network because even if you are increasing dopamine synthesis and slowing down the clearance of the dopamine from the neurons (all through nicotine?); the DAT blocking aspect shouldn't be the cause of newly formed addictive behaviour.

Concerta/ritalin are less dangerous than the amphetamines since amphetamines not only block DAT but they activate TAAR1 directly causing a striatal release of dopamine. But most DAT inhibitors don't target TAAR1 like adderall and meth... I'm pretty sure cocaine doesn't even target it (could be wrong).

The opioid network is more involved with addiction, and I think nicotine's mechanism of addiction is not dopamine related. I don't know exactly what's the underlying MOA of nicotine addiction but it does cause adaptations to opioid receptors...

None of this explains why/how I started developing above mentioned reaction to nicotine after I had already been smoking for years. As I said, it was around the same time when I began drinking beverages with aspartame. I had also been using P5P, L-5-MTHF, methylcobalamin (all cofactors in dopamine synthesis) and TMG for a few months

 

[TsarTsar444]

If you can keep your natural dopamine synthesis high with something like bromantane then 18mg will feel like 90mg... Feeling calm with concerta is probably a sign that you're using too high a dose and stopped producing enough new dopamine because your brain feels there's enough in the synaptic cleft. You'll feel that overwhelming drive with increased dopamine synthesis + DAT blocking, and you don't need a huge dose of concerta to get that drive.

Yeah when I first went on concerta it had that "intense drive" feeling for only a short while but that quickly changed to the slowed down / calm robotic feeling, probably because I was just using too high of a dose of a DAT blocker but wasn't producing a fraction of the dopamine that I should've been naturally (maybe dopamine synthesis got slowed due to the prolonged period of having no dopamine being reuptaken into the neurons? idk..

Interesting, thats exactly what i thought as well, the dopamine already produced got trapped but after that you get a numb feeling because of no new dopamine. So how can this be fixed? Bromantane is one way, any more natural way? Is the lifting and eating 160g of protein with eggs and chicken meat going to change my experience now compared to when i used the concerta while eating just noodles and some shit food?

Also Interesting but what do you mean that 18 can be like 90mg? So i could just use 36mg and be good for the whole day?

 

[Seth Walsh]

None of this explains why/how I started developing above mentioned reaction to nicotine after I had already been smoking for years. As I said, it was around the same time when I began drinking beverages with aspartame. I had also been using P5P, L-5-MTHF, methylcobalamin (all cofactors in dopamine synthesis) and TMG for a few months

I'm not sure man but I don't think something like increased phenylalanine intake combined with smoking can cause such a huge effect

Wish I had a good clue but I don't

 

[Seth Walsh]

Interesting, thats exactly what i thought as well, the dopamine already produced got trapped but after that you get a numb feeling because of no new dopamine. So how can this be fixed? Bromantane is one way, any more natural way? Is the lifting and eating 160g of protein with eggs and chicken meat going to change my experience now compared to when i used the concerta while eating just noodles and some shit food?

Also Interesting but what do you mean that 18 can be like 90mg? So i could just use 36mg and be good for the whole day?

Just anecdotally. I'm absolutely blasted on 18mg if I ever take it now. Full of energy and drive. But when I was on 54mg + 10mg ritalin I felt zombied out.

Yeah my theory is that more dopamine reaches the neurons where the reuptake inhibition can happen, if you focus on increasing natural dopamine synthesis. Also a lower dose of a DAT blocker might allow some dopamine to reach the cytosol which could send positive feedback to naturally keep synthesising more dopamine. Anything that upregulates TH would just amplify the rate and amount of dopamine being synthesised too.

 

[Seth Walsh]

None of this explains why/how I started developing above mentioned reaction to nicotine after I had already been smoking for years. As I said, it was around the same time when I began drinking beverages with aspartame. I had also been using P5P, L-5-MTHF, methylcobalamin (all cofactors in dopamine synthesis) and TMG for a few months

Have you tried quitting the drinks with aspartame?

 

[TsarTsar444]

Just anecdotally. I'm absolutely blasted on 18mg if I ever take it now. Full of energy and drive. But when I was on 54mg + 10mg ritalin I felt zombied out.

Yeah my theory is that more dopamine reaches the neurons where the reuptake inhibition can happen, if you focus on increasing natural dopamine synthesis. Also a lower dose of a DAT blocker might allow some dopamine to reach the cytosol which could send positive feedback to naturally keep synthesising more dopamine. Anything that upregulates TH would just amplify the rate and amount of dopamine being synthesised too.

This is after you started taking bromantane with your concerta right? If so what is your dose and how do you take it, sublingualy is much better then oral

 

[Seth Walsh]

This is after you started taking bromantane with your concerta right? If so what is your dose and how do you take it, sublingualy is much better then oral

Yep after taking a complete 3-4 month break from concerta and using bromantane for the past 2 months, then reintroducing Concerta (just when I need it). Dose is super low. 9-18mg orally. So I need to cut the 18mg in half when taking 9. Can't say it feels "more powerful than" like 108mg concerta even though it does... It feels different though, as if I just took my first ever dose of concerta each time. I guess my dopamine system is just working well and the bromantane is allowing me to produce enough so that huge amounts of dopamine ends up getting blocked at the neuron.

 

[Bewusst]

I'm not sure man but I don't think something like increased phenylalanine intake combined with smoking can cause such a huge effect

Wish I had a good clue but I don't

Well, nicotine increases TYH gene expression. Interestingly, smoking is also associated with significantly lower levels of MAO B, thus inhibiting one pathway of dopamine breakdown: https://pubmed.ncbi.nlm.nih.gov/8602220/

 

[Seth Walsh]

Well, nicotine increases TYH gene expression. Interestingly, smoking is also associated with significantly lower levels of MAO B, thus inhibiting one pathway of dopamine breakdown: https://pubmed.ncbi.nlm.nih.gov/8602220/

Yep but this wouldn't cause a profoundly negative reaction unless taken with something stronger like a DAT blocker. I've drank diet drinks with phenylalanine with bromantane and cordyceps (MAO-B inhibitor) and didn't feel any strong effects.

 

[Pythagoras]

Well, nicotine increases TYH gene expression. Interestingly, smoking is also associated with significantly lower levels of MAO B, thus inhibiting one pathway of dopamine breakdown: https://pubmed.ncbi.nlm.nih.gov/8602220/

Answer in PM

 

[Seth Walsh]

Yep but this wouldn't cause a profoundly negative reaction unless taken with something stronger like a DAT blocker. I've drank diet drinks with phenylalanine with bromantane and cordyceps (MAO-B inhibitor) and didn't feel any strong effects.

Best way to try get rid of it is to just stop the energy drinks if you think they're what cause you to feel uncomfortable when smoking a cig.

 

[TsarTsar444]

Yep after taking a complete 3-4 month break from concerta and using bromantane for the past 2 months, then reintroducing Concerta (just when I need it). Dose is super low. 9-18mg orally. So I need to cut the 18mg in half when taking 9. Can't say it feels "more powerful than" like 108mg concerta even though it does... It feels different though, as if I just took my first ever dose of concerta each time. I guess my dopamine system is just working well and the bromantane is allowing me to produce enough so that huge amounts of dopamine ends up getting blocked at the neuron.

So if i start bromantane and concerta from scratch at the same day should i notice a difference or does it need to build up first? (Speaking about bromantane).

What is your dose and how to you administer it?

 

[Seth Walsh]

Well, nicotine increases TYH gene expression. Interestingly, smoking is also associated with significantly lower levels of MAO B, thus inhibiting one pathway of dopamine breakdown: https://pubmed.ncbi.nlm.nih.gov/8602220/

Does nicotine cause a permanent increase in TYH gene expression?

 

[Seth Walsh]

So if i start bromantane and concerta from scratch at the same day should i notice a difference or does it need to build up first? (Speaking about bromantane).

What is your dose and how to you administer it?

10-15mg orally but I'm trying 5mg x3 at the moment.

I quit concerta 3-4 months ago and started bromantane 2-3 months ago. I do think bromantane has a build up effect and kinda resensitises you to dopaminergics especially after taking a break. It resets the tolerance threshold I feel.

 

[Bewusst]

Yep but this wouldn't cause a profoundly negative reaction unless taken with something stronger like a DAT blocker. I've drank diet drinks with phenylalanine with bromantane and cordyceps (MAO-B inhibitor) and didn't feel any strong effects.

I never mentioned a negative reaction. It's quite the opposite, a very pleasurable feeling

 

[Bewusst]

Does nicotine cause a permanent increase in TYH gene expression?

https://pubmed.ncbi.nlm.nih.gov/12538809/

https://molpharm.aspetjournals.org/content/40/2/193

 

[Seth Walsh]

I never mentioned a negative reaction. It's quite the opposite, a very pleasurable feeling

Oh... If you're trying to understand the exact reason why you feel that feeling it's like finding a needle in a haystack and might not necessarily be due to an interaction between energy drinks and cigarettes. I asked if you ever stopped taking either of the two to see if that feeling went away? Because just trying to guess specific chemical interactions without stopping consumption of what you feel causes the feeling, will leave you unable to find out why you feel that pleasurable feeling in the first place.

 

[Seth Walsh]

https://pubmed.ncbi.nlm.nih.gov/12538809/

https://molpharm.aspetjournals.org/content/40/2/193

Increased TYH gene expression will cause an increased pleasure response over time btw. Maybe that's your answer ^^

 

[Bewusst]

I asked if you ever stopped taking either of the two to see if that feeling went away? Because just trying to guess specific chemical interactions without stopping consumption of what you feel causes the feeling, will leave you unable to find out why you feel that pleasurable feeling in the first place.

Yes. As I said earlier, I get this reaction from smoking now even if I don't have energy drinks or diet soda but they're usually stronger if I combine the two. The reason I pointed out energy drinks and diet soda is that these effects started to occur around the same time when I began drinking them

 

[Bewusst]

Increased TYH gene expression will cause an increased pleasure response over time btw. Maybe that's your answer ^^

That was also one of my guesses

 

[quakociaptockh]

There are many interwinding subsystems in brain: GABA, dopamine/serotonin, nicotinoid, opioid, cannabinoid, steroid etc.

From our perspective the most 2 important are reward system (dopamine/serotonin) and the opioid system (pleasure, pain, emotions) which seems to have some regulatory control over the former one. In short: overactivation of opioid system causes downregulation of reward system. That's why pleasures blunt over time, and also why ascethicism works.

Try what junkies do and do some naltrexone. This will disable your opioid system temporarily, which will cause slight upregulation of opioid and reward system. Then naltrexone fades away, natural opioids (endorphines) kick in and you feel everything strong and fresh.

Bonus: you will cum monstrual loads of jizz next time you fap.

Low dose naltrexone is especially good for chronic depression and chronic anxiety, but it makes you sleepy af so it can be done only when you don't have a job.

 

[Bewusst]

There are many interwinding subsystems in brain: GABA, dopamine/serotonin, nicotinoid, opioid, cannabinoid, steroid etc.

From our perspective the most 2 important are reward system (dopamine/serotonin) and the opioid system (pleasure, pain, emotions) which seems to have some regulatory control over the former one. In short: overactivation of opioid system causes downregulation of reward system. That's why pleasures blunt over time, and also why ascethicism works.

Try what junkies do and do some naltrexone. This will disable your opioid system temporarily, which will cause slight upregulation of opioid and reward system. Then naltrexone fades away, natural opioids (endorphines) kick in and you feel everything strong and fresh.

Bonus: you will cum monstrual loads of jizz next time you fap.

Low dose naltrexone is especially good for chronic depression and chronic anxiety, but it makes you sleepy af so it can be done only when you don't have a job.

You haven't actually read my original post

 

[quakociaptockh]

You haven't actually read my original post

Nope.