Drugs and fantasizing about transexuals?

[JohnBoy2000]

I raise this cause I've read it on various drug harm reduction forums ad nauseum.

Dudes hit methamphetamine then spend the next 24 hours parked in front of their laptop masturbating to a transsexual gang bang porn.

"Nothing in the world like it, most euphoria, best possible escape from reality".

Dudes who are ordinarily, without said VMAT reverser acting inside their nerve terminals, strictly heterosexual.

And that's the question, is it the ultimate escape from reality?

A nice time to check-out if there's a "storm outside" (figuratively speaking) and you just need to have a little shut-in time and wait for it to blow over?

.....

At the moment, for me, given my neural state as a function of my current cognitive state - almost any drug sends me a little hay-wire.

But methamphetamine is like the escapism rocket fuel;
Despite the fact it's a "stimulant", it leaves me kind of comatose staring at nonsensical information feeling like I'm solving universal mysteries whilst actually accomplishing less than squat, never having felt so good in my life.

.....

Is it just me?

 

[bingey]

...........

 

[plumbus-nine]

Lol? I read this before, think here on BL, but I for myself can't imagine changing my sexual preferences due to / while on drugs only. Actually most drugs kill my sexuality, might have to do with antidepressant use. Dissociatives weirdly both increased and killed my libido, here I really found myself masturbating for hours but usually that's not me. Also on amphetamines I have much less problems relating to other men but not in a real sexual way, just usually I am very reserved about my own gender (childhood issue stuff) and stims change that but again, it's not sexual. I can imagine tho that drugs can and will bring out hidden preferences, even such which are hidden from yourself in the subconscious.

 

[JohnBoy2000]

...........

Yeah it was on the "which is the best chem sex drug" thread.

 

[Lil'LinaptkSix]

I have a "thing" for petite transsexuals when on high doses of speed. Mainly high use of good cocaine. It obviously turns me on but if a fine ass girly boy was to approach me in real life I would either pass out or bang til the dawn. lol
YMMV

 

[Las Veghost grower]

sounds like a you problem man …

 

[deficiT]

Bdd ----> SLR

If there's a home for this, it's more likely here then bdd

 

[Kaleida]

Drugs can expand your sexuality in all kinds of wonderful ways. It's just brain chemistry, after all.

Enhaced D2-type receptor activity facilitates the development of conditioned same-sex partner preference in male rats

Animal models have shown that the neural bases of social attachment, sexual preference and pair bonds, depend on dopamine D2-type receptor and oxytocin activity. In addition, studies have demonstrated that cohabitation can shape partner preference via conditioning. Herein, we used rats to explore the development of learned same-sex partner preferences in adulthood as a result of cohabitation during enhanced D2 activity. Experimental Wistar males (N = 20), received saline or the D2 agonist (quinpirole) and were allowed to cohabitate during 24 h, with a stimulus male partner that bore almond scent on the back as conditioned stimulus. This was repeated every 4 days, for a total of three trials. Four days later they were drug-free tested for partner preference between the scented male partner and a sexually receptive female. Sexual partner preference was analyzed by measuring frequency and latency for appetitive and consummatory sexual behaviors, as well as non-contact erections. Social preference was also analyzed by measuring the frequency and latency of visits, body contacts and time spent together. Results indicated that only quinpirole-treated males displayed sexual and social preference for the scented male over the sexually receptive female. They spent more time together, displayed more body contacts, more female-like proceptive behaviors, and more non-contact erections. Accordingly, conditioned males appeared to be more sexually aroused and motivated by the known male than by a receptive female. We discuss the implications of this animal model on the formation of learned homosexual partner preferences.

 

[plumbus-nine]

Yeah it was on the "which is the best chem sex drug" thread.

Indeed, this was it.

But well I mean it's pretty common for drugs to increase libido sometimes to the extent of sleeping with strangers (see alcohol or GHB, the latter became infamous as a date rape drug where the victim actually participates but would not have done so when sober) and guess this includes people which weren't in the dating scheme of the sober individual, but I question dating schemes anyways. Just wanna say, why not - it doesn't seem to be common to turn semi-gay due to drugs but guess you'll sooner or later find others with similar experiences. Possibly you just consciously mask the preference when sober and drugs disinhibit that?

@Kaleida Weird that D2 for me doesn't do any of the supposed stuff, it neither induces psychotomimetic features nor does it make me promiscuous (MXE did so tho, and I'm not exactly proud of, but it was only a disinhibition of stuff already there). It just induces insomnia in me, and reduces brain fog while antipsychotics (D2 antagonists) are anhedonia/dysphoria inducing and increase brain fog.

 

[Juniper Bruhmomentius]

One does not realize that sexuality is a spectrum until one masturbates to traps furiously

 

[Kaleida]

@Kaleida Weird that D2 for me doesn't do any of the supposed stuff, it neither induces psychotomimetic features nor does it make me promiscuous (MXE did so tho, and I'm not exactly proud of, but it was only a disinhibition of stuff already there). It just induces insomnia in me, and reduces brain fog while antipsychotics (D2 antagonists) are anhedonia/dysphoria inducing and increase brain fog.

It's been a really long time since I came upon this, but I know many years ago I found a study that tested different genetic strains of either like rats or mice against D1 an D2 receptor agonists and had results that were things like, in some of them D1 was stimulating and D2 was sedating, in some it was the exact opposite, in some they were both stimulating, etc. I think it's probably one of those things that fluctuates a lot from organism to organism and through evolution maybe just because dopamine is such an important factor in driving survival-oriented behaviors, or something like that. Similarly, even people who have mental disorders that have been linked to high dopaminergic activity don't always experience the same sort of symptoms, like some are more psychotic like schizophrenia, some are more manic like bipolar disorder, and so on. I think psychosis is really interesting, but in general you should probably be happy not to be sensitive to it. Hypersexuality is fun though (when desired), I actually get it from most drugs myself, so I suppose we're pretty opposite in that way.

 

[plumbus-nine]

It's been a really long time since I came upon this, but I know many years ago I found a study that tested different genetic strains of either like rats or mice against D1 an D2 receptor agonists and had results that were things like, in some of them D1 was stimulating and D2 was sedating, in some it was the exact opposite, in some they were both stimulating, etc. I think it's probably one of those things that fluctuates a lot from organism to organism and through evolution maybe just because dopamine is such an important factor in driving survival-oriented behaviors, or something like that. Similarly, even people who have mental disorders that have been linked to high dopaminergic activity don't always experience the same sort of symptoms, like some are more psychotic like schizophrenia, some are more manic like bipolar disorder, and so on. I think psychosis is really interesting, but in general you should probably be happy not to be sensitive to it. Hypersexuality is fun though (when desired), I actually get it from most drugs myself, so I suppose we're pretty opposite in that way.

Possible that SSRI + opioid use skews the picture. I used to have a high libido as an adolescent, before heavy drug use. Guess opioids might be the culprit, I also have pretty low testosterone these days and supplementing it briefly brought back my libido. I'd continue on it but it's pretty expensive and an irreversible choice as endogenous production gets suppressed by substitution.

Very interesting what you found about dopamine, no question that receptor activity varies greatly between individuals and that this is one reason why psychiatric pills don't work as described. I certainly have excitatory D2, maybe overly so as somebody recently suggested, and D1/D3 seems to be inhibitory (pramipexole being a D3 preferring agonist made me sleepy initially) - so far I am the norm but there will be more subtle differences. Still, it's a huge bite that a whole fucking receptor group might work opposed to current science's belief. Wow. Confirms some theorizing of myself. They should approve medicines less rigorously and primarily based on safety. Then let doc + patient chose the right drug.

 

[plumbus-nine]

@Kaleida, would you mind to post a link to that study?

Even more ridiculous is that it's about rats/mice - they just don't know about us humans but diagnose and "treat" the fuck out of stuff.

 

[Kaleida]

@Kaleida, would you mind to post a link to that study?

Even more ridiculous is that it's about rats/mice - they just don't know about us humans but diagnose and "treat" the fuck out of stuff.

Well, the reason I said it the way I did and didn't post the link is just because it was a long time ago and all the keywords I can think of to try to find it again right now are very general, so it's not easy. I'm looking right now, I don't think I've found the specific one I was thinking of yet but there are multiple studies that show how the effects can differ depending on the strains of mice or rat as well as significantly between mice and rats more in general, like this one:

Dopamine D1 and D2 Agonist Effects on Prepulse Inhibition and Locomotion: Comparison of Sprague-Dawley Rats to Swiss-Webster, 129X1/SvJ, C57BL/6J, and DBA/2J Mice

D2 receptors have been studied in relation to therapeutic uses of dopaminergic drugs, and psychomotor stimulant effects [as manifested by decreased prepulse inhibition (PPI) of startle and increased locomotor activity] are hallmark be- havioral effects of D2 agonists in rats. Genetic studies with mutant mice might be useful in this line of investigation; however, recent studies suggest that mice differ from rats with respect to D2 agonist effects. Accordingly, we studied a wide range of doses of the D2-like agonist quinelorane (0.0032–5.6 mg/kg) and the D1-like agonist R-6-Br-APB [R(􏰀)-6-bromo-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5- tetrahydro-1H-3-benzazepine hydrobromide] (0.032–5.6 mg/ kg) in outbred Sprague-Dawley rats, outbred Swiss-Webster mice, and inbred 129X1/SvJ, C57BL/6J, and DBA/2J mice. Whereas the D2 agonist dose-dependently decreased PPI and increased locomotion in rats, neither of these effects was observed in outbred or inbred mice. In contrast, the D1 agonist reduced PPI and increased locomotion in Sprague- Dawley rats and in Swiss-Webster, 129X1/SvJ, and C57BL/6J mice. Neither agonist decreased PPI in DBA/2J mice, although PPI was increased in this strain by a D2 antagonist. Pretreatment with either the D2 antagonist eti- clopride (1 mg/kg) or the D1 antagonist SCH39166 [(􏰁)- trans-6,7,7a,8,9,13b-hexahydro-3-chloro-2-hydroxy-N- methyl-5H-benzo[d]naptho-(2,1-b)azepine] (1 mg/kg) prevented the PPI-disruptive effects of quinelorane in rats and R-6-Br-APB in mice, suggesting receptor interactions in both species. In summary, psychomotor stimulant effects of a D2 agonist that were robustly observed in outbred rats were absent in several outbred and inbred strains of mice. These results may have implications for the study of mutant mice to investigate genes involved in psychomotor function in humans.

I'm still looking so I'll post more if I find that specific one again.

Possible that SSRI + opioid use skews the picture. I used to have a high libido as an adolescent, before heavy drug use. Guess opioids might be the culprit, I also have pretty low testosterone these days and supplementing it briefly brought back my libido. I'd continue on it but it's pretty expensive and an irreversible choice as endogenous production gets suppressed by substitution.

Very interesting what you found about dopamine, no question that receptor activity varies greatly between individuals and that this is one reason why psychiatric pills don't work as described. I certainly have excitatory D2, maybe overly so as somebody recently suggested, and D1/D3 seems to be inhibitory (pramipexole being a D3 preferring agonist made me sleepy initially) - so far I am the norm but there will be more subtle differences. Still, it's a huge bite that a whole fucking receptor group might work opposed to current science's belief. Wow. Confirms some theorizing of myself. They should approve medicines less rigorously and primarily based on safety. Then let doc + patient chose the right drug.

Yeah, I'm not too educated about opioids but I've definitely heard they can have that effect on the sex drive, and I know for sure that SSRIs can too. I didn't know that about endogenous testosterone responding that way to substitution, that's interesting but odd.

I definitely agree that just broadly giving someone one type of drug because they've been given a specific psychiatric label is the wrong way to do it. I think our system somewhat allows a doctor to work with a patient to find the right drug (though not as much as it would with proper drug legislation), but often it seems like that's not what the doctors try to do, they'll just go with what they've been told works, which is definitely too simplistic of a strategy. For me, it's just like working with something like psychedelics - sure, they're functionally similar enough that we can group them together, but still, everyone has a different favorite or favorites, gets different things out of them, wants to use them with different frequency, and so on, and heck, antipsychotics even work through the exact same receptors, so why not do something similar with them?

 

[plumbus-nine]

Yeah, I'm not too educated about opioids but I've definitely heard they can have that effect on the sex drive, and I know for sure that SSRIs can too. I didn't know that about endogenous testosterone responding that way to substitution, that's interesting but odd.

I only know about males but here opioids strongly suppress the production of testosterone, dissociatives do the same and both sum up to dangerous levels. Strangely I only lost my libido, put on some kilos around the belly and rushed into depression, after stopping concomitant use of dissociatives, thus my theory that these both suppress and substitute as steroid-mimetics while opioids only suppress. Oh, I had some severe testicle cramps when starting the bupe alongside DCK, visited a doc and he sent me home probably thinking I made stuff up. Possibly prescribed ibuprofen, I don't remember.

Don't know to which degree T production recovers after ceasing opioids, my hunch is that it doesn't completely so and that it's a major factor in long-term effects of opioids.

I definitely agree that just broadly giving someone one type of drug because they've been given a specific psychiatric label is the wrong way to do it. I think our system somewhat allows a doctor to work with a patient to find the right drug (though not as much as it would with proper drug legislation), but often it seems like that's not what the doctors try to do, they'll just go with what they've been told works, which is definitely too simplistic of a strategy. For me, it's just like working with something like psychedelics - sure, they're functionally similar enough that we can group them together, but still, everyone has a different favorite or favorites, gets different things out of them, wants to use them with different frequency, and so on, and heck, antipsychotics even work through the exact same receptors, so why not do something similar with them?

Agreed. Some/many docs seem to be repelled by the reality of that one just needs to try-fail-retry through the available drugs. When you read a bit about drug discovery etc. you realize that it's pretty random what we have on market and what not. Approval doesn't even help to filter out the toxic ones, I'd say we would probably be better off with a less restrictive approval process which primarily focused on safety and then having docs + pharmacologists (which these days are just glorified salespersons) select the correct drug together with you.

Yeah, drugs with effects opposing to antipsychotics are interesting and somehow make me question the widespread prescription of antipsychs. What if these drugs block neurogenesis? It's already certain that blocking D2 makes your brain shrink. The war on drugs did and does so much damage.

 

[Kaleida]

You know, it's been so long that it's really hard to remember exactly, but I think this might have been the main one I was referring to:

Psychomotor stimulation by dopamine D1-like but not D2-like agonists in most mouse strains

Many neurological and psychiatric disorders are treated with dopamine modulators. Studies in mice may reveal genetic factors underlying those disorders or responsiveness to various treatments, and species and strain differences both complicate the use of mice and provide valuable tools. We evaluated psychomotor effects of the dopamine D1-like agonist R-6-Br-APB and the dopamine D2-like agonist quinelorane using a locomotor activity procedure in 15 mouse strains (inbred 129S1/SvImJ, 129S6/SvEvTac, 129X1/SvJ A/J, BALB/cByJ, BALB/cJ, C3H/HeJ, C57BL/6J, CAST/EiJ, DBA/2J, FVB/NJ, SJL/J, SPRET/EiJ, outbred Swiss Webster and CD-1) and Sprague Dawley rats, using groups of both females and males. Both D1 and D2 stimulation produced hyperactivity in the rats, and surprisingly, only two mouse strains were similar in that regard (C3H/HeJ, SPRET/EiJ). In contrast, the majority of mouse strains exhibited hyperactivity only with D1 stimulation, whereas D2 stimulation had no effect or decreased activity. BALB substrains, A/J and FVB/NJ mice showed only decreased activity following either D1 or D2 stimulation. CAST/EiJ mice exhibited hyperactivity exclusively with D2 stimulation. Sex differences were observed but no systematic trend emerged: For example, of the five strains in which a main factor of sex was identified for the stimulant effects of the D1 agonist, responsiveness was greatest in females in three of those strains and in males in two of those strains. These results should aid in the selection of mouse strains for future studies in which D1 or D2 responsiveness is a necessary consideration in the experimental design.

I only know about males but here opioids strongly suppress the production of testosterone, dissociatives do the same and both sum up to dangerous levels. Strangely I only lost my libido, put on some kilos around the belly and rushed into depression, after stopping concomitant use of dissociatives, thus my theory that these both suppress and substitute as steroid-mimetics while opioids only suppress. Oh, I had some severe testicle cramps when starting the bupe alongside DCK, visited a doc and he sent me home probably thinking I made stuff up. Possibly prescribed ibuprofen, I don't remember.

Don't know to which degree T production recovers after ceasing opioids, my hunch is that it doesn't completely so and that it's a major factor in long-term effects of opioids.

That's interesting, and thanks for the perspective. I never really thought about that with dissociatives but it kind of makes sense too. DXM which is of course a dissociative and a serotonin reuptake inhibitor and even very lightly an opioid (DXO binds reasonably to MOR) is just about the least sexy drug I've ever taken personally even though those kinds of effects usually come easily for me.

Agreed. Some/many docs seem to be repelled by the reality of that one just needs to try-fail-retry through the available drugs. When you read a bit about drug discovery etc. you realize that it's pretty random what we have on market and what not. Approval doesn't even help to filter out the toxic ones, I'd say we would probably be better off with a less restrictive approval process which primarily focused on safety and then having docs + pharmacologists (which these days are just glorified salespersons) select the correct drug together with you.

Yeah, drugs with effects opposing to antipsychotics are interesting and somehow make me question the widespread prescription of antipsychs. What if these drugs block neurogenesis? It's already certain that blocking D2 makes your brain shrink. The war on drugs did and does so much damage.

Yeah, I can't blame them for wanting there to be a quick and easy fix for their patients that minimizes the amount of extra research and work they need to do, but they're definitely often too to quick to accept it when someone claims that there is one. You'd think a doctor would be the kind of person who would actively keep up on drug research and use without even needing to be told - or at least, I would - but I guess some of them just either don't get it or don't care, though some certainly do.

Frankly, I think every drug should be equally legal, publicly owned, and allowed to be marketed (in a legal way, of course) from the instant it's discovered. Take every single cent that was directed towards regulation and approval and put it into drug-related healthcare instead. Create entire programs specifically about helping people find all the drugs of any kind they can imagine that are both the most effective and the least toxic for them personally. No one will pick the damaging shit when they've got access to and information about and help with choosing all the much healthier options, unless they just really want to for recreational purposes or something, in which case they should be able to do that too.

I think of antipsychotics as generally drugs of necessity, personally - like something for treating a disease that will otherwise kill you, the negative potentials are outweighed still by the theoretical benefits. Of course, you still need to make sure you actually get the right drug for it and such to actually make it successfully balanced for you. I would never take antipsychotics if I didn't think they were potentially saving me from something, and I have taken them before briefly for that reason. They do scare me, but so do a lot of drugs for a lot of reasons.

 

[Lil'LinaptkSix]

sounds like a you problem man …

Haha
Ya think? Heard this also ring through the eons "ya got problems ya need help" im ok being who i am be it looney toons or the opposite... its all the same to me.
I have had problematic problemo problems.

 

[Las Veghost grower]

Haha
Ya think? Heard this also ring through the eons "ya got problems ya need help" im ok being who i am be it looney toons or the opposite... its all the same to me.
I have dad problematic problem problems.

Hey I don’t judge anybody for their sexual preferences, my brothers gay and it was pretty obvious from the time he was 10, prolly younger even. So it’s not anything new to me. I just ment it as it’s not the drug its him

 

[Lil'LinaptkSix]

So it’s not anything new to me. I just ment it as it’s not the drug its him

Oh I was wondering at whom the comment was made but thats in the rear view.
I agree that there has to be a core of some sort for this to be expressed and I have never denied my feminine side. Well... never denied being in touch with it not being a slut lol
Ya think anyone who has ever had a thought of any other sexual experience other that + or - has a propensity to become full on gay or is there a limit that we set man ya got me thinkin have to come back to this

 

[Las Veghost grower]

Oh I was wondering at whom the comment was made but thats in the rear view.
I agree that there has to be a core of some sort for this to be expressed and I have never denied my feminine side. Well... never denied being in touch with it not being a slut lol
Ya think anyone who has ever had a thought of any other sexual experience other that + or - has a propensity to become full on gay or is there a limit that we set man ya got me thinkin have to come back to this

It’s such a non issue for me I don’t even think about that kind of stuff, I remember one of my buddy from work came out to me and I guess he was expecting me to freak out so when I was just like “ok…anyway” then right back into whatever we were talking about he kept saying I’m not joking, like he couldn’t comprehend how it literally ment nothing to me, which does make me feel bad that they have to worrie how people will react