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Lysergamides Acid and Leg Pain

Makes sense f&b.

And theres the extra muscle tension you get when you stay up all night on LSD...voila! - pains in the leg :D
 
I have noticed pain in my thighs as well on acid. It was rather intense. I believe that it was due to the vasoconstrictive properties as others have said. I have read the same thing.
 
Do not serotonergic drugs in general vasonconstriction cause- ie: through effects on 5HT receptors?

^Kinda yoda like there...
 
^ No, vasoconstriction is associated with sympathetic asctivity (that mediated by catecholamines eg noradrenaline). Serotonin & associated drugs have their dodgy points (hyperthermia being the biggie), but not vasoconstriction as far as I remember
 
I have noticed pain in my thighs as well on acid. It was rather intense. I believe that it was due to the vasoconstrictive properties as others have said. I have read the same thing.

Why would you notice vasconstriction in your thighs? Why not your fingers or toes?

Isn't it more likely it's just muscle tension from being awake all night under the effects of a psychedelic stimulant?
 
Good thread... I had some pretty intense pains in my groin muscles (inner thighs) on an extremely high dose lsd trip (15-25mg) a few years ago. The pains weren't extremely long lived, perhaps 30min, but i was completely unable to walk during this time. I can't be sure due to the ridiculous time dilation i was experiencing at the time. Until reading f&b's comment I was unaware of lsd's vasoconstrictive properties and had attributed it to what I've called the "acid cringe," which i still believe is responsible for most physical complaints associated with lsd.
 
^ That is a fuckin' huge dose (150 -250 x 100ug 8o) - the most I've ever consumed, without tolerance being an issue, is 2/3rds to 3/4 of a milligram and it did a real number on me. At doses in the milligrams range, LSD is going to have some significant alpha & beta adrenergic receptor activity (hence possible vasoconstriction) as well as lighting up all the 5HT & dopamine receptors
 
The calf pain IS caused by vasoconstriction, through activation of the peripheral serotonin receptors by the LSD. Some people are more sensitive to this effect than others. Some substances do it far more than others. The good thing about LSD is that it is such a potent 5-HT2a agonist, that such low doses are needed to elicit the psychedelic effects that peripheral side effects such as calf pain rarely occur

• schoolgirl of IS years was admitted to hospital on 13lovember 1962 for pain and coldness of the feet. She sufferedcorn migraine for 5 years and for this she took 'migryI'ccasionalIy (a preparation containing ergotamine tartrate). .part from migraine, the past history was essentially normal.iefore the school exanJinations at the end of term, the attackslcreased in frequency and she found that 'migryI' was inefIec-.ve. Her doctor then prescribed methysergide ('deseril' tabs.mg. t.d.s.). Three days later she felt pain in both calves onralking, which was relieved by rest. That night she noticedngling in both her feet and her toes, which recurred in bed8 hours later. Claudication developed again 2 days later,hile dancing, and late that night she experienced paraesthesiae I her feet-being woken by severe pain and coldness feltlore in the outer border of the left foot

These are both molecules similar to LSD but far more effective at vasoconstriction. I have used methysergide before as a psychedelic and ALWAYS get the calf pain at high doses, its unpleasant.
 
^ No, vasoconstriction is associated with sympathetic asctivity (that mediated by catecholamines eg noradrenaline). Serotonin & associated drugs have their dodgy points (hyperthermia being the biggie), but not vasoconstriction as far as I remember

Vasopressors aren't limited to alpha and beta adrenergic agonist ligands. True, epinephrine certainly causes peripheral vasoconstriction, but it's totally not the whole picture. Endogenous vasoconstriction is regulated by various endocrine and neurobiological factors. Oxytocin is an endogenous vasopressor, which causes uterine contractions, and ergoloid drugs (including LSD) do the same by a different mechanism. Specific to this discussion, serotonin in the bloodstream is a factor involved in vasoconstriction under particular circumstances. Exogenous vasopressors are also of a varied nature.

Activation of certain serotonin receptor subtypes is most definitely relevant. With regards to the vasopressor properties of ergoloids, the primary result is from direct serotonergic agonism.

This is absolutely what happens with LSD. (One can even tell from the type of pain experienced - it is a completely different sensation than the pain from muscle fatigue, and totally recognizable as vascular in nature).
 
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^ That is a fuckin' huge dose (150 -250 x 100ug 8o) - the most I've ever consumed, without tolerance being an issue, is 2/3rds to 3/4 of a milligram and it did a real number on me. At doses in the milligrams range, LSD is going to have some significant alpha & beta adrenergic receptor activity (hence possible vasoconstriction) as well as lighting up all the 5HT & dopamine receptors

The main issue I have had with going over a milligram, the highest being about 1400 mics, is the histamine reactions that I had. Tons of mucus production, making it kind of hard to breathe, though no worse than if you have really bad allergies or a cold. Although 15 mg is a whole other story.
 
Vasopressors aren't limited to alpha and beta adrenergic agonist ligands. True, epinephrine certainly causes peripheral vasoconstriction, but it's totally not the whole picture. Endogenous vasoconstriction is regulated by various endocrine and neurobiological factors. Oxytocin is an endogenous vasopressor, which causes uterine contractions, and ergoloid drugs (including LSD) do the same by a different mechanism. Specific to this discussion, serotonin in the bloodstream is a factor involved in vasoconstriction under particular circumstances. Exogenous vasopressors are also of a varied nature.

Activation of certain serotonin receptor subtypes is most definitely relevant. With regards to the vasopressor properties of ergoloids, the primary result is from direct serotonergic agonism.

This is absolutely what happens with LSD. (One can even tell from the type of pain experienced - it is a completely different sensation than the pain from muscle fatigue, and totally recognizable as vascular in nature).

Definitely through the activation of serotonin receptors. That's where the name comes from. Sero=blood , tonin= increased tone of the muscles in the artery walls. Knowledge is power!!
 
Never had pain in legs on acid od have it from benzo withdrawal though.
bicycle day coming up can't wait.
 
If it was vasoconstriction causing the leg-pain I think people taking big doses would be crying out for someone to take off their shoes and rub their toes every trip =D
 
^ That is a fuckin' huge dose (150 -250 x 100ug 8o) - the most I've ever consumed, without tolerance being an issue, is 2/3rds to 3/4 of a milligram and it did a real number on me. At doses in the milligrams range, LSD is going to have some significant alpha & beta adrenergic receptor activity (hence possible vasoconstriction) as well as lighting up all the 5HT & dopamine receptors

yeah it was. It was consumed over about a 20hr period and I was really really high for over 70hrs and had residual visual activity well passed the 100hr mark. Granted the micro-grammage is a rough estimate, but it was between 75-150 dosage units of liquid that was supposedly 250-300mcg a hit, in addition to 4 geltabs, a couple blotters, and a few random other types of liquid. I usually don't give much credence to names, but if anyone has some analysis of the "Spiderman" liquid that was floating around in late 2001 I'd be interested in reading it, if not for anything else just to get a better idea of how much I actually took. However, even if it was only 150mcg and on the low end of dosage units, thats still over 11mg, thus well into the vasoconstriction range. About 5hrs I had taken the geltabs and blotters I wasn't all that buzzed, as they were on the low end of mediocre, if not just bad (based on subjective effects, probably not more than 40mcg per, likely closer to 20, felt like a really stimulating cannabis buzz). Then I ran into a friend that told me about the 250-300mcg stuff he had a copious amount of. I took 3 drops and was higher than I'd ever been before about 2.5hrs later. We went back to his hotel and everyone was so fried we just started squirting the stuff in each others mouths, putting it in drinks, etc. The next day my overly generous friend slid a vial into my hand on the sly and said "Suck on this." I thought it was one of the empty vials from the night before and threw it in my mouth and bit down. It was most definitely not one of the empties from the night before. Ha... I don't know what kind of facial expression I made, but I'm pretty sure it was a lot like his... shock, surprise, laughter, disbelief, etc. It was about 3hrs after this that I experienced the extreme leg pains and was unable to walk or stand for about half an hour (or however long the opening act played). After that I was fine, or as fine as someone on that much lsd can be. Sorry for the digression there, but i felt I should explain myself so no one would think i was confused on my units of measurment.

A little disclaimer here, i wouldn't recommend anyone take this high a dosage. Overall it was a good experience and I enjoyed myself thoroughly at the two concerts I went to, but there were certainly some difficult points and its only due to sheer luck, and to a lesser extent a large base of knowledge about the drug I was on, that nothing went horribly wrong, as it was only my 3rd experience with lsd. For about 2 months after that fateful weekend (that extended into wednsday) I was completely unable to integrate the experience and most of my friends thought i was an "acid casualty." luckily i finally "came back" after a lot of introspection, soul searching and having some temporal distance from the experience.

For a while after that monster trip whenever I took lsd it was usually 10ish dosage units, and occasionally with the stronger stuff I would feel some pain in the same area of my legs, but nothing nearly as intense. I was never sure whether this was some subconscious suggestion from that one overly intense experience or an actual effect of the drug. Since vasoconstriction doesn't seem to manifest until your into the mg range, I suppose its certainly possible that 10 or so hits of good stuff would put you into the mg, and therefore vasoconstriction range.

And a final note, I don't take doses nearly this high anymore. There's only so many times you can walk through that door and find something new. I still enjoy a good LSD trip, but haven't ventured above 750mg in several years, usually stay below 500.

the dose to get significant adrenergic activity is way up in the milligrams region re: dosage (there is a graph somewhere detailing the IC50 for LSD's interaction with various receptors - 5HT/noradrenaline/dopamine/histamine)-
F&B could you direct me to this info? I googled it, but had mostly only quasi-related results.

EDIT: Sorry for the monster post. I've still got such a vivid psychological imprint from that experience, everytime I talk about it i end up going into far too much detail... ha, oh well.
 
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the dose to get significant adrenergic activity is way up in the milligrams region re: dosage (there is a graph somewhere detailing the IC50 for LSD's interaction with various receptors - 5HT/noradrenaline/dopamine/histamine)-
F&B could you direct me to this info? I googled it, but had mostly only quasi-related results.

EDIT: Sorry for the monster post. I've still got such a vivid psychological imprint from that experience, everytime I talk about it i end up going into far too much detail... ha, oh well.

Not relevant.. because it doesn't do it through adrenergic receptors, it does it through serotonin receptors.

How could you be brave to take that much acid on your third trip. what the fuck!
 
^How does activity at adrenergic receptors not cause vasoconstriction?

as for your question, basically we were so trippin we didn't think we could possibly get any higher... then when we figured out we could we thought it was funny... bravery didn't really come into the equation
 
activity at adrenergic receptors does cause vasoconstriction. all i'm saying is that this is not the mechanism through which LSD causes vasoconstriction, because LSD has a relatively lower affinity for adrenergic receptors than it does for serotonin receptors (which also cause vasoconstriction). As such, the dosage needed for the psychedelic effects is so low that the level of adrenergic activation is so small that it it insignificant.

However, that only applies to the normal dosage ranges. I'm not referring to your experience in particular, because 11 milligrams is fucking massive. However, I'm not sure of the exact affinity for the adrenergic receptor of LSD, so it may or may not have come into play in your case. Generally however, the serotonergic activity is responsible for calf pain/vasoconstriction with the use of psychedelics. The peripheral serotonin receptors, when activated, are very effective at causing vasoconstriction. This is because they are not used normally - only used when injury occurs. As such, when you use potent serotonin agonists, these receptors are activated and cause marked vasoconstriction.

However, LSD is a great psychedelic because its affinity at the 5-HT2A receptor (the one causing psychedelic effects) is much stronger than its affinity at the 5-HT1B (the one causing vasoconstriction), meaning that it is less likely to cause the calf pain.
 
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Could a normal dose of LSD really cause vasoconstriction at a level that would be noticed by anyone tho?
 
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