Lisuride - Liquid Lisuride For Lab/R&D

CoconutEffect

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Have not seen anything on lisuride and opioid antagonism. Salt (sodium) is the safest natural opioid antagonist I know of.
Haidut, should I switch my helpless rats off Lithium Carbonate and onto high doses of sodium, don't the two minerals counterbalance one another?
 
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haidut

haidut

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Haidut, should I switch my helpless rats off Lithium Carbonate and onto high doses of sodium, don't the two minerals counterbalance one another?

Ray thinks sodium can do everything lithium can and it is also safer. I have not see any studies comparing effectiveness, so cannot recommend a dose to start. Some of the effects of lithium are due to its ability to chelate brain ammonia, so you may want to also try ceylon cinnamon. If it helps, the the issue may be ammonia toxicity which can be handled in a safer way than with lithium.
 

dand

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After some tinkering, I have found what appears to be a more optimal dose for me with lisuride. I have yet to experience any negative side effects, but 8-10 drops a day gives me pronounced dopaminergic symptoms which are simply wonderful. Colors are brighter and more vivid, mood is high as well as libido. I take a few drops of ritanserin every now and then, but not too frequently. I am curious about the upper limits of lisuride and may try experimenting with even higher doses. So far, 4 in the morning 2 in the afternoon, and 4 in the evening has been outstanding.
 
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haidut

haidut

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After some tinkering, I have found what appears to be a more optimal dose for me with lisuride. I have yet to experience any negative side effects, but 8-10 drops a day gives me pronounced dopaminergic symptoms which are simply wonderful. Colors are brighter and more vivid, mood is high as well as libido. I take a few drops of ritanserin every now and then, but not too frequently. I am curious about the upper limits of lisuride and may try experimenting with even higher doses. So far, 4 in the morning 2 in the afternoon, and 4 in the evening has been outstanding.

There are human studies with hyperprolactinemia in women or Parkison disease using 4mg daily.
 
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Fractality

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Has anyone researched the behavioral effects of this compound compared to LSD on rats? I have experimented with LSD on rats and they exhibited dopaminergic behavior in conjunction with what seemed to be serotonin-mediated effects. I would like to isolate and research the dopaminergic side of these ergoline compounds and am wondering if this compound is one place to start? From my reading it seems like it is.
 

Bodhi

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Nope, exercise elevates serotonin as it does cortisol and estrogen. So, nothing surprising about the effects you are getting from exercise.

Thanks, what about the rise in Testosteron which antagonizes Estrogen with exercise?
 
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haidut

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Thanks, what about the rise in Testosteron which antagonizes Estrogen with exercise?

Why would testosterone antagonize estrogen? If anything, it is a precursor to estradiol and the increased aromatase activity from exercise will convert even more T into E2. And why would testosterone rise during heavy exercise? If anything, prolonged exercise has been found to lower it? Google "athletic hypogonadism" for more info.
 

Greg says

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Experimented with Lisuride 8 drops x2 day now...I am stopping for a while as the side effects for me are too much. Killed my libido, difficulty to urinate (these two symptoms really feel like being on SSRIs), really sleepy and maybe even depressed. I need to stop to remember how it feels off of it. But if it is lowering prolactin then these sides are tolerable, far more doable than bromo for me.

I'm interested to know some experiences of knowledge of what is going on with the prolactin lowering effect. I'm not testing but I wonder how long it takes to lower prolactin and how long it remains lowered for. I feel no effect from it's prolactin lowering effect (if it even has).
 
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haidut

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Experimented with Lisuride 8 drops x2 day now...I am stopping for a while as the side effects for me are too much. Killed my libido, difficulty to urinate (these two symptoms really feel like being on SSRIs), really sleepy and maybe even depressed. I need to stop to remember how it feels off of it. But if it is lowering prolactin then these sides are tolerable, far more doable than bromo for me.

I'm interested to know some experiences of knowledge of what is going on with the prolactin lowering effect. I'm not testing but I wonder how long it takes to lower prolactin and how long it remains lowered for. I feel no effect from it's prolactin lowering effect (if it even has).

In 50mcg-100mcg doses it seems to be strongly pro-libido for both rodents and humans.
 
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marek1989

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Haidut, do you have any idea HOW could lisuride cause someone's libido to drop down, as Greg says reported? This doesn't make any sense. This drug is VERY similar to cabergoline, which is known for its pro-sexual effects. Moreover, lisuride even activates D4 and D5. These two meds are almost identical. Even when comes to serotonin receptors 5-HT1A, 5-HT2A and 5-HT2C. I just don't get it.
 
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haidut

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Haidut, do you have any idea HOW could lisuride cause someone's libido to drop down, as Greg says reported? This doesn't make any sense. This drug is VERY similar to cabergoline, which is known for its pro-sexual effects. Moreover, lisuride even activates D4 and D5. These two meds are almost identical. Even when comes to serotonin receptors 5-HT1A, 5-HT2A and 5-HT2C. I just don't get it.

In high doses lisuride, bromocriptine, and cabergoline are all known to suppress libido. Not sure of the exact mechanism but the mixed serotonin agonism probably has something to do with it. Also, all anti-prolactin drugs lower tissue estrogen. Some estrogen is needed for male libido. DHT has been known to do the same in high doses - i.e. kill libido due to complete estrogen antagonism. Don't take this to mean estrogen is good for you. The amount of estrogen you need for libido is tiny.
 
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Koveras

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Haidut, do you have any idea HOW could lisuride cause someone's libido to drop down, as Greg says reported? This doesn't make any sense. This drug is VERY similar to cabergoline, which is known for its pro-sexual effects. Moreover, lisuride even activates D4 and D5. These two meds are almost identical. Even when comes to serotonin receptors 5-HT1A, 5-HT2A and 5-HT2C. I just don't get it.

In high doses lisuride, bromocriptine, and cabergoline are all known to suppress libido. Not sure of the exact mechanism but the mixed serotonin agonism probably has something to do with it. Also, all anti-prolactin drugs lower tissue estrogen. Some estrogen is needed for male libido. DHT has been known to do the same in high doses - i.e. kill libido due to complete estrogen antagonism. Don't take this to mean estrogen is good for you. The amount of estrogen you need for libido is tiny. A human study showed that estradiol in the bottom 1% of the "normal" range was enough for libido maintenance. But if it is suppressed too much, it will kill libido. Not sure which mechanism exactly is behind the lisuride effects but the libido-suppressive effects of high doses are well-known for all LSD-derivatives. Not sure why people take such high doses, just as I don't understand the same for the 11-keto DHT product. I mean, I never said taking more is better. It should be used in the minimum dose that produces beneficial effects. Even doses of 200mcg are considered pharmacological and used for severe hyperprolactinemia due to pituitary tumor. For libido even 50mcg is plenty.

I would add that some prolactin is necessary for normal HPTA/gonadal function.

Believe two things can happen

1. Dopamine agonists (especially when D2-predominant) may reduce cAMP levels in the brain and lower normal gonadotropin secretion
2. Prolactin itself upregulates gonadotropin receptors in testes, meaning if prolactin tanks, then testicular response to the gonadotropins you do produce will be less then usual. As a result of this, less androgens and estrogen will be available to promote libido.

Believe @haidut has said that a serum prolactin < 5 tends to be ideal, Danny Roddy has said < 3 or < 4, and I would say in my experience 6 or 7 gives the best balance - although this is all individual to someone's particular circumstances and goals as usual.
 

Tarmander

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Not sure why people take such high doses, just as I don't understand the same for the 11-keto DHT product. I mean, I never said taking more is better.

Probably because of lines like this:

I think lisuride probably has a very wide therapeutic profile, which makes it very good for experimentation. I have personally gone up to 1mg in divided doses and tolerated it well up to 0.8mg but the nausea at 1mg became too strong. The positive outlook on life though continued to increase with the dose.

I am still experimenting with this stuff (on rats of course). I will do a write up of my mostly positive experiences here at some point. I have done a couple different doses, but was thinking of ramping up higher to just see if this positive outlook is a thing. Maybe not such a good idea though...
 

natedawggh

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It has been noted in human studies with both bromocriptine and lisuride. And it was fat loss, not muscle :)

I gained 12 lbs in one week on Ritanserin, even though it had some other desireable properties I had to stop taking it or I was going to be as big as I was a year ago. Is lisuride at all potentially a cause of weight (fat) gain? And if not why, and is it known why would ritanserin cause weight gain?
 
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haidut

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I gained 12 lbs in one week on Ritanserin, even though it had some other desireable properties I had to stop taking it or I was going to be as big as I was a year ago. Is lisuride at all potentially a cause of weight (fat) gain? And if not why, and is it known why would ritanserin cause weight gain?

I have never heard of lisuride or other dopamine agonists like it causing weight gain. If anything, it has been shown to help lose weight. The serotonin antagonists on the 5-HT2 receptor seem to all have appetite stimulation as a side effect. I don't think they directly make people fat though. It also depends on the dose. Ritanserin in doses of 6 drops (3mg) daily should not be causing weight gain.
 

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When I was using AL-LAD (LSD analogue) I found the best therapeutic usage was microdoses (around 15-20mcg). At higher dosages the serotonergic effects would become more pronounced and it can also get very hypomanic and overstimulating. My understanding is that lisuride is an even stronger dopamine agonist than LSD so I don't really see the need for such high doses myself. I would think that half a drop of this product would suffice (25mcg). That may even be too much. With LSD microdosing you want to find a dose that's just barely perceptible and the drug is generally taken only every 3-4 days. I haven't tried Lisuride yet and I know its different than LSD, i'm just thinking that maybe people are dosing too high.

Apparently Albert Hoffman called LSD microdosing psychedelic ritalin. He believed that if LSD wasn't so harshly scheduled it could have gone on to treat conditions like ADHD when used in small doses. I know it has pronounced motivating effects at small doses. Too much however will make you crash from overstimulation.
 

DennisX

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@haidut you state in the opening that Lisuride is a punative antagonist on 5-HT2A.

Since I'm new I can't list the URLs but they state that Lisuride is angonist on 5-HT2A

Which is correct?

Google
Prozac, 5HT2C And The Trojan Horse In Lisuride
Lisuride, incredible potential
 

DennisX

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These are the binding affinities for Lisuride
From
Psychedelics and the Human Receptorome
It is also useful to present the npKi data of Fig. S2 in numerical format. In the listing below, the npKi values for each drug are arranged in decreasing order. A value of 0.00 means that the Ki value was measured as >10,000 nm. “ND” indicates that the data is not available. The 5-HT2A and 5-HT2C receptors are also highlighted in bold font for easier location. npKi values below about 2.0 should be imperceptible, while values above about 2.0 should be perceptible, and the higher the npKi value, the more perceptible a receptor should be.

lisuride: 4.00 5ht1a, 3.88 Alpha2C, 3.78 Alpha2B, 3.22 Alpha2A, 3.01 5ht2b, 2.99 5ht5a, 2.90 D4, 2.74 5ht2a, 2.65 D2, 2.64 5ht7, 2.61 5ht6, 2.56 Beta1, 2.27 5ht1b, 2.09 Alpha1A, 1.93 Beta2, 1.83 5ht1e, 1.59 D5, 1.42 H2, 1.34 D3, 1.08 Alpha1B; 0.00: 5ht1d, 5ht2c, D1, DAT, NET, Imidazoline1, M1, SERT, CB2, KOR, MOR, M3, M2, M5, M4, CB1, Ca+Channel; ND: Sigma1, H1, Sigma2, DOR, NMDA
 
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haidut

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@haidut you state in the opening that Lisuride is a punative antagonist on 5-HT2A.

Since I'm new I can't list the URLs but they state that Lisuride is angonist on 5-HT2A

Which is correct?

Google
Prozac, 5HT2C And The Trojan Horse In Lisuride
Lisuride, incredible potential

Actually, the exact profile of lisuride on the 5-HT receptors is not well-known other than its clear antagonism on 5-HT2B, which makes it an excellent anti-fibrotic agent. The links you provide mention 5-HT2C agonism but other studies claim antagonism. Like this one for instance:
Agonist activity of LSD and lisuride at cloned 5HT2A and 5HT2C receptors. - PubMed - NCBI
"...Evidence from studies with phenylisopropylamine hallucinogens indicates that the 5HT2A receptor is the likely target for the initiation of events leading to hallucinogenic activity associated with LSD and related drugs. Recently, lisuride (a purported non-hallucinogenic congener of LSD) was reported to be a potent antagonist at the 5HT2C receptor and an agonist at the 5HT2A receptor. LSD exhibited agonist activity at both receptors."
 
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haidut

haidut

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These are the binding affinities for Lisuride
From
Psychedelics and the Human Receptorome
It is also useful to present the npKi data of Fig. S2 in numerical format. In the listing below, the npKi values for each drug are arranged in decreasing order. A value of 0.00 means that the Ki value was measured as >10,000 nm. “ND” indicates that the data is not available. The 5-HT2A and 5-HT2C receptors are also highlighted in bold font for easier location. npKi values below about 2.0 should be imperceptible, while values above about 2.0 should be perceptible, and the higher the npKi value, the more perceptible a receptor should be.

lisuride: 4.00 5ht1a, 3.88 Alpha2C, 3.78 Alpha2B, 3.22 Alpha2A, 3.01 5ht2b, 2.99 5ht5a, 2.90 D4, 2.74 5ht2a, 2.65 D2, 2.64 5ht7, 2.61 5ht6, 2.56 Beta1, 2.27 5ht1b, 2.09 Alpha1A, 1.93 Beta2, 1.83 5ht1e, 1.59 D5, 1.42 H2, 1.34 D3, 1.08 Alpha1B; 0.00: 5ht1d, 5ht2c, D1, DAT, NET, Imidazoline1, M1, SERT, CB2, KOR, MOR, M3, M2, M5, M4, CB1, Ca+Channel; ND: Sigma1, H1, Sigma2, DOR, NMDA

Right, but binding affinities alone do not show if the drug is agonist or antagonist on that receptor. As you can see, your list also includes 5-HT6 and 5-HT7 on which lisuride is thought to be antagonist.
 
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