Low Serotonin = Lack Of Sexual Discrimination?

kiran

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The authors demonstrated that these mice, lacking serotonin, did not distinguish between sexual partners, mounting male and female mice with seemingly equal fervor. Not only that, the mice showed the same scent preferences for male and female mice and vocalized for male and female mice equally. When the serotonin in these animals was replaced, they preferred female mice over male mice. The authors concluded that serotonin regulates sexual preference in mammals.

http://blogs.scientificamerican.com/gue ... at-simple/

Courtesy of bryan over at peatarian.
 

John Eels

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The authors concluded that serotonin regulates sexual preference in mammals.
Danny Roddy is probably gay by now and has a crush on Ray Peat. The first two men in the world with the lowest serotonin level every achieved (Guinness Book of Records).

It's likely not that simple. Gay = low serotonin, heterosexual = high serotonin, or at the very least higher. Serotonin regulates the desire to copulate. That's the intersting tidbit.
 

juanitacarlos

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John Eels said:
The authors concluded that serotonin regulates sexual preference in mammals.
Danny Roddy is probably gay by now and has a crush on Ray Peat. The first two men in the world with the lowest serotonin level every achieved (Guinness Book of Records).

It's likely not that simple. Gay = low serotonin, heterosexual = high serotonin, or at the very least higher. Serotonin regulates the desire to copulate. That's the intersting tidbit.

That is a really interesting study! The conclusions are total BS, but the study itself was fascinating.
 

kiran

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It's probably more along the lines of low serotonin with high inflammation.
 

Mauritio

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These results are strikingly similar to what some people experience when they take a strong dopamin agonist/ serotonin reducer like cabergoline or bromocriptine: hypersexuality, sometimes even bisexuality and fetishes .
It seems low serotonin leads to a very strong libido up to the point where you hump everyone that's available . Low prolactin might also be involved .
 

Gustav3Y

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These results are strikingly similar to what some people experience when they take a strong dopamin agonist/ serotonin reducer like cabergoline or bromocriptine: hypersexuality, sometimes even bisexuality and fetishes .
It seems low serotonin leads to a very strong libido up to the point where you hump everyone that's available . Low prolactin might also be involved .

I believe you are understating these drugs completely wrong, they work at receptor level.
Cabergoline is not a "serotonin reducer" by any means!
Actually a potent agonist for specific serotoning receptors.
The point of these drugs is to stimulate D2 receptors to stop Prolactin release, and they do that.
Cabergoline is a massive agonist for 5-HT2B, very good agonist for 5-HT2A and 5-HT1D, decent for 5-HT1A
You can see below, how serious the affinity is for those serotonin receptors regarding Cabergoline

Other than that I know several people on these drugs, and in my experience they are uninterested sexually to normal behavior.

 
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Mauritio

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I believe you are understating these drugs completely wrong, they work at receptor level.
Cabergoline is not a "serotonin reducer" by any means!
Actually a potent agonist for specific serotoning receptors.
The point of these drugs is to stimulate D2 receptors to stop Prolactin release, and they do that.
Cabergoline is a massive agonist for 5-HT2B, very good agonist for 5-HT2A and 5-HT1D, decent for 5-HT1A
You can see below, how serious the affinity is for those serotonin receptors regarding Cabergoline

Other than that I know several people on these drugs, and in my experience they are uninterested sexually to normal behavior.

No , I think their net effect is still pro dopaminergic. And dopamin is the strongest endogenous TPH inhibitor ,which will lower serotonin .
They do have some activity on 5ht receptors , especially 5ht2b is bothersome, but for example lisuride is antagonist at this receptor . Also being an agonist at 5ht1a actually reduces serotonin ,since it is the auto receptor.
And if the net effect wasn't anti serotonergic I couldn't see those drugs treating diabetes and be therapeutic for several cancers .

I could send you many reports of people developing hypersexuality on it . It does increase libido in many people . But some seem to be affected in a way that it actually reduces their libido. It's not really black and white ,just as with the serotonin receptors themself!
 
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Gustav3Y

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I specifically gave the example of Cabergoline.
I did not say the effect is not dopaminogenic, where did you get that one from. The sole fact that it agonizes D2 receptors is the entire reason why Prolactin is antagonized, that is the purpose of the drug not to raise dopamine for the sake of dopamine.
It antagonizes several receptors at the same time, there is no inverse agonist specified on any serotonin receptor.

I am talking about people around me family, friend, acquaintances, who took both Cabergoline or Bromocriptine individually I do not need reports to tell me how they felt and how these two drugs act, I saw them puke, having nausea, headaches etc, while before had none of that, all serious people, no drug users, drinkers, or anything like that.

Now if someone felt liberated and super healthy while taking them, who is anybody to tell the opposite to them.
 

Mauritio

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I specifically gave the example of Cabergoline.
I did not say the effect is not dopaminogenic, where did you get that one from. The sole fact that it agonizes D2 receptors is the entire reason why Prolactin is antagonized, that is the purpose of the drug not to raise dopamine for the sake of dopamine.
It antagonizes several receptors at the same time, there is no inverse agonist specified on any serotonin receptor.

I am talking about people around me family, friend, acquaintances, who took both Cabergoline or Bromocriptine individually I do not need reports to tell me how they felt and how these two drugs act, I saw them puke, having nausea, headaches etc, while before had none of that, all serious people, no drug users, drinkers, or anything like that.

Now if someone felt liberated and super healthy while taking them, who is anybody to tell the opposite to them.
Calm down dude . You dont need to be so triggered.
 

tankasnowgod

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I specifically gave the example of Cabergoline.
I did not say the effect is not dopaminogenic, where did you get that one from. The sole fact that it agonizes D2 receptors is the entire reason why Prolactin is antagonized, that is the purpose of the drug not to raise dopamine for the sake of dopamine.
It antagonizes several receptors at the same time, there is no inverse agonist specified on any serotonin receptor.

The dopamine agonism may not be the "sole" method of action of these drugs. Haidut has been posted a few studies about Serotonin's role in diseases like Parkinsons-

Serotonin Excess, Not Dopamine Deficiency, May Be The Cause Of Parkinson
Parkinson Disease (PD) may begin in the gut – To Extract Knowledge from Matter
Serotonin may cause schizophrenia, Parkinson, and Alzheimer diseases – To Extract Knowledge from Matter

In the last one....

"In several of my previous posts I discussed the extensive evidence that both schizophrenia and PD are both caused by serotonin. Aside from the direct imaging studies on brains of people with either condition, as well as rodent studies, there are also recent studies that “stumbled upon” the “shocking” evidence that anti-dopamine drugs commonly used for treating schizophrenia such as haloperidol are actually potent serotonin antagonists as well."

"The new clinical trial below may add the first piece of direct evidence by demonstrating that serotonin is a causative factor in both psychosis and PD. The trial is based on pre-clinical results (with a limited number of patients) demonstrating that the administration of a selective serotonin (5-HT3) antagonist (ondansetron) is capable of stopping the PDP in people with PD. This directly implicates serotonin as a causative factor in both schizophrenia and PDP (and possibly AD as well), because ondansetron is highly selective as 5-HT3 antagonist and does not have any other known effects on monoamine or other mechanisms considered relevant for those conditions. If the trial also demonstrates improvement in other core symptoms of PD then I think serotonin’s fate is sealed. While the full-scale trial won’t start until 2022 the researchers are pretty confident in their preliminary results, which will hopefully lead to more doctors thinking twice before prescribing SSRI drugs to patients with schizophrenia or PD."
 

lampofred

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The effects of high estrogen are often confused with "too low" serotonin (like in depression).
 
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