The High Dopamine & Histamine Personality

Hans

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Hi all,

A while ago I created the high serotonin personality article & more recently the high testosterone personality. Today I finished my article on the high dopamine & histamine personality on request of @Aymen and a few others.


Here is the link to my article: The High Dopamine & Histamine Personality

Hope you enjoy and let me know what you think.

If you liked this article and learned something new, please share this facebook post (MenElite) or share the article on any other social media, it really helps to get the word out.
 

YourUniverse

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Nice article.

You touched on glutamate and its interaction with dopamine. Off-topic, but other than increasing dopamine, do you know of any other ways to reduce glutamate (or increase GABA, which should do the same thing)..?
 
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Hans

Hans

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@Tbone107 @lampofred @Aymen @jamies33 Thanks for reading and for the positive feedback.

A few glutamate antagonists are magnesium (NMDA antagonist), theanine, ketamine (NMDA antagonist), ferulic acid, taurine, valerian, lithium, fixing the kynurenine pathway and lowering estrogen.

For GABA, valerian, taurine, glycine, niacinamide, progesterone, allopregnanolone, lemongrass and skullcap just to name a few.

Finding the cause of the excess glutamate might be the best approach to this, which could most likely be from the gut, estrogen excess, EMF and dirty electricity (too much intracellular calcium), poor sleep and so on.
 

Mauritio

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"D2 is its autoreceptor and activating it lowers dopamine levels."

You sure about that? Lisuride ,bromocriptine cabergoline etc. are all strong dopamin D2 agonists . I know they also have affinity for other dopamin receptors ,but not nearly as high as for D2.
So if the main mechanism of action of those drugs is the activation of the D2 receptor and that supposedly lowers dopamin ,then I doubt those drugs would be therapeutic for prolactinoma ,diabetes and some cancers .
 
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Hans

Hans

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"D2 is its autoreceptor and activating it lowers dopamine levels."

You sure about that? Lisuride ,bromocriptine cabergoline etc. are all strong dopamin D2 agonists . I know they also have affinity for other dopamin receptors ,but not nearly as high as for D2.
So if the main mechanism of action of those drugs is the activation of the D2 receptor and that supposedly lowers dopamin ,then I doubt those drugs would be therapeutic for prolactinoma ,diabetes and some cancers .
From this study:
"Dopamine D2-like receptors are inhibitory. These receptors couple to Gαi/o to inhibit AC and calcium channels, and activate inhibitory G-protein activated inwardly rectifying potassium channels (GIRK) (Neve et al., 2004, Beaulieu and Gainetdinov, 2011). The majority of D2-like receptors are found on non-dopamine neurons and mediate numerous brain functions, playing major roles in regulating locomotor activity, cognition and motivation (Missale et al., 1998, Beaulieu and Gainetdinov, 2011). As such, D2-receptors are important pharmacological targets for treatment of a variety of psychiatric diseases (Missale et al., 1998, Beaulieu and Gainetdinov, 2011). D2-receptors are found at a high density in the striatum, nucleus accumbens, and olfactory tubercle, and to a lower extent in the hippocampus, amygdala, hypothalamus and cortical regions (Missale et al., 1998, Schmitz et al., 2003, De Mei et al., 2009, Beaulieu and Gainetdinov, 2011)."

"Autoreceptors on dopamine neurons are comprised of the D2-subtype of dopamine receptors. These autoreceptors are located on the soma and dendrites of midbrain dopamine neurons in the ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) as well as on their axon terminals in projection areas (Missale et al., 1998, Romanelli et al., 2010, Beaulieu and Gainetdinov, 2011). As feedback regulators, autoreceptors modulate activity directly through the activation of a potassium conductance and indirectly through downstream control of the expression of tyrosine hydroxylase and the plasma membrane dopamine transporter to modulate dopamine dependent transmission. Activation of these receptors decreases both excitability of dopamine neurons and the release of dopamine. Thus, autoreceptors are key regulators of dopamine dependent transmission. While both D2- and D3- receptors are present on dopamine neurons (Rivet et al., 1994, Levant, 1997, Koeltzow et al., 1998, Beaulieu and Gainetdinov, 2011), the D3-receptor likely plays only a minor functional role as an autoreceptor, and the vast majority of autofeedback inhibition is thought to be mediated through the D2-receptor."

"As D2-receptors are found on both the terminals of dopamine neurons and post-synaptically on non-dopamine neurons (heteroreceptors), historically it has been difficult to separate the physiological and behavioral role of autoreceptors from that of heteroreceptors."
 

Mauritio

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From this study:
"Dopamine D2-like receptors are inhibitory. These receptors couple to Gαi/o to inhibit AC and calcium channels, and activate inhibitory G-protein activated inwardly rectifying potassium channels (GIRK) (Neve et al., 2004, Beaulieu and Gainetdinov, 2011). The majority of D2-like receptors are found on non-dopamine neurons and mediate numerous brain functions, playing major roles in regulating locomotor activity, cognition and motivation (Missale et al., 1998, Beaulieu and Gainetdinov, 2011). As such, D2-receptors are important pharmacological targets for treatment of a variety of psychiatric diseases (Missale et al., 1998, Beaulieu and Gainetdinov, 2011). D2-receptors are found at a high density in the striatum, nucleus accumbens, and olfactory tubercle, and to a lower extent in the hippocampus, amygdala, hypothalamus and cortical regions (Missale et al., 1998, Schmitz et al., 2003, De Mei et al., 2009, Beaulieu and Gainetdinov, 2011)."

"Autoreceptors on dopamine neurons are comprised of the D2-subtype of dopamine receptors. These autoreceptors are located on the soma and dendrites of midbrain dopamine neurons in the ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) as well as on their axon terminals in projection areas (Missale et al., 1998, Romanelli et al., 2010, Beaulieu and Gainetdinov, 2011). As feedback regulators, autoreceptors modulate activity directly through the activation of a potassium conductance and indirectly through downstream control of the expression of tyrosine hydroxylase and the plasma membrane dopamine transporter to modulate dopamine dependent transmission. Activation of these receptors decreases both excitability of dopamine neurons and the release of dopamine. Thus, autoreceptors are key regulators of dopamine dependent transmission. While both D2- and D3- receptors are present on dopamine neurons (Rivet et al., 1994, Levant, 1997, Koeltzow et al., 1998, Beaulieu and Gainetdinov, 2011), the D3-receptor likely plays only a minor functional role as an autoreceptor, and the vast majority of autofeedback inhibition is thought to be mediated through the D2-receptor."

"As D2-receptors are found on both the terminals of dopamine neurons and post-synaptically on non-dopamine neurons (heteroreceptors), historically it has been difficult to separate the physiological and behavioral role of autoreceptors from that of heteroreceptors."
Hmm I'm not really convinced , something doesnt add up here . But I'll keep in the back of my head ,in case I might come across something similar.
 
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Hans

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Hmm I'm not really convinced , something doesnt add up here . But I'll keep in the back of my head ,in case I might come across something similar.
Well there is basically auto and heteroreceptors, so some of them will lower/control dopamine secretion whereas others follow out the commands of dopamine so to speak. It's like the 5-HT1A receptor. The auto/presynaptic receptors lower serotonin, whereas the hetero/post synaptic receptors can act to increase dopamine, oxytocin, etc.
 

MitchMitchell

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as someone with naturally high TOTAL testosterone but LOW free T and e2. and low prolactin this article definitely hits home. Whereas the high T article wasn't too relatable (Sadly). High dopamine for sure, I'm always optimistic but the high histamine is where the extra aggression and poor digestion of many foods come from I suppose. I've got high cortisol too - serum, saliva, urine..

Interesting to see that I can fit this box very well.
 
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Hans

Hans

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as someone with naturally high TOTAL testosterone but LOW free T and e2. and low prolactin this article definitely hits home. Whereas the high T article wasn't too relatable (Sadly). High dopamine for sure, I'm always optimistic but the high histamine is where the extra aggression and poor digestion of many foods come from I suppose. I've got high cortisol too - serum, saliva, urine..

Interesting to see that I can fit this box very well.
Poor digestion as in food intolerances or low stomach acid? Histamine stimulates stomach acid secretion so I assume you're talking about food intolerances?
Histamine is broken down by a copper using enzyme as well as through methylation.
Leaky gut can also cause excess absorption of histamine.
 

MitchMitchell

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Food intolerances as histamine causes stronger allergic reactions. Not a big deal though I’ve eliminated many foods. And yeah I have zero problem eating only “acidic” like a good old carnivore.
 

redsun

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Food intolerances as histamine causes stronger allergic reactions. Not a big deal though I’ve eliminated many foods. And yeah I have zero problem eating only “acidic” like a good old carnivore.

Indigestion is low stomach secretions, weak stomach acid. That is food "intolerance".

If you get histamine reaction like sneezing, runny nose, etc from a food that is histamine intolerance because histamine is already very high and you have problems metabolizing histamine in your food. But high histamine types have very strong digestion and basically tolerate any food.
 

Epik

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Great article @Hans ! I've noticed this symptom of high histamine:

"Long and slender fingers. Second toe is often longer than big toe"

My fingers are very slender so that checks. However, my second toe is a hammer toe where it curls all the way down, to the point that the nail is in full contact with the ground when I walk. If try straighting it out, however much I can, it easily passes my big toe. Dose this still fit with this symptom? And does histamine have anything to do with this hammering effect? I've had it since I was a little kid and most of the high histamine symptoms seem to fit with me even as a kid.
 

Motif

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I have histamine intolerance (high histamine) and super
slow digestion. Absolute no great digestion.
 

redsun

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I have histamine intolerance (high histamine) and super
slow digestion. Absolute no great digestion.
Not possible unless you are also B-vitamin deficient, zinc deficient. Histamine strongly stimulates gastric acid secretion but the whole process is still dependent on acetylcholine and CO2 (B-vitamins), electrolytes, carbonic anhydrase (zinc), etc.
 

Motif

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Not possible unless you are also B-vitamin deficient, zinc deficient. Histamine strongly stimulates gastric acid secretion but the whole process is still dependent on acetylcholine and CO2 (B-vitamins), electrolytes, carbonic anhydrase (zinc), etc.

so it’s still possible ;)

im pretty sure I’m high histamine , cause everything anti histamine helps my symptoms and when I , for example , take l histidine my symptoms get crazy shortly after.
I assume low stomach acid , cause food stays in my stomach forever sometimes and taking things that increase stomach acid help with this.


but yeah, I’m zinc deficient. No idea if b- vitamin deficient cause blood tests are confusing. They never showed deficient though.

copper and zinc deficient. Ceruloplasmin and DAO too.
Taking 40 mg zinc sulfate and 6-12 mg copper daily for half a year and still deficient.
 
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