144 replies to this topic

[Zenfood]

Hi.

 

I suffer from ADHD. The only thing that works for focus, motivation and libido is Ritalin (methylphenidate). Ritalin gave me adrenal fatigue when I started with it, because the dosage was way too high and I consumed coffee. I actually stopped methylphenidate for 8 months, but have come to a conclusion that low doses 5-15mg per day actually benefits me. It turns me into a emotional human being again (just like when I was younger).

 

 I've tried everything there is from stimulants to Longvida curcumin, CILTEP, Modafinil, racetams, etc. I don't handle stimulants well and I don't drink coffee (crash, nervousness, anxiety and jitters).

 

My main problems are low libido, dysthymia and anhedonia.

 

According to a gene test from 23andme:

- "The DRD2 TaqIA A1/A2 version causes less dopamine receptors. Doesn't learn from mistakes well. Men may have half the risk of Obsessive Compulsive Disorder but higher risk of ADHD. This is the rs1800497(C;T) gene."
- Also, I am neither a warrior or a worrier, because I have the Rs4680(A;G) gene.

 

What should I do?

 

I found this thread:
http://www.longecity...-dopamine-idea/

 

I believe that the Happy Stack is a good idea (Citicoline, Uridine and DHA) to start with.

What do you guys think about Sulbutiamine? Any more examples you could offer?

Thanks in advance.

 

 

[Area-1255]

D(2) receptor expression....

Well, it's mainly controlled by hormones such as Testosterone and Estrogen. 

Getting to a high testosterone state should help both your low libido and raise D(2) expression; providing you keep estrogen in balance.

D(2)'s correlate with Adenosine and form heteromers with H(3) and A2A receptors as well as possibly NMDA receptors.

Thus increasing the expression of D2's would be possible with chronic caffeine treatment, an H3 antagonist like betahistine, again, with time, and also using DAA or NMDA directly, and with time.

[Zenfood]

Hey!

I do powerlifting. Have been doing this for the past three years, but it hasn't helped. Not sure what you mean with getting to a high testosterone state. The only possible way to do this is to start juicing.

I already eat lots of fats (cholesterol -> pregnenolone -> all kinds of hormones)

 

How about:
"Three-month treatment course of methylphenidate increases plasma levels of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone-sulfate (DHEA-S) in attention deficit hyperactivity disorder."

http://www.ncbi.nlm....pubmed/14586159

Ritalin! Looks promising.

 

Chronic caffeine treatment is not for me, trust me. I have elevated Th2 levels and caffeine makes it worse.

http://selfhacked.co...-th2-dominance/

 

DAA could work (but has to be used chronically then and it could be dangerous/neurotoxic?). I have a bag of 500g DAA at home laying. Do you think I should start using it again? I have used it in the past. I have also experimented with NMDA, took 30mg before sleep for a whole month. Needless to say, it didn't make things better.

Edited by Zenfood, 30 August 2014 - 11:34 AM.

[Area-1255]

Hey!

I do powerlifting. Have been doing this for the past three years, but it hasn't helped. Not sure what you mean with getting to a high testosterone state. The only possible way to do this is to start juicing.

I already eat lots of fats (cholesterol -> pregnenolone -> all kinds of hormones)

 

How about:
"Three-month treatment course of methylphenidate increases plasma levels of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone-sulfate (DHEA-S) in attention deficit hyperactivity disorder."

http://www.ncbi.nlm....pubmed/14586159

Ritalin! Looks promising.

 

Chronic caffeine treatment is not for me, trust me. I have elevated Th2 levels and caffeine makes it worse.

http://selfhacked.co...-th2-dominance/

 

DAA could work, but I'm afraid that it's neurotoxic. I have used it in the past, but I believe that is raises DHEA levels only temporarily. I have also experimented with NMDA, took 30mg before sleep for a whole month. Needless to say, it didn't make things better.

When I say high testosterone, I mean get to the upper limit of your natural production. This is where the right foods and exercise click in.

 

Try a DAT inhibitor (dopamine reuptake inhibitor) a natural one preferably.

Catuaba or Flowering Quince extract.

[Zenfood]

I will look into Catuaba and Flowering Quince. I know that Abelard Lindsay tried/talked about them when he was experimenting with CILTEP.

[Area-1255]

I will look into Catuaba and Flowering Quince. I know that Abelard Lindsay tried/talked about them when he was experimenting with CILTEP.

http://www.ncbi.nlm....pubmed/15991001

 

 

Antidepressant-like effects of Trichilia catigua (Catuaba) extract: evidence for dopaminergic-mediated mechanisms.

Campos MM1, Fernandes ES, Ferreira J, Santos AR, Calixto JB.

Author information

 

Abstract

RATIONALE:

Currently available therapy for depression treatment is often associated with several undesirable side effects, and it is effective only in a certain portion of the population. Therefore, the identification of alternative therapeutic tools for the treatment of depression is still needed.

OBJECTIVE:

The present study analyzed the possible antidepressant-like effects of the Brazilian medicinal plant, Trichilia catigua, in rodents. Attempts were also made to investigate some of the possible mechanisms implicated in its actions.

METHODS:

The antidepressant-like effects of T. catigua extract were assessed in two species of rodents (mice and rats) by means of in vivo (forced swimming test) and in vitro (monoamine reuptake and release in synaptosomal preparations) approaches.

RESULTS:

Acute oral treatment with the extract of T. catigua produced antidepressant-like effects in the forced swimming model in both mice and rats. Anti-immobility actions of T. catigua extract in mice were significantly reversed by haloperidol or by chlorpromazine, but not by pimozide, ketanserin, spiroxatrine or p-chlorophenylalanine. In vitro, T. catigua extract concentration-dependently inhibited the uptake and increased the release of serotonin, and especially of dopamine, from rat brain synaptosomal preparations.

CONCLUSIONS:

The present study provides convincing evidence for a dopamine-mediated antidepressant-like effect of the active principle(s) present in the hydroalcoholic extract of T. catigua in mice and rats when in vivo and in vitro strategies were employed. Therefore, a standardized T. catigua extract or its purified constituents could be of potential interest for the treatment of depressive disorders.

PMID:   15991001   [PubMed - indexed for MEDLINE]  

 

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http://www.ncbi.nlm....pubmed/18485464

 

 

 

 

Pharmacol Biochem Behav. 2008 Sep;90(3):363-71. doi: 10.1016/j.pbb.2008.03.014. Epub 2008 Mar 30. Dopamine transporter inhibitory and antiparkinsonian effect of common flowering quince extract.

Zhao G1, Jiang ZH, Zheng XW, Zang SY, Guo LH.

Author information

 

Abstract

Common flowering quince (FQ) is the fruit of Chaenomeles speciosa (Sweet) Nakai. FQ-containing cocktails have been applied to the treatment of neuralgia, migraine, and depression in traditional Chinese medicine. The present study assessed whether FQ is effective in dopamine transporter (DAT) regulation and antiparkinsonism by utilizing in vitro and in vivo assays, respectively. FQ at concentrations of 1-1000 microg/ml concentration-dependently inhibited dopamine uptake by Chinese hamster ovary (CHO) cells stably expressing DAT (D8 cells) and by synaptosomes. FQ had a slight inhibitory action on norepinephrine uptake by CHO cells expressing the norepinephrine transporter and no inhibitory effect on gamma-aminobutyric acid (GABA) uptake by CHO cells expressing GABA transporter-1 or serotonin uptake by the serotonin transporter. A viability assay showed that FQ mitigated 1-methyl-4-phenylpyridinium-induced toxicity in D8 cells. Furthermore, in behavioral studies, FQ alleviated rotational behavior in 6-hydroxydopamine-treated rats and improved deficits in endurance performance in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. Furthermore, immunohistochemistry revealed that FQ markedly reduced the loss of tyrosine hydroxylase-positive neurons in the substantia nigra in MPTP-treated mice. In summary, FQ is a selective, potent DAT inhibitor and has antiparkinsonian-like effects that are mediated possibly by DAT suppression. FQ has the potential to be further developed for Parkinson's disease treatment.

PMID:   18485464   [PubMed - indexed for MEDLINE]  

 

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Edited by Area-1255, 30 August 2014 - 11:42 AM.

[Zenfood]

This is beautiful. I'm going to dive in forums and read anecdotes about these. Definitely going to try them both out separately. So far it looks promising!

 

And I think you are right about the caffeine thing. I could now also see that it actually decreases Th2, which would be beneficial for me. However it stimulates me too much.

 

Do you think 10-20mg of caffeine daily could work/be enough? I think 5mg of methylphenidate and 10mg of caffeine could be a nice stack actually without stressing out my body. My mind can take it, I really love the stuff, but I just notice that it is toxic to my body in high amounts. Have to find my goldilocks zone.

[Zenfood]

Thanks for all your help and input Area-1255.

Also wanted to check what you think about this:
http://www.ncbi.nlm....pubmed/22791651



I smoke sometimes and I am not prone to get addicted to anything even though I have ADHD. My self-discipline is really good. I don't even drink alcohol even though I live in Finland.

Just a thought. Do you think that smoking high CBD content weed could be beneficial?

[Area-1255]

Thanks for all your help and input Area-1255.

Also wanted to check what you think about this:
http://www.ncbi.nlm....pubmed/22791651



I smoke sometimes and I am not prone to get addicted to anything even though I have ADHD. My self-discipline is really good. I don't even drink alcohol even though I live in Finland.

Just a thought. Do you think that smoking high CBD content weed could be beneficial?

It could be in some cases, most people with OCD can't handle pot though, or it doesn't do anything for them.

The study you linked certainly explains the synergism of CBG / Weed with other drugs and alcohol.

 

Also cannabinoids lower prolactin, but interestingly, also may lower testosterone if used Chronically.

Also read some of my articles; they're worth it and related.

http://area1255.blog...-finishing.html

http://area1255.blog...stosterone.html

http://area1255.blog...e-gels-and.html

Edited by Area-1255, 30 August 2014 - 02:33 PM.

[Haray]

 

Thanks for all your help and input Area-1255.

Also wanted to check what you think about this:
http://www.ncbi.nlm....pubmed/22791651



I smoke sometimes and I am not prone to get addicted to anything even though I have ADHD. My self-discipline is really good. I don't even drink alcohol even though I live in Finland.

Just a thought. Do you think that smoking high CBD content weed could be beneficial?

It could be in some cases, most people with OCD can't handle pot though, or it doesn't do anything for them.

The study you linked certainly explains the synergism of CBG / Weed with other drugs and alcohol.

 

Also cannabinoids lower prolactin, but interestingly, also may lower testosterone if used Chronically.

Also read some of my articles; they're worth it and related.

http://area1255.blog...-finishing.html

http://area1255.blog...stosterone.html

http://area1255.blog...e-gels-and.html

 

 

I think the whole testosterone link hasn't been proven actually. 

 

[Sciencyst]

Hi! Upregulating dopamine receptors could cause undesired results, so make sure to research the implications of upregulation before you attempt it.

That being said, here are the main substances that will actually upregulate dopamine receptors:
-sulbutiamine
-phenylpiracetam (also downregulates nmda which can be quite bad)
-l-tetrahydropalmatine (herbal antipsychotic, antagonizes D1, D2, D3 )

[Bateau]

I will look into Catuaba and Flowering Quince. I know that Abelard Lindsay tried/talked about them when he was experimenting with CILTEP.

 

Babchi or Psoralea corylifolia is another natural DRI, to be specific its an NDRI and MAOI. Ive taken it alongside catuaba and flowering quince and do notice an increase in motivation and drive, and what seems like a mild loss of inhibition. No stimulation or euphoria though.
 

[Area-1255]

 

I will look into Catuaba and Flowering Quince. I know that Abelard Lindsay tried/talked about them when he was experimenting with CILTEP.

 

Babchi or Psoralea corylifolia is another natural DRI, to be specific its an NDRI and MAOI. Ive taken it alongside catuaba and flowering quince and do notice an increase in motivation and drive, and what seems like a mild loss of inhibition. No stimulation or euphoria though.
 

 

Interesting, I'll have to look into that one.

[Kewell357]

Hi! Upregulating dopamine receptors could cause undesired results, so make sure to research the implications of upregulation before you attempt it.

That being said, here are the main substances that will actually upregulate dopamine receptors:
-sulbutiamine
-phenylpiracetam (also downregulates nmda which can be quite bad)
-l-tetrahydropalmatine (herbal antipsychotic, antagonizes D1, D2, D3 )

 

I'm just curious.

 

Can Phenylpiracetam be used to reduce amphetamine tolerance? since it upregulates dopamine receptors.

[Bateau]

Try a DAT inhibitor (dopamine reuptake inhibitor) a natural one preferably.

Catuaba or Flowering Quince extract.

 

What source did you use for your Catuaba? Ive used both Solaray and Stakich, neither are concentrates or very effective. The Solaray mislabeled the scientific name and the Stakich brand is ridiculously overpriced.

 

Also what subjective effects did you experience?

[Area-1255]

 

Try a DAT inhibitor (dopamine reuptake inhibitor) a natural one preferably.

Catuaba or Flowering Quince extract.

 

What source did you use for your Catuaba? Ive used both Solaray and Stakich, neither are concentrates or very effective. The Solaray mislabeled the scientific name and the Stakich brand is ridiculously overpriced.

 

Also what subjective effects did you experience?

 

Don't waste money on mainstream brands, go with an independent seller and herbalist --> http://barlowesherba...extract-41.html

 

Michael Barlowe is a good guy, and trustworthy. Prices can't be beat.

 

In regards to effects, let's just say Catuaba is one of the few herbal stimulants that seems to produce the perfect balance; especially in combination with Caffeine and Muira Puama (which are the only ones I was testing at the time). There was some euphoria, particularly the euphoric outlook of a child (desire to explore,seeing things in brighter colors,just overall +++).

 

Keep in mind that catuaba is also found in some energy drinks (Alternative Energy) which you can buy at Wegmans. 

It's the same brand that makes the drink "Urban Detox" which is spreading quickly in many stores.

 

Alternative Energy is the only one I know of with such a unique ingredient matrix.

 

It's one of the only energy drinks I would feel safe with.

http://www.functiond...ternativeenergy

 

 

 rsz_label.jpg   210.75KB   16 downloads

 

-Guarana                            (like caffeine, a cAMP-specific PDE inhibitor)

-Horny Goat Weed           (an antihistamine, MAO inhibitor and PDE-5 inhibitor)

-Muira Puama             (5-HT2A agonist, Beta-adrenergic agonist, Dopamine D1 agonist and AcHe inhibitor)

-Catuaba      ( a DSRI - dopamine serotonin reuptake inhibitor )

Edited by Area-1255, 31 August 2014 - 04:16 PM.

[Bateau]

Don't waste money on mainstream brands, go with an independent seller and herbalist --> http://barlowesherba...extract-41.html

Michael Barlowe is a good guy, and trustworthy. Prices can't be beat.

 

In regards to effects, let's just say Catuaba is one of the few herbal stimulants that seems to produce the perfect balance; especially in combination with Caffeine and Muira Puama (which are the only ones I was testing at the time). There was some euphoria, particularly the euphoric outlook of a child (desire to explore,seeing things in brighter colors,just overall +++).

 

Keep in mind that catuaba is also found in some energy drinks (Alternative Energy) which you can buy at Wegmans. 

It's the same brand that makes the drink "Urban Detox" which is spreading quickly in many stores.

 

Alternative Energy is the only one I know of with such a unique ingredient matrix.

 

It's one of the only energy drinks I would feel safe with.

http://www.functiond...ternativeenergy

 

 

rsz_label.jpg

 

-Guarana                            (like caffeine, a cAMP-specific PDE inhibitor)

-Horny Goat Weed           (an antihistamine, MAO inhibitor and PDE-5 inhibitor)

-Muira Puama             (5-HT2A agonist, Beta-adrenergic agonist, Dopamine D1 agonist and AcHe inhibitor)

-Catuaba      ( a DSRI - dopamine serotonin reuptake inhibitor )

 

 

Catuaba, muira puama, and caffeine? essentially Catuama right? does a pinch of ginger (to fully mimic catuama) have any effects?
 

I've tried muira puama as a nootropic. Didnt notice any effects, gave it to my sister as an "herbal nootropic", forgetting to mention its aphrodisiac properties. She called me two days later freaking out saying that she was so insanely horny that she was genuinely worried about it. I laughed so hard. Apparently its libido improving aspects are quite potent.

 

Thanks for the link. Just bought 2 bottles.

 

How much of the Catuaba extract would you take and how much caffeine would you co-ingest?

Edited by Bateau, 31 August 2014 - 04:56 PM.

[Flex]

Better You look out for something modulating i.e. that increase D2 mrna,than something that You have to use every day.

But since its genetically set, dont know.

You could try a MAO-B and/or MAO-A inhibitors. this works at least for me and "could" be safer than DRI.

 

The problem with 23andMe is that the result could distract from another problem.

This was IIRC the Reason why it was forbidden to diagnose Your results.

What if it turns out that You have a damaged dopamine system which is loosely related to the genetics ?

E.g. chronic stress is known to cause damage.

I would think about it.

 

I would advise You to stay away from Methylphenidate.

Prefrontal cortical and striatal transcriptional responses to the reinforcing effect of repeated methylphenidate treatment in the spontaneously hypertensive rat, animal model of attention-deficit/hyperactivity disorder (ADHD)

http://www.behaviora...content/10/1/17

 

Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice

http://www.plosone.o...al.pone.0033693

 

Anyway I could uptill now only find this:

Pukatein is a DRI and a Dopamine agonist.

If You have trouble to find the solely compound, look out for the Herb/ Herb extract.

Dopaminergic pharmacology and antioxidant properties of pukateine, a natural product lead for the design of agents increasing dopamine neurotransmission.

http://www.ncbi.nlm....pubmed/10211594

http://en.wikipedia.org/wiki/Pukateine

 

But I dont know nothing about Pukateine and DAWS ( dopamine agonist withdrawal syndrom) or anything.

Usually an increase in Dopamine means sometimes an icrease in oxidation, so damage.

Therefore use it on Your own risk.

 

Not only dopamine D2 receptors involved in Peony-Glycyrrhiza Decoction, an herbal preparation against antipsychotic-associated hyperprolactinemia.

....Consistent with a D(2)-action, PGD did not affect PRL in rat pituitary lactotropic tumor-derived GH3 cells that lack the D(2) receptor expression but significantly increased the expression of D(2) receptors and dopamine transporters (DAT) in PC12 cells...

http://www.optimalrx..._1349155441.pdf

http://www.ncbi.nlm....pubmed/22796279

 

But if You look in the ingredients of this below, You´ll find vitamins, aminoacids &etc.

So either, simple compounds or a mixture of them are responsible for this and do work, or they are selling Snakeoil...

 

Natural Dopaminergic Activator Improves Outcomes of Addiction Recovery

SynaptaGenX will increase proliferation of D2 receptors, enhancing dopamine sensitivity and increasing the sense of happiness, particularly in carriers of DRD2 A1 allele.

http://www.holisticp...ction-recovery-

Edited by Flex, 31 August 2014 - 05:05 PM.

[chemicalambrosia]

 

Hey!

I do powerlifting. Have been doing this for the past three years, but it hasn't helped. Not sure what you mean with getting to a high testosterone state. The only possible way to do this is to start juicing.

I already eat lots of fats (cholesterol -> pregnenolone -> all kinds of hormones)

 

How about:
"Three-month treatment course of methylphenidate increases plasma levels of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone-sulfate (DHEA-S) in attention deficit hyperactivity disorder."

http://www.ncbi.nlm....pubmed/14586159

Ritalin! Looks promising.

 

Chronic caffeine treatment is not for me, trust me. I have elevated Th2 levels and caffeine makes it worse.

http://selfhacked.co...-th2-dominance/

 

DAA could work, but I'm afraid that it's neurotoxic. I have used it in the past, but I believe that is raises DHEA levels only temporarily. I have also experimented with NMDA, took 30mg before sleep for a whole month. Needless to say, it didn't make things better.

When I say high testosterone, I mean get to the upper limit of your natural production. This is where the right foods and exercise click in.

 

Try a DAT inhibitor (dopamine reuptake inhibitor) a natural one preferably.

Catuaba or Flowering Quince extract.

 

 

Where are you getting your flowering quince extract from?
 

[Bateau]

Where are you getting your flowering quince extract from?

 

I second this question.

 

I would get mine here

 

Funnily enough, in the "Customers Who Bought This Item Also Bought" section, Psoralea corylifolia (Babchi) pops up which, not to sound self centered (but its SOO going to anyway), has to be from my doing. So does mucuna derived L-DOPA though, which is a ballzy combo, not of my doing, and not something I would suggest. L-tyrosine (not NALT) would be a safer alternative.

 

The Psoralea tastes much better than the quince, Quince tastes very sour and somewhat savory. Psoralea tastes almost like mild cinnamon.

 

EDIT: They are severely discounted for some reason, mine cost ~$37 + $5 shipping, they're $11-16 plus shipping right now. LOL .

Edited by Bateau, 31 August 2014 - 07:11 PM.

[Area-1255]

 

Where are you getting your flowering quince extract from?

 

I second this question.

 

I would get mine here

 

Funnily enough, in the "Customers Who Bought This Item Also Bought" section, Psoralea corylifolia (Babchi) pops up which, not to sound self centered (but its SOO going to anyway), has to be from my doing. So does mucuna derived L-DOPA though, which is a ballzy combo, not of my doing, and not something I would suggest. L-tyrosine (not NALT) would be a safer alternative.

 

The Psoralea tastes much better than the quince, Quince tastes very sour and somewhat savory. Psoralea tastes almost like mild cinnamon.

 

EDIT: They are severely discounted for some reason, mine cost ~$37 + $5 shipping, they're $11-16 plus shipping right now. LOL .

 

I thought the Quince tastes good actually, kinda lemony sour type thing. Yeah that's the one I bought though. 

In regards to Catuaba, take anywhere from 1-2 capsules twice a day. Start low though, it's a potent stimulant.

Though less dangerous than ritalin, Adderall, caffeine, 1,3 dimethylamylamine (Geranamine).

 

Since it's a reuptake inhibitor it doesn't share vasoconstricting effects of other stimulants; in fact, it's a more vasodilator because of this.

Though there are some exceptions though (such as when combining catuaba with MAO,COMT inhibitors) which in these cases serotonin syndrome and / or hyperadrenalism may occur. So be careful when using MAOI's etc Serotonin Syndrome is NOT fun.

 

Catuaba also helps improve platelet generation and also has a mild blood thinning effect. 1/4 if the potency of Ginkgo, which isn't much - but still worth noting.

 

Catuaba interacts with Phospholipace C and inhibits Phospholipase A2 - this can help explain it's anti-inflammatory effects as well.

 

http://eurekamag.com...6/004206993.php

http://www.raysaheli...om/catuaba.html

Edited by Area-1255, 31 August 2014 - 07:30 PM.

[Area-1255]

My recent article on histamine may shed some light as well OP - Histamine H(3) antagonists are probably the best bet for actually increasing D(2) mRNA Expression.

They also are under investigation for treatment of schizophrenia and ADHD.

http://www.sciencedi...006295207000159

 

 

Abstract

The interactions in the rat striatum between H₃ receptors (H₃Rs) and D₂ receptors (D₂Rs) were investigated with the [³⁵S]GTPγ[S] binding assay. The H₃R agonist (R)α-methylhistamine increased [³⁵S]GTPγ[S] binding to striatal membranes with an EC₅₀ = 14 ± 5 nM and a maximal effect of +19 ± 1%. This effect was inhibited by the H₃R antagonist ciproxifan with a K_i = 1.0 ± 0.3 nM. The D₂R agonist quinpirole increased [³⁵S]GTPγ[S] binding to the same membranes with an EC₅₀ = 1.5 ± 0.5 μM and a maximal effect of +28 ± 2%. Its effect was blocked by haloperidol with a K_i = 0.3 ± 0.1 nM. The maximal effects of the H₃R and D₂R agonists were additive (+46 ± 3%). However, D₂R ligands did not modify the effects of H₃R ligands and vice versa. Ciproxifan behaved as an H₃R inverse agonist and decreased [³⁵S]GTPγ[S] binding. Haloperidol had no effect and did not change the inverse agonist effect of ciproxifan. Administrations for 10 days of ciproxifan (1.5 mg/kg/day) or haloperidol (0.5 mg/kg/day) did not change the effects of quinpirole and (R)α-methylhistamine, respectively. These data suggest that striatal H₃Rs and D₂Rs do not interact through their coupling to G-proteins. However, a hyperactivity of histaminergic and dopaminergic neurons being observed in schizophrenia, the additive activations of H₃Rs and D₂Rs suggest that they cooperate to generate some schizophrenic symptoms. Such a postsynaptic mechanism may underlie the antipsychotic-like effects of H₃R inverse agonists and supports their therapeutic interest, alone or as adjunctive treatment with neuroleptics.

 

 

http://www.ncbi.nlm....les/PMC2435196/

 

 

 

Radioligand binding experiments in striatal membrane preparations showed the existence of a strong and selective H3-D2 receptor interaction at the membrane level. In agonist/antagonist competition experiments stimulation of H3 receptors with several H3 receptor agonists significantly decreased the affinity of D2 receptors for the agonist. This kind of intramembrane receptor-receptor interactions are a common biochemical property of receptor heteromers. In fact, by using Bioluminescence Resonance Energy Transfer techniques in co-transfected HEK-293 cells, H3 (but not H4) receptors were found to form heteromers with D2 receptors. The present study demonstrates an important role of postsynaptic H3 receptors in the modulation of dopaminergic transmission by means of a negative modulation of D2 receptor function.

 

http://www.ncbi.nlm....pubmed/23109919

 

 

 

 

 

Abstract

Histamine H3 receptor (H3R) antagonists/inverse agonists possess potential to treat diverse disease states of the central nervous system (CNS). Cognitive dysfunction and motor impairments are the hallmark of multifarious neurodegenerative and/or psychiatric disorders. This review presents the various neurobiological/neurochemical evidences available so far following H3R antagonists in the pathophysiology of Alzheimer's disease (AD), attention-deficit hyperactivity disorder (ADHD), schizophrenia, and drug abuse each of which is accompanied by deficits of some aspects of cognitive and/or motor functions. Whether the H3R inverse agonism modulates the neurochemical basis underlying the disease condition or affects only the cognitive/motor component of the disease process is discussed with the aim to provide a rationale for their use in diverse disease states that are interlinked and are accompanied by some common motor, cognitive and attentional deficits.

 

Edited by Area-1255, 31 August 2014 - 11:22 PM.

[Flex]

No offence, but I couldnt find any statements that Histamine increases or decreases D2 expression.

I could have them overlooked.

Because changes in binding affinity could be caused by various causes.

 

[Area-1255]

No offence, but I couldnt find any statements that Histamine increases or decreases D2 expression.

I could have them overlooked.

Because changes in binding affinity could be caused by various causes.

I posted it above. Here it is again.

http://www.ncbi.nlm....pubmed/18547596

 

 

 

Radioligand binding experiments in striatal membrane preparations showed the existence of a strong and selective H

3-D2 receptor interaction at the membrane level. In agonist/antagonist competition experiments stimulation of H3 receptors with several H3 receptor agonists significantly decreased the affinity of D2 receptors for the agonist. This kind of intramembrane receptor-receptor interactions are a common biochemical property of receptor heteromers. In fact, by using Bioluminescence Resonance Energy Transfer techniques in co-transfected HEK-293 cells, H3 (but not H4) receptors were found to form heteromers with D2 receptors. The present study demonstrates an important role of postsynaptic H3 receptors in the modulation of dopaminergic transmission by means of a negative modulation of D2 receptor function.

Edited by Area-1255, 01 September 2014 - 02:20 AM.

[Flex]

This kind of intramembrane receptor-receptor interactions are a common biochemical property of receptor heteromers. In fact, by using Bioluminescence Resonance Energy Transfer techniques in co-transfected HEK-293 cells, H(3) (but not H(4)) receptors were found to form heteromers with D(2) receptors. This study demonstrates an important role of postsynaptic H(3) receptors in the modulation of dopaminergic transmission by means of a negative modulation of D(2) receptor function.

 

Heteromers have nothing to do with the expression of receptors.

 

Or would based on this, an alteration of CB1 also Skyrocket the D2 mRNA like via H3 ?

 

CB1/D2 heteromers

Antagonistic cannabinoid CB1/dopamine D2 receptor interactions in striatal CB1/D2 heteromers. A combined neurochemical and behavioral analysis.

http://www.ncbi.nlm....pubmed/18262573

 

Or Sigma receptors ?

Cocaine disrupts histamine H3 receptor modulation of dopamine D1 receptor signaling: σ1-D1-H3 receptor complexes as key targets for reducing cocaine's effects.

http://www.ncbi.nlm....pubmed/24599455

Edited by Flex, 01 September 2014 - 03:26 PM.

[Area-1255]

This kind of intramembrane receptor-receptor interactions are a common biochemical property of receptor heteromers. In fact, by using Bioluminescence Resonance Energy Transfer techniques in co-transfected HEK-293 cells, H(3) (but not H(4)) receptors were found to form heteromers with D(2) receptors. This study demonstrates an important role of postsynaptic H(3) receptors in the modulation of dopaminergic transmission by means of a negative modulation of D(2) receptor function.

 

Heteromers have nothing to do with the expression of receptors.

 

Or would based on this, an alteration of CB1 also Skyrocket the D2 mRNA like via H3 ?

 

CB1/D2 heteromers

Antagonistic cannabinoid CB1/dopamine D2 receptor interactions in striatal CB1/D2 heteromers. A combined neurochemical and behavioral analysis.

http://www.ncbi.nlm....pubmed/18262573

 

Or Sigma receptors ?

Cocaine disrupts histamine H3 receptor modulation of dopamine D1 receptor signaling: σ1-D1-H3 receptor complexes as key targets for reducing cocaine's effects.

http://www.ncbi.nlm....pubmed/24599455

Doesn't matter, it's still a negative modulator of D(2) function; so the net effect would still be enhanced D1 and D2-mediated neurotransmission. Also saying heteromers have nothing to do with expression would be contradictory, if there are interactions on one receptor level and considering how sensitive dopamine D2RL is in general, the only presumption can be made that you would have the effect based on receptor reactivity. I suggest you do a little more research so you can understand things aren't that clear cut and linear.

It's about the indirect actions of blocking a regulator, just like H1 antagonists can downregulate or upregulate H1R's themselves, depending on potency, ligand/natural agonism/antagonism. H(1)R's interestingly when activated, cause their own upregulation. Histamine also increases tyrosine hydroxylase (!) activity, leading to MORE dopamine synthesis right from the start. 

 

From a biological understanding and knowing the human brain, it makes sense to say that H(3)R antagonism Would upregulate D2R expression...wanna know why?Homeostasis/Negative Feedback is one reason, by blocking H3R's we induce a potent cAMP response, to protect against excess cAMP  the body naturally upregulates it's key cAMP inhibiting receptor - Dopamine D2R.

Why?

Because too much cAMP causes excess Thyroid hormone and will beat up the stress response system if not controlled, however this only occurs at very VERY HIGH levels of cAMP, but H3R's represent a major cAMP regulation system, so significant that by blocking them the level of cAMP would be increased over 144% just by doing that alone.

 

 

Take a look at these threads on here.

You will see why people are so interested.

 

http://www.longecity...tropic-effects/

http://www.longecity...-3-antagonists/

http://www.longecity...ntidysenterica/

 

 

 

 

Take a look at these threads on here.

You will see why people are so interested.

 

http://www.longecity...tropic-effects/

http://www.longecity...-3-antagonists/

http://www.longecity...ntidysenterica/

 

 

Stimulation of histamine H1 receptor up-regulates histamine H1 receptor itself through activation of receptor gene transcription.

Das AK1, Yoshimura S, Mishima R, Fujimoto K, Mizuguchi H, Dev S, Wakayama Y, Kitamura Y, Horio S, Takeda N, Fukui H.

Author information

 

Abstract

Histamine is a major mediator in allergy acting mainly through the histamine H(1) receptor (H1R). Although H1R up-regulation has been suggested as an important step for induction of allergic symptoms, little is known about the regulation of H1R level. Here we report that the activation of H1R up-regulates H1R through augmentation of H1R mRNA expression in HeLa cells. Histamine stimulation significantly increased both H1R promoter activity and mRNA level without alteration in mRNA stability. H1R protein was also up-regulated by histamine. An H1R antagonist but not histamine H(2) receptor antagonist blocked histamine-induced up-regulation of both promoter activity and mRNA expression. A protein kinase C (PKC) activator, phorbol-12-myristate-13-acetate, increased H1R mRNA expression, whereas an activator of PKA or PKG (8-Br-cAMP or 8-Br-cGMP, respectively) did not. Furthermore, histamine-induced up-regulation of both promoter activity and mRNA level were completely suppressed by the PKC inhibitor Ro-31-8220. H1R antagonists have long been thought to block H1R and inhibit immediate allergy symptoms. In addition to this short-term effect, our data propose their long-term inhibitory effect against allergic diseases by suppressing PKC-mediated H1R gene transcription. This finding provides new insights into the therapeutic target of H1R antagonist in allergic diseases.

 

 

One more thing, H3R antagonists are found to significantly decrease MAO activity...this ALSO leads to enhanced dopaminergic transmission..how much more proof do you need?

Just look at the forum links I gave you and see what people had to say.

 

 

 

 

Brain Res. 2001 Jul 6;906(1-2):180-3. Effects of histamine H3-receptor ligands on brain monoamine oxidase in various mammalian species.

Sakurai E1, Sakurai E, Tanaka Y, Watanabe T, Singh Jossan S, Oreland L.

Author information

 

Abstract

The effects of an H3 agonist, R-alpha-methylhistamine (alpha-MeHA), and an H3 antagonist, thioperamide, on monoamine oxidase (MAO) activity in the hypothalamus of rat, monkey and human brains were compared in vitro. The histamine H(3)-receptor ligands competitively inhibited MAO-B, but noncompetitively inhibited MAO-A in all three mammalian species. However, alpha-MeHA inhibited MAO-A more potently than MAO-B at high concentrations in all three species. The K(i) values for MAO-A of alpha-MeHA in hypothalamic homogenates of rat, monkey and human brains were estimated to be 1.1, 1.2 and 1.9 mM, respectively, suggesting that alpha-MeHA cannot behave as a substrate for the MAO inhibitor. In contrast, rat, monkey and human brain MAO-B activities were inhibited by thioperamide, with respective K(i) values of 174.6, 8.2 and 10.8 microM, more potently than MAO-A activity. These results indicate that thioperamide, which elicits a strong activation of histamine release and turnover to N-tele-methylhistamine from histamine, competitively inhibits the conversion of N-tele-methylhistamine to N-tele-methylimidazoleacetic acid in human and monkey brains where MAO-B predominates.

PMID:   11430877   [PubMed - indexed for MEDLINE]  

 

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Edited by Area-1255, 01 September 2014 - 04:34 PM.

[Area-1255]

 

This kind of intramembrane receptor-receptor interactions are a common biochemical property of receptor heteromers. In fact, by using Bioluminescence Resonance Energy Transfer techniques in co-transfected HEK-293 cells, H(3) (but not H(4)) receptors were found to form heteromers with D(2) receptors. This study demonstrates an important role of postsynaptic H(3) receptors in the modulation of dopaminergic transmission by means of a negative modulation of D(2) receptor function.

 

Heteromers have nothing to do with the expression of receptors.

 

Or would based on this, an alteration of CB1 also Skyrocket the D2 mRNA like via H3 ?

 

CB1/D2 heteromers

Antagonistic cannabinoid CB1/dopamine D2 receptor interactions in striatal CB1/D2 heteromers. A combined neurochemical and behavioral analysis.

http://www.ncbi.nlm....pubmed/18262573

 

Or Sigma receptors ?

Cocaine disrupts histamine H3 receptor modulation of dopamine D1 receptor signaling: σ1-D1-H3 receptor complexes as key targets for reducing cocaine's effects.

http://www.ncbi.nlm....pubmed/24599455

Doesn't matter, it's still a negative modulator of D(2) function; so the net effect would still be enhanced D1 and D2-mediated neurotransmission. Also saying heteromers have nothing to do with expression would be contradictory, if there are interactions on one receptor level and considering how sensitive dopamine D2RL is in general, the only presumption can be made that you would have the effect based on receptor reactivity. I suggest you do a little more research so you can understand things aren't that clear cut and linear.

It's about the indirect actions of blocking a regulator, just like H1 antagonists can downregulate or upregulate H1R's themselves, depending on potency, ligand/natural agonism/antagonism. H(1)R's interestingly when activated, cause their own upregulation. Histamine also increases tyrosine hydroxylase (!) activity, leading to MORE dopamine synthesis right from the start. 

 

From a biological understanding and knowing the human brain, it makes sense to say that H(3)R antagonism Would upregulate D2R expression...wanna know why? Homeostasis/Negative Feedback is one reason, by blocking H3R's we induce a potent cAMP response, to protect against excess cAMP  the body naturally upregulates it's key cAMP inhibiting receptor - Dopamine D2R.

Why?

Because too much cAMP causes excess Thyroid hormone and will beat up the stress response system if not controlled, however this only occurs at very VERY HIGH levels of cAMP, but H3R's represent a major cAMP regulation system, so significant that by blocking them the level of cAMP would be increased over 144% just by doing that alone.

 

 

Take a look at these threads on here.

You will see why people are so interested.

 

http://www.longecity...tropic-effects/

http://www.longecity...-3-antagonists/

http://www.longecity...ntidysenterica/

 

 

Stimulation of histamine H1 receptor up-regulates histamine H1 receptor itself through activation of receptor gene transcription.

Das AK1, Yoshimura S, Mishima R, Fujimoto K, Mizuguchi H, Dev S, Wakayama Y, Kitamura Y, Horio S, Takeda N, Fukui H.

Author information

 

Abstract

Histamine is a major mediator in allergy acting mainly through the histamine H(1) receptor (H1R). Although H1R up-regulation has been suggested as an important step for induction of allergic symptoms, little is known about the regulation of H1R level. Here we report that the activation of H1R up-regulates H1R through augmentation of H1R mRNA expression in HeLa cells. Histamine stimulation significantly increased both H1R promoter activity and mRNA level without alteration in mRNA stability. H1R protein was also up-regulated by histamine. An H1R antagonist but not histamine H(2) receptor antagonist blocked histamine-induced up-regulation of both promoter activity and mRNA expression. A protein kinase C (PKC) activator, phorbol-12-myristate-13-acetate, increased H1R mRNA expression, whereas an activator of PKA or PKG (8-Br-cAMP or 8-Br-cGMP, respectively) did not. Furthermore, histamine-induced up-regulation of both promoter activity and mRNA level were completely suppressed by the PKC inhibitor Ro-31-8220. H1R antagonists have long been thought to block H1R and inhibit immediate allergy symptoms. In addition to this short-term effect, our data propose their long-term inhibitory effect against allergic diseases by suppressing PKC-mediated H1R gene transcription. This finding provides new insights into the therapeutic target of H1R antagonist in allergic diseases.

 

 

One more thing, H3R antagonists are found to significantly decrease MAO activity...this ALSO leads to enhanced dopaminergic transmission..how much more proof do you need?

Just look at the forum links I gave you and see what people had to say.

 

 

 

 

Brain Res. 2001 Jul 6;906(1-2):180-3. Effects of histamine H3-receptor ligands on brain monoamine oxidase in various mammalian species.

Sakurai E1, Sakurai E, Tanaka Y, Watanabe T, Singh Jossan S, Oreland L.

Author information

 

Abstract

The effects of an H3 agonist, R-alpha-methylhistamine (alpha-MeHA), and an H3 antagonist, thioperamide, on monoamine oxidase (MAO) activity in the hypothalamus of rat, monkey and human brains were compared in vitro. The histamine H(3)-receptor ligands competitively inhibited MAO-B, but noncompetitively inhibited MAO-A in all three mammalian species. However, alpha-MeHA inhibited MAO-A more potently than MAO-B at high concentrations in all three species. The K(i) values for MAO-A of alpha-MeHA in hypothalamic homogenates of rat, monkey and human brains were estimated to be 1.1, 1.2 and 1.9 mM, respectively, suggesting that alpha-MeHA cannot behave as a substrate for the MAO inhibitor. In contrast, rat, monkey and human brain MAO-B activities were inhibited by thioperamide, with respective K(i) values of 174.6, 8.2 and 10.8 microM, more potently than MAO-A activity. These results indicate that thioperamide, which elicits a strong activation of histamine release and turnover to N-tele-methylhistamine from histamine, competitively inhibits the conversion of N-tele-methylhistamine to N-tele-methylimidazoleacetic acid in human and monkey brains where MAO-B predominates.

PMID:   11430877   [PubMed - indexed for MEDLINE]  

 

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• Share on Google+[/

 

 

 

 

Doesn't matter, it's still a negative modulator of D(2) function; so the net effect would still be enhanced D1 and D2-mediated neurotransmission. Also saying heteromers have nothing to do with expression would be contradictory, if there are interactions on one receptor level and considering how sensitive dopamine D2RL is in general, the only presumption can be made that you would have the effect based on receptor reactivity. I suggest you do a little more research so you can understand things aren't that clear cut and linear.

It's about the indirect actions of blocking a regulator, just like H1 antagonists can downregulate or upregulate H1R's themselves, depending on potency, ligand/natural agonism/antagonism. H(1)R's interestingly when activated, cause their own upregulation. Histamine also increases tyrosine hydroxylase (!) activity, leading to MORE dopamine synthesis right from the start. 

 

From a biological understanding and knowing the human brain, it makes sense to say that H(3)R antagonism Would upregulate D2R expression...wanna know why?Homeostasis/Negative Feedback is one reason, by blocking H3R's we induce a potent cAMP response, to protect against excess cAMP  the body naturally upregulates it's key cAMP inhibiting receptor - Dopamine D2R.

Why?

Because too much cAMP causes excess Thyroid hormone and will beat up the stress response system if not controlled, however this only occurs at very VERY HIGH levels of cAMP, but H3R's represent a major cAMP regulation system, so significant that by blocking them the level of cAMP would be increased over 144% just by doing that alone.

 

 

Take a look at these threads on here.

You will see why people are so interested.

 

http://www.longecity...tropic-effects/

http://www.longecity...-3-antagonists/

http://www.longecity...ntidysenterica/

 

Edited by Area-1255, 01 September 2014 - 04:32 PM.

[Zenfood]

Thanks for your input.

I believe that methylphenidate does more good than harm for me in low doses. E.g. the rats were fed 5 mg/kg, that's megadosing. I take 5-15mg a day (really low dose).

 

"SynaptaGenX will increase proliferation of D2 receptors, enhancing dopamine sensitivity and increasing the sense of happiness, particularly in carriers of DRD2 A1 allele."

Very interesting. I have the DRD2 A1 allele.

 

 

Better You look out for something modulating i.e. that increase D2 mrna,than something that You have to use every day.

But since its genetically set, dont know.

You could try a MAO-B and/or MAO-A inhibitors. this works at least for me and "could" be safer than DRI.

 

The problem with 23andMe is that the result could distract from another problem.

This was IIRC the Reason why it was forbidden to diagnose Your results.

What if it turns out that You have a damaged dopamine system which is loosely related to the genetics ?

E.g. chronic stress is known to cause damage.

I would think about it.

 

I would advise You to stay away from Methylphenidate.

Prefrontal cortical and striatal transcriptional responses to the reinforcing effect of repeated methylphenidate treatment in the spontaneously hypertensive rat, animal model of attention-deficit/hyperactivity disorder (ADHD)

http://www.behaviora...content/10/1/17

 

Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice

http://www.plosone.o...al.pone.0033693

 

Anyway I could uptill now only find this:

Pukatein is a DRI and a Dopamine agonist.

If You have trouble to find the solely compound, look out for the Herb/ Herb extract.

Dopaminergic pharmacology and antioxidant properties of pukateine, a natural product lead for the design of agents increasing dopamine neurotransmission.

http://www.ncbi.nlm....pubmed/10211594

http://en.wikipedia.org/wiki/Pukateine

 

But I dont know nothing about Pukateine and DAWS ( dopamine agonist withdrawal syndrom) or anything.

Usually an increase in Dopamine means sometimes an icrease in oxidation, so damage.

Therefore use it on Your own risk.

 

Not only dopamine D2 receptors involved in Peony-Glycyrrhiza Decoction, an herbal preparation against antipsychotic-associated hyperprolactinemia.

....Consistent with a D(2)-action, PGD did not affect PRL in rat pituitary lactotropic tumor-derived GH3 cells that lack the D(2) receptor expression but significantly increased the expression of D(2) receptors and dopamine transporters (DAT) in PC12 cells...

http://www.optimalrx..._1349155441.pdf

http://www.ncbi.nlm....pubmed/22796279

 

But if You look in the ingredients of this below, You´ll find vitamins, aminoacids &etc.

So either, simple compounds or a mixture of them are responsible for this and do work, or they are selling Snakeoil...

 

Natural Dopaminergic Activator Improves Outcomes of Addiction Recovery

SynaptaGenX will increase proliferation of D2 receptors, enhancing dopamine sensitivity and increasing the sense of happiness, particularly in carriers of DRD2 A1 allele.

http://www.holisticp...ction-recovery-

 

[abelard lindsay]

In regards to Catuaba, take anywhere from 1-2 capsules twice a day. Start low though, it's a potent stimulant.

Though less dangerous than ritalin, Adderall, caffeine, 1,3 dimethylamylamine (Geranamine).

 

Since it's a reuptake inhibitor it doesn't share vasoconstricting effects of other stimulants; in fact, it's a more vasodilator because of this.

Though there are some exceptions though (such as when combining catuaba with MAO,COMT inhibitors) which in these cases serotonin syndrome and / or hyperadrenalism may occur. So be careful when using MAOI's etc Serotonin Syndrome is NOT fun.

 

Catuaba also helps improve platelet generation and also has a mild blood thinning effect. 1/4 if the potency of Ginkgo, which isn't much - but still worth noting.

 

Catuaba interacts with Phospholipace C and inhibits Phospholipase A2 - this can help explain it's anti-inflammatory effects as well.

 

http://eurekamag.com...6/004206993.php

http://www.raysaheli...om/catuaba.html

 

 

Catuaba is great stuff.   I was researching it originally when I was looking into popular Amazonian herbs.  I found out that it's extremely popular in Brazil.  If you search Twitter for "catuaba" you'll see lots and lots of happy Brazilians.

 

In regards to its effects, I find it raises my core body temperature such that I feel comfortable outside in cold weather and it gives me a lot of energy.

Edited by abelard lindsay, 01 September 2014 - 10:53 PM.

[Area-1255]

 

Thanks for your input.

I believe that methylphenidate does more good than harm for me in low doses. E.g. the rats were fed 5 mg/kg, that's megadosing. I take 5-15mg a day (really low dose).

 

"SynaptaGenX will increase proliferation of D2 receptors, enhancing dopamine sensitivity and increasing the sense of happiness, particularly in carriers of DRD2 A1 allele."

Very interesting. I have the DRD2 A1 allele.

 

 

Better You look out for something modulating i.e. that increase D2 mrna,than something that You have to use every day.

But since its genetically set, dont know.

You could try a MAO-B and/or MAO-A inhibitors. this works at least for me and "could" be safer than DRI.

 

The problem with 23andMe is that the result could distract from another problem.

This was IIRC the Reason why it was forbidden to diagnose Your results.

What if it turns out that You have a damaged dopamine system which is loosely related to the genetics ?

E.g. chronic stress is known to cause damage.

I would think about it.

 

I would advise You to stay away from Methylphenidate.

Prefrontal cortical and striatal transcriptional responses to the reinforcing effect of repeated methylphenidate treatment in the spontaneously hypertensive rat, animal model of attention-deficit/hyperactivity disorder (ADHD)

http://www.behaviora...content/10/1/17

 

Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice

http://www.plosone.o...al.pone.0033693

 

Anyway I could uptill now only find this:

Pukatein is a DRI and a Dopamine agonist.

If You have trouble to find the solely compound, look out for the Herb/ Herb extract.

Dopaminergic pharmacology and antioxidant properties of pukateine, a natural product lead for the design of agents increasing dopamine neurotransmission.

http://www.ncbi.nlm....pubmed/10211594

http://en.wikipedia.org/wiki/Pukateine

 

But I dont know nothing about Pukateine and DAWS ( dopamine agonist withdrawal syndrom) or anything.

Usually an increase in Dopamine means sometimes an icrease in oxidation, so damage.

Therefore use it on Your own risk.

 

Not only dopamine D2 receptors involved in Peony-Glycyrrhiza Decoction, an herbal preparation against antipsychotic-associated hyperprolactinemia.

....Consistent with a D(2)-action, PGD did not affect PRL in rat pituitary lactotropic tumor-derived GH3 cells that lack the D(2) receptor expression but significantly increased the expression of D(2) receptors and dopamine transporters (DAT) in PC12 cells...

http://www.optimalrx..._1349155441.pdf

http://www.ncbi.nlm....pubmed/22796279

 

But if You look in the ingredients of this below, You´ll find vitamins, aminoacids &etc.

So either, simple compounds or a mixture of them are responsible for this and do work, or they are selling Snakeoil...

 

Natural Dopaminergic Activator Improves Outcomes of Addiction Recovery

SynaptaGenX will increase proliferation of D2 receptors, enhancing dopamine sensitivity and increasing the sense of happiness, particularly in carriers of DRD2 A1 allele.

http://www.holisticp...ction-recovery-

 

Did you read my post about histamine?