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Antidepressant effect of D3 preferring dopamine agonists

also guys, in some mental issues overmethylation is the problem, this is barely ever mentioned, atleast theres a new sup coming differeneD so there might be a hype about it soon, hippys will promote it like samE, you know the hippys that say meds are bad and sups are the solution, haha if only that was true, pharm companys wouldnt have to synth chemicals out of plant components.

One sup shop here allways give away magazines with insane claims that depression allways a nutrition imbalance or other nonesense.
holland and barret is a big offender of advising nonesense, with the idiotic uses they have in their book regarding sups, im a big fan of sups but look at science, not the traditional use of back in the day ppl lived in the forest and were eating flowers.
 
medievil, what about someone with reduced expression and low receptor density at D2, what do you recommend they take?
 
MeDieViL said:
also guys, in some mental issues overmethylation is the problem, this is barely ever mentioned, atleast theres a new sup coming differeneD so there might be a hype about it soon, hippys will promote it like samE, you know the hippys that say meds are bad and sups are the solution, haha if only that was true, pharm companys wouldnt have to synth chemicals out of plant components.

One sup shop here allways give away magazines with insane claims that depression allways a nutrition imbalance or other nonesense.
holland and barret is a big offender of advising nonesense, with the idiotic uses they have in their book regarding sups, im a big fan of sups but look at science, not the traditional use of back in the day ppl lived in the forest and were eating flowers.
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Damn I sounded stupid on some rcs haha.

medievil, what about someone with reduced expression and low receptor density at D2, what do you recommend they take?
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Same as for all, experimentation to find something that works well for you personally, itsn very complicated and I dunno how you can know wheter you have low receptor density.
 
MeDieViL said:
you must have been sensitive to the anticholinergic side effects, which prob rules hypercholinergic activity as a possible cause in your depression out, scopolamine works for like 90% of ppl that try it for depression with long lasting results.

i like that ketamine induces long lasting antidepressant effects rather then only when you take the stuff like ssris.
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What could possibly give rise to poor "methylation", or conversion?
Just a clinical condition, or any precipitating factors?

Ketamine lasts maybe a week or two, according to a clinical trial conducted in a private hospital around my way recently.
Certainly not "months", as some claim.
I did examine that in depth and, basically gave up on it as a potential treatment option.
I believe it is administered in cases of extreme suicidal tendencies, but not beyond that.
 
Is there any symptomology that would indicate specifically the chances of poor conversion or methylation?

By example, noradrenaline being the implicated receptor in a specific type of depression, is associated with low energy, fatigue, low motivation.

Serotonin being implicated - more, "sadness", rumination.
 
I just had my doc take bloods for homocystiene levels.

If they come back high - does that mean I'm a poor converter?

If they're normal, does that mean I won't benefit from the addition of l-methylfolate?

In the UK, the brands listed on amazon seem to come in 1 mg.
Where the AD dose is 7.5 to 15 mgs.

Anyone got decent source for these and methyl b12, possibly SAMe for someone in the UK?
 
lol.

This may be the miracle drug - but - do you know how expensive this shit is?

Deplin.

500 units of currency for 90x pills?

lolruserious?
 
https://www.ncbi.nlm.nih.gov/m/pubmed/3110847/

Regarding ketamine, while it is true that some treatment resistant depression patients relapse after a course of ketamine produces remission (for example in one patient who had undergone 200+ ECT treatments and tried 24 medications), it is possible that some patients could be sustained on maintence therapy (as said patient was).

But those patients could be very different situations than some other patients. Especially if one is towards the maladaptive daydreaming disorder spectrum and may not have typical depressive physiology.
 
JohnBoy2000 said:
Given that, I'm guessing I'll try taking the pramipexole at night to start off with, and see how that goes.

In terms of it's half life or length of action, should the tiredness be gone by the morning time pretty much??
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Plasma concentration half lives don't always correlate very well with brain concentrations. Haloperidol for example is known to build up in the brain. But every drug (and person) is unique.
 
MeDieViL said:
claiming they are more effective are absurd, it dpends wheter the individual has a favorable response, other ppl benefit from differened strategts like da agonists while they wont work for others. According to that logic one ssri would be enough as a ssri would be "that" good, its more complicated then that
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Regarding tricyclic's greater efficacy, this is statistically noted especially in Amitriptyline https://www.ncbi.nlm.nih.gov/pubmed/11157426 https://www.ncbi.nlm.nih.gov/pubmed/10760555

Amitriptyline is thought to be an agonist at neurotrophic receptors like TrkB https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2844702/

BDNF is especially important for anti-depressant response, although impaired signaling could be a bottleneck.

https://www.ncbi.nlm.nih.gov/pubmed/27620841 - this is a key study.

Many people can acutely alter their neurotransmission with drugs of abuse to relieve depression momentarily, but that is not the same thing as truly treating depressive pathology.
 
adder said:
Stuff like that doesn't sound appealing at all as fluoxetine is useless for depression in my opinion as are all SSRIs, SNRIs etc. At best they were mania-inducing for me which is clearly not what an antidepressant should do. I bet many tests done in lab that supposedly show whether there is an antidepressant activity or not give results that poorly correlate with the presence of antidepressant activity. For instance increased motor activity as opposed to lack of it is not really a sign of depression gone, right?
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I think the reason why animal models like the forced swim test are used (or models more akin to learned helplessness type behavior/biology that you can see with chronic defeat stress in both humans and animals) is because they do actually have predictive value when it comes to human anti-depressant response, I don't think scientists would use those animal models if they didn't have some predictive value. But those animal models are seemingly often used just to identify therapeutic targets/do pilot studies, while efficacy focused clinical trials (phase II and III) are a different matter.
 
JohnBoy2000 said:
What could possibly give rise to poor "methylation", or conversion?
Just a clinical condition, or any precipitating factors?
Click to expand...

Single nucleotide polymorphisms, see rs1801131 and rs1801133, also known as A1298C and C677T respectively. But be cautious when entering this area of genomic data. Its okay to do the whole 23andme - Promethase thing but don't be freaking out thinking that a fundamental metabolic pathway is broken or something and start ruminating to all hell. It's probably best to just try methylfolate and P-5-P (carefully at first, same with SAMe) if you so desire. People do have weird reactions to SAMe anecdotally.
 
Cotcha Yankinov said:
Single nucleotide polymorphisms, see rs1801131 and rs1801133, also known as A1298C and C677T respectively. But be cautious when entering this area of genomic data. Its okay to do the whole 23andme - Promethase thing but don't be freaking out thinking that a fundamental metabolic pathway is broken or something and start ruminating to all hell. It's probably best to just try methylfolate and P-5-P (carefully at first, same with SAMe) if you so desire. People do have weird reactions to SAMe anecdotally.
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Are
you advising P-5-P as an adjunct to l-methylfolate?

A lot of the clinical trials involving l-methylfolate didn't seem to use other active enzyme/vitamin adjuncts of any kind.

I've been searching for articles that support the use of these adjuncts: l-tyrosine, P5P, SAMe etc - but haven't found a whole lot of info.

It also seems the effective dose of l-methlyfolate, is 15 mg, as oppose to 7.5.

But if you have any links to papers that expound on this more....?
 
I wouldn't personally bother with P-5-P, nothing wrong with taking a multivitamin with B-vitamins or just B-6 https://www.ncbi.nlm.nih.gov/m/pubmed/14584010/

If you choose to take various supplements, I would advise doing so carefully, taking small dosages at first and trying one thing at a time.

https://www.ncbi.nlm.nih.gov/m/pubmed/27113121/

https://www.ncbi.nlm.nih.gov/m/pubmed/24813065/

The dosage of methylfolate is probably only particularly consequential on cancer cell growth in the long run, but because it's fairly potent I don't think you'd need more than 15mg. Cells that divide very quickly, such as cancer cells, need folate (hence folate supplementation during pregnancy). So I don't know if I would heroic dosage it daily for years but I wouldn't bat an eye at a month trial.
 
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