36 replies to this topic

[computeTHIS]

Oh, and if someone could tell me how I can edit/delete a double post, that would be awesome.  

[computeTHIS]

Delta Gamma, on 03 October 2011 - 05:28 PM, said:

I really don't understand why everyone here loses their minds over selegiline and other MAO-B inhibitors, MAO-B is mainly present in subcortical structures, not the PFC. Lower levels of DA and NE are consistantly seen in the PFC of ADHD individuals and in the PFC its mainly COMT and the NE transporter which remove them from the synaptic cleft. Granted almost everyone on this board seems to have some bizarre treatment-resistant form of ADHD-PI so it might be working through a different pathway than most.

If its working for you sweet, but the science points to COMT being by far the more relevant target.

I'm curious what you might recommend based on this.  Most COMT inhibitors that I've seen seem to be used for Parkinson's Disease and I've never heard of them.

[sam7777]

an excerpt
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Most traditional chemical dependency treatment programs are not holistic, and make no attempts to tailor therapy based on individual differences in adrenal function, thyroid function, hormone imbalances, tissue levels of heavy metals like mercury, or genetic polymorphisms affecting the dopaminergic system. All of these influence addiction behavior, and must be considered carefully. People addicted to drugs typically carry at least one of the following risk alleles: DRD2=A1; SLC6A3 (DAT) =10R; DRD4=3R or 7R; 5HTTlRP = L or LA; MAO= 3R; and COMT=G.

[Delta Gamma]

The whole COMT thing is a bit of a nightmare to test for as its primary associated with inattentive symptoms and ADHD is far from a single gene based illness. But more recent studies are more consistently showing that the val158met substitution has significant effects on alertness and inattentive symptoms. But, it does seem to predict response to some medications.

Selegiline is really popular as it more effects the subcortical structures damaged in Parkinson's and there's a larger grey market for it than COMT inhibitors. Granted this is a vast oversimplification, but you get what I mean.

http://www.biomedcen...44-9081-5-8.pdf
http://onlinelibrary...mg.b.30704/full
http://onlinelibrary...mg.b.30831/full

If you really want to see what's going on and maybe tailor a stack to better suit your genotype it might be looking at a service like 23andme.

[devinthayer]

Delta Gamma, on 04 October 2011 - 08:10 PM, said:

The whole COMT thing is a bit of a nightmare to test for as its primary associated with inattentive symptoms and ADHD is far from a single gene based illness. But more recent studies are more consistently showing that the val158met substitution has significant effects on alertness and inattentive symptoms. But, it does seem to predict response to some medications.

Selegiline is really popular as it more effects the subcortical structures damaged in Parkinson's and there's a larger grey market for it than COMT inhibitors. Granted this is a vast oversimplification, but you get what I mean.

http://www.biomedcen...44-9081-5-8.pdf
http://onlinelibrary...mg.b.30704/full
http://onlinelibrary...mg.b.30831/full

If you really want to see what's going on and maybe tailor a stack to better suit your genotype it might be looking at a service like 23andme.

23andme sounds like a goal.  Don't have $99 to play with right now, but when I do, I will consider the investment.

I agree that is why Selegiline is popular.  There are also studies at 10mg that suggest it could compete in effectiveness with methylphenidate.  This, to me, is quite a positive thing.

From what i read about the COMT gene variation, val158met, it seems as those with the Val allele would be inattentive while those with Met allele would be more aggressive.  I guess Val allele makes it function properly?  If my logic serves me, increased (accurate) COMT activity would mean less dopamine & norepinephrine stimulation in the pre-frontal cortex.  Which would mean that the Val Allele actually makes COMT hyperactive, chomping more dopamine and norepinephrine into (useless) metabolites.

Makes me wonder if ADHD is the "old" genetics and "normal" is a result from mutation and natural selection.  I.E. cavemen had ADHD.

[magniloquentc0unt]

Is there chance to hear from you? An update on how sustainable the treatment is, and if you were permanently healed? Any cognitive decline or improement?

[magniloquentc0unt]

computeTHIS, on 04 October 2011 - 05:32 AM, said:

Delta Gamma, on 03 October 2011 - 05:28 PM, said:

I really don't understand why everyone here loses their minds over selegiline and other MAO-B inhibitors, MAO-B is mainly present in subcortical structures, not the PFC. Lower levels of DA and NE are consistantly seen in the PFC of ADHD individuals and in the PFC its mainly COMT and the NE transporter which remove them from the synaptic cleft. Granted almost everyone on this board seems to have some bizarre treatment-resistant form of ADHD-PI so it might be working through a different pathway than most.

If its working for you sweet, but the science points to COMT being by far the more relevant target.

I'm curious what you might recommend based on this.  Most COMT inhibitors that I've seen seem to be used for Parkinson's Disease and I've never heard of them.

so how did it go long term?