30 replies to this topic

[thedevinroy]

The COMT enzyme is much like the MAO enzyme. It's purpose is to break down neurotransmitters and other look-a-likes. See diagram here of noradrenaline breakdown: http://en.wikipedia....e_breakdown.svg . I'm ADHD, so my norepinephrine is precious.

One problem that I see with natural COMT inhibitors like catechins such as EGCG and bioflavanoids such as quercetin is that they all can cause potential DNA damage by inhibiting Topoisomerase I & II. The thing with catechins is that they tend to be more peripheral, which is good because EGCG is also known to inhibit Dopa Decarboxylase. EGCG is also hurts the folate cycle. Quercetin is probably one of the better ones out there for guys due to its anti-oestrogen properties, but a lot of other polyphenol bioflavanoids are estrogen receptor agonists. However, quercetin does act as an adenosine receptor antagonist, but this effect is over 10x less potent than caffeine and probably negligible when compared to the COMT inhibition effects of increased norepinephrine.

IC50 Values of Common Polyphenols for COMT Inhibition:

• EGCG: 0.2uM
• Quercetin: 0.48uM or 0.9uM
• Catechin: 1.64uM
• Epicatechin: 1.96uM
• Fisetin: 3.3uM

I was wondering if there is some type of synergy I can get from taking natural COMT inhibitors, like those above, in order to cut back on the ill effects of EGCG. I have been taking green tea supplements for general energy for a while... 6 months or so. Time to find an alternative to throw in the mix.

Does anyone have any experience with an increase in focus from supplementing with a natural COMT inhibitor?

Also, does anyone know of a natural central COMT inhibitor that does not inhibit the Topoisomerase enzymes?

Edited by devinthayer, 04 July 2011 - 06:50 AM.

[Logan]

Luteolin might be what your looking for. If I'm understanding this correctly, since it is believed luteolin does not prevent binding to DNA, despite being a topoisomerase inhibitor, it might not incur the same kind of damage that quercitin could? I might be totally off on this one. I got this information from figure 7 of this paper: http://www.google.co...37SxcDS-yl9Iqqg

[thedevinroy]

Just remembered that Quercetin is often taken with Resveratrol to enhance the antioxidant effects of both. Please note also that COMT breaks down estriol metabolites, but Resveratrol prevents those metabolites from even happening, because it is a CYP1B1 substrate. There are more potent CYP1B1 inhibitors...http://www.ncbi.nlm....58998/table/T1/

Edited by devinthayer, 04 July 2011 - 07:50 AM.

[thedevinroy]

Luteolin might be what your looking for. If I'm understanding this correctly, since it is believed luteolin does not prevent binding to DNA, despite being a topoisomerase inhibitor, it might not incur the same kind of damage that quercitin could? I might be totally off on this one. I got this information from figure 7 of this paper: http://www.google.co...37SxcDS-yl9Iqqg

Yeah it sounds like a lesser Top inhibitor than some other bioflananoids. It inhibits the catalyst. Cool. That might be a mechanism of bacteria only?

I think Luteolin is a substrate of COMT. Methylated metabolites were reduced in the urine of rats after being coadministered a COMT inhibitor. http://www.ncbi.nlm....pubmed/21209248

Pretty cool! That might work. I don't know how powerful it is as an inhibitor, but it is most likely broken down by the COMT enzyme. It should provide at least a little temporary elevation in catecholamines, being a competitor for the enzyme.

Edit: This would explain why I can't go a day without vegetables. Veggies have a lot of antioxidants like quercetin, luteolin, resperatrol, etc. Without at least one green veggie in a day, I feel totally deprived of mental and emotional energy. Natural COMT substrates must be in a lot of healthy things.

Edited by devinthayer, 04 July 2011 - 08:19 AM.

[Logan]

Luteolin might be what your looking for. If I'm understanding this correctly, since it is believed luteolin does not prevent binding to DNA, despite being a topoisomerase inhibitor, it might not incur the same kind of damage that quercitin could? I might be totally off on this one. I got this information from figure 7 of this paper: http://www.google.co...37SxcDS-yl9Iqqg

Yeah it sounds like a lesser Top inhibitor than some other bioflananoids. It inhibits the catalyst. Cool. That might be a mechanism of bacteria only?

I think Luteolin is a substrate of COMT. Methylated metabolites were reduced in the urine of rats after being coadministered a COMT inhibitor. http://www.ncbi.nlm....pubmed/21209248

Pretty cool! That might work. I don't know how powerful it is as an inhibitor, but it is most likely broken down by the COMT enzyme. It should provide at least a little temporary elevation in catecholamines, being a competitor for the enzyme.

Edit: This would explain why I can't go a day without vegetables. Veggies have a lot of antioxidants like quercetin, luteolin, resperatrol, etc. Without at least one green veggie in a day, I feel totally deprived of mental and emotional energy. Natural COMT substrates must be in a lot of healthy things.

I've been taking luteolin in the Lutimax formulation for different reasons than you(though I could probably always use a little extra boost in catecholamines at the right amount). My only concern about taking too much is that it appears it may inhibit nitric oxide production, which I feel may be a reason for me feeling a bit deflated after taking high amounts. Right now I take 100 mg at bedtime and 25 in the morning.

Edited by MorganM, 04 July 2011 - 04:23 PM.

[abelard lindsay]

Careful with COMT inhibitors. You don't want to get too much dopamine going through the MAO pathway or else you may build up the DOPAL intermediary which can be neurotoxic if alcohol dehydrogenase can't get to it fast enough.


Here's the study that talks about MAO degrading dopamine into DOPAL and then the non-neurotoxic DOPAC via alcohol dehydrogenase:

Chem Biol Interact. 2011 Jun 30;192(1-2):118-21. Epub 2011 Jan 13.
Dopamine-derived biological reactive intermediates and protein modifications: Implications for Parkinson's disease.
Jinsmaa Y, Florang VR, Rees JN, Mexas LM, Eckert LL, Allen EM, Anderson DG, Doorn JA.
Source

Division of Medicinal and Natural Products Chemistry, College of Pharmacy, The University of Iowa, Iowa City, IA 52242-1112, USA.
Abstract

Dopamine (DA) undergoes monoamine oxidase catalyzed oxidative deamination to 3,4-dihydroxyphenylacetaldehyde (DOPAL), which is metabolized primarily to 3,4-dihydroxyphenylacetic acid (DOPAC) via aldehyde dehydrogenase (ALDH). Previous studies demonstrated DOPAL to be neurotoxic, more so than DA and other metabolites, and implicated the aldehyde intermediate as a factor in the pathogenesis of Parkinson's disease (PD). However, the mechanism for generation of DOPAL at aberrant levels and the pathways for toxicity are not conclusively known. Various models for DA catabolism revealed the susceptibility of DOPAL biotransformation (e.g., ALDH) to products of oxidative stress, e.g., 4-hydroxy-2-nonenal, at physiologic/pathologic levels and agents that induce oxidative stress. An elevated concentration of DOPAL correlated with increased protein modification with subsequent work demonstrating significant reactivity of the DA-derived electrophile toward protein nucleophiles compared to DA and other metabolites, e.g., DOPAC. The addition of DOPAL to proteins proceeds via reaction of the aldehyde with Lys residues, yielding a Schiff base; however, post-adduction chemistry occurs for the DOPAL-modification resulting in protein cross-linking. Preliminary work indicates enzymes in DA synthesis and catabolism to be cellular targets for DOPAL. Functional consequences for elevated levels of the DA-derived aldehyde and protein modification may include adverse cellular effects. These data implicate DOPAL as a toxic and reactive intermediate potentially serving as a "chemical trigger" for some stage of PD pathogenesis.

Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

PMID:
21238438
[PubMed - in process]
PMCID: PMC3109112
[Available on 2012/6/30]

More on DOPAL, an endogenous neurotoxin that causes parkinsons like symptoms:
http://www.ncbi.nlm....pubmed/21179455


IMHO, MAOI-B inhibitors are safer than COMT inhibitors because the COMT dopamine degradation pathway does not carry the risk of generating the DOPAL toxic intermediary while the MAO degradation pathway may do so under certain circumstances.

Edited by abelard lindsay, 05 July 2011 - 06:37 PM.

[thedevinroy]

Careful with COMT inhibitors. You don't want to get too much dopamine going through the MAO pathway or else you may build up the DOPAL intermediary which can be neurotoxic if alcohol dehydrogenase can't get to it fast enough.


Here's the study that talks about MAO degrading dopamine into DOPAL and then the non-neurotoxic DOPAC via alcohol dehydrogenase:

Chem Biol Interact. 2011 Jun 30;192(1-2):118-21. Epub 2011 Jan 13.
Dopamine-derived biological reactive intermediates and protein modifications: Implications for Parkinson's disease.
Jinsmaa Y, Florang VR, Rees JN, Mexas LM, Eckert LL, Allen EM, Anderson DG, Doorn JA.
Source

Division of Medicinal and Natural Products Chemistry, College of Pharmacy, The University of Iowa, Iowa City, IA 52242-1112, USA.
Abstract

Dopamine (DA) undergoes monoamine oxidase catalyzed oxidative deamination to 3,4-dihydroxyphenylacetaldehyde (DOPAL), which is metabolized primarily to 3,4-dihydroxyphenylacetic acid (DOPAC) via aldehyde dehydrogenase (ALDH). Previous studies demonstrated DOPAL to be neurotoxic, more so than DA and other metabolites, and implicated the aldehyde intermediate as a factor in the pathogenesis of Parkinson's disease (PD). However, the mechanism for generation of DOPAL at aberrant levels and the pathways for toxicity are not conclusively known. Various models for DA catabolism revealed the susceptibility of DOPAL biotransformation (e.g., ALDH) to products of oxidative stress, e.g., 4-hydroxy-2-nonenal, at physiologic/pathologic levels and agents that induce oxidative stress. An elevated concentration of DOPAL correlated with increased protein modification with subsequent work demonstrating significant reactivity of the DA-derived electrophile toward protein nucleophiles compared to DA and other metabolites, e.g., DOPAC. The addition of DOPAL to proteins proceeds via reaction of the aldehyde with Lys residues, yielding a Schiff base; however, post-adduction chemistry occurs for the DOPAL-modification resulting in protein cross-linking. Preliminary work indicates enzymes in DA synthesis and catabolism to be cellular targets for DOPAL. Functional consequences for elevated levels of the DA-derived aldehyde and protein modification may include adverse cellular effects. These data implicate DOPAL as a toxic and reactive intermediate potentially serving as a "chemical trigger" for some stage of PD pathogenesis.

Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

PMID:
21238438
[PubMed - in process]
PMCID: PMC3109112
[Available on 2012/6/30]

More on DOPAL, an endogenous neurotoxin that causes parkinsons like symptoms:
http://www.ncbi.nlm....pubmed/21179455


IMHO, MAOI-B inhibitors are safer than COMT inhibitors because the COMT dopamine degradation pathway does not carry the risk of generating the DOPAL toxic intermediary while the MAO degradation pathway may do so under certain circumstances.

Good advice! MAOI-B makes DOPAL which is suspected to be the reason for Parkinson's. Haha, I shake enough as is, and I'd rather not make it worse.

[abelard lindsay]

Good advice! MAOI-B makes DOPAL which is suspected to be the reason for Parkinson's. Haha, I shake enough as is, and I'd rather not make it worse.

Pretty much. Just to get all the acronyms right, MAOB makes neurotoxic (if it builds up) DOPAL out of Dopamine which is then quickly turned into DOPAC by alcohol dehydrogenase. Inhibiting COMT and thus sending more Dopamine through the MAOB pathway thus might cause problems.

[niner]

Regarding luteolin and topo inhibition, in the abstract of the link MorganM posted, it says:

we show that luteolin completely inhibits the catalytic activity of eukaryotic DNA topoisomerase I at a concentration of 40 uM, with an IC50 of 5 uM.

This suggests to me that it isn't going to be a problem, because attaining even 5 micromolar, much less 40 is pretty tough with a polyphenol like luteolin.

[thedevinroy]

Regarding luteolin and topo inhibition, in the abstract of the link MorganM posted, it says:

we show that luteolin completely inhibits the catalytic activity of eukaryotic DNA topoisomerase I at a concentration of 40 uM, with an IC50 of 5 uM.

This suggests to me that it isn't going to be a problem, because attaining even 5 micromolar, much less 40 is pretty tough with a polyphenol like luteolin.

I wonder how that translates to an oral dose in vivo? Molecular weight is 286.24 g/mol ... is there a theoretical calculator for vitro to vivo oral dose? Ya figure with all the biochem engineers, they would have meticulously concocted some online calculator or even an Excel spreadsheet... I tried looking, but it wasn't easier than 30 seconds on Google.

[niner]

Regarding luteolin and topo inhibition, in the abstract of the link MorganM posted, it says:

we show that luteolin completely inhibits the catalytic activity of eukaryotic DNA topoisomerase I at a concentration of 40 uM, with an IC50 of 5 uM.

This suggests to me that it isn't going to be a problem, because attaining even 5 micromolar, much less 40 is pretty tough with a polyphenol like luteolin.

I wonder how that translates to an oral dose in vivo? Molecular weight is 286.24 g/mol ... is there a theoretical calculator for vitro to vivo oral dose? Ya figure with all the biochem engineers, they would have meticulously concocted some online calculator or even an Excel spreadsheet... I tried looking, but it wasn't easier than 30 seconds on Google.

It's a lot more complicated than that. Every compound is behaves differently, and any given compound will behave differently indifferent people depending on their genetics, size, body composition, gut flora, and what they've had to eat recently. For the typical polyphenol to hit 5 uM in human plasma for more than a few minutes, the dose would be in the 'whopping' range. Maybe a fistful, plus or minus a lot.

[thedevinroy]

Good advice! MAOI-B makes DOPAL which is suspected to be the reason for Parkinson's. Haha, I shake enough as is, and I'd rather not make it worse.

Pretty much. Just to get all the acronyms right, MAOB makes neurotoxic (if it builds up) DOPAL out of Dopamine which is then quickly turned into DOPAC by alcohol dehydrogenase. Inhibiting COMT and thus sending more Dopamine through the MAOB pathway thus might cause problems.

Trying to find an MAOi-B supplement... there are a couple herbs listed on the wiki article, two of which are hard to find, and Kava Kava... which causes liver damage over time. I think most herbs are MAOi-A... harmala alkaloids, rosavins, to a name a couple. I think PEA might be a substrate of MAO-B? Possibly hordenine? I take 100-200mg of hordenine a day... so I might be good.

EDIT: Found and selected these from a post on the Bluelight Forums:


Camellia Sinensis [Green Tea, Black Tea, White Tea, Oolong Tea] (Catechin, Epicatechin)
Olea Europaea [Olive Oil] (Hydroxytyrosol)
Paeonia Suffruticosa [Cortex Moutan, Mudanpi, Peony] (Paeonol)
Piper Longum/Nigrum [Long Pepper/Black Pepper] (Piperine)
Uncaria Tomentosa [Cat's Claw] (Catechin, Epicatechin)

Turns out some inhibit both COMT and MAOi-B. Piperine inhibits a whole bunch of other enzymes too.

Edited by devinthayer, 06 July 2011 - 03:12 AM.

[thedevinroy]

Regarding luteolin and topo inhibition, in the abstract of the link MorganM posted, it says:

we show that luteolin completely inhibits the catalytic activity of eukaryotic DNA topoisomerase I at a concentration of 40 uM, with an IC50 of 5 uM.

This suggests to me that it isn't going to be a problem, because attaining even 5 micromolar, much less 40 is pretty tough with a polyphenol like luteolin.

I wonder how that translates to an oral dose in vivo? Molecular weight is 286.24 g/mol ... is there a theoretical calculator for vitro to vivo oral dose? Ya figure with all the biochem engineers, they would have meticulously concocted some online calculator or even an Excel spreadsheet... I tried looking, but it wasn't easier than 30 seconds on Google.

It's a lot more complicated than that. Every compound is behaves differently, and any given compound will behave differently indifferent people depending on their genetics, size, body composition, gut flora, and what they've had to eat recently. For the typical polyphenol to hit 5 uM in human plasma for more than a few minutes, the dose would be in the 'whopping' range. Maybe a fistful, plus or minus a lot.

A fistful? Haha I'm not a gorilla sized man... 170 pounds of pure muscle flab. And 25 pounds of the other flab.

Interesting... well, you've only listed off 5 variables, of which some can be simplified for the sake of simplicity. Genetics, size, and body composition could be instead height, weight, and gender. Gut flora can be averaged for the population or simply negated in a general play variable. Recently ate could be a checkbox. There's also molecular weight, IC50 of effect, and a time integral. There's 9 variables...

[jlspartz]

Regarding luteolin and topo inhibition, in the abstract of the link MorganM posted, it says:

we show that luteolin completely inhibits the catalytic activity of eukaryotic DNA topoisomerase I at a concentration of 40 uM, with an IC50 of 5 uM.

This suggests to me that it isn't going to be a problem, because attaining even 5 micromolar, much less 40 is pretty tough with a polyphenol like luteolin.

I wonder how that translates to an oral dose in vivo? Molecular weight is 286.24 g/mol ... is there a theoretical calculator for vitro to vivo oral dose? Ya figure with all the biochem engineers, they would have meticulously concocted some online calculator or even an Excel spreadsheet... I tried looking, but it wasn't easier than 30 seconds on Google.

It's a lot more complicated than that. Every compound is behaves differently, and any given compound will behave differently indifferent people depending on their genetics, size, body composition, gut flora, and what they've had to eat recently. For the typical polyphenol to hit 5 uM in human plasma for more than a few minutes, the dose would be in the 'whopping' range. Maybe a fistful, plus or minus a lot.

A fistful? Haha I'm not a gorilla sized man... 170 pounds of pure muscle flab. And 25 pounds of the other flab.

Interesting... well, you've only listed off 5 variables, of which some can be simplified for the sake of simplicity. Genetics, size, and body composition could be instead height, weight, and gender. Gut flora can be averaged for the population or simply negated in a general play variable. Recently ate could be a checkbox. There's also molecular weight, IC50 of effect, and a time integral. There's 9 variables...

Stay far away from luteolin if you are ADHD. It does the exact opposite of what ADHD meds do. It's a monoamine transporter activator that mainly targets dopamine, majorly speeding up dopamine's reuptake. Amphetamine and methylphenidate are effective because they decrease the amount of these transporters.

[thedevinroy]

Stay far away from luteolin if you are ADHD. It does the exact opposite of what ADHD meds do. It's a monoamine transporter activator that mainly targets dopamine, majorly speeding up dopamine's reuptake. Amphetamine and methylphenidate are effective because they decrease the amount of these transporters.

Good to know! It's funny how many monoamine (and neurotransmitters in general) activities have their own negative feedback loops. It's a COMT substrate and activates transport to enzymes... haha.

[ailambris]

I'm a tad confused by your table. You've EGCG with the lowest half maximal inhibitory concentration, and then you've got catechin and epicatechin above it, but those are categories, and if I'm not mistaken EGCG is a catechin, so what is this, an average?

[sam7777]

Rhodiola is a COMT inhibitor.

"

Pretty cool! That might work. I don't know how powerful it is as an inhibitor, but it is most likely broken down by the COMT enzyme. It should provide at least a little temporary elevation in catecholamines, being a competitor for the enzyme.

Edit: This would explain why I can't go a day without vegetables. Veggies have a lot of antioxidants like quercetin, luteolin, resperatrol, etc. Without at least one green veggie in a day, I feel totally deprived of mental and emotional energy. Natural COMT substrates must be in a lot of healthy things.

I would always get a boost in clarity if I ate raw organic cucumbers. honestly I oughta just pay someone to make like a gallon of organic raw cucumber juice a day. It is rightous stuff.

[rwac]

So, here's a question, why do you want to reduce COMT activity?
High COMT activity is related to things like better problem solving on the fly.

Edited by rwac, 24 September 2011 - 04:16 AM.

[thedevinroy]

I'm a tad confused by your table. You've EGCG with the lowest half maximal inhibitory concentration, and then you've got catechin and epicatechin above it, but those are categories, and if I'm not mistaken EGCG is a catechin, so what is this, an average?

Catechin refers to the compound (2R,3S)-2-(3,4-dihydroxyphenyl)-3,4-dihydro-2H-chromene-3,5,7-triol which also goes by catechol interestingly enough. Epicatechin refers to the compound (-)-Epicatechin. Both structures are in the links provided. See page 318 of this http://toxsci.oxford.../2/316.full.pdf excerpt.

[thedevinroy]

So, here's a question, why do you want to reduce COMT activity?
High COMT activity is related to things like better problem solving on the fly.

On the premise of what you are saying is indeed correct, I would say that it is most likely due to an abundance of catechols that the body would induce the enzyme COMT to mark them for deletion by the kidney. However, this "on the fly" thing may be refering to an individual's ability to make out-of-the-box decisions which would be characteristic of someone with lowered monoamine levels (ADD-Pi) which has caused the brain to "work around" using the pre-frontal cortex and use creative solutions to get even the most ordinary things accomplished.

[thedevinroy]

Just a found a couple more natural compounds: http://www.ncbi.nlm....4329/figure/F1/

Caffeic Acid, Chlorogenic Acid, and Caffeic Acid Phenethyl Ester. These inhibit some DNA functions, too.

It seems as though anything with the catechol (Phenyl ring plus two OH molecules on side by side hydrogen replacements) ring qualifies as a COMT inhibitor. I wonder if Telomerase and other DNA workers are confused by all smaller COMT substrates able to pass into the nucleus. Perhaps we should be looking for a larger molecule.

Here is a short list of a few COMT substrate suspects: http://en.wikipedia....xycinnamic_acid

Edited by devinthayer, 04 October 2011 - 05:54 PM.

[thedevinroy]

Chlorogenic Acid inhibits some Telomerase activity indirectly: http://www.ncbi.nlm....pubmed/21835418 because it is a ligand for G-gruadruplex. Basically, it messes up your DNA to tangle in a certain way. More information here: http://en.wikipedia....ki/G-quadruplex

[Ampa-omega]

darn, coffee is a source of Chlorogenic acid. its hepatoprotective but if it inhibits telomerase that kinda sucks.

thanks for sharing.

[thedevinroy]

Cichoric acid and rosmarinic acid are a bit bigger molecules: http://www.jstage.js.../74/7/1350/_pdf THey also are potent antioxidants. Cichoric acid seems to up-regulate choline receptors. That's a pretty cool bonus.

[thedevinroy]

darn, coffee is a source of Chlorogenic acid. its hepatoprotective but if it inhibits telomerase that kinda sucks.

thanks for sharing.

Very indirectly. It stabilizes a DNA structure that snags Telomerase from doing its job properly. This is helpful in fighting viruses and cancer, too. Never knew coffee was an antiviral cancer fighter, did ya? It slows Telomerase down, but not completely inhibits its function.

[thedevinroy]

Found a neat little study: http://www.ncbi.nlm....cles/PMC152928/

There is a graph explain different substrates of COMT. Caffeic acid is the primary substrate. Being that both rosmarinic acid and cichoric acid have caffeic acid as metabolites, I would dare say that these two compounds are my favorite. Rosmarinic acid is pretty easy to get, but it is also GABAergic as well, which would mean that it would only make sense to take with Ginkgo (partial GABA antagonist), which I haven't any at the moment.

A pure cichoric acid extract is going to be hard to get. I'd rather not get it from Echinacea, since it also has cannibinoids that would increase my appetite. Reserve that for skinny people. This source: http://www.springerl...78p45728081233/ says that I can get some from dandelion and bilberry. I wonder if there are any good bilberry extracts optimized for their cichoric acids...

Anyone had any success with Alibaba?

Edited by devinthayer, 05 October 2011 - 01:54 AM.

[Valor5]

Effect of rosmarinic acid on sexual behavior in diabetic
male rats

"Level of sexual behavior (according video
observation) and testosterone significantly increased in groups that received Ro, in comparison to the
whole groups (P < 0.05)."

[Valor5]

I would like to add to the above post that apparently INGESTION OF ROSEMARY OIL IS TOXIC!!!

[thedevinroy]

I would like to add to the above post that apparently INGESTION OF ROSEMARY OIL IS TOXIC!!!

What compound and in what amount?

[Valor5]

I would like to add to the above post that apparently INGESTION OF ROSEMARY OIL IS TOXIC!!!

What compound and in what amount?

The study below is fairly thorough. Before I knew it was toxic I boiled about 4-6 grams of it and drank it without going into a coma or anything two days in a row (BUT THIS IS JUST ME, PLEASE BE CAREFUL and read the study for interactions etc.).

The amount of rosmarinic acid is in the first study I eluded to.
This study talks about carnosic acid. Has no relation to COMT that I know of.
This study talks about how Ro can protect testicles from EMF. For those of you with laptops. Sorry a little off topic.
I ran into this product FWIW. This is another product.
I don't know what your purpose is but the fragrance of certain plants are proven to be very therapeutic. Two specific compounds are linalool and of course cineol from rosemary. Interestingly st. John's wort has most of these and COMT properties.

Attached Files

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