Green tea for protecting memory…good or bad?

Portrait of young happy smiling man drinking coffee or tea outdoors

It works by suppressing one particular enzyme…

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Green tea for protecting memory…good or bad?

Everyone has an enzyme called catechol-O-methyltransferase in their bodies, or COMT for short.

Everyone has it in either the low-activity, or the hyperactive form. Evidence suggests that the low-activity form is preferred.

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This enzyme converts much-needed dopamine to O-methyldopamine.

Dopamine is an essential neurotransmitter, methyldopamine is not.

Not only does it displace dopamine from the brain and nerves, it can actually inhibit transmission.

It interferes directly with nerves.

Methyldopamine causes imprecise and spontaneous movements, and it is actually this alone which causes the effects generally-attributed L-dopa after ingestion.

But fortunately, there is a perfectly-safe way to inhibit this enzyme — a natural and effective plant molecule.

Parkinson’s is characterized by low dopamine levels. The lack of dopamine is what’s actually causing it.

Parkinson’s is mostly caused by certain pesticides, entering the brain and destroying the dopamine-producing region.

Raising dopamine through L-dopa supplementation has sometimes led to paradoxical results, for this reason.

Too much conversion of dopamine to O-methyldopamine can cause problems.

Doctor Feuerstein was the first to notice this.

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He examined the relationship between blood methyldopa levels and abnormal involuntary movements.

This led us to plot all the plasma 0-methyl-dopa levels of the L-dopa combined with PDI-treated patients with abnormal involuntary movements,… ―Feuerstein

He found that dyskinesia was highly-associated with the methyldopa levels.

The methyldopa blood levels were nearly twice as high in people showing these side-effects.

The plasma 0-methyl-dopa levels were 2.75 pg/ml, while in the former, they were 5.09 pg/ml, which is 1.85 times higher. The difference is highly significant: ―Feuerstein

He had also found that there was essentially no difference in the normal L-dopa levels between the two groups, so this cannot be explained on account of varying L-dopa levels.

You could almost pass this finding off as speculative — as an anomaly — but this article sparked further interest, leading some to validate the results.

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Rivera published even more proof in the very same year.

He found that in every case among his patients, the “non-responders” had more methyldopa in their blood.

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The ratio of methyldopa/dopa was always higher in the “non-responders.” It was greater than one in every case.

And these people suffered from involuntary movements, just like Feuerstein’s patients.

The people who did just fine with extra dopamine always had a ratio of less than one — much less than one.

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Now this seems to be a general rule: dopamine is preferred to methyldopamine, and methyldopamine causes dyskinesia.

Parkinson’s can be reversed with L-dopa, but only if you inhibit the COMT enzyme — preventing the formation of methyldopa.

But this happens to everyone, all the time.

Methyldopamine is being constantly produced within the body — in variable amounts.

Methyl-dopa is produced from L-dopa, and methyldopamine is produced from dopamine.

Just one enzyme, COMT, does all of this.

These methylated versions are always anesthetic, and they cause uncoordinated movements.

This enzyme is everywhere, it’s even in the brain.

So people naturally have varying levels of methyldopamine, and some more than others.

This is largely due to the two different forms of COMT which can be inherited.

These two enzyme types can be called the hyperactive one, and the low-activity one.

The only physical difference is that one of them has valine in position #158, where the other has methionine.

Studies have shown that people with the low-activity, methionine form consistently score higher on tests than those with the other form — the hyperactive valine form.

By having the methionine form or COMT, you are constantly producing lower levels of methyldopamine — naturally. 

Also, carriers of the methionine form would be expected to have higher dopamine levels.

They would also be expected to have lower homocysteine levels — which is another product of this reaction.

The enzyme’s cofactor is S-adenosylmethionine, which becomes S-adenosylhomocysteine after transferring its methyl group to dopamine.

Two studies which highlight the difference in test scores between the two different types were published in quick succession between 2002 and 2004:

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Both showed higher test scores with the methionine form. You can be certain that they had lower methyldopamine and higher dopamine levels.

The principal finding of this study is that Met-hemizygous patients performed significantly better than Val-homozygous patients on a composite measure of executive cognition. ―Bearden 

Results from the two studies are presented side-by-side: intelligence tests on the left, and error tests on the right.

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The methionine form is shown in blue, while the valine form gets… fuschia.

The experimenters actually had enough contempt for this allele to depict it in fuschia, and you should too.

The valine form creates methyl-dopa at a faster rate — between two and four times that of the methionine form.

In the same instant, this enzyme transforms dopamine into methyldopamine.

Taken together, these data provide evidence that reductions in COMT function, whether induced by a pharmacological agent, gene knockout, or the presence of a low-function allele, are associated with improved cognitive performance. ―Malhotra

Each form of this dopamine-destroying enzyme is common.

It is split about 50%-50% in the Western world. This leads to three different combinations: Val-Val, Met-Val, and much preferred Met-Met.

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The preferred form is variable among different countries.

So for a European or American, you would expect a population of about 25% Val-Val, 50% Met-Val, and 25% Met-Met.

But regardless of what genetic form may be present, the dopamine/methyldopamine ratio can be shifted with a COMT inhibitor. 

In fact, the ratio can be improved to a much greater extent than what you will find between the Met-Met and Val-Val forms.

You can lower methyldopamine and raise dopamine even further.

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Catechol-O-methyltransferase inhibitors are used clinically, and they do work well.

But many of the synthetic ones, the patentable ones, are toxic to the liver.

They are overpriced, and Nature has provided one that is exceedingly-selective, cheap, convenient, and just as effective.

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It has been demonstrated on multiple occasions that epicatechin gallate inhibits COMT more than any natural molecule found.

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And it inhibits COMP at a concentration similar to that of treatments designed expressly for this purpose, making them seem like pointlessly-redundant and overpriced cons.

Entacapone, used to lower methyldopamine levels pharmacologically, is the classical pharmaceutical COMT inhibitor. It has an IC₅₀ between 10 and 160 nM.

Moreover, COMT gene knockout mice display better memory than wild-type mice under conditions of environmental stress. ―Malhotra

The IC₅₀ for epicatechin gallate, in this study, was measured at 70 nM.

Out of the 15 inhibitors studied, this was certainly the most powerful.

Most other polyphenols studied, such as genistein and biochanin, were completely without effect.

And Tomonori Unno showed in 2014 that these concentrations are achievable by just one cup of green tea.

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So it’s absorbable, and concentrations which inhibit COMT by 50% can be found after drinking only one cup, after about two hours.

This is probably why there are so many studies showing green tea improving memory and concentration — they are probably doing this by inhibiting COMT. 

Asians, despite having more of the valine form, are actually some of the smartest people. Green tea could be part of the answer.

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The only downside of tea, that I know of, is its relatively-high fluoride levels.

This can be counteracted with boron, the natural antidote, which forms boron trifluoride which can then be excreted.

There are other benefits to taking a little boron, besides that.

But epicatechin gallate can be found in capsule form. So nobody really has to ingest tea at all for this molecule. 

The enzyme catechol-O-methyltransferase only works on dopamine, epinephrine, and the catechol-estrogens.

Inhibiting this enzyme will not affect methylation elsewhere in the body.

And it has a long history of use in Asia, lending support to the safety of this molecule — and the safety of COMT-inhibition in general. I personally recommend the benefits of coffee more often than tea, but you may want to consider epicatechin gallate as a supplement.

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Matt Cook is editor-in-chief of Daily Medical Discoveries. Matt has been a full time health researcher for 26 years. ABC News interviewed Matt on sexual health issues not long ago. Matt is widely quoted on over 1,000,000 websites. He has over 300,000 daily newsletter readers. Daily Medical Discoveries finds hidden, buried or ignored medical studies through the lens of 100 years of proven science. Matt heads up the editorial team of scientists and health researchers. Each discovery is based upon primary studies from peer reviewed science sources following the https://www.dailymedicaldiscoveries.com/what-is-cialis-5-mg-used-for/ to ensure accuracy.
Männistö, Pekka T., and Seppo Kaakkola. "Catechol-O-methyltransferase (COMT): biochemistry, molecular biology, pharmacology, and clinical efficacy of the new selective COMT inhibitors." Pharmacological reviews 51.4 (1999): 593-628. http://pharmrev.aspetjournals.org/content/51/4/593.short Chen, Dapeng, et al. "Inhibition of human liver catechol-O-methyltransferase by tea catechins and their metabolites: structure–activity relationship and molecular-modeling studies." Biochemical pharmacology 69.10 (2005): 1523-1531. http://www.sciencedirect.com/science/article/pii/S0006295205000602 Palmatier, Meg A., A. Min Kang, and Kenneth K. Kidd. "Global variation in the frequencies of functionally different catechol-O-methyltransferase alleles." Biological psychiatry 46.4 (1999): 557-567. http://www.sciencedirect.com/science/article/pii/S0006322399000980 Bearden, Carrie E., et al. "Effects of a functional COMT polymorphism on prefrontal cognitive function in patients with 22q11. 2 deletion syndrome." American Journal of Psychiatry 161.9 (2004): 1700-1702. https://pdfs.semanticscholar.org/1223/67d32c2c29d79198151b8778f7a6b768a56a.pdf Unno, Tomonori, et al. "Analysis of (–)-epigallocatechin gallate in human serum obtained after ingesting green tea." Bioscience, biotechnology, and biochemistry 60.12 (1996): 2066-2068. http://www.tandfonline.com/doi/pdf/10.1271/bbb.60.2066 Malhotra, Anil K., et al. "A functional polymorphism in the COMT gene and performance on a test of prefrontal cognition." American Journal of Psychiatry 159.4 (2002): 652-654. http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.159.4.652