MAO stands for monoamine oxidase.
It's an enzyme that breaks down certain neurotransmitters in the brain like dopamine, serotonin, and dimethyltryptamine. All of which are crucial to brain function in various ways.
There are actually 2 types of MAO in the body, and although similar, have different preferences for the monoamines they break down (deaminate). MAO-A, and MAO-B.
Kia,
Just yesterday was looking for natural MAO-B. Amazon have Neuroignite with very good review vs Optimind, but our forum don't have any posts regarding this subject.
Good article, thank you. I'm using Dopa Mind - Wild Green Oat Extract along with Green Tea every morning. I sent this article over to my acupuncture Dr asking if he could recommend any of the Chinese herbs mentioned. We used to say "you are what you eat". With PD treatment it's more like "you are what you suppress".
😁 John G
Im using the same protocol.
Thanks for that link. The information was simple, easy to read, and enlightened me about terms I've avoided learning about because I spend all of my time looking for ways to improve energy.
Great article. So consuming green tea, turmeric, black pepper and licorice during the day should be beneficial overall and very easy to do.
Interesting and maybe I missed it, but what is the expertise of the party presenting this information?
Why not just take rasagiline? Purified, characterised, many years of clinical experience to support efficacy and safety, off patent, cheap. Best of all, there is evidence of slowing progression of PD (not definitive but positive).
Not impressed by the article, particularly expressing IC50 (the concentration that gives 50% inhibition) as mg/ml with no pharmacokinetics.
Azilect (rasagiline) is an Interesting drug (which has passed several Phase III trials) as an alternative to deprenyl (selegiline) , but certainly not "natural". Azilect is about 4 times the cost of its generic equivalent, rasagiline. Both usually come in either .5 and 1 mg tablets. Selegiline generic is about 50% the cost of rasagiline.
Do not combine Rasagiline with Selegiline. Serious reactions can and do occur.
Sharon,
Which one better?
Selegiline (generic name for Eldepryl, Zelapar) is a dopamine agonist (DA) of a relatively weak chemical nature that some of this forum think is detrimental to all PD patients (speaking of all DAs) . I disagree, as do most neurologists, but each to his//her own belief system.
Azilect (generic Rasagiline) on the other hand is a MAO irreversible inhibitor which is still studied very intensively to this day not only for PD but depression.
Historical clinical trials suggest Rasagiline or Azilect is a better choice than Selegiline, but IMO as a biochemist it all depends on the individual and their drug cocktail and how extensive or varied that drug cocktail is. Multiple variables to consider for each individual.
What is extremely interesting to me about Azilect (rasagiline) is that two peer review clinical trials of very recent origin (2018 and 2019) have come out of Japan and China of all places .Both positive about controlling PD progression but not overwhelming. Another very interesting trial that has not yet been completed is the use of Rasagiline with two popular dopamine agonists (Prami is one) that might show that the use of both is synergistic for PD. Don't know, but it is an interesting theory of combining two drug classes that are generally (almost to a fault) considered non-compatible.
Of all the MAO inhibitors, only selegiline and rasagiline have been found to be useful in treating the progression of PD.
correction: only rasagiline.
Sharon,
Thank you, but Selegiline is also from Mao-B group.
Examples of MAO-B inhibitors used in Parkinson’s disease
Selegiline
:
Selegiline is one of the most commonly used MAO-B inhibitors and is the active ingredient in medications such as Eldepryl, Carbex and Zelapar.
Rasagiline
:
Rasagiline is as an irreversible MAO-B inhibitor and the active agent of Azilect. It is frequently prescribed to manage symptoms of Parkinson’s disease.
It is better review for Rasagiline, but much more expensive...
Yes, they are both MAOIs although selegiline acts somewhat differently than rasagiline.
Some chemists consider selegiline a DA ( which is technically incorrect IMO) as well as a MAOI(B) so it can get confusing at times. From a primary point of view, both selegiline and rasagiline are all about reducing the breakdown of dopamine. DAs in contrast (such as pergolide, cabergoline) presumably stimulate striatal dopamine receptors.
The problem with selegiline (whatever brand you choose to use) is its very low bioavailability. So, take it with some fat if you are going to use it.
In sum, rasagiline is far more potent than selegiline. Thus, it can be much more cost effective when considering its potency.
OK, but original post was regarding natural MAO-B.
I agree. The discussion got diverted into drugs...unfortunately.
So you consider that Selegiline is not a DA. But you used selegiline as your DA example in another thread and call it a DA in this thread too. Each to his own I guess.
Hikoi: I didn't address you, so please, please when you address me get off your broom stick. I would really appreciate it.
As to whether selegiline is a DA, some chemists consider selegiline both a DA and a MAOI because selegiline is a acetylenic derivative of phenethylamine (which is basically a stimulant which can release dopamine and serotonin), unlike other MAOIs such as Rasagiline ... and therefore in most cases can and does act as a DA.
More importantly from a PD perspective, selegiline (as with Rasagiline) may inhibit the negative action of the protein "Alpha Synuclein" which can interfere with the brain's neuroprotective pathway. This protein "kills" TrkB activities leading to the cell death of dopamine...leading to increased vunerability to PD in the long run.
Does this inhibition action increase dopamine? I would argue it does. Granted, it doesn't bind to dopamine receptors in the brain, but that is a technical issue.
So, selegiline is a unique chemical drug which can serve dual purposes in the treatment of PD. Is it perfect? No drug is.
As an aside Hikoi, glad you asked.
OK I am to speak to you only when spoken to and off a broom stick. Noted.
As an aside, dopaminergic cell death is not a trivial issue. It is the basis of our understanding the nature of PD.
To clarify my comment about Rasagiline, it has no amphetamine like metabolites, like Selegiline, but it has the capability of increasing the release of DA. So, again here is a MAOI class of drug which can also function in releasing DA. Bioavailability with Rasagiline is about 35% versus about 10% with Selegiline, hence the difference in potency although studies have not shown very much difference between the two drugs in terms of efficacy in "real time".
Combining sinemet with selegiline also does not work
Casey: You might want to read the 1991 study by Elizan before you repeat that statement. Further, selegiline has been found to increase the effect L-DOPA. Therefore, it has been used routinely with sinemet.
should have made it clear that it did not work for me . Felt like death warmed over , nauseous etc. and stopped at week six when even sipping water caused me to throw up. At that point typed into google 'can I take sinemet and selegeline and got an enhanced list of side effects. At that time stopped taking everything except sinemet and thyroid medication and am starting to feel better. Would be interested in other experiences and will read the study.
Do you have link to study?
Here is the abstract of the Elizan study. You should note carefully that they examined the combination of 10 mgs. of Selegiline (initially!) and then combined with a LOW DOSE LEVEDOPA (Sinemet 3-4 times per day) to examine the combination's efficacy. A relatively small population of NEWLY DIAGNOSED(!) PD patients but over a credible period of time (26 months). The authors maintain the combination of the two (2) drugs was far more effective than Selegiline alone which has been found subsequently.
****
Arch Neurol. 1991 Jan;48(1):31-4.
Early combination of 10 mg. of selegiline and low-dose levodopa as initial symptomatic therapy in Parkinson's disease. Experience in 26 patients receiving combined therapy for 26 months.
Elizan TS1, Moros DA, Yahr MD.
Author information
Abstract
Thirty-eight patients newly diagnosed as having Parkinson's disease (mean age, 57.3 years; mean Parkinson's disease duration, 2.7 years) in the earlier phase of the disease (mean Hoehn/Yahr stage, 2; mean motor scores, 11.4) were given selegiline (Deprenyl), 10 mg daily, and maintained on this drug alone until significant clinical worsening warranted the addition of low-dose levodopa (Sinemet, 25/100 three to four doses per day). Five of these patients were not yet receiving additional levodopa despite some worsening of motor scores. Of the 33 patients now taking combined therapy, seven have been followed up for 6 months or less. Twenty-four (92%) of the 26 patients taking combined therapy for a mean of 26 months (8.5 to 99 months) who have had Parkinson's disease for 6 years showed a dramatic improvement in their parkinsonism shortly after the addition of levodopa, with significant decreases in their rated motor scores, such improvement being maintained at their latest neurologic evaluation. Eighteen (75%) of these 24 patients responded to the combined selegiline/levodopa therapy with degrees of improvement equal to or greater than 50%, compared with their motor status at the start of combined therapy just before the addition of levodopa. This degree of "reversal" of parkinsonism on addition of levodopa (mean carbidopa/levodopa dose, 98/389 mg) was not observed in any of these same patients receiving selegiline alone for an average of 13.8 months. Four patients taking combined therapy developed mild, transient, abnormal involuntary movements, and end-of-dose pattern of response after more than 2 years of combined therapy (24.75 and 33.5 months, respectively).(
'Cheap' is a relative term. According to GoodRx, it costs $200/month with a coupon, $500 without:
I should think someone who has need would go ahead and buy it, but then there are people with diabetes in the US who have died because they rationed their insulin.
Hi Rhyothemis - sorry, when I said cheap, I was giving a UK perspective. The "drug tariff", what the National Health Service pays the manufacturer and the pharmacist, is £2.03 ($2.65) for 28x1mg tablets. Each prescription would cost the individual £9.00 ($11.70) per item, unless you're eligible for free prescriptions, like anyone over 60 or on benefits.
It's so good to live in a country with socialised medicine!
Is there some way we know that these substances work, and how? And that as supplied? By the way, kava kava is positively researched to demonstrate liver damage (I personally knew one of the active proponent researchers in the 1980-90s who published extensively in peer reviewed journals, the final association to liver damage did not make him happy but he said he accepted the science as valid.)
A neurologist who prescribed Azilect to me years ago said the FDA won’t sanction but many doctors believe it slows progression. 1 mg day is optimal. Studies did not show higher doses to be more effective. I get generic now. $5 copay.
Rasagiline by Teva was approved I believe in 2004 by the FDA (long time ago) for PD with a follow up clarification on tyramine (which many physicians still haven't read) in 2009. Several Phase III clinical trial results clearly show it slows progression of PD.
I would be interested to see the citations for those studies. The only ones I can find say it "may" slow the progression. That is also what I have been told by several neurologists, including top researchers.
Go to Teva.
FDA approvals are not "studies".
"Several Phase III clinical trial results clearly show it slows progression of PD," from your comment above. Trials are also referred to as studies. Below is the link to the Teva trial, please note in the title it uses "may." If it was so clear every neurologist would be insisting that their patients take it. If it was so clear every person with PD would be taking it if they could afford it.
clinicaltrials.gov/ct2/show...
Trials are rarely classified as studies in my experience. But perhaps your clinical trial experience has been different than mine. Studies almost always refer to "meta-analysis" of data or a individual clinical case study. Splitting hairs, but usually the way it is done.
I think we are getting lost in the weeds here with MAOIs. Think about the basic situation with PD patients. They have reduce levels of dopamine. MAOIs act as chemical agents to reduce the breakdown of dopamine, not to enhance it. This distinction and difference is CRITICAL.....Therefore, if a PD patient has reduced levels of dopamine, which most do unless in its earliest stages, a MAOI is going to have a limited effect. It is why MAOIs are rarely used beyond a certain level of PD dysfunction.
If what I say doesn't make sense, then go back to the underlying cause of PD and understand why l-dopa is the preferred choice of treatment by many physicians (because it s a dopamine precursor).
Hi Sharon, don't forget that MAOI-Bs will prolong the effect of exogenous levodopa by delaying its breakdown, even if endogenous dopamine production is low.
Yes, it is the main and primary function of this class of drugs, although rasagiline does it much better than selegiline and without some of the potential side effects of selegiline used with L-DOPA.
Julie: go back an re-read the results from the "delayed-start "trial" of Resagiline in PD" in the NEJM ( Sept 24, 2009) or re-read the quote from ADAGIO "results of the study show that early treatment with once-daily rasagiline 1mg tablets provided significant clinical benefits ...
Or....
ADAGIO trial results show Azilect® slows progression of Parkinson's disease
--- Lundbeck 27 August 2008
I hope this clarifies your confusion.
Julie:
"ADAGIO showed that previously untreated PD patients randomized to initiate therapy with rasagiline (Azilect(R)) 1 mg per day had benefits at 18 months that were not achieved when the same drug was initiated at nine months. These results are consistent with the possibility that the drug has a disease-modifying effect which slows disease progression. The study examined both 1- and 2-mg doses of rasagiline using a rigorous design that included three primary endpoints. The 1-mg dose met all three primary endpoints. The 2-mg dose did not."
The probable most useful use of MAO-Bs is their presumed ability to reduce DOPAL. If they actually do it, a big presumption certainly, then they will subsequently increase the levels of dopamine floating around in the brain.
The TrkB/BDNF study attempts to validate this assumption.
Hi Julie! Don't they all (meds and supplements) MAY help, MAY slow, may, may, may! No definitive results for anything. Even PD meds might/might not work for all. Anything that raises hope should be welcome to try. Dr. Mischley and our Vanderbilt MDS have both suggested Azilect (Rasagiline). I actually asked our MDS for Xadago, but he wouldn't prescribe it, said it is extremely expensive. That is the only med (MAO-B inhibitors) I believe MAY (as you suggested) slow the progression. My husband started taking it a week ago.
In all the Phase III trials for rasagiline (if I remember correctly) the UPDRS scale showed a smaller increase (which is a positive) over a period of 1 year or longer. 1 mg. dose was preferable to 0.5 mg. All versus a placebo of unknown origin IMO.
So glad you mentioned, was going to myself, the commercially driven now-universal standard of "better than placebo" that replaced earlier comparisons to known other agents, typically those of competitors, significantly diluted the clinical value of so many studies, it is virtually impossible to get a clean comparison pre-approval, if ever. That and seriously longitudinal studies went bye-bye long ago, even though by now they could have been long performed. Also over time have to remember that over time the number of dopamine producing cells declines, so then too must the eventual effectiveness of agonists and uptake- and MAO inhibitors, from that cell-number decline alone. But the specific mechanisms of all agents are often sufficiently variable that it is always worth shopping around. But some of the new investigation drugs do offer good promise.
Meanwhile, if we are talking about exptra-pyramidal motion effects, then at least an agent doesn't have to cross the blood-brain barrier to help, and that would mean worth trying fava beans, dopamine supplements. And mucuna seems always to be worth trying, at least from subjectively watching comments on this site.
And B-1 hcl is important to remember that it is supposed to be a supplement, not replacement, to any therapy that works, and can take several months to kick in and also find the right dosage. Still is remarkable that it seems to work for so many people.
I wonder why no mention of Rhodiola... I guess because it in not selective (MAO-A as well as MAO-B)?
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