General Category > Contributing Factors - Physical

methylation genes - MAO A (monoamine oxidase) and COMT (Catechol-O-methyl transf

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no_longer_numb:
Well, as you may know, I began taking supplements for methylation due to getting tested positive for the mthfr mutation.  There are many other genes tested in the methylation pathway, and one of them that I had the mutation for was MAO A.  Apparently males only get one copy of this gene, and it comes from the mother's side.

Monoamine Oxidase apparently breaks down adrenaline, noradrenaline, melatonin, serotonin and also dopamine (in combination with MAO B which I was not tested for).  It gets really complicated, as I was also tested for another gene called COMT (who knows the COMT may be more relevant) which is apparently another enzyme that breaks down dopamine, epinephrine, norepinephrine.

I am heterozygous for two of the tested COMT genes, so

I should breakdown adrenaline, noradrenaline, melatonin, serotonin, and possibly dopamine slower than normal (MAO A mutation)
I should breakdown epinephrine, norepinephrine, and dopamine slower than normal (2 COMT heterozygous mutations)

Here's where I find it interesting.  I know that a lot of people get ejaculatory anhedonia after taking SSRI antidepressants.  I've had weird health problems most of my life, and on occasion I remember taking cold medicine and having strange reactions, like increased intensity of libido (don't go try it I doubt they put the same ingredients in cold medicine anymore).  Then I found out that a side effect of MAOI medications is "difficulty reaching orgasm." (monoamine oxidase inhibitors - basically people take these as antidepressants, though not used much anymore, because it keeps the neurotransmitters from breaking down so fast - but my body is doing this already due to the MAO and COMT mutations).  

I'm sure it's been noted here before, but what if our problem isn't too little neurotransmitter, but too MUCH!  What if our chemical receptors are DOWNREGULATED because they are always SWIMMING in neurotransmitters....I believe this is documented to be able to occur physiologically if I recall from my abnormal psychology class long ago.  If you have 100 molecules of serotonin in the synapse, you don't need 100 receptors, whereas someone who has 3 molecules may need 200 (made up these numbers for illustration only).

I was curious and tried to google around for things that encourage the production of monoamine oxidase, but I couldn't find anything.  My theory being that a slight reduction in these brain chemicals might spur some new process in the synapse, perhaps lead to an UPREGULATION of receptors.  Yes, basically we are talking about a sensitization process here.  Maybe one of the reasons we are not getting spontaneous cures is because there isn't a whole lot of research, much less medication that DOWNREGULATES neurotransmitters or speeds up their breakdown?

I will be getting an amino acid urine test soon, and I will be curious to see if anything is way out of balance.  Amino acids are the building blocks of the "amines" in "monoamines" by the way, and some of that stuff is in cold medicine also sometimes.  One additional thing that I found out is that smoking reduces MAO B by 40% and also reduces MAO activity.  You would think it would be good to have more of these neurotransmitters in the synapse, but maybe it is paradoxical.  

This is only one of my new theories, I have another theory simultaneously that is contradictory to this somewhat.  It involves something called BH4, and the interesting thing is it helps build neurotransmitters, and royal jelly, which is mentioned here all the time, contains some BH4 or promotes it in some way.  Some people who have the mthfr A1298C mutation (which I do) are low on BH4.  Also people who have aluminum toxicity.  I am going to be taking another test that should help me see if my BH4 is low.

The one thing I don't understand is how this (as well as all of my other health problems) started literally overnight at age 26.  I suppose I may have flipped some genetic switch.  This is also roughly the time that I began to smoke cigarettes daily (see the above note about smoking)

no_longer_numb:
This just gets even more interesting. No idea if this will help me find a reliable treatment, but I'm guessing that my theory above about impaired breakdown of neurotransmitters causing fatigued receptors is a likely culprit.  I, along with many of you, have noticed that my libido and some sensation are improved after sleep deprivation and even hangovers.  Last night I couldn't sleep the entire night due to stress and all of a sudden i'm way more horny than normal and I can tell there is some increased sensation!  I don't know how this exactly relates to the quote below - but I'm guessing I may not be getting enough NREM sleep or perhaps too much REM sleep?


A noted 2002 University of California animal study indicated that non-rapid eye movement sleep (NREM) is necessary for turning off neurotransmitters and allowing their receptors to "rest" and regain sensitivity which allows monoamines (norepinephrine, serotonin and histamine) to be effective at naturally produced levels. This leads to improved regulation of mood and increased learning ability. The study also found that rapid eye movement sleep (REM) deprivation may alleviate clinical depression because it mimics selective serotonin reuptake inhibitors (SSRIs). This is because the natural decrease in monoamines during REM is not allowed to occur, which causes the concentration of neurotransmitters in the brain, that are depleted in clinically depressed persons, to increase. Sleep outside of the REM phase may allow enzymes to repair brain cell damage caused by free radicals. High metabolic activity while awake damages the enzymes themselves preventing efficient repair. This study observed the first evidence of brain damage in rats as a direct result of sleep deprivation.[25]

http://en.wikipedia.org/wiki/Sleep_deprivation

no_longer_numb:
This is crazy...I am suspecting that my answer may be very paradoxical.

When I first got sick with many ailments at age 25, one of the first symptoms was a horrible ongoing insomnia.  This has improved a bit over the years as I have treated my gluten allergy and taken other medication (not sleep medication).  However, I still have to take a variety of herbal, melatonin, etc in order to sleep fairly normally, which I found very odd.

Well, after not having slept at all due to stress the other night, I had an unmistakable surge of libido the following two days, better sensitivity and much improved quality of erection.  Yes, not a cure, but a step in that direction.

Well, my theory at present is this.  I have abnormally high neurotransmitters due to gene mutations such as MAO A and COMT which means that my body breaks down neurotransmitters much too slowly.  Combine this with my chronic sleep problem - essentially never reaching deep sleep, and therefore the lack of NREM sleep means that NREM doesn't have a chance to break down my already high neurotransmitters. 

So, why would another random night of no sleep improve my libido and sensitivity?  This is the paradoxical part.  The answer is that it is my RECEPTORS for the neurotransmitters that are abnormally sensitized, not the neurotransmitters themselves.  Therefore, the one night lack of sleep leads to low production of neurotransmitters temporarily, which gives the RECEPTORS a partial break after chronically bathing in neurotransmitters, and allows them to partially function appropriately for a short period of time, until the neurotransmitter levels go back up and stay up.

More paradox - the cure, according to my own theory here, is to achieve deep sleep - NREM sleep.  I am considering a sleep study to try to address this component.  Also, quitting cigarette smoking, since I found articles that smoking drastically reduces the effectiveness of MAO B and perhaps MAO A which breakdown various neurotransmitters.

So essentially here is the information:  I have gene mutations which prevent my body from effectively breaking down neurotransmitters, leaving them floating around the synapse.  Secondly, I have chronic sleep problems preventing NREM deep sleep which leads to further inability to break down neurotransmitters.  The final blow is that I smoke, which further reduces the effectiveness of my MAO genes.  Therefore I am left awash in neurotransmitter levels that must be much, much higher than normal, which causes my receptors to be overly sensitized and not function.  It is as if your eye was made to stare into a spotlight until all you could see was white, and even when you closed your eyes you saw white - fatigue, neural fatigue or receptor fatigue perhaps.

If I am right the following should cure my anhedonia:

1.  Improve sleep quality, specifically acheive more NREM sleep
2.  Quit smoking

The only thing I am unsure of is how the methylation treatment will work with all of this.  Some of the methyl vitamins supposedly increase neurotransmitters.  I have an idea why royal jelly might work, at least for a short time.  Royal jelly increases something called BH4 which increases neurotransmitters.  Even though high neurotransmitters are the problem in my theory, the extra boost takes things above the baseline (a high baseline for me) enough to shake and rattle the neurotransmitter receptors into some function.  Of course, if I am correct, the relief with royal jelly would be temporary, as it would just be exacerbating the problem of too high neurotransmitters fatiguing the receptors.

Feedback welcome.

andrew_b:
Someone way back on the old board once reported that improving his sleep resulted in a cure. This was basically discounted and ignored as being far too simple to be an actual solution, but maybe he was onto something. It does sound very possible based on what you've researched. I work shifts, intact I'm working nights as I write this, so maybe this could be a contributing factor.

no_longer_numb:
A little bit more to report.  I have been trying numerous things now as part of my methylation treatment in addition to the EA.

First I added the regular (non DGL) licorice root I had bought some time back.  When I tried the DGL licorice, I definitely noticed an increase in precum, which had also been abnormally reduced as a symptom of my sexual dysfunction.  However, with the DGL licorice, I did not notice any benefit to my libido, sensation, orgasm, or erection.

I took one Nature's way licorice capsule at noon with lunch, and one a few hours later and I experienced some form of orgasm, some normality coming back - I didn't have to work for it, it flowed through me.  My erection was also much better the whole time and sex was much more enticing, but it wasn't a miracle cure.  However, it was something, and I have to say, Licorice root (non-DGL) has been the only supplement so far that has had any benefit on my orgasm (methylcobalamin and other things seem to help other areas, such as sensation and erection but haven't modified my orgasm).  One very noticeable improvement has been that I am ejaculating normally for the first time in years - I can feel everything going out - which makes me wonder if the reason I had been thinking I had reduced semen is because I was suffering retrograde ejaculation?

I was doing a lot of google searches about licorice root and found a lot of interesting tangents to follow up on.  Somewhere I found that it can be a MAO inhibitor - if this is true, it leads me to believe that the effect will be temporary, as it would only worsen things in the long term, although shake things up in the short term (via disturbing the recepter sensitization)

I am also considering licorice root in the following regards:

1.  It increases cortisol, the stress hormone (is this related to why libido/orgasm improves with no sleep/hangover)
2.  Phytoestrogens....I read that licorice root actually decreases testosterone, maybe it someone addresses estrogen dominance or something?
3.  non-DGL licorice can raise blood pressure
4.  Adrenal insufficiency - licorice is considered a treatment for adrenal insufficiency (this is VERY intersting to me as I am pretty sure that I have had some long term adrenal malfunction)


and perhaps MOST interesting, I found something with a google search that Licorice could be a treatment for cocaine withdrawl.  More and more I am beginning to think that this is akin to my problem - not due to drug abuse, but due to my messed up genes that don't break down neurotransmitters and therefore sensitize receptors....this genetic basis along with viewing of porn may have sensitized the receptors and licorice might be undoing this sensitization.  Like I said earlier, however, if the beneficial effect of licorice is due only to even MORE OF A REDUCTION in BREAKING DOWN neurotransmitters - then I should relapse very very hard and go back to being completely an anesthesia dick at orgasm.

Well, we will see.  I am not in a hurry to report back to the endocrinologist, because as enticing as the cortisol hypothesis is, all of my endocrinology reports were completely normal, I still think this is a neurotransmitter/receptor issue. 

I am also very intrigued by a chemical that used to be in cold medicine in the USA prior to being banned, called phenylpropanalomine.  I recall growing up that when I took certain cold medications I had a huge boost in orgasm and libido.  Several of the brands of cold medicine that I highly regarded (I never abused them only took them when I had a cold or flu) were alka seltzer plus cough and cold and I think Contact.  I found that both of these at one time (not any longer) had this PPA in them.  Apparently this PPA contains phenylalanine which believe is synthesized into tyrosine and dopamine.  In the USA, PPA is now only approved for veterinary use for incontinence in dogs, which is also ironic since I have longstanding stress urinary incontinence that is unexplained.  Cold medicine containing PPA remains legal in Europe.  It was pulled from the USA due to alleged incident of stroke in women - PPA was in those lose weight quick drugs like dexatrim etc.  I also think that I read that PPA has been looked at as a treatment for retrograde ejaculation.

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