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I also have the "Warrior gene" 3r version of this gene.Which means I'm missing a segment of DNA of this gene that apparently causes inconsistant production of, and therefore unstable levels of, important neurotransmitters. I will say that a MAOI inhibitor helped me tremendously with depression.I had to stop taking it for health reasons.

I'd really like to understand MAO-A +/+ better. I have addicted-type behaviors, but why would I if I have plenty of dopamine and serotonin? Or maybe I don't? I often get carb/sugar cravings which means low serotonin. Can anyone shed light on this?

That's great info! Thanks.

My daughter shares this mutation and we have found the following supplements have improved her crippling anxiety and depression enormously (they include the building blocks of neurotransmitters and must be taken in this ratio to keep all the neurotransmitter in balance long term - she takes this dose twice a day with meals and the results have been amazing and without the side effects of the prescription drugs she was prescribed initially)

100 mg 5-hydroxy-tryptophan
100 mg vit B6
1000 mg (1g) L-tyrosine
1000 mg (1g) L-cysteine

Good luck!

Regarding Maoa rs6323 G and mao inhibitor, i have the same G variant and i tried mao inhibitor (only 4 days though) and results where similar to ssri medication, but less side effects and the effect was more subtle. It seems to me that more serotonin in synaps blocks emotions and feelings. That's why ssri's work better for panic and anxiety problems than for depression imo. Im also C on rs909525.

Hi My first time post too. I am also homozygous for Mao-a rs6323 (TT). I have spent the first couple of weeks trying to get a grip of my MTHFR gene variation. I was just working out a way forward when I saw this thread. How on earth is it possible to get a grip on all of my gene variants, all the information and ideas which I am finding really overwhelming! Is there a hierachy of what to concentrate on first? This is all new to me and potentially exciting if only my brain would allow!

You could be right.It may be hormones or other genes.But there is no avalible test for MAO-A right now.You say your your serotonin is high and your dopamine is low.Have you checked your MAO-B enzyme for for homozygosity? That could explain the low dopamine.But I agree with you about the supplements,the body knows best.

This gets complicated, but I think I'm cracking the puzzle ... at least for myself. I've had my share of anxiety to the point where I experienced A-fib, burnout, etc. Doing much better now. And in the improvements I've made, I feel there's more that needs to be considered as part of this equation. Like many of you, I am MAOA +/+ (encodes for lower enzyme activity which means higher serotonin). I'm also COMT -/- (encodes for higher COMT enzyme activity which means lower dopamine). MAO inhibitors may help, but there's a big BUT. The purpose of an MAO inhibitor is to prevent the degrading of serotonin or dopamine depending which type you take, right? Maybe you have high levels for some other reason besides your genes. Well in my case, I'm also MTHFR as I came to find out recently. So I wasn't producing BH4 which is a precursor to these neurotransmitters in the first place. It makes so much sense now when I look at my neurotransmitter test which says my dopamine is zilch and my serotonin, while much higher, is still below reference range. I would say it's prudent to get ... More

This gets complicated, but I think I'm cracking the puzzle ... at least for myself. I've had my share of anxiety to the point where I experienced A-fib, burnout, etc. Doing much better now. And in the improvements I've made, I feel there's more that needs to be considered as part of this equation. Like many of you, I am MAOA +/+ (encodes for lower enzyme activity which means higher serotonin). I'm also COMT -/- (encodes for higher COMT enzyme activity which means lower dopamine). MAO inhibitors may help, but there's a big BUT. The purpose of an MAO inhibitor is to prevent the degrading of serotonin or dopamine depending which type you take, right? Maybe you have high levels for some other reason besides your genes. Well in my case, I'm also MTHFR as I came to find out recently. So I wasn't producing BH4 which is a precursor to these neurotransmitters in the first place. It makes so much sense now when I look at my neurotransmitter test which says my dopamine is zilch and my serotonin, while much higher, is still below reference range. I would say it's prudent to get a neurotransmitter test through your doc, and then take natural supplements like 5-HTP (to increase serotonin) or mucuna pruriens (to increase dopamine) as needed. PROCEED VERY SLOWLY WITH THE DOSING. It's easy to go overboard with supplementing for neurotransmitters, and I'll tell you first hand it can give you anxiety and worse symptoms from the other end. P.S. doctors can guide you in the supplementation, but ultimately you have to listen to your body to tell you if you need more or if you're taking too much. It's not really practical to get frequent neurotransmitter tests. Less

Thank you for responding and not being the only human suffering this way. For many years I was pretty sure about this! For your understanding my health practitioner meant that I do not have MAO in my body so taking Inhibitors would make it more worse. I am also heterozygous on three SNP s and homozygous on COMT rs4646312. Strange at all... Because you can t buy sublinguar Hydroxycobalmin here in Germany I try Adenosylcobalamin since a few days and folat. I feel slightly better now. The brain fog has gone and I do not feel dizzy and strange in my head anymore. I will take this a few months and have a look how it is going on. I go for a walk nearly every day and drive my bike and this helps a bit but my social phobia and anxiety is really bad... Have you ever heard about taking B2 Riboflavin which should handle the lack of MAO-A??

To @VA3782. I think you're probably right in not taking a MAO-A inhibitor because rs6323 is,according to my reading, a good indicator for low or high activity of the enzyme.(you have the low activity snp,T) Don't know what your doctor is talking about when he says there is "No mao-a that can be inhibited" Inhibitors do inhibit mao enzymes, and there are many studies that can prove it.As far as your anxiety,have you checked out your COMT genes,especially rs4680.I am heterozygous for four snp's and homozygous for one according to my Nutrahacker report.I also have quite a bit of anxiety as well.Nutrahacker recommends a form of B12 called Hydroxycobalamin (Hydroxy B12) taken sublingually, for all these snp's.I have also found that cardiovascular exersise two to three times a week is VERY helpful for anxiety.Try it for a month if you haven't already.Wish I could help more,bro.Good luck.

Hello all, my first post, too. .I am homozygous for Mao-a rs6323-T and I suffer from anxiety nearly my whole life. Trying so much and wasting so much doctors who are unable to help because they don t understand anything about genes. Always I hear "You have an anxiety disorder, take your drugs 'escitalopram' and get lost". Escitalopram never helped. Nothing ever helped. Going to work every day, sitting here with always on anxiety without a reason but unable to do anything against it I ask YOU if you already found some help in handling this life consuming "bug". MAO-A inhibitors MUST be avoided as explained by my health practitioner because there is NO MAO-A which could be inhibited. Any suggestions are gratefully appreciated!!

Here's why I took selegiline. Back at the end of 2011, I realized that I was suffering from a dopamine deficiency. In one of my journals from 2008 I have a notation that I was suffering from a "happy lethargy" that was crippling because I had no drive. I worked my job, but other than that I felt like doing nothing but watching sitcoms after work, and when I got up in the morning to go to work. No bills got paid, no dishes got washed. It was a weird time, but I could see outside of myself that this was not normal. I knew somehow that it wasn't an issue with serotonin and strangely it dissipated when I took adequate levels of vitamin D3. Well, I learned later that vitamin D via the enzyme tyrosine hydroxylase becomes LDOPA.

The other thing that brought me relief was caffeine, but caffeine's ability to augment dopamine levels has a half-life of approximately 5 hours and if you DON'T want to live a life of insomnia you can't utilize it past 1 PM. I ordered selegiline from overseas in a desperate attempt halt this weirdness. Although coffee and ... More

Here's why I took selegiline. Back at the end of 2011, I realized that I was suffering from a dopamine deficiency. In one of my journals from 2008 I have a notation that I was suffering from a "happy lethargy" that was crippling because I had no drive. I worked my job, but other than that I felt like doing nothing but watching sitcoms after work, and when I got up in the morning to go to work. No bills got paid, no dishes got washed. It was a weird time, but I could see outside of myself that this was not normal. I knew somehow that it wasn't an issue with serotonin and strangely it dissipated when I took adequate levels of vitamin D3. Well, I learned later that vitamin D via the enzyme tyrosine hydroxylase becomes LDOPA.

The other thing that brought me relief was caffeine, but caffeine's ability to augment dopamine levels has a half-life of approximately 5 hours and if you DON'T want to live a life of insomnia you can't utilize it past 1 PM. I ordered selegiline from overseas in a desperate attempt halt this weirdness. Although coffee and vitamin D were effective, you can't use either effectively forever. In the case of vitamin D, there's the danger of vitamin D toxicity. I have sodium channel mutations, but was just learning about my disorder. When I tried selegiline in January of 2012, what it did was inhibit calcium channels and I couldn't walk. I chose selegiline because it used to be prescribed to Parkinson's sufferers. Anyway, the next month my new neurologist prescribed Mestinon, an acetylcholinestarase inhibitor, and it mitigated the dopamine lows, but this was strange because acetylcholine and dopamine exist in a see-saw relationship, not parallel to one another. It wasn't until later that I realized that green tea extract had the same effect as selegiline, inhibiting calcium channels, and research showed that it, too, was an MAO inhibitor, especially in a concentrated extract form. Oh, I should also note that the Mestinon initiated an autoimmune reaction called dermagraphia urticaria, a condition that only 1% of the population experience. The weirdness continues in that I started a ketogenic diet to control my sodium channelopathy disorder and the dermagraphia stopped.

Choline supplementation also helps I found out in November of 2014. I keep learning about my body, and still there are mysteries as I use choline to augment Mestinon because my dosage requirements keep increasing. I found out this week that I suffer from an acute from of fatty liver disease, but its effects are producing symptoms that are reminiscent of both Parkinson's and Congenital Myasthenic Syndrome. Many Americans suffer from some form of nonalcoholic fatty liver disease, but my genetics indicate I have an extreme case. Women become predisposed as they enter the postmenopausal phase of their life as estrogen is critical to the production of choline. I, however, am currently on 23 times the dosage cited for fatty liver disease when in the form of lecithin, and 10 times the amount when using choline chloride.

In addition, I became aware that I was suffering from cholinergic dysautonomia November of 2013, requiring dosage with Mestinon else I don't produce bodily fluids without it (no saliva, tears, sweat, bronchial mucous, nasal mucous, reduced urine output, tachycardia, heart stroke variation, pupillary dilation, fast-gastric emptying, my pee smells like ammonia and my underarms smell noxious, and let me not forget to mention that I have Hypertensive Postural Orthostatic Tachycardia, which again is rare as most with POTS suffer from Hypotensive POTS). All these symptoms disappear along with the dopamine lows with either choline or Mestinon, and I take both together as Mestinon works within 5 minutes so I get a quick boost while the choline is just getting started. I see a Hepatologist in a couple of weeks as my case is so complex, and I'll show her the PNPLA3 gene mutation. Choline also has a positive effect on skeletal muscle strength in my chest. I downloaded some abstracts and articles to research, so I'm hoping for more insight into my personal weirdness.

Oh, I'm also @XS6386 above as my 23andme raw data didn't include the SCN4A gene, but the raw data from Ancestry DNA did. Two different logins to differentiate. Less

Well for me on Survivor, haha, I'd say it's less about energy and more about character, like being tenacious. That's where the aggressiveness is.

That's interesting.I also have the tendency to keep things bottled up.(BOOM!) Do your MAOA genes code for high or low activity of the enzyme? or both? I'm thinking it's low if you have the energy to win Survivor.

Interesting. I'm all red on this one! I'm generally not an aggressive person, but you also don't want to get me mad. And I totally know that I have capabilities, as in, I would kick ass if the Walking Dead was my reality, and I've always known I'd win Survivor if I was on the show.

In response to @XS6386.Have you read the Wikipedia page on Selegiline? It states that Selegiline is a MAO-B inhibitor and only inhibits MAO-A at high doses.Question: Are you taking Selegiline for depression/anxiety or for something else,like Pakinsons? I can't anwser your question about the correlation between MAO genes and SCN4A.But I can tell you that I take a MAO inhibitor called Nardil and it works very well for depression,despite the crappy side effects,insomnia,constipation,low blood pressure.I am homozygous for rs6323 with the G variant,which codes for high activity of MAO-A.When I take the medication at higher doses (above 45mg) I experience muscle tightness,especially in the ankles and generally below the waist.I also experience some very mild loss of coordination.All easily tolerable to me because I can't take being depressed half the time,a condition beyond my control,until now.MAO inhibitors are presribed to parkinson patients because they increase dopamine levels,which help with the symtoms of Parkinsons disease,especially MAO-B inhibitors.(MAO-B metabolizing primarily dopamine.) MAO-A metabolizes primarily serotonin.So if it's depression,MAYBE a MAO-A inhibitor might work better.Something to discuss with your doctor.Sorry I couldn't be more helpful.I really hope you find some anwsers and start feeling better.Good luck.

* do I have the warrior gene, can anyone translate my MAOA.
Gene variation Genotype Phenotype
MAOA R297R rs6323 TG +/-
MAOA rs2235186 AG +/-
MAOA rs3027399 -
MAOA rs909525 CC +/+

Since January 2012, I've known I had an issue. While on the drug Selegiline, an MAO inhibitor, my muscles became unresponsive. Later, while using green tea extract capsules, I got the same reaction. Green tea is also an MAO inhibitor. Interestingly, I have a muscle disorder, and take the medication, Mestinon. My reaction pre-Mestinon using Selegiline was exactly the same reaction I had post-Mestinon with the green tea extract. I'm trying now to see if there are any correlations between the MAO gene cluster and those for my muscle disorders on THE SCN4A gene. Unfortunately, I don't believe the SCN4A gene was genotyped by 23andme. The Medical genetics lab, Athena Diagnostic, revealed the SCN4A mutations in tests ordered by my neurologist. Of course, there may be no correlation at all. Just looking for answers.

The reason why Livewello results may look different from others is because Livewello flags a SNP as red, yellow, or green (++, +-, or --) based purely on how common the allele is, and lower frequency does not always mean more problematic. For this particular one, it also seems that there is not good and bad, but rather just higher or lower activity of the enzyme. Back to the original question, it would seem logical (although I don't know if there is empirical support for it) that an MAO inhibitor might make sense if you had the higher activity of the enzyme. If you have the lower activity, its almost like you already have a naturally occurring MAO inhibitor. MAO inhibitors do also have a lot of side-effects, and you need to avoid certain food, so I wouldn't want to take one.

@ZC5238 Thanks so much for your response. Very much appreciated.

Just to clarify my first confusion arose because my livewello results for MAO A are rs6323 are TT -/- . The result also comes up as 'green' indicating no variation. Whereas on GeneticGenie.com MAO A is donated as rs 6323 TT +/+ indicating a homozygous variation.

My previous research also indicates that TT +/+ is the low activity ('worrier' variant), which displays lower levels of neurotransmitters. This also fits with my experience from previous lab tests which have always shown low levels of serotonin, VMA and HVA. I have also suffered from depression, sadness and tearfulness often for no apparent reason all my life. Even as a child I was 'moody'.

As I have got older, I also do tend to have temper outbursts and fly off the handle. I also have hormonal imbalances due to oestrogen dominance (I also have genes that slow down oestrogen metabolism). The latter may go some way to explaining the mood swings along with a combination of the MAO A genes and other methylation/ detox mutations. I also notice that when I ran a general MAO SNP report that I had a number of MAO homozygous mutations ... More

@ZC5238 Thanks so much for your response. Very much appreciated.

Just to clarify my first confusion arose because my livewello results for MAO A are rs6323 are TT -/- . The result also comes up as 'green' indicating no variation. Whereas on GeneticGenie.com MAO A is donated as rs 6323 TT +/+ indicating a homozygous variation.

My previous research also indicates that TT +/+ is the low activity ('worrier' variant), which displays lower levels of neurotransmitters. This also fits with my experience from previous lab tests which have always shown low levels of serotonin, VMA and HVA. I have also suffered from depression, sadness and tearfulness often for no apparent reason all my life. Even as a child I was 'moody'.

As I have got older, I also do tend to have temper outbursts and fly off the handle. I also have hormonal imbalances due to oestrogen dominance (I also have genes that slow down oestrogen metabolism). The latter may go some way to explaining the mood swings along with a combination of the MAO A genes and other methylation/ detox mutations. I also notice that when I ran a general MAO SNP report that I had a number of MAO homozygous mutations.

My understanding through research is that those with the low activity TT+/+ variant who has experienced childhood trauma tend to be more affected by it, hence the outbursts and PTSD I now suffer with. This also fits in with my experiences as a child where I did not fight back like one of my brothers did, but rather played dead.

The high activity variant (not sure which alleles) however when exposed to childhood trauma have less propensity to suffering trauma/ becoming aggressive as adults as they have the 'warrior' gene which allows them to fight back and not feel victimized. I suspect my brother has this gene.

Thanks once again for your help. Less