Depleting Serotonin Levels

[trainman04]

Hello Guys.. I always thought I had high serotonin levels.. I was trying different stuff and finaly I decided to do a genetic test.. Well if you wanna call it that. I used 23andme DATA on a few websites to look for genetic mutations in my genes.

And I was right.. I had mutations for high serotonin.

So I made a very long story short but this is where I am at now.
Every Human has Either 2 Long form of 5-HTTLPR (5-HTTLPR = serotonin transporter..) , 2 short form of 5-HTTLPR or 1 short form 5-HTTLPR and 1 long form 5-HTTLPR

2 long forms = Low Serotonin
2 short forms = high serotonin
1 short and 1 long = balance

But I have 4 short forms of 5-HTTLPR..... So I have twice as much serotonin than people with 2 short form in the synapse.
So Now I wanna reduce them... This mutation has ruined my life from the beginning , I tried searching on google but I cant find anything about having more than two 5-HTTLPR forms, having more than 2 must be rare.
My 2 SNPS for this serotonin are:
rs11867581 - AA= 2 short
then another SNP rs2020934 - AA = 2 short again
Have you guys ever seen something like this?


I have a few things I wanna try .

1. Evodiamine ( Wu Zhu Yu ) + berberine
Increases SERT expression which is perfect for my situation it basically reduces serotonin faster in the synapse ofc.
https://www.ncbi.nlm.nih.gov/pubmed/21647174
forskolin + bacopa also increases SERT.
https://area1255.blogspot.se/2017/12/natural-herbal-sert-serotonin.html

2. Progesterone Increases MAO-A and MAO-B which breaksdown serotonin and other neurontransmitters it also increases GABA which reduces neuron firing further decreasing serotonin. But only if taken ORALLY , cream progesterone doesent work. So you will have to take like 100mg orally because the bioavailability is low when taking oral progesterone (swallow not sublingual).
https://neuroendoimmune.wordpress.c...ansmitters-the-under-recognized-relationship/
https://pdfs.semanticscholar.org/1f3b/c62a4e8370e5da8b8f5668ceb2634ad72add.pdf

3. acute tryptophan depletion
Only eat/drink steak , water and 20GRAMS of gelatin to counteract against the tryptophan from the steak.
Take all amino acids except tryptophan with food.
L-alanine 5.5 g, L-arginine 4.9 g, L-cysteine 2.7 g, glycine 3.2 g, L-histidine 3.2 g, L-isoleucine 8 g, L-leucine 13.5 g, L-lysine monohydrochloride 11 g, L-methionine 3 g, L-phenylalanine 5.7 g, L-proline 12.2 g, L-serine 6.9 g, L-threonine 6.9 g, L-tyrosine, 6.9 g, and L-valine 8.9 g.
http://www.nutrientsreview.com/proteins/amino-acids
https://en.wikipedia.org/wiki/Essential_amino_acid
doesent have to be the exact dosage just over 5G will do I would guess.
So you do all this Once a day with food should deplet tryptophan in a few days.

4. block serotonin receptors with OTC supplements.


5. Fenclonine or AGN-2979
These are selective and irreversible inhibitor of tryptophan hydroxylase. So serotonin cant even be made and they are potent too.. Last resort..

Anyway I just wanted to post this .. Im gonna try all these beginning with step 1 of course. Feel free to post advice or anything or if you have any ideas.

 

[Cotcha Yankinov]

1. It's impossible to have 4 short forms of 5-HTTLPR - you can only have 2 at the maximum
2. It's not actually clear to me that you have 2 short forms (others feel free to chime in) - the SNPs seem to indicate you have at least one short form, but I'm not certain that it indicates that you have two short forms. I believe you could still have one short and one long.

Having two short forms is also not rare, and isn't very strongly correlated with mental illness (there have actually been a lot of negative results when looking for a correlation between having a short form/two short forms and having increased risk of mental illness).

So I certainly wouldn't tunnel vision on this in some sort of "I have this rare mutation, this is the source of all my problems and I'm completely screwed" manner. I'm pretty sure we have the exact same genetic situation as far as 5-HTTLPR is concerned.


As for your plan... I guess I'll just say that all the ideas are no good. Especially #3 and #4. People with the short form are actually more vulnerable to the mood altering/depressing effects of tryptophan depletion, even though I don't think the #3 regimen would actually work to induce tryptophan depletion. Normally its done very carefully experimentally to temporarily worsen mood in those with a short form and depression.

Number 4 is a horrible idea. Whatever you do, don't do that.
Whatever your problems are, they may not actually have much to do with variation at 5-HTTLPR or "high serotonin" anyways.

I highly suggest seeking professional help from a psychiatrist and psychologist. If you're interested, you could ask them about vortioexetine (spelling?), a serotonin reuptake enhancer that is approved as an anti-depressant, but for now I advise mindfulness meditation and cardio. Please note that many people with the short form have success treating their depression and other issues with SSRIs, but this is all something that should be done under the careful supervision of a doctor.

Take care,
CY

 

[trainman04]

1. It's impossible to have 4 short forms of 5-HTTLPR - you can only have 2 at the maximum
2. It's not actually clear to me that you have 2 short forms (others feel free to chime in) - the SNPs seem to indicate you have at least one short form, but I'm not certain that it indicates that you have two short forms. I believe you could still have one short and one long.

Having two short forms is also not rare, and isn't very strongly correlated with mental illness (there have actually been a lot of negative results when looking for a correlation between having a short form/two short forms and having increased risk of mental illness).

So I certainly wouldn't tunnel vision on this in some sort of "I have this rare mutation, this is the source of all my problems and I'm completely screwed" manner. I'm pretty sure we have the exact same genetic situation as far as 5-HTTLPR is concerned.


As for your plan... I guess I'll just say that all the ideas are no good. Especially #3 and #4. People with the short form are actually more vulnerable to the mood altering/depressing effects of tryptophan depletion, even though I don't think the #3 regimen would actually work to induce tryptophan depletion. Normally its done very carefully experimentally to temporarily worsen mood in those with a short form and depression.

Number 4 is a horrible idea. Whatever you do, don't do that.
Whatever your problems are, they may not actually have much to do with variation at 5-HTTLPR or "high serotonin" anyways.

I highly suggest seeking professional help from a psychiatrist and psychologist. If you're interested, you could ask them about vortioexetine (spelling?), a serotonin reuptake enhancer that is approved as an anti-depressant, but for now I advise mindfulness meditation and cardio. Please note that many people with the short form have success treating their depression and other issues with SSRIs, but this is all something that should be done under the careful supervision of a doctor.

Take care,
CY

How do you know its only possible to have max 2?maybe scientists just havent found someone like me with 4.
then what does this mean?
rs11867581 - AA= 2 short
then another SNP rs2020934 - AA = 2 short again
2 + 2 = 4
two different mutations for short.
I never said having 2 short is rare.. I said Having 4 SHORTS are rare.. I have 2 different SNP mutations which cause 2 short ones each total of = 4.
rs11867581 linked to the gene SERT. Your genotype is AA, which is observed in 31% of all individuals reported.

AA= Short Allele 91% of the time.

The A (minor) allele is associated with:

Short allele= lower transporter, higher 5HT.


rs2020934 linked to the gene SERT. Your genotype is AA, which is observed in 30% of all individuals reported.
rs2020934 (A) (Me=AA)= Short allele (r2=0.72)S=lower transporter, higher 5HT

 

[trainman04]

These all are the SNPs I have which I think are related to serotonin:

rs1049353 TT = The T allele of rs1049353 may cause lower receptor numbers and less activation. With this variation, the receptors also don't become significantly less sensitive when activated - i.e. you don't build up tolerance. Less SERT Expression = more serotonin?

rs11174811 AA = The activity of this receptor is mediated by G proteins which activate a phosphatidyl-inositol-calcium second messenger system .

GOOD SERT(?)
rs4251417 CC = ???

rs2129785 TT = Short Allele 91% of time.

Then the ´´bad´´ ones I talked about in the thread:

rs2020934 AA = rs2020934 (A) (Me=AA)= Short allele (r2=0.72)S=lower transporter, higher 5HT

rs11867581 AA = AA= Short Allele 91% of the time. The A (minor) allele is associated with: Short allele= lower transporter, higher 5HT.


The last 2 bad ones are how I came to the conclusion I had 4 Short sert forms..

---------------------------thats from one website this is from another which says I have 1 SHORT but 2 LONG?)----
gs288

You have two long form 5-HTTLPR. You likely have two long-form 5-HTTLPR (serotonin-transporter-linked polymorphic region). Variations in the region have been extensively investigated in connection with neuropsychiatric disorders. Identification of tag haplotypes for 5HTTLPR for different genome-wide SNP platforms

gs289

You have one short form 5-HTTLPR. You probably have one short-form 5-HTTLPR (serotonin-transporter-linked polymorphic region). Variations in the region have been extensively investigated in connection with neuropsychiatric disorders. Identification of tag haplotypes for 5HTTLPR for different genome-wide SNP platforms

Its weird that in the text it says 1 short but on the right side of the genetic website bar it says magnitude 2 so that means two short forms but the text says 1 short?

Anyone can help me understand this?

 

[sekio]

There's only two sets of 5-HT transporter genes, one on each chromosome, of which there are two. So you can at maximum express two different 5-HTP transporter protiens.

If you have a SNP for the short type on both genes then you will express two short-type transporter protiens. It looks to me that you have two short forms, that second website is in error telling you that you have two long form and one short.

As for treatment, don't bother trying to mess with serotonin levels... just because you have a mutated SERT protien doesn't mean you are guaranteed to have serotonin regulation issues, there are many other things that keep 5-HT levels in check like autoreceptors and the like.

Whatever your problems are, they may not actually have much to do with variation at 5-HTTLPR or "high serotonin" anyways.

I second this - nobody has ever treated their depression successfully by worrying about serotonin levels exclusively.

 

[trainman04]

There's only two sets of 5-HT transporter genes, one on each chromosome, of which there are two. So you can at maximum express two different 5-HTP transporter protiens.

If you have a SNP for the short type on both genes then you will express two short-type transporter protiens. It looks to me that you have two short forms, that second website is in error telling you that you have two long form and one short.

As for treatment, don't bother trying to mess with serotonin levels... just because you have a mutated SERT protien doesn't mean you are guaranteed to have serotonin regulation issues, there are many other things that keep 5-HT levels in check like autoreceptors and the like.



I second this - nobody has ever treated their depression successfully by worrying about serotonin levels exclusively.

what you mean? BOTH websites say I have . first site says 4 shorts the second 1 short but 2 long.

rs2020934 AA = 2 short


rs11867581 AA = 2 short again

so = 4 shorts
am i missing something?

tell me more about autoreceptors and other that keep 5-ht in check.


Tell me any site you trust and I will upload my 23andme so I can prove I have 4 shorts. I have already uploaded to 2 sites promethus and selfdecode which first one say 1 short 2 long and second 4 shorts..

 

[trainman04]

There are some OTC serotonin antagonists too, you can google them pretty easily, wouldn't those be good in your situation?

Nop my problem is Low SERT expression with 4 short forms Sertonin transporters.
SERT is supposed to get rid of your serotonin so if you have high SERT activity = less serotonin
Low Sert (me) = More Serotonin in the synapse
Thats why Increasing it would benefit me if I am right about all this.
But if you block a serotonin receptor with a supplement you will still have high serotonin activity in the synapse floating around . So I need to increase SERT in order to break it down . there are also 14 serotonin receptors which do different things.
The serotonin has to go trough SERT (I think) before it goes to the receptors.
I could be wrong about all of this.. so dont take my word for it.

 

[Cotcha Yankinov]

what you mean? BOTH websites say I have . first site says 4 shorts the second 1 short but 2 long.
rs2020934 AA = 2 short
rs11867581 AA = 2 short again
so = 4 shorts
am i missing something?
tell me more about autoreceptors and other that keep 5-ht in check.

I'm no genetic guru, but here's an analogy for what seems to be confusing you -

Imagine there is only one bridge ahead, but multiple "bridge ahead" sign posts. Just because there are multiple sign posts doesn't necessarily mean there is more than one bridge.

The gene sequence interpretation technology is looking for sequences of genes that suggest you may have a certain gene, but there can be multiple markers that correlate with having a gene, and they're going to report all the markers because that's more useful information (if the markers or signposts aren't 100% correlated with the SNP, its good to have more than one signpost).

As sekio has pointed out, you can only have two 5-HTTLPR forms in total.

I'm not quite sure about the gs288 marker that says you have two long forms. I would be careful about how you go about doing all of this, it can be really easy for a laymen like you and I to misinterpret the data here.

CY

 

[Cotcha Yankinov]

Nop my problem is Low SERT expression with 4 short forms Sertonin transporters.
SERT is supposed to get rid of your serotonin so if you have high SERT activity = less serotonin
Low Sert (me) = More Serotonin in the synapse
Thats why Increasing it would benefit me if I am right about all this.
But if you block a serotonin receptor with a supplement you will still have high serotonin activity in the synapse floating around . So I need to increase SERT in order to break it down . there are also 14 serotonin receptors which do different things.
The serotonin has to go trough SERT (I think) before it goes to the receptors.
I could be wrong about all of this.. so dont take my word for it.

I've seen some fundamental misunderstandings in your post that suggest to me you should start with the basics if you wish to learn more about neuroscience and mental health, but I wouldn't obsess with it to cure you of your own issues. It tends to only increase neuroticism, which is one of the traits the short form is a bit associated with

 

[sekio]

The serotonin has to go trough SERT (I think) before it goes to the receptors.
I could be wrong about all of this.. so dont take my word for it.

Nope, SERT is the protein that removes serotonin from the synapse *after* it has interacted with the receptors on the other cells.

Serotonin-releasing cell gets stimulated -> releases serotonin into the synapse -> serotonin binds to post-synaptic receptors (activates other cells) and pre-synaptic autoreceptors (receptors for serotonin on the same cell that released the serotonin, used to monitor how much serotonin is in the synapse and regulate release based upon that) -> after the signal is transmitted most serotonin is returned to the cell that released it via the SERT protein (but some is also degraded by MAO, etc)

You can only have two different copies of the SERT protien, assuming you're not a genetic chimera or anything rare and weird. Humans have two sets of every gene because they have two pairs of every chromosome (one inherited from each parent). Most of the time the two chromosomes match and only one protien is coded for but occasionally one will have a different code for a gene than the other, and in that case you produce two separate proteins. You can't produce more than two though.

SERT is supposed to get rid of your serotonin so if you have high SERT activity = less serotonin

SERT does not "get rid" of serotonin, it just moves it from place to place. Like I said before too, autoreceptors on the cells that release serotonin can compensate for low activity of SERT - if they sense too much serotonin in the synapse then the cell will not release more, it's like a "volume control" for the amount of serotonin released. There's also the VMAT transporter which can do a similar thing, transporting monoamines like serotonin back inside the cell. And monoamine oxidase enzymes are still there to remove serotonin even if the SERT is totally blocked. There's a bunch of regulatory systems that can compensate for a lazy SERT.

Please consider treating yourself symptomatically rather than worrying about the effect of one protein in your brain, it's not as if all your problems are caused by SERT alone. Nature vs nurture and all that. Situational stressors and life experiences are way larger contributors to mood.

 

[trainman04]

Nope, SERT is the protein that removes serotonin from the synapse *after* it has interacted with the receptors on the other cells.

Serotonin-releasing cell gets stimulated -> releases serotonin into the synapse -> serotonin binds to post-synaptic receptors (activates other cells) and pre-synaptic autoreceptors (receptors for serotonin on the same cell that released the serotonin, used to monitor how much serotonin is in the synapse and regulate release based upon that) -> after the signal is transmitted most serotonin is returned to the cell that released it via the SERT protein (but some is also degraded by MAO, etc)

You can only have two different copies of the SERT protien, assuming you're not a genetic chimera or anything rare and weird. Humans have two sets of every gene because they have two pairs of every chromosome (one inherited from each parent). Most of the time the two chromosomes match and only one protien is coded for but occasionally one will have a different code for a gene than the other, and in that case you produce two separate proteins. You can't produce more than two though.




SERT does not "get rid" of serotonin, it just moves it from place to place. Like I said before too, autoreceptors on the cells that release serotonin can compensate for low activity of SERT - if they sense too much serotonin in the synapse then the cell will not release more, it's like a "volume control" for the amount of serotonin released. There's also the VMAT transporter which can do a similar thing, transporting monoamines like serotonin back inside the cell. And monoamine oxidase enzymes are still there to remove serotonin even if the SERT is totally blocked. There's a bunch of regulatory systems that can compensate for a lazy SERT.

Please consider treating yourself symptomatically rather than worrying about the effect of one protein in your brain, it's not as if all your problems are caused by SERT alone. Nature vs nurture and all that. Situational stressors and life experiences are way larger contributors to mood.

so basically SERT makes your serotonin less active in places in the brain ? IE it would be like you had reduced serotonin if you increased sert. So Increasing SERT expression could make your serotonin receptors less active.

But what if you have Low MAO-a + 2 short ... there is a thing called warrior gene people with this have low MAO activity. So with this I could have more serotonin circaling around my brain and my brain never gets to break it down because when its almost done finnish breaking all the serotonin I will have had another meal and AGAIN my serotonin levels rise.. so it never gets the chance to go down? makes sense? Or what if you have any other mutations so you cant break down serotonin well none of it is working.. ever thought of that?
The serotonin transporter (5-HTT) is important in the termination and modulation of serotonergic neurotransmission by sodium-dependent reuptake of serotonin into the presynaptic neuron, which thus terminates the synaptic actions of serotonin and recycles it into the neurotransmitter pool.

But still there has to be a reason I got
rs2020934 AA = 2 short
rs11867581 AA = 2 short again

it doesent just happen by misstake.. Selfdecode is a very good site and they know what they are doing.\

 

[Cotcha Yankinov]

But still there has to be a reason I got
rs2020934 AA = 2 short
rs11867581 AA = 2 short again
it doesent just happen by misstake.. Selfdecode is a very good site and they know what they are doing.

Just copying and pasting my explanation again in case you missed it -

Imagine there is only one bridge ahead, but multiple "bridge ahead" sign posts. Just because there are multiple sign posts doesn't necessarily mean there is more than one bridge.

The gene sequence interpretation technology is looking for sequences of genes that suggest you may have a certain gene, but there can be multiple markers that correlate with having a gene, and they're going to report all the markers because that's more useful information. If the markers or signposts aren't 100% correlated with the SNP, its good to have more than one signpost.

So lets say you had one region (Not the 5-HTT linked polymorphic region) that was linked/correlated to having a short form of the 5-HTTLPR 75% of the time, and another region that was linked to having a short form 85% of the time. It would make sense to report both of these together because its more evidence that the 5-HTTLPR region is the short form.

Personally I think people get way too into their genetics, especially with regards to warrior vs. worrier et cetera. People tend to think they're discovering some deep, profound secret about their brain when it could be playing an extremely minor role in how their brains have turned out, and could be playing a very minor role in how their brains continue to change.

Brains are capable of extraordinary change, given the right encouragement and time. As sekio has said, I would focus on the symptoms that you're having trouble with and ignore genetics for now.

Get to a mental health professional - the answer to your problems does not lie in obsessing over your genome

 

[trainman04]

@Cotcha

what im saying is selfdecode the site I tested my genes they would have thought of any errors etc that could happen and have something that prevents it. Also why do you never see anyone else get this error with 4 serotonin forms? You would think many others would have gotten it too if its an error.

 

[Cotcha Yankinov]

Others do get calls for the exact markers that you have because those (as I understand it) are surrogate markers for having a short form region.

rs2020934 AA
rs11867581 AA
- are not actually measurements of the entire 5-HTTLPR sequence, they are simply sign posts, and as I said earlier, there can be more than one sign post for a bridge but that does not mean that there will be multiple bridges. When you see those "rs2020934" et cetera markers, that is not the same as seeing a bridge itself, that is just seeing a sign post telling of a bridge.

There are different places they can look in your sequence to try to determine what form of 5-HTTLPR you have, and they are simply looking in more than one area for such a surrogate marker. Because they've looked in more than one area, they are reporting more than one sign post. Hopes this makes some sense. I assure you that you do not have 4 short forms.

The makers of these genome sequencing sites and the other sites that interpret the raw data are probably putting too much faith in the users to correctly interpret the results. Or maybe they're just selling a product/service and don't care too much about holding laymen's hands through the process of understanding one's results.

 

[trainman04]

Others do get calls for the exact markers that you have because those (as I understand it) are surrogate markers for having a short form region.

rs2020934 AA
rs11867581 AA
- are not actually measurements of the entire 5-HTTLPR sequence, they are simply sign posts, and as I said earlier, there can be more than one sign post for a bridge but that does not mean that there will be multiple bridges. When you see those "rs2020934" et cetera markers, that is not the same as seeing a bridge itself, that is just seeing a sign post telling of a bridge.

There are different places they can look in your sequence to try to determine what form of 5-HTTLPR you have, and they are simply looking in more than one area for such a surrogate marker. Because they've looked in more than one area, they are reporting more than one sign post. Hopes this makes some sense. I assure you that you do not have 4 short forms.

The makers of these genome sequencing sites and the other sites that interpret the raw data are probably putting too much faith in the users to correctly interpret the results. Or maybe they're just selling a product/service and don't care too much about holding laymen's hands through the process of understanding one's results.

But does anyone have BOTH? you usually just have one of the AA SNPs. and thats what I am saying. If it was an ERROR more people would have shown have BOTH together but they dont they just have 1 of the snp that cause short when they test their genes. Also these results can give me an IDEA what I might have...

 

[Cotcha Yankinov]

But does anyone have BOTH? you usually just have one of the AA SNPs.

Like I said, I believe they are just surrogate markers for having a short form. Just because you have two markers showing that you are homozygous for the short form doesn't mean that you have 4 short forms. They are different markers correlated to the same thing, just by proxy. See the road sign analogy again.

4 road signs warning of a bridge in this case does not mean that there are 4 bridges.

You seem to be claiming things about other people's test results as if nobody else has been called as you have (homozygous AA for both of those rs markers). I'm sure plenty of people have been called homozygous AA for both of those, why do you claim otherwise?

CY

 

[trainman04]

Like I said, I believe they are just surrogate markers for having a short form. Just because you have two markers showing that you are homozygous for the short form doesn't mean that you have 4 short forms. They are different markers correlated to the same thing, just by proxy. See the road sign analogy again.

4 road signs warning of a bridge in this case does not mean that there are 4 bridges.

You seem to be claiming things about other people's test results as if nobody else has been called as you have (homozygous AA for both of those rs markers). I'm sure plenty of people have been called homozygous AA for both of those, why do you claim otherwise?

CY

show me 1 person that has the same results as me and I will Believe you.

 

[sekio]

what im saying is selfdecode the site I tested my genes they would have thought of any errors etc that could happen and have something that prevents it.

SelfDecode actually explicity tells you that their site can report contradictory results, you should not rely on it to dictate medical treatment, and is not 100% accurate in predicting phenotype.

From the SelfDecode FAQ:

How should you behave based on the information presented?
You should never take any drastic action or an action that has significant side effects based on your genetics. Currently, the best way to use your genes is to motivate you to take a healthy action that you should already be taking.

If you see something that may alarm you, make sure to speak with your doctor to understand what these results mean.

The FDA says that it has the ability to regulate genomic interpretation (whether we like it or not) because people sometimes take drastic action based on genetic results.

You shouldn't make any changes in medical behavior based on your genes without discussing with your doctor.

However, if you see something in your genetics that will motivate you to take a healthy action, then that's always a good thing.

[...]

Is your interpretation guaranteed or just a probability?
Any interpretation or information presented is simply a probability.

How reliable is the SNP Analyzer?
The SNP analyzer is a way to aggregate information, often from contradicting SNPs. You shouldn't use the information as factual, but rather as something to look more into. Often, there will be SNPs that contradict each other in the SNP analyzer. This is because people are made up of millions of SNPs that often do contradictory functions and it's the totality of these functions that decide what your biology is like.

The SNP analyzer aims to integrate information from a certain function to come up with a clearer picture. You should rely on it as a rough estimation of what you're like.

Because most genetic self testing kits rely on SNPs and do not sequence the whole genome, it's not possible to say with certainty if you have a long or short form SERT... in fact it's possible you may have an entirely new genotype or express both.

So with this I could have more serotonin circaling around my brain and my brain never gets to break it down because when its almost done finnish breaking all the serotonin I will have had another meal and AGAIN my serotonin levels rise.. so it never gets the chance to go down? makes sense? Or what if you have any other mutations so you cant break down serotonin well none of it is working.. ever thought of that?

If you lacked the ability to break down serotonin at all you'd die in the womb before being born because every cell that used serotonin for signalling would be hopelessly overstimulated and you'd effectively be in a permanent state of serotonin syndrome. You'd need to have two copies of a defective SERT, two copies each of defective MAO-A and MAO-B, and probably two copies of a defective VMAT gene. So a minimum of eight mutations, probably more. Seems unlikely to me.

Given that you aren't in tonic-clonic seizures and could take the time to coherently type out a post, I can almost certainly guarantee you that you possess the ability to degrade serotonin. Besides, there are urinary markers of serotonin degradation people can test for. (indole acetic acid etc) .. get one of those tests if you are so worried.

Also keep in mind that serotonin is far from the only neurotransmitter that controls mood. There's a lot more to human biology than "serotonin = happy".

Also also, if my memory serves, when serotonin levels are higher than usual, production of more serotonin via tyrosine hydroxylase is downregulated... the body has a lot of these feedback loops.

So, in conclusion, treat symptomatically and quit worrying about what a SNP analysis tells you. Nobody has ever treated their depression/mental issues by focusing exclusively on serotonin levels.

 

[trainman04]

when I was younger before puberty age 12 I didnt have any problems. I found this " The Amygdala: An Agent of Change in Adolescent Neural Networks"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3781589/

so yeah Im sure that can apply to many other things in the brain that changes when you grow up . my serotonin was normal but when I grew up it changed. I still belive high serotonin is my problem and nothing is gonna change that. The best you guys can do is help me but if you dont want to help thats fine but im done arguing about if I have high serotonin or not.

Blood of SIDS infants contains high levels of serotonin
https://www.nih.gov/news-events/news-releases/blood-sids-infants-contains-high-levels-serotonin

 

[Cotcha Yankinov]

when I was younger before puberty age 12 I didnt have any problems.

Story of our lives

my serotonin was normal but when I grew up it changed. I still belive high serotonin is my problem and nothing is gonna change that. The best you guys can do is help me but if you dont want to help thats fine but im done arguing about if I have high serotonin or not.

Blood of SIDS infants contains high levels of serotonin
https://www.nih.gov/news-events/news-releases/blood-sids-infants-contains-high-levels-serotonin

I think you're barking up the entirely wrong tree here. Also, correlation does not equal causation. There are many cases where something (for example, elevated serotonin) is noticed in a set of people with certain symptoms/conditions, but that does not mean the condition is caused by the noted abnormality. Something entirely different could be causing both elevated serotonin in the serum of SIDS infants and the SIDS at the same time.

If you are unable to change your beliefs about what is causing your issues then its just going to take longer for you to get the treatment you need. Try to let go of this high serotonin fixation and get yourself to a mental health professional.
CY