Dopamine concern

[Hip]

@ppodhajski
Can you show me any evidence that interventions which specifically address the shortcomings of a particular person's SNPs have led to improvements or remission in that person's diseases?

 

[ppodhajski]

@ppodhajski
Can you show me any evidence that interventions which specifically address the shortcomings of a particular person's SNPs have led to improvements or remission in that person's diseases?

You are talking to one. And I worked with others that do not have ME. (arthritis, anxiety, anger, heart palpitations). @ahmo is another on the board. I called out his need for B2 as well by looking at his genetics.

But even if there is no one else there always has to be a first. Maybe if you read those links and try to understand the science more it ill help you grasp what I am doing.

But I do not understand your need? Are you here to just doubt me or do you want to try to understand what I did so we can see if it can work for others. This is not a regimen. It is a method of looking at peoples genes and lifestyle to find what is putting pressure on there antioxidant system to cause autoimmune issues.

Let me ask you this, forget about the evidence, what in the science makes you doubt what I told the original poster about his genes and what might work?

And, you could always try it and see for your self.

 

[Hip]

You are talking to one. And I worked with others that do not have ME. (arthritis, anxiety, anger, heart palpitations). @ahmo is another on the board. I called out his need for B2 as well by looking at his genetics.

As I mentioned, you did not take any supplements which specifically address the shortcomings of your particular SNPs. You took R5P, which will be involved with the SNPs of most people.

So as I said, you are not using an approach tailored to your SNPs. I don't see how your taking R5P relates to your SNPs in particular.

But I do not understand your need? Are you here to just doubt me or do you want to try to understand what I did so we can see if it can work for others.

Not you personally; I am generally doubtful about any treatments that are supposedly chosen on the basis of someone's SNPs. Lots of people come to this forum with a long list of their SNPs, expecting that the answer to their problems is going to be found in these SNPs. Then we get long and highly, highly speculative discussions about these SNPs, which mostly read like pseudoscience, but generally no improvements in health.

I am not saying that occasionally knowledge of one's SNPs can lead to some useful health interventions; but generally these SNP discussions seem like a lot of hot air.

Let me ask you this, forget about the evidence, what in the science makes you doubt what I told the original poster about his genes and what might work?

To repeat myself: because you have not demonstrated either anecdotally, nor via published studies, that supplements which specifically address the shortcomings of a particular person's SNP can lead to improvements in health.

 

[ppodhajski]

As I mentioned, you did not take any supplements which specifically address the shortcomings of your particular SNP. You took R5P, which will be involved with the SNPs of most people.

So as I said, you are not using an approach tailored to your SNPs. I don't see how your taking R5P relates to your SNPs in particular.

First, I do not call it R5P, I call it FMN. There is a reason I do so.

What is it exactly that you think vitamins do if they do not effect gene expression?

You do not understand Nutritional Genomics. Read for a few days, watch some videos. You do not want to learn anything from me so learn it for your self. You could not have read all those links and that hour long video yet.

I have slow MAOA and MAOB enzymes this is determined by my PERSONAL SNPs. That is my biology based on my SNPs. Someone else might have faster MAOA and MAOB SNPs. When they take FMN they will get depressed. When I take it I go from having crippling anxiety to no anxiety. I never thought of taking riboflavin until I saw my genetics.

Not you personally; I am generally doubtful about any treatments that are supposedly chosen on the basis of someone's SNPs. Lots of people come to this forum with a long list of their SNPs, expecting that the answer to their problems is going to be found in these SNPs. Then we get long and highly, highly speculative discussions about these SNPs, which mostly read like pseudoscience, but generally no improvements in health.

A lot of people come inhere and talk about a lot of stuff that goes nowhere.

Yet when someone comes in, with a different method, you just doubt and do not try to be skeptical. There is a difference. You will not take the time to read any material I post. I have been studying nutritional genomics for a year straight and I have been studying nutrition for 15 years full time.

I am not saying that occasionally knowledge of one's SNPs can lead to some useful health interventions; but generally these SNP discussions seem like a lot of hot air.

To repeat myself: because you have not demonstrated either anecdotally, nor via published studies, that supplements which specifically address the shortcomings of a particular person's SNP can lead to improvements in health.

I proved it anecdotally..it is me.

Watch this video, and there is your proof as well. But while you are looking for 100% proof you will still be sick. I am better. If you have a better explanation of how I am better I would like to hear it. And if you want proof for yourself you can investigate the method and try it for yourself.

 

[Gondwanaland]

you did not take any supplements which specifically address the shortcomings of your particular SNPs. You took R5P, which will be involved with the SNPs of most people.

So what if someone is deficient precisely in B2?

Lots of people come to this forum with a long list of their SNPs, expecting that the answer to their problems is going to be found in these SNPs. Then we get long and highly, highly speculative discussions about these SNPs, which mostly read like pseudoscience, but generally no improvements in health.

Obviously because people with different SNPs AND different deficiency conditions do not benefit from the standard protocols proposed all over the internet

because you have not demonstrated either anecdotally, nor via published studies, that supplements which specifically address the shortcomings of a particular person's SNP can lead to improvements in health.

Nutrigenomics is based on science, it is so obvious, if you have the SNPs and have the symptoms of deficiency in the specific co-factor so it is only logical what to take. The problem resides in the way it has been done by some practitioners who are only inerested in selling the same expensive supplements to each and everyone.

@ppodhajski approach is very appealing to me because it is something I can understand and IS well supported by research.

I find it so puzzling that @Valentijn doesn't agree, because she always says "you've got to read the reaseach" and this is precisely what this is about. Then she says "you are choosing random SNPs" - I disagree, because the SNPs chosen are the ones about which there is research!

 

[Valentijn]

I find it so puzzling that @Valentijn doesn't agree, because she always says "you've got to read the reaseach" and this is precisely what this is about. Then she says "you are choosing random SNPs" - I disagree, because the SNPs chosen are the ones about which there is research!

Then why does @ppodhajski keep trotting out SNPs which don't have research saying they have an impact? In one of his posts he explicitly says that he focuses on some SNPs solely because they are on relevant pathways and they are rare. And when he does cite research, he doesn't seem to read it well enough to give an accurate interpretation of it.

As a very recent example from this thread:

That PTS rs3819331 CC is interesting and it uses ZInc as a cofactor. Looks like it could lead to BH4 deficiency which will leave you low in all the neurotransmitters.

http://ghr.nlm.nih.gov/gene/PTS
http://www.uniprot.org/uniprot/Q03393
http://www.nature.com/jhg/journal/v57/n2/full/jhg2011146a.html

There is scant research on this SNP but it seems associated with Autism:
http://onlinelibrary.wiley.com/doi/10.1111/j.1601-183X.2009.00521.x/pdf

First of all, another study contradicts the one listed (final link, from Wiley) - it found no significant associations with the same and other SNPs in autism. So the study he cited failed to be replicated, which usually means it was a false positive.

Another problem with the Wiley study is that no effect sizes are given. So maybe they found that having one genotype results in a 0.01% increase in risk of having autism. Which would indicate that the SNP is having almost no impact on anyone - but we don't know, because they aren't telling us. It's not a good sign.

And the really big problem is that if you actually read the study, you'll find that the rarer allele (C) is reported being associated with decreased autism risk. So that means that the CC and CT people supposedly have less risk of autism and it's the other 75% of the population which is supposedly at increased risk.

So it's important to find out which allele is the risk allele. You can not assume it's the rare one, even when there is a risk allele found. Once again, this failure to read and understand the research has resulted in @ppodhajski spreading disinformation, and giving advice based on that disinformation.

Do. Not. Trust. SNPedia.
Read. The. Research.
Find. The. Effect. Size.
Find. The. Risk. Allele.
Find. The. Dissenting. Research.

I don't know how many times I need to say it. But I will keep saying it until it sinks in.

 

[ppodhajski]

Then why does @ppodhajski keep trotting out SNPs which don't have research saying they have an impact? In one of his posts he explicitly says that he focuses on some SNPs solely because they are on relevant pathways and they are rare. And when he does cite research, he doesn't seem to read it well enough to give an accurate interpretation of it.

As a very recent example from this thread:


First of all, another study contradicts the one listed (final link, from Wiley) - it found no significant associations with the same and other SNPs in autism. So the study he cited failed to be replicated, which usually means it was a false positive.

Another problem with the Wiley study is that no effect sizes are given. So maybe they found that having one genotype results in a 0.01% increase in risk of having autism. Which would indicate that the SNP is having almost no impact on anyone - but we don't know, because they aren't telling us. It's not a good sign.

And the really big problem is that if you actually read the study, you'll find that the rarer allele (C) is reported being associated with decreased autism risk. So that means that the CC and CT people supposedly have less risk of autism and it's the other 75% of the population which is supposedly at increased risk.

So it's important to find out which allele is the risk allele. You can not assume it's the rare one, even when there is a risk allele found. Once again, this failure to read and understand the research has resulted in @ppodhajski spreading disinformation, and giving advice based on that disinformation.

Do. Not. Trust. SNPedia.
Read. The. Research.
Find. The. Effect. Size.
Find. The. Risk. Allele.
Find. The. Dissenting. Research.

I don't know how many times I need to say it. But I will keep saying it until it sinks in.

I am not talking about how the SNP causes Autism. Just mood disorders in general. That is the issue you have with trying to understand Nutritional Genomics and Metabolic Pathways.

If I did everything you said I would not be better. So there is that as well.

 

[Valentijn]

I am not talking about how the SNP causes Autism. Just mood disorders in general. That is the issue you have with trying to understand Nutritional Genomics and Metabolic Pathways.

No, you are talking about SNPs being relevant when they are not. You are also frequently badly misinterpreting the pretty basic research involving SNPs. You are making blatantly incorrect claims about it.

If I did everything you said I would not be better. So there is that as well.

Right. So to "heal" we need to do every random thing we can imagine, ignore the research as much as possible, and/or do exactly the opposite of what the research indicates. Thanks for the clarification.

 

[ppodhajski]

No, you are talking about SNPs being relevant when they are not. You are also frequently badly misinterpreting the pretty basic research involving SNPs. You are making blatantly incorrect claims about it.

Right. So to "heal" we need to do every random thing we can imagine, ignore the research as much as possible, and/or do exactly the opposite of what the research indicates. Thanks for the clarification.

OK

 

[ahmo]

I can only say here that from the time I got my 23andme results, I have been treating myself according to snps. Maybe this has not been in as precise a manner as doubters might like, but it's how I've been healing. At times I've thought I could have done it w/o my snps, but it would have been far more by chance. As it is, I've used Yasko RNA supps at the outset, which helped. And I've followed advice for CBS, MTHFR, others. @ppodhajski's recommendation of FMN for MAO changed my life considerably.

 

[Hip]

First, I do not call it R5P, I call it FMN. There is a reason I do so.

Riboflavin-5′-phosphate (R5P) and flavin mono nucleotide (FMN) are just synonyms for the exactly same chemical compound, a compound specified by CAS number 146-17-8. For more synonyms of this compound, see here.

I have slow MAOA and MAOB enzymes this is determined by my PERSONAL SNPs. That is my biology based on my SNPs. Someone else might have faster MAOA and MAOB SNPs. When they take FMN they will get depressed.

Are there published studies on this, that people with fast MAOA and MAOB will get depressed if they take R5P? Or if not studies, have you or anyone else gathered any anecdotal evidence showing that the speed of people's MAOA and MAOB enzymes correlates to whether R5P improves or worsens their depression?

So what if someone is deficient precisely in B2?

Then they likely will find vitamin B2 beneficial. That does not necessarily mean however that the benefits they get from taking vitamin B2 are explained by their SNPs. There could be any number of biochemical reasons why B2 may benefit a patient, and I would think that most will have nothing to do with SNPs.

Very often we can follow a speculative theory, and find supplements that help. However, just because we were following a theory, and that led us to trying a supplement than helped, that does not mean that the theory is correct. The supplement may help for reasons entirely unconnected to the theory.

I can only say here that from the time I got my 23andme results, I have been treating myself according to snps.

When you say according to your SNPs, do you mean that the treatments you are taking are specific to your SNPs, such that they would not work for anyone else with different SNPs?

@ppodhajski's recommendation of FMN for MAO changed my life considerably.

What symptoms did riboflavin-5′-phosphate improve, can I ask?

 

[ppodhajski]

Riboflavin-5′-phosphate (R5P) and flavin mono nucleotide (FMN) are just synonyms for the exactly same chemical compound, a compound specified by CAS number 146-17-8. For more synonyms of this compound, see here.

Riboflavin-5′-phosphate and Riboflavin-5′-phosphate Sodium is not the same.

Are there published studies on this, that people with fast MAOA and MAOB will get depressed if they take R5P? Or if not studies, have you or anyone else gathered any anecdotal evidence showing that the speed of people's MAOA and MAOB enzymes correlates to whether R5P improves or worsens their depression?

No. But someone has to be the first to discover something. I have seen this in action in two people. And look at here on this forum:
http://forums.phoenixrising.me/inde...-of-b2-here-a-warning-about-riboflavin.31639/

Then they likely will find vitamin B2 beneficial. That does not necessarily mean however that the benefits they get from taking vitamin B2 are explained by their SNPs. There could be any number of biochemical reasons why B2 may benefit a patient, and I would think that most will have nothing to do with SNPs.

But what you keep ignoring is that I see this in the SNPs. That is how I foudn out it worked for me. I saw the MAOA and MAOB SNPs were slow, saw they needed riboflavin. I took it. My anxiety went away. Tried it on others. Discovered it made them depressed. Saw there MAOA and MAOB genes were different than mine.

Dude, this is just a theory of mine but it seems to be working out. Where is the explorer in you?

Very often we can follow a speculative theory, and find supplements that help. However, just because we were following a theory, and that led us to trying a supplement than helped, that does not mean that the theory is correct. The supplement may help for reasons entirely unconnected to the theory.

If you can tell me the alternative theory I would be willing to hear it. But you are not offering me that theory. If more people try this method and it works that would keep proving my theory. You already heard from a few in here that saw it work.

When you say according to your SNPs, do you mean that the treatments you are taking are specific to your SNPs, such that they would not work for anyone else with different SNPs?

Yes, everyone will have a different treatment. Everyone need to understand their genetics and environment and how it might put pressure on their specific slow metabolic pathways.

I am not offing a protocol, I am offering a method.

What symptoms did riboflavin-5′-phosphate improve, can I ask?

 

[Hip]

Riboflavin-5′-phosphate and Riboflavin-5′-phosphate Sodium is not the same.

What's that go to do with anything?

No. But someone has to be the first to discover something. I have seen this in action in two people. And look at here on this forum:

So one minute you are making the statement that people with fast MAOA and MAOB will get depressed if they take R5P, as if it were a fact. But now from your above statement, you admit that there is no evidence for this whatsoever.

Really, this is an issue of language: if you have a hypothesis that people with fast MAOA and MAOB will get depressed if they take R5P, then say that. Say this is your hypothesis. That's fine.

But don't state this as a fact, when there is as yet no evidence for it. This normal scientific etiquette: you should not present your speculations and hypotheses as facts until they are proven by some sort of evidence.

If you can tell me the alternative theory I would be willing to hear it. But you are not offering me that theory. If more people try this method and it works that would keep proving my theory. You already heard from a few in here that saw it work.

Don't you think you yourself should be open to and looking for alternative explanations and theories? Every supplement or drug gets involved in hundreds of metabolic pathways. I have found several supplements that have benefitted me, and I have come up with some biochemical speculations as to the mechanism, but I am always on the lookout for other possible explanations. I would never just get stuck on the first possible explanation that I found.

Yes, everyone will have a different treatment. Everyone need to understand their genetics and environment and how it might put pressure on their specific slow metabolic pathways.

So why do you keep suggesting R5P to everyone, if everyone will have a different treatment?

 

[ppodhajski]

So one minute you are making the statement that people with fast MAOA and MAOB will get depressed if they take R5P, as if it were a fact. But now from your above statement, you admit that there is no evidence for this whatsoever.

Really, this is an issue of language: if you have a hypothesis that people with fast MAOA and MAOB will get depressed if they take R5P, then say that. Say this is your hypothesis. That's fine.

But don't state this as a fact, when there is as yet no evidence for it. This normal scientific etiquette: you should not present your speculations and hypotheses as facts until they are proven by some sort of evidence.

Give me a break with this stuff. We all know we all are just putting our own hypothesis out here. No one has scientifically studied my method so there is no evidence. There is plenty of evidence for the subsets of my theory.

Don't you think you yourself should be open to and looking for alternative explanations and theories? Every supplement or drug gets involved in hundreds of metabolic pathways. I have found several supplements that have benefitted me, and I have come up with some biochemical speculations as to the mechanism, but I am always on the lookout for other possible explanations. I would never just get stuck on the first possible explanation that I found.

I did. I cannot find a single hole in my method. Because I started from theory and experimented with it. Unlike you, who tries something and them sets up a theory around it. I think my method is more scientific. You need to be on the look out for other explanations because you did not START with the explanation. I saw the explanation and therefore the cure of my illness in my genes.

And then you send a protocol out for people to try and by your own admission it only works half of the time.
http://forums.phoenixrising.me/inde...nxiety-symptoms-with-three-supplements.18369/
And what evidence but your own anecdotal evidence do you have? You just want to GUESS that if might work for people without knowing their genetics? For all you know if could be placebo effect at 50%!

So why do you keep suggesting R5P to everyone, if everyone will have a different treatment?

I am not suggesting it to everyone. HOWEVER, it might be that FMN is needed by a majority of ME people.

Why don't you try my method?

 

[ahmo]

When you say according to your SNPs, do you mean that the treatments you are taking are specific to your SNPs, such that they would not work for anyone else with different SNPs?

I can't answer what anyone else might experience. I followed Yasko, as some call it, Yasko-lite, to give me directions re how to proceed. It worked for me. I attended to things in the order she suggested, to prepare for each next step in methylation.

What symptoms did riboflavin-5′-phosphate improve, can I ask?

See my signature for FMN blog account. It's almost eliminated my need for antihistamines and mast cell stabilizers, dramatically reduced my insatiable need for antioxidants. I had been assured that there was no connection between MAO and histamines, but it seems otherwise in my experience. Of course, you might say that this shows no relationship. But ppodhajski suggested FMN for MAO, MAOA is my sole homozygous methylation snp, and it worked as well as he predicted. When I tried taking increased doses of B2, prior to FMN, as far as I know I was not depressed, but felt as if I was drowning in ammonia.

Dude, this is just a theory of mine but it seems to be working out. Where is the explorer in you?

 

[ppodhajski]

I can't answer what anyone else might experience. I followed Yasko, as some call it, Yasko-lite, to give me directions re how to proceed. It worked for me. I attended to things in the order she suggested, to prepare for each next step in methylation.

See my signature for FMN blog account. It's almost eliminated my need for antihistamines and mast cell stabilizers, dramatically reduced my insatiable need for antioxidants. I had been assured that there was no connection between MAO and histamines, but it seems otherwise in my experience. Of course, you might say that this shows no relationship. But ppodhajski suggested FMN for MAO, MAOA is my sole homozygous methylation snp, and it worked as well as he predicted. When I tried taking increased doses of B2, prior to FMN, as far as I know I was not depressed, but felt as if I was drowning in ammonia.

Interesting about you histamine a but it makes sense! The enzyme that breaks down histAMINE is Diamine Oxidase (DAO) and guess what it used as a cofactor.......FAD!

So I will guess if we look at you DAO SNPs we would see a lot of lie frequency genes.

The next gene in that pathway is HNMT which uses SAMe as a coenzyme. It is important that someone is making enough SAMe on the methionine cycle before taking the FMN since it can cause issues.

When I have someone's gene I look at these two together and ask about symtoms I see it play out in the genes. For me, my allergies are not bad, they only get bad when my anxiety acts up. I believe this is because I will use us B2 trying to assist my bad MAO genes that it will eventually slow down my not so bad DAO genes.

And when people have bad allergies it will eventually cause mood issues if their DAO is worse than their MAO.

Interesting that riboflavin made you feel worse, never heard that but something I will look out for. I can see if one took it the RFK gene could use up zinc and magnesium which it needs to change the B2 into FMN and those deficiencies can effect other symptoms.

 

[ppodhajski]

Oh my, @ahmo, look at this! I never looked this up before. It suddenly dawned on me this morning that I never looked up the cofactor for FLAD1 which turns FMN into FAD and there iit is, it uses MAGNESIUM as a cofactor! AND it uses an ATP molecule as well. No wonder why magnesium relaxes most people and now I know why when I take magnesium it no longer relaxes me but drains too much ATP. This makes me think of lowering my FMN and adding a low dose of magnesium to keep things balanced.

I know when my magnesium is low my dandruff and sebhoric dermatitis crops up. This I fault to the COMT gene.

So now we can imagine some one with low riboflavin, magnesium and zinc getting very little FAD from either B2 or FMN which I turn will slow down all the enzymes that need it like MTHFR DAO MAO MTRR, etc. Someone who did not have SNPs in these genes would be less effected by someone who does.

Fantastic!

 

[Violeta]

When I tried taking increased doses of B2, prior to FMN, as far as I know I was not depressed, but felt as if I was drowning in ammonia.

@ahmo , do you mean that when you took B2 you felt like you had too much ammonia but FMN relieved that?

B2 is supposed to help with purine metabolism, but maybe there is something still missing downstream. I would like to find out what that might be, if anything, as I do think I have ammonia problems to the point of having difficulty when I eat protein high in purines.

Anyone?

 

[ahmo]

@ahmo , do you mean that when you took B2 you felt like you had too much ammonia but FMN relieved that?

No. Actually, it was you who started this for me. The post for the B2 thread, re B2 helps process folate, which I received in my email, but you deleted from the thread...I tried B2, and had a terrible reaction. I did not have FMN at that time. And I was titrating from a 100mg capsule, so that likely contributed to the poisoning.

This is actually pretty interesting, when I look closer. Id' already been getting 25mg r5p in my B complex, for at least a year. But adding the 18mg FMN made an enormous change.

I've just now increased my meat intake, do not appear to be having problems.

 

[Violeta]

No. Actually, it was you who started this for me. The post for the B2 thread, re B2 helps process folate, which I received in my email, but you deleted from the thread...I tried B2, and had a terrible reaction. I did not have FMN at that time. And I was titrating from a 100mg capsule, so that likely contributed to the poisoning.

This is actually pretty interesting, when I look closer. Id' already been getting 25mg r5p in my B complex, for at least a year. But adding the 18mg FMN made an enormous change.

I've just now increased my meat intake, do not appear to be having problems.

When I look at that post, it's confusing, because whoever is asking me the question didn't represent the way I think about B2, and I don't remember deleting anything. I'll look at it more closely, but it seems so twisted that it's hard to straighten it back out.

So even though you had been taking r5p, when you added in FMN you felt better. Interesting.