intro and genetic testing 8-2015

[phoenix76]

Hi There,

This is what I have for the promethease report. I included a copy of exactly what is on it for my SNPs you listed above for yourself...hopefully this is what you wanted me to do and not look up my signature line values instead. What is the difference between the first and second letters? Some of mine match up and others are different. Thanks again!

MAOA
rs909525(A;A) this looks good; it is green in the report

MAOB
rs2283729(G;G) gray--not red nor green
rs1799836(A;G) red shading

COMT
rs4633(C;T) red shading
rs4680(A;G)
rs165722(C;T)

 

[phoenix76]

I am not sure I need less estrogen...it is the balance with progesterone. I took a few saliva tests over the past few years, which indicated that I am slightly estrogen dominant but my estrogen numbers were not really all that high either. Adrenals were a bit whacked out at night when on the merry go round of meds...but has recovered nicely and within normal limits on future tests. I take daily dose, sometimes double it if feeling under the weather, of Carlson's Cod Liver Oil. It is rich in Omega-3s, A and D. Cruciferous veggies in excess are a no-no for hypothyroid. Or so I have read. I still each them here and there cooked but it is not a mainstay for me.

Not sure why I have the hypothyroid with all of this...it is not too bad though. I take a low dose of generic for Synthroid. I would love to get off of it though. My mom has a lot of autoimmune disorders with Hashimoto's being one of them.

I need to find someone who can do the hair analysis or can you do it yourself? If so, where can I find info on how to do it myself?

GI tests (just copying and pasting...sorry for the BIG letters)--all negative
--stool sample for ENTEROHEMORRHAGIC E COLI EIA, SALMONELLA/SHIGELLA SCREEN, CAMPYLOBACTER CULTURE, OVA+PARASITES EXAM, ROUTINE
--H. PYLORI STOOL ANTIGEN
--C DIFFICILE TOXIN GENE NAA
--Celiac Disease Profile (mom has it) -- and I have not been eating it consistently for months--accurate??
ENDOMYSIAL ANTIBODY IGA, T-TRANSGLUTAMINASE (TTG) IGA, Immunoglobulin A, Qn, Serum

average
--LACTOFERRIN, FECAL, QUANT.
--VITAMIN D, 25-HYDROXY 30.0 - 100.0 ng/mL my value 59.8--I supplement because it used to be low end of avg
--Vitamin B12 211 - 946 pg/mL my value 905
FOLATE (FOLIC ACID), SERUM >3.0 ng/mL my value >20.0-- I take B Healthy by Emerald that has methylated B vitamins in a complex
--FERRITIN 8-388 ng/mL my value 39
--Iron, Serum 50-175 µg/dL my value 86
TIBC 250-450 µg/dL my value 285
Saturation Percent 20-55 % my value 30.2
--C-Reactive Protein 0.00-0.90 mg/dL my value 0.14
--Erythrocyte Sedimentation Rate 0-25 mm/hr my value 13
--Fecal fats normal

Ultrasound of abdominal--nothing remarkable but could not fully see pancreas

So I still have this nagging little scratching sort of feel on the left side even after I have a morning sip of water. And have soft IBS-D but not full out D quite a bit. FODMAPs diet is okay but I do notice fructans, FOS, some polyols if I eat too many of these fruits and veggies, dairy are all culprits.

This is a lot of information...and I know you are not a doctor but thanks for helping me out.

 

[ppodhajski]

Hi There,

This is what I have for the promethease report. I included a copy of exactly what is on it for my SNPs you listed above for yourself...hopefully this is what you wanted me to do and not look up my signature line values instead. What is the difference between the first and second letters? Some of mine match up and others are different. Thanks again!

MAOA
rs909525(A;A) this looks good; it is green in the report

MAOB
rs2283729(G;G) gray--not red nor green
rs1799836(A;G) red shading

COMT
rs4633(C;T) red shading
rs4680(A;G)
rs165722(C;T)

The first and second letters are each a separate alleles, one from each chromosome. We inherit one from our mother and one from our father.

Do not go by the colors on prometehase. While they consider that MAOA (A;A) SNP good in that we are probably not "fighters", But if we are not fighters what are we? We are probably FLIGHTERS (anxiety).

The G allele makes the higher active enzyme, so that means that the A allele is slower. The slower it is the more serotonin, dopamine, and epinephrine we keep around. There is a good discusion on this here:
http://www.anthrogenica.com/archive/index.php/t-3074.html

Your MAOB is not slow, but it primarily breaks down dopamine. Not serotonin and epinephrine.

Your COMT is heterozygous and that reduces COMT activity. COMT breaks down dopamine and epinepherine.
http://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/83301

So we can assume that you are in general slower at breaking down catecholamines but probably break down more dopamine.

But I do not stop there, next we need to look at the receptors and the transporter genes of these neurotransmitters. For a good video of all this see:

But I will wait for that until after you ask any questions about MAOA MAOB and COMT.

 

[phoenix76]

I enjoyed the videos but am still unclear about the alleles--which one is the fastest speed, slowest speed, recessive, etc. I see that there are A, C, G, T types. I keep finding other aspects of genes during searches. So I am not sure if things are this cut and dry for which types are fast vs. slow.

I understand that COMT reduces speed and has an affinity with dopamine and adrenaline.
MAO speeds things up and -A likes serotonin and -B likes dopamine and adrenaline.
I am not sure if this applies to everyone or people who have some mutations but I learned that MAO speeds things up pre-synaptically and COMT slows things down post-synaptically and this can lead to a build of too much neurotransmitters in the synapse--anxiety, tremors, Raynaud's (?--thought that was interesting), etc. Do I have this right? Is there something that I have not mentioned that is important to know?

I wonder what these plant nutritional treatments are that the speaker alluded to but did not explain...perhaps cofactors? =o)

I do feel as if I have had to become a fighter and more assertive but I am not always comfortable with it...other times I am. But I definitely can get revved up. I can see that both of my parents do not like conflict and avoid it rather than confront it. Also, I can see that when I do get stressed or disappointed, it sticks around a lot longer than say my husband, who seems to be able to shrug stuff off better. I know men who are like and women you are not...so it is not just gender here...it is genes and environment.

So what would you like to share going forward? Thanks again. Hope you are having a great day!

 

[phoenix76]

also...on another note, what is the talk of methyl donors and certain gene mutations? I found what looks like a good resource for methyl donors on some of my value at http://www.knowyourgenetics.com/media/pdf/Simplified Protocol.pdf

and this is what it shows as a cofactor for B12 (hydroxy b12 and adenosyl b12)--pure encapsulation carries this. Sometimes when I take B healthy vitamins by emerald, I can feel a little bit too energized for a while and then it tapers off--it has all the b vitamins and I like this. But if there is something better for me, I am willing to take what could work better for me--not just because it looks good on a label.

 

[Valentijn]

What is the difference between the first and second letters? Some of mine match up and others are different.

The letters are your two alleles for each SNP. If they're the same, they are homozygous. If they're different, they are heterozygous.

rs1799836(A;G) red shading
rs4633(C;T) red shading

Both alleles are extremely common for each of these. So by being heterozygous for each, you have the most common version of each. Hence it would be inaccurate to say either gene is "slow" or "fast". They're both the most normal version available.

Some people theorize that they impact tolerance of methyl donors in supplements, such as methylB12. But a great many of people tolerate or don't tolerate methyl donors in a manner which is contrary to that theory. The only way to really know if methylB12 will be tolerated is to try it.

 

[ppodhajski]

What @Valentijn keeps confusing is Allele Frequency and Genotype Frequency..While any SINGLE allele may be common, the Genotype, meaning the combination of the TWO allele may be less common even though the single allele is common. And I feel this is why she thinks every genotype is "common" and does not matter.

In fact, when we look at the Genotype distribution of rs1799836 we can see that Valentjn is absolutely wrong, that in fact, AG is the LEAST common genotype even though both of those alleles are common.

I would not say that what looks like an 18% Genotype distribution is common.

Why is this? Because there is no heterozygous combination for this SNP in men because MAO is only carried on the X chromosome.

For the COMT SNP, your Genotype does appear more often, in about 45% of the population, but.to say that these SNPs do not reveal any fast of slow activity flies in the face of the voluminous research on the subject and it saddens me as well because the research has exactly to do with FM pain.

Pain sensitivity in fibromyalgia is associated with catechol-O-methyltransferase (COMT) gene
http://onlinelibrary.wiley.com/doi/10.1002/j.1532-2149.2012.00153.x/abstract
According with previous research, our findings revealed that haplotypes of the COMT gene and genotypes of the Val158Met polymorphism play a key role on pain sensitivity in FM patients.

I want to say as well that it is curious to me that she choose to focus on those that particular COMT SNPs and left the rest out. Because if she looked at ALL the COMT SNPs when would see the relevance, ie rs4680 above.

And for MAOB rs1799836,
Genetic Variants of Neurotransmitter-Related Genes and miRNAs in Egyptian Autistic Patients
http://www.hindawi.com/journals/tswj/2013/670621/
Plasma MAOB activity was significantly reduced in G than in A allele carrying males.

But why do I look at these genes in CFS and FM? Because the researchers do as well:

A comparison of classification methods for predicting Chronic Fatigue Syndrome based on genetic data
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2765429/
Candidate genes
In the present study, we only focused on the 42 SNPs as described in Table Table22[18]. As shown in Table Table22[18], there were ten candidate genes including COMT, corticotropin releasing hormone receptor 1 (CRHR1), corticotropin releasing hormone receptor 2 (CRHR2), MAOA, MAOB, NR3C1, POMC, solute carrier family 6 member 4 (SLC6A4), tyrosine hydroxylase (TH), and TPH2 genes. Six of the genes (COMT, MAOA, MAOB, SLC6A4, TH, and TPH2) play a role in the neurotransmission system [8]. The remaining four genes (CRHR1, CRHR2, NR3C1, and POMC) are involved in the neuroendocrine system [8]. The rationale of selecting these SNPs is described in detail elsewhere [8]. Briefly, most of these SNPs are intronic or intergenic except that rs4633 (COMT), rs1801291 (MAOA), and rs6196 (NR3C1) are synonymous coding changes [8].

 

[Valentijn]

What @Valentijn keeps confusing is Allele Frequency and Genotype Frequency.

I know the difference.

While any SINGLE allele may be common, the Genotype, meaning the combination of the TWO allele may be less common even though the single allele is common. And I feel this is why she thinks every genotype is "common" and does not matter.

In fact, when we look at the Genotype distribution of rs1799836 we can see that Valentjn is absolutely wrong, that in fact, AG is the LEAST common genotype even though both of those alleles are common.

Seriously? Fine. For WOMEN, of which the poster is one, the heterozygous type is by far the most common. And 49.6% of women are heterozygous with CT, while 29.5% are homozygous with TT, and 20.9% are homozygous for CC. The heterozygous CT variation is by far the most common variation for females with two X chromosomes.

And of course, 45.7% of men are hemizygous for C and 54.3% of men are hemizygous for T, but I'm not sure why you think that is pertinent. Perhaps you could explain why you think hemizygous male variations are at all relevant in the current thread, where a female forum member was asking for information about her specific situation? Personally I find it preferable to stay on point and avoid detailed information which is completely irrelevant to the questions being asked.

I would not say that what looks like an 18% Genotype distribution is common.

Well, as long as SNPedia is your primary source of information, don't expect to get an in-depth understanding of anything. At any rate, the heterozygous version is the most moderate. Not "fast", and not "slow". And even if it were the slow or fast homozygous or hemizygous versions, that wouldn't mean a helluva lot. The body manages to cope pretty well with either version, as evidenced by the billions of people walking around without any obvious problems.

And ... 18% of 7 billion people is still 1,260,000,000 people who have exactly the same genotype. I'd say that's pretty damned common.

Pain sensitivity in fibromyalgia is associated with catechol-O-methyltransferase (COMT) gene
http://onlinelibrary.wiley.com/doi/10.1002/j.1532-2149.2012.00153.x/abstract
According with previous research, our findings revealed that haplotypes of the COMT gene and genotypes of the Val158Met polymorphism play a key role on pain sensitivity in FM patients.

1) Don't quote a paper unless you have full access to it. Abstracts give a partial picture at best, and it's often a misleading one. 2) You forget to mention this bit, which says that only those homozygous for the "A" allele report increased pain:

FM patients were more sensitive to experimental pain than healthy volunteers and, in particular, FM individuals with the met/met genotype (Val158Met SNP) or the HPS-APS haplotypes showing higher sensitivity to thermal and pressure pain stimuli than patients carrying the LPS haplotype or val alleles (Val158Met SNP).

I want to say as well that it is curious to me that she choose to focus on those that particular COMT SNPs and left the rest out. Because if she looked at ALL the COMT SNPs when would see the relevance, ie rs4680 above.

It's the version which is not causing problems, according the abstract of the paper you cited.

Most of what you say involving SNPs is consistently complete nonsense. I recommend taking classes in understanding research papers, statistics, genomics, and bioinformatics. I've found them all to be very helpful in understanding a complex subject, and all are available for free via Coursera.

 

[Valentijn]

What @Valentijn keeps confusing is Allele Frequency and Genotype Frequency.

I know the difference.

While any SINGLE allele may be common, the Genotype, meaning the combination of the TWO allele may be less common even though the single allele is common. And I feel this is why she thinks every genotype is "common" and does not matter.

In fact, when we look at the Genotype distribution of rs1799836 we can see that Valentjn is absolutely wrong, that in fact, AG is the LEAST common genotype even though both of those alleles are common.

Seriously? Fine. For WOMEN, of which the poster is one, the heterozygous type is by far the most common. And 49.6% of women are heterozygous with CT, while 29.5% are homozygous with TT, and 20.9% are homozygous for CC. The heterozygous CT variation is by far the most common variation for females with two X chromosomes.

And of course, 45.7% of men are hemizygous for C and 54.3% of men are hemizygous for T, but I'm not sure why you think that is pertinent. Perhaps you could explain why you think hemizygous male variations are at all relevant in the current thread, where a female forum member was asking for information about her specific situation? Personally I find it preferable to stay on point and avoid detailed information which is completely irrelevant to the questions being asked.

I would not say that what looks like an 18% Genotype distribution is common.

Well, as long as SNPedia is your primary source of information, don't expect to get an in-depth understanding of anything. At any rate, the heterozygous version is the most moderate. Not "fast", and not "slow". And even if it were the slow or fast homozygous or hemizygous versions, that wouldn't mean a helluva lot. The body manages to cope pretty well with either version, as evidenced by the billions of people walking around without any obvious problems.

And ... 18% of 7 billion people actually is very common. That's in excess of 1.26 billion people.

Pain sensitivity in fibromyalgia is associated with catechol-O-methyltransferase (COMT) gene
http://onlinelibrary.wiley.com/doi/10.1002/j.1532-2149.2012.00153.x/abstract
According with previous research, our findings revealed that haplotypes of the COMT gene and genotypes of the Val158Met polymorphism play a key role on pain sensitivity in FM patients.

1) Don't quote a paper unless you have full access to it. Abstracts give a partial picture at best, and it's often a misleading one. 2) You forget to mention this bit, which says that only those homozygous for the met

I want to say as well that it is curious to me that she choose to focus on those that particular COMT SNPs and left the rest out. Because if she looked at ALL the COMT SNPs when would see the relevance, ie rs4680 above.

And for MAOB rs1799836,
Genetic Variants of Neurotransmitter-Related Genes and miRNAs in Egyptian Autistic Patients
http://www.hindawi.com/journals/tswj/2013/670621/
Plasma MAOB activity was significantly reduced in G than in A allele carrying males.

But why do I look at these genes in CFS and FM? Because the researchers do as well:

A comparison of classification methods for predicting Chronic Fatigue Syndrome based on genetic data
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2765429/
Candidate genes
In the present study, we only focused on the 42 SNPs as described in Table Table22[18]. As shown in Table Table22[18], there were ten candidate genes including COMT, corticotropin releasing hormone receptor 1 (CRHR1), corticotropin releasing hormone receptor 2 (CRHR2), MAOA, MAOB, NR3C1, POMC, solute carrier family 6 member 4 (SLC6A4), tyrosine hydroxylase (TH), and TPH2 genes. Six of the genes (COMT, MAOA, MAOB, SLC6A4, TH, and TPH2) play a role in the neurotransmission system [8]. The remaining four genes (CRHR1, CRHR2, NR3C1, and POMC) are involved in the neuroendocrine system [8]. The rationale of selecting these SNPs is described in detail elsewhere [8]. Briefly, most of these SNPs are intronic or intergenic except that rs4633 (COMT), rs1801291 (MAOA), and rs6196 (NR3C1) are synonymous coding changes [8].[/QUOTE]

 

[ppodhajski]

I know the difference.

Seriously? Fine. For WOMEN, of which the poster is one, the heterozygous type is by far the most common. And 49.6% of women are heterozygous with CT, while 29.5% are homozygous with TT, and 20.9% are homozygous for CC. The heterozygous CT variation is by far the most common variation for females with two X chromosomes.

And of course, 45.7% of men are hemizygous for C and 54.3% of men are hemizygous for T, but I'm not sure why you think that is pertinent. Perhaps you could explain why you think hemizygous male variations are at all relevant in the current thread, where a female forum member was asking for information about her specific situation? Personally I find it preferable to stay on point and avoid detailed information which is completely irrelevant to the questions being asked.

Well, as long as SNPedia is your primary source of information, don't expect to get an in-depth understanding of anything. At any rate, the heterozygous version is the most moderate. Not "fast", and not "slow". And even if it were the slow or fast homozygous or hemizygous versions, that wouldn't mean a helluva lot. The body manages to cope pretty well with either version, as evidenced by the billions of people walking around without any obvious problems.

And ... 18% of 7 billion people is still 1,260,000,000 people who have exactly the same genotype. I'd say that's pretty damned common.

1) Don't quote a paper unless you have full access to it. Abstracts give a partial picture at best, and it's often a misleading one. 2) You forget to mention this bit, which says that only those homozygous for the "A" allele report increased pain:

It's the version which is not causing problems, according the abstract of the paper you cited.

Most of what you say involving SNPs is consistently complete nonsense. I recommend taking classes in understanding research papers, statistics, genomics, and bioinformatics. I've found them all to be very helpful in understanding a complex subject, and all are available for free via Coursera.

You said all of that without one reference or citing anything but your own opinion. You can make up all those numbers and ideas but they mean nothing. While you say these genes are not important scientists seem to keep studying them.

I have access to the full research articles, do you? If you did you would know I cannot post non abstracted portions. And yet while you tell me to not make assumptions based on an abstract, you make assumption from an abstract. =^/

You push my buttons, I admit, I see what you are doing but I cannot explain it and I can only hope others can see through it. If it is not a misunderstanding I would have to say it is manipulative to say 18% is common in a population because 1 billion people have it. I would say that the 82% who do not have it are be MORE common. But that is the trick with that word you use,"common", it means nothing in statistics, it is a squishy word that lawyers love to use. Yes, you can say that 18% is common, but 82% is more common. And if you said to anyone on the street that 18 out of a hundred was more common than even 40 out of a hundred they would certainly laugh at you. The problem with "free courses" online is that they do not give grades...

It is funny that use use that 18% number and toss it away as "common: and "unimportant". Did you know that 18% of the people in the U.S. also have an anxiety disorder? (This is the part where I cite, like a scientist and a researcher, and look! It is a full paper!)
http://sites.oxy.edu/clint/physio/article/Epidemiologyofanxietydisorders_Michael_2004.pdf

Hmmm, I wonder if MAOB is implicated in anxiety disorders? Well, i better not put up a link because it will not be good enough.

But all my understanding would mean nothing if I was not better. I am better. Are you? If you can HELP ME explain why my understanding lead to a treatment that worked 100% for me I will welcome it. Can you help me understand WHY you think FMN was pivotal in my recovery getting rid of my OCD and Anxiety and CFS and chronic pain? Can you help me understand WHY when I lowered dietary amines a lot of my other issues vanished? Otherwise your comments are just making noise and are not helpful.

 

[Valentijn]

But all my understanding would mean nothing if I was not better. I am better. Are you? If you can HELP ME explain why my understanding lead to a treatment that worked 100% for me I will welcome it. Can you help me understand WHY you think FMN was pivotal in my recovery getting rid of my OCD and Anxiety and CFS and chronic pain? Can you help me understand WHY when I lowered dietary amines a lot of my other issues vanished? Otherwise your comments are just making noise and are not helpful.

I have ME. Not OCD or anxiety or CFS. This is an ME forum. I don't know or care if or why you think something helped you with something else.

And one guy's opinion on the internet is not a reputable source. Especially when he persists in displaying a stunning lack of understanding regarding the basics of genetics and research.

 

[ppodhajski]

I have ME. Not OCD or anxiety or CFS. This is an ME forum.

This is also a CFS forum. See the banner at the top of the page?

I don't know or care if or why you think something helped you with something else.

You don't care. Got it. Your not caring adds no value. If you do not care I suggest you stop responding and making noise with citeless responses. From now on I will do my best to stop responding to you, but not because I don't care, it is because I see that you do not care that I care.

http://pro.psychcentral.com/psychia...ephalomyelitis-andor-fibromyalgia/001226.html
There are 3 common patterns of syndrome comorbidity between ME, FM, and psychiatric conditions. The patterns can be identified by their temporal relationship.

Antecedent (comorbid) psychiatric condition. Patients can have antecedent depression or anxiety—the psychiatric symptoms predate the onset of physical symptoms, often by many years. In these cases, the psychiatric and physical conditions respond independently to treatment. The comorbid psychiatric condi-tions respond to the usual recommended psychiatric and psychological treatments.

Coincident psychiatric condition. Although rare, in some patients, such as Ben (Case 2), psychiatric symptoms develop concurrently with the onset of ME or FM. In these patients, the psychiatric condition seems to be a part of the physical symptom constellation and all the symptoms vary in parallel. For example, on a bad energy or pain day, mood or anxiety will always be worse. These patients are difficult to treat because the psychiatric conditions do not generally respond to common psychiatric treatments. The focus needs to be on improving physical health. This is best accomplished through symptom management.16 Improvement in psychiatric symptoms will be concurrent with physical improvement.

Grief/secondary depression/anxiety. The most common psychiatric/psychological symptoms in patients with ME and FM are feelings of grief and worry due to multiple life losses and uncertainty about the future. These symptoms develop after the onset of physical symptoms, often when the chronicity of and losses due to the conditions become clear. Grief and worry lessen with improved physical health. Psychological support and psychiatric treatments are indicated if symptoms are severe.

 

[Valentijn]

This is also a CFS forum. See the banner at the top of the page?

Yeah, because ME isn't an official diagnosis in the US. But when people refer to ME/CFS, they are referring to something which includes PEM. Not chronic fatigue.

You don't care. Got it. Your not caring adds no value. If you do not care I suggest you stop responding and making noise with citeless responses. From now on I will do my best to stop responding to you, but not because I don't care, it is because I see that you do not care that I care.

I don't care about some things. But I do care when you repeatedly report blatant misinformation and your personal speculations as if they were fact. For example, your inability to understand a pretty straight-forward abstract which directly contradicted your interpretation of it.

http://pro.psychcentral.com/psychia...ephalomyelitis-andor-fibromyalgia/001226.html
There are 3 common patterns of syndrome comorbidity between ME, FM, and psychiatric conditions. The patterns can be identified by their temporal relationship.

Again you are referring to a paper which does not say what you seem to think it does. The author is discussing the existence of psychiatric conditions unconnected to ME, or occurring in reaction to ME. It does not suggest that they are somehow related in a special manner, beyond what would be seen in relationship to any other chronic illness.

 

[phoenix76]

Very interesting posts...I am not sure what to say. I am wondering if this volley has occurred before in other threads between the two of you. I have studied enough research in my career area of psychological science. Have studied neuropsychology, memory, learning, etc. for over 15 years. Even wrote a thesis. Research is never 100% correct and have to keep some skepticism.

Anyhow, I felt like I was getting somewhere in learning about genetics--an area completely new to me. But I really do not want battles breaking out. I know people become very emotionally invested in their information that they share--passionate--especially if the have seen a change for the better--this comes through in my therapy practice toward my clients so I get it.

At this point can we continue with learning about genetics 101? Are there any good reference books out there as well? I like the YouTube videos as well. Thanks for what has been shared so far.

 

[Valentijn]

At this point can we continue with learning about genetics 101? Are there any good reference books out there as well? I like the YouTube videos as well. Thanks for what has been shared so far.

Coursera has some good options regarding both basic and more advanced genetics topics, for free.

 

[phoenix76]

Thanks. I will check into it...along with all the other recommendations people have offered. I am not sure if this is a gut issue or not...or if supplementing with cofactors will help. I am willing to try things out but want to be as informed as possible. I will say this...Ayurveda's food combining has worked for me. Sugar after a meal--whether fruits, fruit juices, or desserts are disastrous for me depending on how much sugar is consumed. It is better to eat fruit alone and follow up with a protein 15 minutes later so that blood sugar does not go crazy OR eat it first in any meal (this goes for a little dessert as well). Sugar can be mind clogging as well...That's my $.02.

I have seen things get ugly in the name of research in the schools in which I have worked...correlation does not mean causation. And I have also found that everything is interconnected in some way--perhaps everyone is right! Have a great day =o)

 

[phoenix76]

@ppodhajski---how's it going? I enjoyed watching the youtubes and seeing how MAO-A and -B work with COMT. What is next in the line up of information that you are willing to share? The student is here...

Thanks again...and have a great evening.

 

[phoenix76]

seeketh out @caledonia and peruse her links.

Thanks pogoman for reaching out to me earlier on ... I am catching up with my thanks you today! Where can I find such links? Take care.

 

[ppodhajski]

@ppodhajski---how's it going? I enjoyed watching the youtubes and seeing how MAO-A and -B work with COMT. What is next in the line up of information that you are willing to share? The student is here...

Thanks again...and have a great evening.

Let me know what you have questions about and we will go from there!

 

[ppodhajski]

The letters are your two alleles for each SNP. If they're the same, they are homozygous. If they're different, they are heterozygous.


Both alleles are extremely common for each of these. So by being heterozygous for each, you have the most common version of each. Hence it would be inaccurate to say either gene is "slow" or "fast". They're both the most normal version available.

http://forums.phoenixrising.me/index.php?threads/when-common-snps-matter.39635/