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Maybe some know about this gene mutation than I do. I've heard about it but have ignored it pretty much.
One thing I can say, my integrative MD started testing my homocysteine levels (related to heart disease) about 3 yrs ago and my levels were elevated...so for 3 yrs I've been taking a Homocysteine Formula which includes Methyfolate, B12, TMG. My homo levels are coming down.
A person on another health group finally found out she has the MTHFR mutation gene. She has a history of depression. And some other health issues. This person is on a food based drug Deplin which is high in Methyfolate but I believe it's much too high a dose she is taking. I think so many doctors don't know how to treat these mutations. Or maybe don't even know about them.
Maybe some know about this gene mutation than I do. I've heard about it but have ignored it pretty much.
One thing I can say, my integrative MD started testing my homocysteine levels (related to heart disease) about 3 yrs ago and my levels were elevated...so for 3 yrs I've been taking a Homocysteine Formula which includes Methyfolate, B12, TMG. My homo levels are coming down.
A person on another health group finally found out she has the MTHFR mutation gene. She has a history of depression. And some other health issues. This person is on a food based drug Deplin which is high in Methyfolate but I believe it's much too high a dose she is taking. I think so many doctors don't know how to treat these mutations. Or maybe don't even know about them.
Anyone up on this.
I am up on it. The link between MTHFR and depression is there but taking Deplin (5-MTHF) for is is just silly.
MTHFR uses FAD as a cofactor. what that means is that the more FAD you have in your body the faster that enzyme will work. It seems people with this variant need more FAD to make their MTHFR enzyme work well. Also, for each milligram of folate that they eat they will loose more FAD than someone without the variant. so eventually the will become FAD deficient. Since FAD is used as a cofactor for other enzymes in the body, soon they will experience other issues,
Also, if the enzyme runs slow it will produce less NADPH, which is used in the antioxidant cycle. So low MTHFR means low glutathione which means more H2O2 which means more depression.
Back to 5-MTHF and FAD. So if MTHFR is slow we can do two things. One is to just add the product, 5-MTHF (Deplin). That will kind of work but we did not solve the real problem, not enough FAD to make the MTHFR run faster. FAD is made from riboflavin, so to make more FAD we need to take more riboflavin (B2) and magnesium (magnesium helps turn B2 into FAD). Taking B2 will speed up MTHFR and the body will make the exact amount of 5-MTHF it needs and you will not have to guess and pay a ton of money for it. And it is shown in studies that B2 helps speed up MTHFR. Here are all the studies to prove it. And you will see in these studies how riboflavin lowers homocysteine.
Yet doctors keep prescribing the overpriced Deplin instead of just giving people the extremely cheap and effective B2. I wonder why that i$?
I have that variant as well and I take B2 and it helped a lot. You might want to check out my blog.
Moderator cut: link removed, read our terms of service
Thanks and I take some B's but get low amounts of B2 so I just ordered some. I had to look up FAD. Very interesting...and don't get me started on the drug $$... I'll be checking into your blog. I will share your info with the Deplin taking person. J
Such a crime and so many dying. Thinking of my own sister who has taken mega drugs from her MS specialists for the "slowing of the MS", this is what they have told her, and her condition has so advanced. She's even lost her vocal chords and can barely speak.
Yes, the fact that MTHFR SNPs do not always lead to high homocysteine is well know. If you knew the pathways it would make sense.
Those of us who study nutrigenomics know its role in concert with other gene variants however. The body is a symphony, not a solo act.
You seem to be missing the point of the article. Many people with various polymorphisms still produce adequate amounts of the enzyme. They need no treatment.
The simplest thing to do is measure homocysteine. If it is not elevated, nothing needs to be done. If it is, then supplementation with B6, B12, and folate can be offered. Looking for MTHFR polymorphisms is not even necessary.
Last edited by suzy_q2010; 03-13-2016 at 09:26 PM..
[quote=suzy_q2010;43347544]You seem to be missing the point of the article. Many people with various polymorphisms still produce adequate amounts of the enzyme. They need no treatment.
The simplest thing to do is measure homocysteine. If it is not elevated, nothing needs to be done. If it is, then supplementation with B6, B12, and folate can be offered. Looking for MTHFR polymorphisms i, this is still me, the o Moderat
I did not miss the point.
MTHFR variants decrease enzyme activity
Quote:
There are two commonly recognized polymorphic variants in the gene encoding for this enzyme: the “thermolabile” variant c.665C→T (p.Ala222Val), histori-cally more commonly referred to as C677T, and the c.1286A→C
(p.Glu429Ala) variant; both are missense changes that are known to decrease enzyme activity.
And that, when giving them folic acid homocysteine did not decrease homocysteine. (This is silly and I will talk about it later)
Quote:
a meta-analysis of homocysteine-lowering trials did not find evidence that supplementation with B vitamins, including folic acid,
So they conclude that it is useless for two reasons. One, that if has no DIRECT effect on venous thromboembolism alone.
Quote:
The American Congress of Obstetricians and Gynecologists does not recommend the measurement of homocysteine or MTHFR polymorphisms in the evaluation of the etiol-ogy of venous thromboembolism.
Why? Because...
Quote:
Because MTHFR polymorphism is only one of many factors contributing to the overall clinical picture, the utility of this testing is currently ambiguous.
So your see, MTHFR variants are only ONE gene in a BIG genetic pathway that can effect homocystiene levels and even high homocystene is not even a 100% cause for VT.
But the part about giving folic acid to MTHFR variants is just bad science. The cofactor that increases MTHFR activity is FAD, which is a derivative of Riboflavin. Now what happens when they give these people Riboflavin?
(Yes, giving people folic acid for MTHFR was probably making them worse because it creates a FAD deficiency which is used as a cofactor for so many other enzymes.)
http://www.clinchem.org/content/49/2/295.short
Effect of Riboflavin Status on the Homocysteine-lowering Effect of Folate in Relation to the MTHFR (C677T) Genotype
Although previously overlooked, homocysteine is highly responsive to riboflavin, specifically in individuals with the MTHFR 677 TT genotype. Our findings might explain why this common polymorphism carries an increased risk of coronary heart disease in Europe but not in North America, where riboflavin fortification has existed for >50 years.
http://nfsr.sbmu.ac.ir/browse.php?a_..._lang=fa&sid=1
Although the precise mechanism linking this polymorphism to hypertension remains to be established, it would appear that the biological perturbation, which leads to higher blood pressure in individuals with MTHFR 677TT genotype, is modifiable by correcting the variant MTHFR enzyme through enhancing riboflavin status.
Listen, there is so much bad information out there about Nutrigenomics right now, and even many scientists do not understand how to apply it. There is a deep truth out there if you keep studying it.
Last edited by in_newengland; 03-16-2016 at 03:36 AM..
You seem to be missing the point of the article. Many people with various polymorphisms still produce adequate amounts of the enzyme. They need no treatment.
The simplest thing to do is measure homocysteine. If it is not elevated, nothing needs to be done. If it is, then supplementation with B6, B12, and folate can be offered ...
I did not miss the point.
MTHFR variants decrease enzyme activity
And that, when giving them folic acid homocysteine did not decrease homocysteine. (This is silly and I will talk about it later)
So they conclude that it is useless for two reasons. One, that if has no DIRECT effect on venous thromboembolism alone.
Why? Because...
So your see, MTHFR variants are only ONE gene in a BIG genetic pathway that can effect homocystiene levels and even high homocystene is not even a 100% cause for VT.
But the part about giving folic acid to MTHFR variants is just bad science. The cofactor that increases MTHFR activity is FAD, which is a derivative of Riboflavin. Now what happens when they give these people Riboflavin?
(Yes, giving people folic acid for MTHFR was probably making them worse because it creates a FAD deficiency which is used as a cofactor for so many other enzymes.)
Effect of Riboflavin Status on the Homocysteine-lowering Effect of Folate in Relation to the MTHFR (C677T) Genotype
Effect of Riboflavin Status on the Homocysteine-lowering Effect of Folate in Relation to the MTHFR (C677T) Genotype
Although previously overlooked, homocysteine is highly responsive to riboflavin, specifically in individuals with the MTHFR 677 TT genotype. Our findings might explain why this common polymorphism carries an increased risk of coronary heart disease in Europe but not in North America, where riboflavin fortification has existed for >50 years.
http://nfsr.sbmu.ac.ir/browse.php?a_..._lang=fa&sid=1
Although the precise mechanism linking this polymorphism to hypertension remains to be established, it would appear that the biological perturbation, which leads to higher blood pressure in individuals with MTHFR 677TT genotype, is modifiable by correcting the variant MTHFR enzyme through enhancing riboflavin status.
Listen, there is so much bad information out there about Nutrigenomics right now, and even many scientists do not understand how to apply it. There is a deep truth out there if you keep studying it.
Most "MTHFR variants decrease enzyme activity".
Yes, but most still result in sufficient activity. Decreased does not mean absent. The mere presence of a variant does not mean it is clinically significant and needs treatment.
Folic acid does decrease homocysteine in subjects with MTHFR variants and increased homocysteine:
"We conclude that after folic acid fortification in the US, measurement of tHcy (total homocysteine) rather than genotyping of MTHFR 677TT should be used as the primary assay for the diagnosis and monitoring of moderate hyperhomocysteinemia."
If you look at the entire riboflavin study you cite, which was done in the UK, their final conclusion is
"In conclusion, our results indicate a high prevalence of riboflavin deficiency in our study population and suggest that riboflavin status could be compromised further by folate supplementation in the absence of additional riboflavin."
In short, that was probably not an ideal population to study.
In addition, the clinical benefit of lowering homocysteine levels, even in conditions for which high levels are associated with increased risk, has yet to be established.
This all came to me since homocysteine levels are elevated when my MD started testing about 3 yrs ago. The levels have been coming down and I need to get them tested this year.
Then it became more interesting when another person found she did have the MTHFR mutation.
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