Dr. A explains how MTHFR gene variants affect your body's ability to detoxify, balance hormones, and regulate mood. The video covers which genetic mutations matter most, why adding methyl donors without testing related genes like MTRR and CBS can backfire, and how addressing methylation improves outcomes in some patients.
You really want to support everybody instead of just one thing. So this is why I don't advocate people just guessing they've got a problem and then taking a bunch of methyl donors because you're going to jack up one part of the cycle that might have breakdowns elsewhere. I'm Dr. A. I use this YouTube channel to answer questions. Been involved in research and teaching for over 30 years now in medicine, especially in the naturopathic and integrative space. And I've been seeing patients a long time who have chronic illness. And I've actually done human research around MTHFR. So I'm just going to give you a big picture here, and I promise you we're going to do other content on genomic single nucleotide polymorphism mutation, et cetera. So MTHFR is methylene tetrahydrofolate reductase. It's an enzyme, and enzymes are things that help you go from one form of a molecule to another. Generally, what MTHFR does is it helps with the methyl cycle, and the methyl cycle is is critical for giving what we call methyl donors for making new cells, running nucleotide metabolism, and a whole bunch of other things really. So when people talk about, I have an MTHFR defect, what they're really saying is that there's something about their coding to make the enzyme that's different. So when you have SNP, single nucleotide polymorphism, it means that you don't have the native or wild-type pair of genes to make the MTHFR. MTHFR enzyme, of which there are many, and you either inherited one or 2 single nucleotide polymorphisms that then came down from your parents, and now you have 2. And if somebody has normal MTHFR gene activation, they're both the wild type or normal nucleotides, so they code normally. If you have one that doesn't work and one that does work, it decreases the function of that enzyme about 25 or so percent. If you have 2 that don't work, it decreases it 50 to 65% or And so when people say they have a SNP in MTHFR, that's what they mean. So then it means that the enzyme that codes for this transfer to help with methylation is slower. Now, as I said, there's a bunch of MTHFR SNPs. The ones that seem to be the most biochemically important in human physiology anyway are 2, and they have different numbers on them. And we'll do other content on the, all the, you know, getting into the weeds of the specifics. But if you have a higher grade defect, so 1 or 2, to heterozygous or homozygous, then what happens is your ability to transfer in the methyl cycle decreases. Quick plug here, if you're a healthcare practitioner working with patients with these issues, I have a CE website and I do webinars on this topic and others. So we're going to put a link in the description below to the CE website link and the particular webinar of interest. Thank you. In the human research we did that I will talk about in a separate thing, the punchline was in a chronic fatigue community of people, if you had MTHFR and you had one gene that was not good in the critical one, then you would have about a 20% increase in therapeutic outcome with chronic fatigue if you treated that. If you had 2 genes in the critical one, you would have up to a 75% increase in treatment outcome by treating your methyl cycle and getting it normal. Now, that sounds great. So sometimes people will say, well, then why doesn't everyone just go and take methyl donors, which is the treatment? Well, the reason is if you methylate normally and you take a bunch of methyl donors, you might get really overstimulated because methylation triggers the formation of a ton of things, some of which are your excitatory neurotransmitters. So your brain might wake up and be going a little bit too fast. The other thing is, is if you don't need extra methyl donors, it's just going to be overstimulating to your body. So you do have to be thoughtful about this. Now, the other part of this, and we'll get more into this in other content, but it's MTHFR is the famous gene because It was one of the first ones that was tested widely. It was one of the first SNP patterns that were outlined. My human research with it was about, gosh, 13 years ago now. And some very critical groundlaying research in psychiatry was done at the same time. I had communication with those researchers as well, and very, very important. So we've known about it not that long in human history, but you know, it's been around. What you need to remember for safety and also for the big picture is you have SNPs all over in your body. If you look at a SNP There can be tens and tens of thousands of data points there. Well, that's going to be a little bit overwhelming, but just in the methyl cycle, you have other enzymatic— it's a cycle. So MTHFR is kind of the name brand one that helps you to get the folate, the active folic acid created, but it goes in a cycle and there's MTRR, there's, there's many other, you know, BHMT, there's all sorts of other checkpoints along the way. And so what we found is after we did just, you know, pure MTHFR research, What we found clinically moving forward, once the technology to test these things became more affordable, is if you're going to mess with your methyl cycle, you're better to know all of it. So is everything else fine and it's just MTHFR? Then you can probably get away with a little bit of support for methylation. But what if the interface between the methyl cycle and the thiol cycle, which is CBS, cystathionine beta-synthase, what if that's broken? And then you hypermethylate, you're going to get stuck down here at CBS because it's down below that in the cycle. Or what if the BHMT is broken? Well, then you're going to get stuck there. So you really want to support everybody instead of just one thing. So this is why I don't advocate people just guessing they've got a problem and then taking a bunch of methyl donors, because you're going to jack up one part of the cycle that might have breakdowns elsewhere. Now, as I said, we're going to do a bunch of other content on this. We'll get into what are the other checkpoints of the cycle and what do they need. What they need are largely other B vitamins and some minerals to help them run. And we'll also get into therapeutically How do we interact with the methyl cycle in a safe way that is not overstimulating and helps balance out these natural slowdowns that we inherit? All right, Dr. A, thank you for listening. We'll put some other content for you to see and stay tuned for other genomic methylation, et cetera, content. See you on the next one.
