Defining Treatment Aims for Methylation, MTHFR and Pyroluria

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Defining Treatment Aims for Methylation, MTHFR & Pyroluria

So you've tested a patient for MTHFR SNPs and for Mauve Factor/Kryptopyrroles. What now?

Methylation and Pyrroles are hot topics in integrative medicine, yet controversy surrounds both their clinical significance and the best way to treat patients who have demonstrated aberrant biochemical results.

In today's podcast, Belinda Reynolds takes us through the complexities, the realities and the traps which practitioners sometimes find themselves in when oversimplifying these seemingly simple biochemical "wheels."

Covered in this episode

[01:38] Welcoming Belinda Reynolds
[02:10] What is methylation?
[11:17] Health concerns associated with inadequate folate
[16:30] Homocysteine metabolism
[24:04] What tests should we be using? 
[29:48] What are pyrroles and how do they fit into the picture?
[36:06] Treatment options

Andrew: This is FX Medicine, and I am Andrew Whitfield-Cook. Joining me in the studio today is Belinda Reynolds, who's a dietitian with over 15 years experience in the integrated medicine industry. She is an acclaimed senior educator with BioCeuticals, who regularly presents to audiences throughout Australia and New Zealand, and she's known for her practical and easy style, bringing complex biochemical processes into an easily digestible format, with practical clinical applications. Welcome, Bel.

Belinda: Thank you, Andrew. Great to be here.

Andrew: Belinda, today we're going to be discussing some highly topical issues, such as methylation, histamine, SNPs, and pyrroles. And we're going to try and shed some light as to the practicalities of treating patients with these disorders because I think people can get caught up in compounds rather than what happens in the body. So, Belinda, firstly, can you take me through just, what are we dealing with here, with regards to that thing called methylation?

Belinda: So, methylation in itself is a huge area, and I think what people have become very focused on at the moment is the MTHFR SNP, or the single nucleotide polymorphism, on the gene that encodes for the MTHFR enzyme. And as a result, we're developing a huge concern over certain supplements, people are moving away from certain things and believing that they're dangerous, when potentially that's not so much the case. And we're also, I think, at times losing sight of the big picture. I think that looking at the SNP is certainly warranted, and we definitely need to take it into account when we're looking at our patients, but we need to look beyond this, and also analyse the patient to determine how much the presence of that SNP is actually impacting their health, and then treat accordingly.

Andrew: Yeah. I think you said a crucial thing there, and that was, "The MTHFR is an enzyme." And the whole problem is that people have a gene mutation, whereby this enzyme doesn't work. And I think people get caught up on the compounds rather than the enzymes.

Belinda: Yeah, I think that does happen, and there's an idea that if you do have the MTHFR SNP that you're not producing any of the enzyme at all, which isn't actually the case. There's just simply a reduced expression of that enzyme. 

Andrew: Yeah.

Belinda: So, what we need to do is really take a step back and have a look at what else is going on. 

Andrew: Yeah.

Belinda: So, rather than simply just test for the MTHFR SNP, it's really important to look also at factors that can be impacted by this. So, look at homocysteine levels. We know that the function of the MTHFR enzyme is to reduce 5,10-Methenyltetrahydrofolate to the active form of folate, which is 5-MTHF. The 5-MTHF acts as a methyl donor, donating a methyl group to homocysteine to convert it to methionine. And that then, as a result, keeps homocysteine levels under control. If we have an MTHFR SNP, and therefore a reduced functioning of that enzyme, we can get lower than ideal levels of that active folate, and as a result, homocysteine can accumulate.

Andrew: Build up. Yeah.

Belinda: Yeah. So measuring homocysteine can be a good indication of how significantly someone is being impacted by the presence of that gene SNP in their body. However, if the homocysteine is identified to be elevated, we need to also be mindful of the fact that the MTHFR SNP isn't the only thing which could be contributing to that homocysteine elevation.

Andrew: Yeah.

Belinda: There’s an enzyme which catalyzes the donation of the methyl group from 5-MTHF to the homocysteine, and that enzyme is methionine synthase, and it's dependent on the presence of methyl B-12. 

Andrew: Yeah.

Belinda: So, we could have a methyl B-12 deficiency, which is actually in fact what is impacting the homocysteine levels. So, we really do need to be looking at a variety of different factors, not getting bogged down in one individual thing.

Andrew: I think the important thing for our listeners to try and conceptualise is that there's a lot of circular patterns here, if we like, circular enzyme systems. And I say "circular" to conceptualise it, right? And what happens is, these circles are integrated in a way that they're sort of like, if you can imagine, cogs of a watch…

Belinda: Yep.

Andrew: …or a machine, running together to turn some greater hand, some greater movement, some greater machine. So, these intertwine, these work together. It's not one entity.

Belinda: No.

Andrew: It's very often all of the entities. And although you might have a problem with one or more of these enzymes, these nutrients are still, as Bob here says, famously, they're biological spare parts. And I think this is one of the premises of nutritional medicine, is using these biological spare parts to, at wild, we need to bluster our way through, and at other wild, we need to really ease back, if there's an issue there. Because some people can say, "Oh, I'll just use methyltetrahydrofolate." Well, that can still cause a problem if your cogs aren't working. Is that right?

Belinda: Yeah. So, I think there's definitely the idea, and it's quite correct in most situations, that MTHF, which is the actual active form of folate, is the best thing to use for people with an MTHFR SNP. And this makes total sense… 

Andrew: Yeah.

Belinda: …because what you're putting into the body is a purely active form, and you're bypassing the need for the MTHFR enzyme in one step.

Andrew: Yeah.

Belinda: So, what you have there is active folate, which is able to donate its methyl group onto homocysteine. However, once the MTHF has donated its methyl group to the homocysteine to yield methionine, you have tetrahydrofolate, which then is required to be re-methylated to form the 5,10-Methenyltetrahydrofolate, which then needs to be reduced again by the MTHFR enzyme before it can become MTHF, to ultimately go through that process again. So, it's really important that we're aware that although, yes, you are putting the active form of folate into the body, it's only able to perform its functions of donating a methyl group once, and then you're back at the beginning again, and it becomes a similar form to that which your other forms of folate are similar to. So, we need to be ensuring that we're supporting all aspects of that folate cycle, not simply just putting in the active form of folate.

But, when we look at comparing folic acid to folinic acid to MTHF, I think it's definitely correct that MTHF is the superior form. But we also need to be aware of the fact that it's not the be-all and end-all. And we need to be considering, is there enough B-12? And do we need to supplement with the methyl B-12 if there's a gut issue going on which is impacting someone's ability to absorb their B-12 from their diet? Do we need to look at other nutrient levels? So for example, vitamin B-6 is important for the methylation of tetrahydrofolate, to yield the 5,10-Methenyltetrahydrofolate. We also need to ensure that we have sufficient levels of vitamin B-2, because MTHFR function is reliant on vitamin B-2. So, if we're ensuring that there's a good nutritional status overall, we're going to assist that folate cycle in its ability to continue to turn.

And it's interesting when you mentioned, we really need to look at enzymes, because so many enzymes in the body rely on sufficient zinc, sufficient magnesium, B-6, also selenium. So, we need to make sure that all of those essential co-factors are available so that our enzymes are functioning. We need to make sure that we don't have a buildup of potentially toxic heavy metals in the body, which can push co-factors like zinc out of their enzyme...

Andrew: Out. That's right.

Belinda: ...and replace them. Like binding to the thiol group in that enzyme and efficiently destroying the functioning of that enzyme. So, mercury and copper are some...

Andrew: Cadmium.

Belinda: Yeah, cadmium, are some really good examples of that. So, when we're looking at somebody who appears to have issues with their methylation, who has elevations in homocysteine, are expressing symptoms of this under-methylation or elevated histamine-type mood disorders or other functional problems, we need to not just be looking at the one nutrient, although, yes, you'll likely get a very good improvement in their symptoms with that nutrient. But, if we're going to really look at addressing their health overall, we need to be addressing multiple factors which could be contributing to their ill-health.

Andrew: So let’s… I want to take this to a population, sort of, arena, if you like, and concentrating on three issues that are commonly associated with folate problems. First one is, cardiovascular disease with homocysteine. The second one is the poster child, if you like, of folic acid supplementation, and that's protection against neural tube defects. The other one is a very controversial one, and that's a potentially raised incidence in cancers, especially bowel cancer. Very controversial and not proven. And not in all studies. Otherwise, they would cease folate supplementation overnight.

So the first one is cardiovascular disease. And there was a very good study, I think it was around about 2005, 2006, that showed, in somebody who has stable angina, forgive me if this is wrong, I'm trying to remember, but in somebody who has preexisting cardiovascular disease, lowering the homocysteine is not going to help them. And the basic analogy for that is similarly, if you already have somebody with a cleft palate, giving them folic acid is not going to get rid of that cleft palate. The damage is done. The horse has bolted. So, in that instance, where there's already preexisting disease, homocysteine becomes a marker that something is wrong, rather than a target for somebody to hit, to lower it. It's not going to help them.

Belinda: Mm-hmm.

Andrew: The cleft palate issue is, getting back onto that, is protection, not treatment. That's an obvious one. But then moving over from that is the wholesale supplementation, at least in Australia, certain other countries as well, with all breads fortified with folic acid except organic breads. And then there was a couple of controversial studies showing that there might be an increased risk of cancer. But if that was so glaringly obvious, we wouldn't be doing it. So, is it only in those sub-populations who have a gene SNP? And is it like, if...people are purporting that, at minimum, 30% of the population's got a gene SNP. It can't be 30% of the population that's getting cancers. So, how big is that issue?

Belinda: Yeah. I think it's something that we still don't completely understand. When you look around at the evidence that's there, there's a lot of conflicting evidence. There's so many studies which support the safety and the benefit of folic acid. When we did start fortifying foods with folic acid, we did see a reduction in the incidence of spinal tube defects, and that was a really positive outcome. What we're starting to see now though, however, is the potential that over-consumption of these foods, together with supplementation of folic acid, is potentially contributing to some imbalances in the system, and I guess it's that whole idea that too much of a good thing isn't necessarily a good thing.

Andrew: On its own.

Belinda: Yeah. So, it's an example of one of those things where we've looked at one nutrient…

Andrew: Yep.

Belinda: …and decided that that's going to solve our problem. And we're suddenly just started fortifying foods and supplementing people with that one nutrient, rather than paying attention to what's going on as a whole. And I think when we've looked at studies that show a great incidence of certain conditions, based on a high intake of foods that are fortified with folic acid, what really is the issue there? Is it the folic acid in itself? Or is it the types of foods that they're consuming? The foods that are rich in folic acid are generally highly processed, often stripped of their nutritional value, and they're taking up space in the diet, which may otherwise be filled with natural folate-rich foods.

So, folic acid is synthetic. There's no folic acid which exists naturally in our food sources. It's an artificial form of folate which has been added into our food supply. And potentially, there's the theory that it's competing for uptake into the cells against the natural folates that do exist in our food and are more easily utilised. So I think, again, we need to take a step back and look at that big picture…

Andrew: Yep.

Belinda: …and understand what really is the problem. Is it the consumption of the wrong types of foods? 

Andrew: That’s right.

Belinda: Is it too much of one particular nutrient without us providing all of the other nutrients which support its function in the body and keep those cogs turning? So, yeah, I think it's something that we...there's more research that needs to be done. We need to gain a better understanding of what is happening. But what we really need to do right now is, again, look at that big picture and get back to the very basics.

Andrew: Talking on that point of, you know, how do we metabolise homocysteine, how do we affect its level? There was a dose-ranging study done in 2005. Now, the author is, actually it's a group, the Homocysteine Lowering Trialists' Collaboration. And it's called "The Dose-Dependent Effects of Folic Acid on Blood Concentrations of Homocysteine: A Meta-Analysis of the Randomized Trials." And I remember they talked about in there that adding B-12 in there only gave, you know, like a 3% additive effect. So it was basically folic acid and B-6 that had the major effects. And if you think about the cogs, it sort of makes sense and sort of doesn't.

Belinda: Yeah.

Andrew: You think, "Hmm. How can B-12 isn't having more of an effect?"

Belinda: So, B-6 is actually involved in a few different steps there. So, not only is it involved in the assisting in the activation of folate, but it's also involved in the transsulfuration pathway, as well, so it helps...

Andrew: And that's what gets rid of the compounds, if you like, out of the cycle, and helps it to actually be turned a "antioxidant" glutathione.

Belinda: Yep. Yes, and serine plays an important role there too.

Andrew: Serine as well.

Belinda: So, yeah. I guess it's a matter of what that population were more deficient in, too. I guess they could have been a population who were more deficient in B-6 than they were in B-12. But, yeah, and it can depend on at how many different points that particular nutrient is essential for the control of homocysteine. But if you looked at another parameter, you may have found a more significant improvement after the addition of the B-12. So, probably depends on what you're looking at, and the population.

Andrew: That would be a very interesting thing for our listeners to give us some feedback on. If they have any information on maybe some trials that were done on certain sub-populations with certain SNPs, maybe they could followup FX Medicine on Twitter or Facebook, or indeed the FX Medicine page, and give us some feedback or enlighten our other practitioners with that research. That'd be lovely.

Belinda: Yeah, that'd be great. Yeah. For sure.

Andrew: So, what about histamine? Now, this is something that really gets me. I am not up with this.

Belinda: I'm still learning as well.

Andrew: Aren't we all? But, please teach me. Let's go.

Belinda: I mean, histamine, we generally think of to be something that's released from mast cells in response to an allergic-type reaction. But a lesser-known fact, to some people at least, is that it's a neurotransmitter. 

Andrew: Yep.

Belinda: And it plays a number of different roles in our sense of alertness, and our arousal, and even our sensation of pain. And what could happen is that, if we have issues in the functioning of our methylation cycles, that can lead to changes in histamine levels.

So, methyl groups RM or SAMe, is involved in the metabolism of histamine. So if we have, say an MTHFR SNP, or for some reason we have an issue of under-methylation, where homocysteine is accumulating due to the body's inability to convert that homocysteine to methionine, which would then, via a number of different steps, be converted to SAMe, which would go on to assist with histamine metabolism, that will lead to a histamine accumulation, and it can contribute to a variety of different mental concerns and other symptoms as well.

But we also need to be mindful of the fact, too, that there are other enzymes involved in histamine metabolism, such as the DAO enzyme, or diamine oxidase. So, it's another one of those things where if people observe an elevation in histamine, they may automatically assume it's an under-methylation issue. But that may not be the case. We need to consider what else might be going on for that individual, of course, we also need to consider the mast cell immune dysfunction side of things.

And on the flip side of that, I guess too often, people will see the MTHFR SNP and make an assumption that someone will be high in histamine because they're not producing sufficient active folate, and therefore there'll be the assumption that we have a deficiency of SAMe, and therefore an accumulation of histamine. But it is worth actually checking that, because what can happen is that, within any individual we can have thousands of different SNPs on different genes encoding for different enzymes. 

Andrew: Yep.

Belinda: And yes, someone may have an MTHFR SNP, but they may also have a variety of different SNPs on enzymes involved in the utilisation of SAMe. For example, the conversion of the SAMe to creatine.

Andrew: Yep.

Belinda: I learned this from a Dr. Bill Walsh seminar, actually. And what he was discussing was the fact that there then is a push and pull between the SNPs. So we've got an issue where, yes, there's something which would suggest an under-methylation issue on one side…

Andrew: Yeah. 

Belinda: …but there's a number of other SNPs which are actually contributing to potential issues with over-methylation on the other side.

Andrew: Ah.

Belinda: So, someone could have the MTHFR SNP, but still be an over-methylator, because what SAMe that is being produced isn't being efficiently utilised, and is accumulating and contributing to different problems, such as the over-metabolism of histamine, which causes that to drop. But then you're actually getting a depletion of, or a reduced production of creatine, for example. 

Andrew: Right.

Belinda: So, there's a broad variety of different responses you can get based on what combination of SNPs you have occurring in your body. On the other hand, if you were to only look at histamine, and you saw that histamine was low, you may think, "Oh, that person's an over-methylator, I better not give them any SAMe…”

Andrew: Yep.

Belinda: “…or I better not give them any methyl folate, because that could create a problem." But copper is also involved in histamine metabolism, so it could be a copper excess, which is contributing to that low level of histamine. And we know copper excess to be a common culprit in a lot of mood and anxiety-type concerns. Copper can actually bind to the GABA receptor and act as an antagonist there. That's why providing lots of zinc is great, because it can displace copper from that receptor and enhance GABA functioning. The copper also is involved in the conversion of dopamine to noradrenaline and adrenaline. So, it can lead to anxiety-type issues there as well.

So, it's important that we're, again, considering all potential aspects. So, if someone has histamine issues, yes, consider MTHFR as a culprit, but also consider other aspects of methylation, consider certain toxicities, consider what's going on in the immune system, and what other potential SNPs are sort of interacting with that issue.

Andrew: You know, one of the things...I'm just thinking, when you were saying all of this, I'm just thinking two things. First one is, does that lead us to either over-test? You know, test for copper, test for all the SNPs in the body, test for this. And where does that clinically lead you? Or, do you just throw up your hands and do nothing, no testing, and do what we always did, and that was, you treat responsibly?

Belinda: Yep. I...

Andrew: What I think's interesting as well is that, looking at high histamine foods, you know, and I'm trying to, in my mind, trying to draw a picture with this folic acid supplementation cancer thing. And I'm just wondering, wouldn't it be interesting if anybody out there has looked at histamine-rich foods, like fermented beverages, wine, champagne, beer...

Belinda: Cheeses.

Andrew: ...cheeses, fermented foods, even sauerkraut, vinegar. Those people that might have an adverse reaction to vinegar, a real adverse, not just, you know, the stifling reaction of the taste, but something like soy sauce gives somebody a really truly adverse reaction. Cured meats, the bacon, the things...and then, I'm not going to lead into it now, but I'm just going to mention it. When you're talking about these cured meats, bacon, salami, pepperoni, luncheon meats, hotdogs, have just recently been implicated as the worst foods for an increase...or the worst meats for an increase in cancer. 

Belinda: Hmm.

Andrew: Hmm. Are we then talking about an inability to, not just metabolise folate, but over-dose, if you like, on histamine? And we can't use it? Where does that lead us all? So, what's your opinion of how to test, and what are appropriate tests? And then where do you lead from that? Where do you go from that?

Belinda: Look, I think it's's an individual thing. It's very much determined by the patient that you're presented with, their situation, what they're able to spend on testing. I think that testing certainly does play a really important role because it can help to confirm your suspicions. I've often heard Beth Bundy make mention of the fact that people love to see themselves in colour, and you often get a better buy-in from the patient…

Andrew: Yep.

Belinda: …and better compliance when they've actually seen on paper that this is what is happening with them. But it also can give you a baseline, too, so that you can remeasure after a number of months, and show the patient what they've achieved by working well with you.

Andrew: But you're not going to be changing a SNP. So…

Belinda: Sorry. So that' the SNP, that's a separate thing. So the SNP won't change, but if you do take a measure of homocysteine or whole blood histamine or look at folate levels and B-12 levels, those things can certainly change for the better with a good treatment-type program.

Andrew: I think in all of this, we know that medicine is going to be genomically testing things. They already are for certain things, like tamoxifen, I've banged on about this heaps. There's certain other things, where they're...certain other SNPs where they're looking at mainly CYP enzyme interactions, where they're looking at personalised medicine for drugs. That's going to be a fact in medicine. And so, I think it can give any practitioner an idea of what is there. Then you have to take, "Okay, what's going to be my treatment, or my management of that? And how am I going to measure that objectively? Now, as a baseline, and in the future to address change?"

Belinda: Yes. And I think to take it on just as one part of your process of diagnosis, and determining what sort of intervention, because how the patient is presenting is one of the best ways to really give an indication of what needs to be addressed, and simply talking with them and finding out what issues are the biggest concern for them, it can help give you an idea of what aspect of their health that you need to prioritise. But, it's also important too, that people themselves don't get fearful of seeing these genetic SNPs that they have. 

Andrew: Yeah.

Belinda: I think people think, "I have MTHFR. I'm going to get cancers. I'm at a greater risk of all of these terrible diseases." And it's important that we're also educating the patients well to help them understand that this is just giving us an indication of how best to proceed with your particular case. 

Andrew: Yeah.

Belinda: Everyone has different SNPs within their body that can potentially increase their risk of different illnesses, but the most important things is the epigenetic factors, and what our diet and our lifestyle is doing to influence the expression of different genes in our body. So it's important that we're focusing more on the dietary, the intervention, the lifestyle changes more so than getting bogged down and fearful of the presence of any particular gene issue.

Andrew: Bel, I've got to say, you're awesome. Thank you so much for taking all of our listeners through that, because you really cleared so much up for me.

Belinda: Yeah, and's an area that's, you know, our knowledge is growing still. So I know that I definitely have more learning to do. I think we all do.

Andrew: We all do.

Belinda: But it's definitely an interesting topic to discuss.

Andrew: I've often said, anybody who thinks they know everything about a subject, please hang up your shingle and go and do something else. You've just turned arrogant. This all is changing.

Belinda: Yeah.

Andrew: We're learning more and more each day. Let's go on to another topical point, and that is pyrroles. And this ties into this methylation issue, but it's got some particular attributes on its own. What are we talking about here?

Belinda: Yeah. So, with pyrroles, there's, again, this is another area where there's limited evidence. A lot of what we know is based on sort of anecdotal evidence or research which is being done by practitioners who specialise in the field. So, what I'll be discussing is based on their findings that I've learned from watching seminars, but also from reading what papers there are available.

But, what it seems is that what pyrroles, or hydroxyhemopyrrolin, is something which is produced by the body naturally, but due to potentially a gene SNP or due to a lot of oxidative stress in the body, there's a greater production of that. It is normally released within the bile into the gut. If you have the presence of leaky gut, or just due to normal processes of re-circulation, those pyrroles, or the HPL, enters into the bloodstream. It's quite efficiently excreted by the kidneys.

So, the pyrroles themselves don't really create a huge issue. The problems associated with high pyrroles, and the conditions which tend to stem from it, occur due to the fact that the pyrroles in the blood, or in the body, bind zinc and vitamin B-6. And as they're excreted via the kidneys and the urine, they're taking that zinc and that B-6 with them. Therefore, the higher the pyrroles in the body, the higher the pyrroles in the urine, the greater the loss of zinc and the greater the loss of B-6.

The issue is that zinc plays an important role in gastrointestinal integrity. So, as more zinc is lost, gastrointestinal integrity is further diminished, you get a greater re-absorption of the pyrroles, pyrrole levels go up, excretion of the pyrroles go up, zinc loss goes up, and it becomes quite a nasty self-perpetuating cycle.

Andrew: Mmm.

Belinda: We know that a good amount of zinc is important to protect against copper toxicity. So what you can potentially develop is elevated levels of copper, which compromise healthy GABA functioning, which result in greater production of noradrenaline and adrenaline, and low dopamine. Zinc is essential then, not only for protecting against that copper accumulation, but it's also an important promoter of brain-derived neurotrophic factor, which protects our serotonergic neurons from damage and assists with neuroplasticity. So, you're also contributing to a greater risk of depression and cognitive decline if this is allowed to persist over a long period of time. 

Further to that, the deficiency of B-6 can impact your healthy methylation, but B-6 is also important for healthy GABA synthesis. So, as you can start to understand is that, what will end up happening as a result of these high pyrroles, we get a lot of the potential for the development of anxious-type disorders, an inability to relax and calm down after a stressful event, potentially depression, potentially long-term cognitive decline. But due to the importance of zinc for the immune system, for gut integrity, we can get immune dysfunction, because of B-6 role in healthy methylation, we can get methylation problems.

And down the track, that could also potentially even contribute to oestrogen-dominant type problems. We know that zinc deficiency can contribute to elevated aromatase activity, which can lead to a greater buildup in oestrogen. We often see high copper with high oestrogen, and we also know that oestrogen is metabolised to a degree via the methylation pathway.

Andrew: Yep, yep.

Belinda: And in addition to that, if we have, say, dysbiosis in the gut occurring at the same time as this pyrrole issue, you'll get a greater production of beta-glucuronidase, which can actually cleave oestrogen from its conjugate in the bowel. That combined with the leaky gut, which is commonly associated with pyrroles sees free oestrogen reentering into the circulation.

Further to that, you have an increased passage of LPS, which initiate inflammation. That pushes up aromatase activity and contributes to sort of systemic inflammatory issues, which activate the HPA access, and you actually get quite a messy situation.

Andrew: And the normal proliferative actions of oestrogen, which, as you know, if you have a long, or prolonged, non-cyclical level, or, that's probably an incorrect term, an increased circulating level of oestrogens, without getting rid of them, then you have that additive proliferative action, which can lead to cancers. Hmm, folic acid cancers.

Belinda: Yeah. It really start to see how it all interacts, and no matter what situation you're dealing with, you do need to consider methylation. We do need to make sure that that process is functioning properly. But, MTHF, yes, is probably the best form of folate that we can give, generally, and your methyl B-12 is probably the best form of B-12 you can give. B-6 is absolutely essential there as well, we can't forget B-6's importance. 

Andrew: Yep.

Belinda: You mentioned the homocysteine study earlier, that B-6 had a more significant impact on returning homocysteine levels to normal than the B-12 did. But we also need to consider the zinc. We need to consider our gut health. We need to ensure the absence of dysbiosis. We need to be encouraging people to take part in mindfulness, and meditation, and gratitude, in order to try and actively pull themselves out of that sympathetic dominant-type state.

Andrew: Yeah. Absolutely.

Belinda: So, it doesn't matter what issue you're talking about...

Andrew: And wasting of minerals.

Belinda: Yeah.

Andrew: Rather than being esoteric about, you know, lovely feelings, I'm always thinking about it on a biochemical level. If you're increasing stress hormones in your body, you're weeing out minerals, and B vitamins with them.

Belinda: Yeah. And magnesium, and, yeah.

Andrew: Yeah. So, what I think's interesting though, is looking at the Australian Bureau of Statistics, and this was for something that I did quite...separate for this, I was just very interested in following this up. So this is the Australian Bureau of Statistics, ABS, Australian Health Survey, Usual Nutrient Intakes, 2011-2012.

And I picked out just a few graphs of zinc, B-6, magnesium, and iron. And iron, we know, it's a real issue. You know, around about 8% of people don't have enough iron. Usually women show up as being more deficient as men, because men don't have a way, a physiological way of getting rid of iron. And the only reason that women do is because they menstruate. So, snapshot of iron, just because I mentioned it, is if you look at the graph you see that it's an issue up until really when menstruation ceases, and then it's no issue. That's iron out of the way. But the big ones I see here are zinc, B-6, and magnesium. 

Belinda: Mm-hmm.

Andrew: And the graphs are huge. And they just have an upward trend, from childhood into adulthood. More males are zinc deficient than females, more females are B-6 deficient than males, but males and females are both highly deficient in magnesium. This is just a hugely disproportionate amount of people in Australia who aren't getting enough of these extremely basic components, that run 200, 300 enzymes in our body. Hmm.

Belinda: Yeah. And it's no surprise then that...

Andrew: I think we have to start back at food.

Belinda: Yeah. Yeah.

Andrew: You know?

Belinda: We need to improve our diet, and then, like as you said, address the stress which is contributing to the increased excretion of these nutrients from the body.

Andrew: Absolutely, the wasting of them.

Belinda: Yeah.

Andrew: And then you're talking about oestrogens before, and what's a way to get rid of oestrogens is to increase fibre, which, unfortunately, can sometimes bind to zinc. So, it's this...

Belinda: It's a balancing act, isn't it?

Andrew: It's a real balancing act. But, we certainly need more fibre in our diet.

Belinda: We do.

Andrew: That's for sure. So I think as a treatment type thing, we really need to be concentrating on starting digestion…

Belinda: Yep.

Andrew: …having a good, balanced, healthy diet, and I disagree with the Standard Australian Diet, but a healthy diet, with loads of nutrient-dense, calorie-poor, plant-based foods.

Belinda: Mm-hmm. Agree.

Andrew: Less red meat. What else?

Belinda: We also, I think we need to really focus on the health of the microbiome. So, probiotics are really important there. We haven't even touched the sides or gotten close to what we...

Andrew: No. Touched the sides?

Belinda: Yeah.

Andrew: Sorry. Pun. Microbiota bowel. Touch the...okay.

Belinda: We haven't even gotten a full understanding of what these...

Andrew: No.

Belinda: ...microbes can do for our health. And so it's really important that we're ensuring that that microbial diversity. And we also need to consider supplementing, where it's necessary. I think would be great if we could get all of our nutrients from our diet. The reality is, most people aren't very compliant with their diet. The sources of our foods that we have available to us are often deplete of a lot of different nutrients that are very essential for us. And in a lot of cases, supplementation can be necessary...

Andrew: Yeah, that's practical.

Belinda: ...when people are presenting with these real health issues, which are impacting the quality of their life. So, if we're focusing on the pyrroles, the gut healing, the fibre, the good diet, the probiotics, but also some zinc and B-6, and also magnesium supplementation is important.

Consider the potential presence of high copper. You may need to help turn up detoxification processes, and it is really important that we're addressing that sympathetic dominance as well, and helping people to calm down and relax, and find some coping mechanisms that can help calm them down. Because when we are in a sympathetic state, and when we're adrenally overworked, that actually turns down our detoxification processes.

Andrew: Yep. Absolutely.

Belinda: So, our cellular...

Andrew: It's part of digestion.

Belinda: Yeah. Our normal detoxification and antioxidant defence mechanisms that our cells are equipped with simply aren't functioning effectively enough.

Andrew: We're trying to get away from the lion.

Belinda: Yeah. We're running away from those lions, as opposed to focusing on detoxification. So, I think definitely zinc, magnesium, B-6. And then considering detox, addressing stress, and just also taking a step back and looking at what other approaches are required for that particular individual's current state of health.

Andrew: Belinda Reynolds, fantastic practical aspects that you bring to treating what can ostensibly seem over-complicated and just overwhelming to many practitioners. And I do totally agree with you, that we really are at the tip of the iceberg, with regards to, you know, gene SNPs and where we have to go with methylation, and what it means to bring about a change in patients' health. And I urge practitioners, yes, you know, if you're interested in it and certainly if you think there's a clinical need, do a gene test, where it's appropriate.

But I think we also have to fundamentally be looking at a basement and a treatment measure of some objective parameter, that we can say, "My treatment definitely worked," to improve the health of the patient.

Belinda: Yes. I agree.

Andrew: So thank you once again for taking us through that.

Belinda: Thanks so much for having me. It's great to be here again.

Andrew: This is FX Medicine, and I'm Andrew Whitfield-Cook.

Belinda Reynolds is a dietitian and Education Manager at BioCeuticals. She graduated with an Honours Degree in Nutrition and Dietetics, and has been involved in the complementary medicine industry for over 15 years. Her key interests are immune modulation, the human microbiome and the impact they have on overall health.



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FX Medicine is at the forefront of ensuring functional and integrative medicine gains the recognition it deserves and ultimately establishes itself as an integral part of standard medical practice. Hosted by Andrew Whitfield-Cook, our podcasts are designed to promote research and evidence-based therapeutic practises, acting as a progressive force for change and improvement in patient health and wellbeing.