MAO-A Fast And the Carbohydrate Rollercoaster

MAO-A is an enzyme that has the power to determine a lot of who you are, and the gene SNPs that change its activity have additive effects, just like the COMT gene SNP that we spoke about previously, The various SNPs add up to give you either fast or slow action.

MAO-A stands for Monoamine Oxidase A, and it is a breakdown pathway for your monoamine neurotransmitters, which means serotonin, dopamine, and norepinephrine. Unfortunately, those three little things, serotonin, dopamine, and norepinephrine, determine so much of how you feel and act in the world.

An interesting aside about the MAOA gene that we mentioned last week as well: most of the genes SNPs we talk about are linked to regular chromosome pairs, meaning there are two functioning copies of each one. The MAO-A gene is X-linked, meaning that it sits on the X chromosome or chromosomes that are responsible for physiological gender determination. Men have only one copy of the MAOA gene and women have two, but one is silent. On women’s genetic tests there is no way to tell which copy of the MAO-A gene is active and which is silent so symptoms are the best place to look.

Fast MAO-A means that breakdown of the neurotransmitters is faster than average, therefore levels of these neurotransmitters are lower than they would be in a person with the wild-type genetics.

Low neurotransmitters is a challenge that people tend to self-medicate, and in this case the easiest and most available self-medication is carbs. Carbohydrate foods are an amazing short-term boost to neurotransmitters, but it really is very short-lived. Sadly, this method fails spectacularly in the long run.

The Carbohydrate Rollercoaster

The carbohydrate rollercoaster is a pretty familiar place for a lot of people. You feel down, or blue, maybe hopeless or even just bored. You know you shouldn’t reach for a cake or chocolate bar, but it’s like you can’t help yourself. You eat the twinkie and feel a burst of goodwill and hopefulness that pretty soon transitions into guilt for packing another twinkie in the saddle bags. Your mood gets darker and soon enough, you’re reaching for a ho-ho to ease the pain. You might even wake up in the middle of the night and need a snack to fall back to sleep.

I’m exaggerating for comic effect, but surely some of you out there recognized your own all too painful cycle. This sad cycle is an easy reality to fall into with a fast MAO-A picture, but in good news, if you know it’s MAO-A it is also reasonably easy to get out of.

What You Can Do To Balance A Fast MAO-A

One of the key factors with a fast MAO-A is helping your psychology and physiology stay balanced, and there are a number of things that can help you to do that.

  • Balanced B vitamins – for a slow MAO-A we talked about how important riboflavin is, but for a fast MAO-A we want to make sure you’re gettin all the Bs and not too much riboflavin, which will make this enzyme even faster.
  • Complex carbs and protein – Instead of the starch and sugar rollercoaster, the most important thing you can do is to get three regular meals that are high in complex carbs and protein for stable blood sugars and neurotransmitters. This type of carbs, which includes whole grains and lots of fiber, digest slowly and so keep a steady stream of serotonin coming rather than the peaks and valleys that quick carbs produce.
  • Remove stressors – Stress is not your friend with any MAO-A imbalance. Life has lots of stressors, but a lot of them are self-imposed. Let go of the food sensitivities, the blood sugar ups and downs, the toxic friends, and any extra jobs or tasks that you’ve picked up that don’t need to be there. Do a stress edit on your life.
  • Boost your Glutathione – We’ve talked for ages about this so check out Season 1, Episode 14: MTHFR and Glutathione, and Season 2, Episode 32: Glutathione Review. Glutathione helps to decrease inflammation and reduce some of the negative side effects of burning through neurotransmitters too quickly.
  • Eliminate Food Sensitivities – Eating foods that your body is sensitive to raises your inflammation, which in turn drives your body to make more stress hormones and pushes the peaks and valleys of your neurotransmitter levels even higher .
  • Meditate – Meditation is one of the most effective non-drug methods of balancing neurotransmitters with any kind of gene SNPs. Even something as simple as 3 minutes of mindfulness meditation daily can have huge results over time.
  • Watch your warning signs – With a fast MAO-A you know you’re not keeping the right dietary balance when you’re’ waking up in the middle of the night hungry, or when your emotions are pushing you to the pantry for that sweet treat. If you see these warning signs, make sure your next meal has plenty of complex carbs, a moderate amount of protein, and good fats to feed your neurotransmitters.
  • Boost your tryptophan Intake – Tryptophan is the precursor to serotonin and melatonin and the tryptophan that crosses into the brain most easily is found in complex carb-heavy foods. Keep snacks with a good balance of complex carbs and protein at hand to stabilize blood sugars and give you a steady flow of tryptophan. Think yogurt, oatmeal, nuts and seeds, or some turkey slices rolled in iceberg lettuce.

Thanks so much for listening and great news this week! The Beta test group for MTHFR Live is going to start in early July and enrollment is secretly open now, but I won’t advertise that to anybody but my listeners for a week so that you have a chance to get in. The Beta test version is 75% off the regular price, plus if you enroll in the free course, MTHFR Basics, you can have a coupon for an additional

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MAO-A Slow and Your Short Fuse

MAO-A is an enzyme of singular importance, and the gene SNPs that alter its activity have additive effects, just like the COMT gene SNP that we spoke about some months ago, to produce either fast or slow action.

MAO-A stands for Monoamine Oxidase A, and it is the primary breakdown pathway for your monoamine neurotransmitters, which means serotonin, dopamine, and norepinephrine. I’m hoping just that tiny introduction is raising red flags in your thoughts because those three little things, serotonin, dopamine, and norepinephrine, determine so much of how you behave, feel, and present in the world.

An interesting note about the MAOA gene – most of the genes SNPs we’ve talked about are linked to regular chromosome pairs, meaning there are two functioning copies of every gene. This particular gene is X-linked, meaning that it sits on the X chromosome or chromosomes that are responsible for physiological gender determination. This means men have only one copy of the MAOA gene and women have two, but one is silent. In women’s genes there is no way, from a genetic report, to tell which copy of the MAO-A gene is active so symptoms are the best place to look.

As with COMT that we spoke of before, MAO-A slow means that breakdown of the neurotransmitters is slow, therefore levels of these neurotransmitters are higher than they would be in a person with the wild-type genetics.

High neurotransmitters sounds amazing, right? Extra serotonin – who doesn’t want that? Well, as with everything else in health, the key factor here is balance. Excess is not balance.

Neurotransmitters are one of the ways you respond to life and the things around you. If neurotransmitters are too high, that can lead to too much response.

Signs of a Slow MAO-A and Signs of Excessive Neurotransmitters

  • Irritability or aggression in a heartbeat – swift acceleration from 0 to 100 on the anger scale.
  • Jumpy, anxious, easily startled
  • Difficult to calm down or regulate moods after stress, anger, or excitement.
  • General anxiety or irritable mood.

The hallmark here is rapid escalation that is difficult to normalize.

What You Can Do To Balance A Slow MAO-A

One of the key factors with a slow MAO-A is helping your psychology and physiology to calm down, and there are a number of things that can help you to do that.

  • Riboflavin – Make sure you’re getting enough riboflavin or vitamin B2. MAO-A needs this vitamin as a cofactor.
  • Blood sugars – Stabilize your blood sugars with three regular, higher protein meals per day with no sugary drinks or snacks in between.
  • Remove stressors – Stress is not your friend with a slow MAO-A. Life has lots of stressors, but a lot of them are self-imposed. Let go of the toxic friends, the extra duties at work that aren’t actually going anywhere, the projects you think you should do but don’t actually want to. Do a stress edit on your life.
  • Boost your Glutathione – We’ve talked for ages about this so check out Season 1, Episode 14: MTHFR and Glutathione, and Season 2, Episode 32: Glutathione Review. Glutathione helps to decrease inflammation and reduce some of the hydrogen peroxide caused by high stress hormones.
  • Eliminate Food Sensitivities – Eating foods that your body is sensitive to raises your inflammation, which in turn boosts stress hormones. The goal with a slow MAO-A is to keep stress hormones under control.
  • Meditate – Meditation is one of the most effective non-drug methods of balancing neurotransmitters with any kind of gene SNPs. Even something as simple as 3 minutes of mindfulness meditation daily can have huge results over time.
  • Step Away From The Trigger – Because of the tendency to explode into anger or irritability, if you encounter a situation that causes anger, instead of fully engaging and boosting your neurotransmitters even more, step away. Take a brisk walk for a few minutes, do some jumping jacks in your office, or even just take a few minutes to look at a painting you love or listen to a song that makes you happy. Once you’ve used this technique a few times, you’ll figure out what works for you.
  • Reduce your tryptophan Intake – Tryptophan is the precursor to serotonin and is mostly found in protein-heavy foods. Often, people with a slow MAO-A will crave carbs, but eating too many carbs is like dousing the angry fire with gasoline. It isn’t the best idea. Make sure your meals are protein heavy and carb-lite.

Next week, we’ll talk about the corollary MAO-A fast picture. Thank you so much for listening today and if you are looking for an amazing community of folks who are also working with their genes to get better, then Genetic Rockstars is for you. Enjoy a free two-week trial at community.tohealthwiththat.com

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Low Histamine, Gene SNPs, and MTHFR

Low histamine is generally not recognized as a problem within the medical community or even in the media, but histamine is emerging as a target in research for conditions like cancer, cardiac protection, and alzheimer’s so I think in the next decade or so, we will begin to see some talk about low histamine and not just high histamine. Histamine is there for a reason and present in different levels in different humans, so it is equally likely that there are problems from low levels just like there are from high levels.

Histamine is involved in so many things beyond the allergies we usually attribute to it.

Histamine is involved in:

  • Allergic reactions – this is the part everyone knows about.
  • Immune response
  • Opening blood vessels (or vasodilation)
  • Neurotransmission
  • Signaling within your stomach

Histamine levels depend on two factors.

  1. How much histamine is being produced – this depends on your gut microbiome, how easily your mast cells degranulate, allergies, and the action of your basophils, which are one of your white blood cells.
  2. How much histamine is being broken down – this depends on MTHFR, and two histmine-specific enzymes called DAO and HNMT.

Histamine has an incredibly diverse range of effects including:

  • Promoting wakefulness, or stopping you from sleeping all the time.
  • Constricting airways
  • Increasing stomach acid secretion
  • Modulating pain signals
  • Itch perception

Histamine interconnects with MTHFR in a couple of ways. Histamine breakdown is dependent on healthy methylation just like other monoamine neurotransmitters. Also, the HNMT enzyme needs a methyl group from SAMe in order to function. That means if you have an overactive methylation cycle, then you break down histamine more quickly than average and you are more likely to have a low histamine picture.

Keep in mind that low histamine states are one of the characteristics of the “overmethylation” basic state – these are the folks I like to call the Black Sheep. Of course, far more than just your MTHFR status goes into your histamine levels but it is still really useful for us MTHFR folks to know which side of the basic state picture we fall on. I believe this simply because the general patterns between over- and under-methylators, especially as it pertains to probable drug and supplement tolerances, are surprisingly accurate..

Gene SNPs That Affect Histamine

  1. MTHFR and other genes in the methylation pathway – including MTR and MTRR. Also, even if these gene SNPs are “wild type” (or “normal”), this can look impaired if your folate status is low, your folic acid intake is too high, or your riboflavin levels are too low.
  2. DAO – DAO is one of the major breakdown pathways of histamine and gene SNPs can cause problems.
  3. HNMT – HNMT is the other major breakdown pathway and it needs a SAMe (from the methylation cycle) in order to function.

Low Histamine Symptoms Include

  • Seasonal allergies that present as general symptoms for a season but aren’t the typical allergy picture. This could include a seasonal headache, body pain, muscle tightness, brain fog, and more long-term, non-specific symptoms. If your allergies don’t look like hay fever, but repeat seasonally and don’t feel any better with antihistamines, you might fall into this category.
  • Fatigue, lack of alertness, and difficulty feeling awake in the morning. Keep in mind there are a number of other factors involved here like the MAOA or COMT gene SNP which may lower dopamine, epinephrine and norepinephrine and that will also feel like fatigue and lack of alertness in the morning.
  • Digestive symptoms including low stomach acid and reflux related to low stomach acid, cramping, and bloating
  • High blood pressure
  • Alzheimer’s disease – this is not actually a symptom of low histamine, but an interesting association has been found specifically with low brain levels of histamine and the progression of Alzheimer’s. Raising brain levels of histamine is being explored as a new treatment strategy.
  • Increased heart damage in heart attack – new research is showing that histamine levels rise sharply in the first moments of a heart attack, and that if they don’t rise appropriately then the level of damage the heart sustains is likely to be worse.

Managing Low Histamine Naturally

Low histamine isn’t typically regarded as a problem by the medical community, but balancing histamine levels can make you feel better on a day to day basis, especially if you struggle with lack of alertness, high blood pressure for no clear reason, or low stomach acid and digestive power. If you find, like I do, that you generally feel better with high-histamine foods like aged cheeses, smoked meats, bone broth, and leftovers, then your histamine might be on the lower end of normal.

  • Eat a higher histamine diet – some foods are extremely high in histamine including alcohol, fermented foods, processed or smoked meats, aged cheeses, and shellfish. Adding those into your diet can help to boost histamine levels
  • Embrace the leftovers – food that sits for a while, like leftovers, accumulates histamine while it sits so if you generally have a low histamine picture then leftovers are great for you. Batch cook your favorite foods and enjoy for a few days.
  • Exercise exercise has been shown to boost histamine levels, which is part of your body’s mechanism to increase blood flow to muscles and to decrease pain perception. If you tend to have low histamine symptoms, exercise can be a great way to boost your numbers.
  • Boost your folate levels if you can tolerate it – histamine increases with increasing folate, and so boosting your folate levels can help to boost a flagging histamine. Just don’t flip over into a too-high histamine picture.

Thank you so much for listening today, and be sure to check out courses.tohealthwiththat.com for the Free MTHFR Basics class and to sign up so you’re the first to know about beta testing opportunities with the MTHFR for life class at 1/4 of the usual price.

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Vitamin D, MTHFR, and the VDR Gene SNPs

Like everything else we talk about, MTHFR and vitamin D have a curious relationship. Vitamin D doesn’t link into the folate cycle, the methylation cycle, or the BH4 pathway so it isn’t an obvious connection, but it’s thought to be linked through the sharply named “Folate-Vitamin D-UV Hypothesis of Skin Pigmentation.” So let’s break this down along with a couple of gene SNPs that affect vitamin D specifically.

Vitamin D

Vitamin D is a fat soluble vitamin that is sounds like a miracle in the research, helping to prevent everything from depression to cancer. It helps you build strong bones by increasing absorption and retention of calcium and phosphorus. It reduces cancer cell growth, helps control infections, and reduces inflammation. Research also found a link between high vitamin D levels and protection from the most severe consequences of Covid-19.

Research has been booming about vitamin D for the last fifteen to twenty years, and startlingly it has shown that roughly 24% of the US population is vitamin D deficient and almost 6% of the population is severely so. Vitamin D deficiency has been implicated in:

  • Autoimmune conditions like lupus and MS
  • Diseases of aging like Alzheimer’s and dementia
  • Mental health issues like schizophrenia and depression
  • Atopic conditions like asthma and eczema
  • Bone diseases like osteoporosis and rickets
  • Hormone issues like PMS and repeat pregnancy loss
  • Inflammatory conditions like IBD and tooth and gum decay
  • Other conditions like cancer, ADHD, and erectile dysfunction

Vitamin D is found in a small number of foods including egg yolk, oily fish, red meat, mushrooms, and liver. The bulk of the vitamin D in your body, however, is produced via a chemical reaction between sunlight and your skin. Specifically, it needs ultraviolet radiation on your skin.

Gene SNPs that Affect Vitamin D Levels VDR Bsm and VDR Taq.

VDR gene SNPs actually code for vitamin D receptors, so this isn’t in the manufacture of vitamin D per se, it’s in the ability to metabolize, transport, and use Vitamin D. There are other gene SNPs that are emerging for Vitamin D, but these are the most frequently studied.

VDR Taq

This gene is associated with both vitamin D levels in the blood and also with muscle growth and bone density on strength training. The CC variant, which is the wild type, is generally linked to high vitamin D levels, as well as greater muscle growth and bone density with strength training exercise. The TT variant, is associated with lower vitamin D status and less muscle growth and bone density in response to strength training. The CT form is somewhere in the middle.

BDR Bsm

This gene is associated with immunoprotection, bone mineral density, and also short stature. The wild type, or GG allele, has lower risk of bone density issues, normal stature, and more typical immunity. The AA allele has a higher risk of bone density problems, is more likely to be short in stature, and may have specific types of immune compromise. The AG allele is somewhere in the middle of those two states.

Managing VDR Gene SNPs

The relationship between these gene SNPs and pathology depends entirely on vitamin D levels, so the clear path to balancing out VDR gene SNPs lies in boosting vitamin D levels. This is where we leave solid research and enter my own musings and supposition, so take this as a well educated guess and nothing more.

The typical “normal” range for vitamin D on blood tests is broad – between 20 ng/mL and 100 ng/mL. Although there is some debate about what constitutes an optimal number, for most people I think hovering somewhere around the 40 – 50 ng/mL mark seems logical. Not too close to the lower limit, but also not pushing crazy high numbers for no reason. For people with VDR polymorphisms, I encourage numbers closer to 70-80 ng/mL simply because if your body has trouble transporting, metabolizing, or using vitamin D, then giving it a higher background level may help to compensate. Again, this is my own supposition and hasn’t been particularly well researched yet.

The complicated relationship between Folate and Vitamin D.

This is actually interesting, because it’s a departure from the usual chemical pathways that we typically talk about. Folate is sensitive to ultraviolet radiation, so the more time you spend with your skin in direct sunlight, especially on high UV-index days, the more folate is used within your skin. This happens because UV light generates free radicals within your skin, and folate acts as an acceptor for those free radicals, essentially doing the duty of an antioxidant in this situation, to help protect your vulnerable tissues from damage.

Folate also works overtime donating methyl groups to DNA that gets damaged by UV radiation, essentially helping to protect your skin from the mutations that would lead to skin cancers.

The bottom line here is that UV exposure uses up folate reserves while UV exposure generates Vitamin D.

There is a remarkable theory of human evolution, the afore mentioned “Folate vitamin D UV-hypothesis of skin pigmentation” that states that skin pigment evolved as humans migrated northward out of Africa to maximize and balance levels of both folate and vitamin D because they are both so pivotal for successful reproduction as well as overall health.

This theory states that skin pigments were concentrated and skin remained dark in areas close to the equator to buffer some of the effects of the tremendous amount of UV exposure, but still allow enough for vitamin D processing. Therefore, people with darker skin pigment actually need more sunlight exposure to manufacture enough vitamin D, and their folate is well protected by the pigments. People who migrated northward were becoming vitamin D deficient due to lack of adequate UV exposure and so evolution favored lighter skin pigments that require less UV exposure to make adequate vitamin D, but that also leave folate more vulnerable to UV-related breakdown.

Vitamin D and MTHFR – A Supportive Relationship?

Because of the contrary relationship between folate and vitamin D with UV exposure, it’s becoming a research target. An interesting study published in the journal neurology, found that in children with ADHD, which has known linkages with both MTHFR and low vitamin D status, the effects of MTHFR on vitamin D weren’t entirely what the researchers predicted.

Children with the C677T homozygous polymorphism (so TT or two mutant copies) actually had higher vitamin D levels than individuals with the CC allele or the “wild type.” Individuals with a heterozygous mutation, or CT allele, were somewhere in the middle.

The researchers theorized that because people with MTHFR need to conserve folate, and therefore need to avoid prolonged UV radiation exposure, they have developed some mechanism to manufacture or maintain vitamin D levels more efficiently.

“As such, individuals with MTHFR TT may manufacture and/or maintain vitamin D more efficiently due to their genetic need to avoid prolonged UVR exposure. Hence, vitamin D levels may be higher at baseline in children with MTHFR TT status.”

Methylenetetrahydrofolate Reductase (MTHFR) C677T polymorphism and associated vitamin D levels in children with Attention-Deficit/Hyperactivity Disorder (ADHD) (P5.6-043)
Sarah Silverstein, Keith Pecor, Asher Junger, Jeffrey Kornitzer
Neurology Apr 2019, 92 (15 Supplement) P5.6-043;

Thank you so much for listening today.

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Mercury Toxicity, Fibromyalgia, and Arsenic. Answers to Questions From Listeners.

I love it when listeners leave questions – the questions are always interesting and thought provoking and it helps me to understand what you’re interested in, so if you have a question for me please use the video ask feature at tohealthwiththat.com. I try to do at least one listener questions episode per quarter.

Detoxing Arsenic Toxicity with MTHFR

Someone wrote in with the question:

Hi, what would be the best option for detoxing arsenic toxicity?

Great question, human. It probably goes without saying, but finding the source of all of that arsenic is probably a great first step. Arsenic can come from drinking water, especially if you’re on a well, contaminated food, and even some medications. But step one is always going to be to minimize your exposure as much as you can.

Arsenic does rely on the MTHFR enzyme in that it needs SAMe to be detoxified so step two is going to be to work on optimizing your methylation. Make sure you’re getting all the b vitamins and right dose of methylfolate or another methylation driver for your body. Arsenic also needs glutathione for detox and so the GST gene SNP also has an effect here, specifically GSTO1.

Anything that will boost your glutathione will help your body to eliminate arsenic, and that includes getting adequate selenium. A wonderful longitudinal study published in the journal Toxicology and Applied Pharmacology showed that higher selenium status in people with chronic arsenic exposure was protective against arsenic induced skin lesions. Other things you can do to boost your glutathione include NAC, which I feel like I’m forever talking about.

NAC, along with selenium, is necessary to make glutathione. It competes with other proteins, so it’s best taken on an empty stomach. You can also take a liposomal glutathione if you don’t tolerate NAC, but it tends to be a bit harder on the wallet.

Boosting other antioxidants seems to help arsenic toxicity as well – vitamins A, C, and E were all mentioned in the research, along with reducing factors that make arsenic toxicity worse like cigarette smoking.

So in short, make sure your folate status and methylation are in place. Boost your selenium and glutathione precursors, and get your antioxidants. Above all, avoid arsenic.

Mercury Toxicity and MTHFR

“Hey Amy, my name is Clair and I have been sick most of my life. I got diagnosed with MTHFR C677T roughly 8 years ago but before that I got tested and had severe mercury poisoning and went through chelation therapy. That was 20 years ago. I just started some adrenal treatment and they found that I have it again and I just keep thinking that the root cause of all of this is MTHFR, so why am I not treating that? I know that I cannot take a lot of folate. I’m just highly sensitive to everything. I don’t know if I’m an overmethylator or an undermethylator. Which level do you think I should join?

Amazing question, Claire. Honestly i do think MTHFR is behind a lot of what is going on – this repeating mercury toxicity really drags your system down and it sounds like it’s been hard for you to get methylation drivers in there.

I feel like your best course of action would be to actually work one-on-one, simply because you have two big medical things – the mercury toxicity and the adrenal fatigue – going on with the MTHFR and it’s best to have someone like me or another experienced practitioner looking at the big picture.

In a situation like this, doing it yourself can be a bit dicey because with mercury toxicity, anything that actually pushes your body to detoxify – like balancing your methylation – is also a little bit scary because there are some big bad toxins in there. So it has to be done gently and slowly over time. Chelation for mercury is a good option if you have a dangerous level of mercury, but it is harsh and it can strip other minerals from your body and so it isn’t a great long-term solution.

Fibromyalgia

Dan writes:

Have you discussed fibromyalgia? I had it but was able to reverse it. After a quick scroll through your podcast I’m really interested to hear your thoughts about fibro and how it forms and if you think it can be reversed. Oh .. I’m a 49 year old male and former professional football player… So not your typical fibro sufferer.

This is a great question, Dan and honestly it deserves an entire podcast season to itself, but I’ll offer some thoughts.

It absolutely can be reversed – you are proof and I’ve seen a number of clients who have been able to master fibromyalgia and move on.

In terms of how fibromyalgia forms. There are so many theories, and as is the case in a lot of complex disease, like autoimmunity or chronic fatigue, I think it’s never just one thing. I think there is always a combination. There are some gene SNPs that have been associated – the only one we’ve talked about here is COMT. MTHFR, so far as research has shown to date, isn’t linked.

Other factors that I believe play a role are:

  • Neurotransmitter imbalance
  • Past trauma
  • Magnesium deficiency or excess calcium
  • Toxicity
  • Sleep defecit
  • Hormonal imbalance
  • Inflammation

As you can see, it’s a long list and not every person suffering with fibromyalgia will have all of those factors, and some of them will have other disease processes that play in. Also, this is mostly a connective tissue disease and while we don’t really understand why the connective tissue here becomes so reactive and congested, it is clear that it does and that must be directly addressed. I feel like fibromyalgia is a whole person condition and so things that benefit the whole person will work best. This includes:

  • Finding and eliminating food sensitivities – this is huge in fibromyalgia.
  • Balancing magnesium levels
  • Lots and lots of bodywork
  • Balancing hormones if that is a factor. This includes thyroid and adrenals.
  • Working on sleep quality and quantity
  • Neurotransmitters and also therapy if it’s appropriate.

The path is going to be different for everyone struggling with fibromyalgia, but it is really important to look at it as a combination of factors. There isn’t just one thing, the person as a whole has to be healed.

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High Histamine, gene SNPs, and MTHFR

Histamine and MTHFR are bound together for so many reasons. One, is because just like MTHFR, histamine has its fingers in so much more than just allergies.

Histamine is involved in:

  • Allergic reactions – this is the part everyone knows about.
  • Immune response
  • Opening blood vessels (or vasodilation)
  • It’s a neurotransmitter!
  • Signaling within your stomach

Histamine levels in your body depend on two factors.

  1. How much histamine is being produced – this depends on your gut microbiome, how easily your mast cells degranulate, and allergies and the action of your basophils, which are one of your white blood cells.
  2. How much histamine is being broken down – this depends on MTHFR, and two histmine-specific enzymes called DAO and HNMT.

Histamine is mostly formed in your mast cells, which are immune cells that protect sites vulnerable to injuries like mucus membranes in your nose and mouth, your internal body surfaces, and the insides of your blood vessels. Also, in your basophils, which are white blood cells in your immune system that respond to allergins. It is also scattered throughout your body tissues and has an incredibly diverse range of effects including:

  • Promoting wakefulness (otherwise known as stopping a good night’s sleep)
  • Constricting airways
  • Increasing stomach acid secretion
  • Modulating pain signals
  • Itch perception

Histamine is important with MTHFR for a couple of other reasons as well. Histamine breakdown is dependent on healthy methylation just like other monoamine neurotransmitters, and the HNMT enzyme needs a methyl group from SAMe in order to function. That means if you have a sluggish MTHFR, then it is much harder to break down histamine and you are more likely to have a high histamine picture.

Keep in mind that high histamine states are one of the characteristics of the “undermethylation” (legacy term) basic state – these are the folks I like to call the Achievers. Of course more than just your MTHFR status goes into high histamine – there are several gene SNPs that can affect it including DAO and HNMT – the two major histamine breakdown pathways – but it is still really useful for us MTHFR folks to know. I believe this simply because the general patterns between over- and under-methylators (again, that’s a legacy term handed down from the Walsh Research Institute and doesn’t necessarily describe what is happening physiologically) are still really useful.

The most useful aspect, in my opinion, is the drug and supplement reactions in each group, which I find to be shockingly accurate.

Gene SNPs That Affect HIstamine

  1. MTHFR and other genes in the methylation pathway – especially MTR (or MTRR which affects MTR’s ability to function. Remember that MTHFR is dependent on riboflavin as well, so low riboflavin status can look like difficult methylation.
  2. DAO – DAO is one of the major breakdown pathways of histamine and gene SNPs can cause problems.
  3. HNMT – HNMT is the other major breakdown pathway and it needs a SAMe (from the methylation cycle) in order to function.

High Histamine Symptoms Include

  • Seasonal allergies that present as hayfever type allergies – sneezing, watery eyes and runny nose, itching, hives, itchy nose, sudden symptoms.
  • Headaches and migraines
  • Shortness of breath
  • Skin itching for no apparent reason, or because of any and everything that happens, and low pain tolerance
  • Digestive symptoms including cramping, diarrhea, and bloating
  • Wakefuless, insomnia, anxiety
  • Drop in blood pressure, dizziness on change of position, or irregular heart beat.

Managing High Histamine Naturally

HIgh histamine can be seasonal, or it can be constant in the case of something called Histamine Intolerance. Either way, here are some steps you can take toward managing high histamine levels.

  • Eat a low histamine diet – some foods are extremely high in histamine including alcohol, fermented foods, processed or smoked meats, aged cheeses, and shellfish. Avoid these and focus on fresh unprocessed foods.
  • Ditch the leftovers – food that sits for a while, like leftovers, accumulates histamine while it sits so if you generally have a high histamine picture then leftovers may not be your friend. Make enough food for one sitting and cook fresh each time.
  • Vitamin C – vitamin C helps to prevent mast cell degranulation, which is the histamine-release event. In my own clinical experience, it is quite often a larger than average dose of vitamin C, and a buffered vitamin C product like Ester-C can be most effective.
  • Calcium – calcium helps to lower histamine levels in brain tissues and has a generally complicated relationship with histamine in mast cells – stimulating histamine release in some circumstances and regulating it in others. Some people seem to feel a direct and clear improvement in their symptoms with calcium supplementation and some people don’t notice anything.
  • Watch your folate levels – histamine increases with increasing folate, and often people with folic acid toxicity have problems with high histamine levels. Also, people who are supplementing with too much folate in any form – even the good ones like 5-LMTHF – can experience high histamine symptoms.
  • DAO enzyme – DAO, remember, is one of your main histamine breakdown pathways and a DAO supplement can help tremendously, especially if you experience a lot of histamine release directly related to foods. Still eat a low histamine diet if possible, but supplement a DAO enzyme to help your body calm down.
  • Try Quercetin – quercetin is well known and well researched to inhibit histamine production and to reduce pro-inflammatory mediatiors. For allergies it should be taken in a higher dose. Around 400 mg twice daily away from food is most common.

Thank you so much for listening today and it’s official – a free MTHFR Basics course has launched at courses.tohealthwiththat.com and an in-depth MTHFR for Life course is coming soon. That one will need beta testers who will be able to attend the course for 1/4 of the usual price, so please do sign up for the mailing list at tohealthwiththat.com, or on the courses page.

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Nitric Oxide, MTHFR, and NOS3

MTHFR is well known for causing heart health issues. It’s directly responsible for raising homocysteine levels, it’s implicated in troublesome blood clotting, and it’s indirectly responsible for making it harder to make adequate nitric oxide.

All of this is compounded if you have MTHFR and another gene SNP called NOS3.

What is Nitric Oxide?

Nitric oxide is the primary substance responsible for keeping your blood vessels open and relaxed so that blood can flow through easily. Without it, your blood vessels tighten and constrict, which drives up blood pressure and reduces oxygenation of your tissues. The primary function of your blood is to carry oxygen to all of the muscles, organs, and tissues that need it, and nitric oxide helps make that happen.

Nitric oxide also helps to keep your platelets, those tiny flakes in your blood that make up blood clots, nice and smooth and slippery. It inhibits platelet aggregation and adhesion, and even helps to destabilize any small clots that have formed.

Blood that clots when you’re injured are a good thing – they keep you from losing too much blood. Blood clots that happen for no reason, are deadly. That is what lies underneath the bulk of the heart attacks and strokes out there. You want blood that is smooth and free of clots.

Nitric oxide also helps with the growth and formation of new blood vessels.

Why Does MTHFR Affect Nitric Oxide?

MTHFR is part of the folate cycle, turning inactive folate into the active form, which is 5-LMTHF. The folate cycle needs to spin in order for a linked pathway, the BH4 pathway, to also spin. The BH4 pathway is most known for neurotransmitter formation because this is where we see serotonin and dopamine formation. BH4 is also necessary for nitric oxide synthesis. There is a detailed pathway document in the show notes, if you really want to dive in, but suffice to say if MTHFR is sluggish, then nitric oxide synthesis is also sluggish.

Let’s Talk NOS

NOS stands for nitric oxide synthease and there are three different forms, depending on where they are located in your tissues. NOS1, is also called neuronal NOS (or nNOS). NOS2 is also called iNOS, or inducible NOS, and NOS3 is epithelial NOS, or eNOS. eNOS, or NOS3 is extremely important here because it is most represented in the epithelium, which lines your blood vessels and so has the greatest direct impact on vessel dilation as well as clotting.

Nitric oxide is made from arginine, which is one of the building blocks of protein, and so that matters for proper functioning, as does calcium. Under normal circumstances, NO synthesis is dependent on the level of calcium within the cell and so that must be adequate. NO synthesis can also be influenced by injuries, such as shear stress, that require changes to blood flow.

NOS “Uncoupling”

There are many factors, mostly implicated in heart disease, that can set up a bad situation with your NOS. These factors include diabetes, ongoing high blood pressure, high cholesterol, aging, and metabolic syndrome and they all lead to higher percentages of oxygen radicals, which can in turn cause NOS to break off of BH4, or “uncouple” and bond with a reactive oxygen species. This establishes a cascades of enhanced free radical production that does nobody any good. This is part of why your doctor is so eager to treat diabetes, high blood pressure, and cholesterol before they have a chance to do long-term damage.

NOS3 Gene SNP

The NOS3 gene SNP, as you might have guessed, has its biggest consequences in heart and cardiovascular health, but also influences some tissues that rely heavily on constant, tightly regulated blood flow like your brain or a developing fetus. It is especially likely to create problems in situations with overlapping pathology, like NOS3 Gene SNP with diabetes, which also decreases circulation.

Common signs of NOS3 problems:

  • Chest pain with exertion or away from it
  • Cold hands and feet (poor circulation)
  • High blood pressure
  • Erectile dysfunction
  • Migraines
  • Stroke
  • Chronic sinus issues
  • Blood clots
  • Congenital heart defects (in babies born from mothers with untreated NOS3 polymorphisms)
  • Arteriosclerosis or hardening of the arteries
  • Preeclampsia in pregnancy (this is also a risk with MTHFR alone).
  • Family or personal history of Alzheimer’s disease.

Supporting a NOS3 Polymorphism

There are many ways you can support nitric oxide synthesis in your body, with or without a NOS3 gene SNP. Here are just a few:

  • Eliminate Folic Acid – folic acid causes a decrease in BH4, which is bad for your nitric oxide synthesis and your neurotransmitter production (also, your methylation).
  • Hum! – eNOS is highly expressed in your sinuses, and humming causes a 15-20 x increase in nitric oxide synthesis in those tissues. This is part of why breathing through your nose at night is so important for tissue oxygenation. A wonderful study published in the journal Medical Hypothesis showed that not only will strong humming for an hour every evening clear up nasal blockages and sinus infections, it also increases your functional nitric oxide.
  • Eat a low glycemic index diet – lowering your blood sugar fluctuations as well as your blood sugar in general will help your NOS, your heart, and your risk of diabetes in the long term. This means that every meal and snack should have a balance of proteins, good fats, fiber, complex carbs and sugars. A big pop or candy bar in the middle of the afternoon with no real food to back it up is the opposite of this.
  • Breathe through your nose– talk with your doctor about mouth breathing (Especially at night), try mouth taping, and make sure any larger issues like deviated septum get addressed. Deep breathing exercises for one minute three times per day can really help as well.
  • Exercise – exercise is great for everything and a healthy NOS3 is no exception.
  • Stop smoking and stay away from chemicals – chemicals in your environment can impair your NOS function by reducing the amount of BH4 produced, as well as impacting glutathione levels and NOS needs support from glutathione so it doesn’t get into the uncoupling situation.
  • Good dietary sources of arginine, calcium, and B2. Arginine comes from high protein foods like meat, dairy, and legumes which you will be eating more of with a low glycemic index diet. Calcium also comes from dairy, dark ark leafy greens, and broccoli. Riboflavin can be found in eggs, liver, lamb, mushrooms, spinach and almonds.

Whether you have a NOS3 polymorphisms or not, supporting a healthy nitric oxide function is crucial for a healthy heart, brain, and sinuses. It is especially important if you have an MTHFR polymorphism because we do have tendencies toward compromise in this area. Plus, most of the steps here overlap with the MTHFR lifestyle – so if you do the MTHFR lifestyle plus some deep breathing or humming, you’re there.

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S2E33: GST and GPX – Gene SNPs the Affect Glutathione

Last week we reviewed glutathione and its absolutely crucial importance in the body. We also spoke about it in S1E14: MTHFR and Glutathione that details some of the symptoms and diseases linked to low glutathione status and goes over the basics about how MTHFR affects glutathione.

This week, let’s talk about the two most well documented gene SNPs that affect glutathione in particular detoxification pathways. Those are GST and GPX.

GST, Which I Like to Call “Genetically Sensitive To Everything”

GST stands for glutathione S-transferase, and there are a number of different GST genes including GSTA1, A4, M2, M3, O1, O2, and P1. Outside of the necessary genetic alphabet soup, all of these genes code for enzymes that attach glutathione to some kind of xenobiotic, which is a fancy word for a chemical that is foreign to your body.

The reason you need to attach a glutathione to foreign chemicals is so that your body can actually make them water soluble and eliminate them from your body. If the GST enzymes don’t work correctly then the chemicals build up quickly and start doing damage and nobody feels this damage more than folks with a GST polymorphism. This can include cigarette smoke, heavy metals, pesticides, herbicides, carcinogens, air pollutants, and pharmaceutical drugs.

Signs and Symptoms of a GST Polymorphism

  • Hypersensitivity to chemicals – you know when there’s a scented candle in the house and if someone walks past with strong perfume, it’s game over.
  • Fatigue – because let’s face it. You’re toxic.
  • Brain fog – especially with chemical exposure but it can feel like it’s all the time.
  • Increased inflammation – which can look like joint or tissue pain, headaches, or mood issues like anxiety or depression
  • Cancer – higher than average amounts of cancer in your family tree or personal history of cancer.
  • Asthma – several GST polymorphisms have a strong association with asthma, especially asthma triggered by air pollutants or particulates.
  • Trouble with fertility – some GST mutations are linked to poor spermatogenesis in men and adverse pregnancy outcomes in women.

GST Does Have Some Superpowers

Thank god for small mercies. GST folks tend to have a higher than average response to chemotherapy, which is a blessing. This is essentially because the chemicals in the chemotherapy are also difficult to clear. Folks with this polymorphism also naturally tend to keep a more chemical-free home and have an innate ability to detect chemicals that other people might not notice and so can take proactive steps to keep them out of their lives.

GPX, or Glutathione Peroxidase

Just like the name suggests, glutathione peroxidase helps your body to eliminate peroxide.

You might be thinking, “But, Amy. I don’t drink a lot of peroxide.”

While I’m happy to hear that, but the sad truth is that your body makes its own peroxide in fairly large quantities. Hydrogen peroxide is a common metabolic by-product and is formed from normal activities of daily living and especially during stressful times.

Like with the GST polymorphism, there is a family of GPX mutations conveniently numbered from GPX-1 to GPX-7.

Signs and Symptoms of a GPX Polymorphism

  • Prematurely grey hair – turns out that peroxide internally leeches the color out of your hair as well as it does from the surface.
  • Increased inflammation – which can look like joint or tissue pain, headaches, or mood issues like anxiety, depression, irritability, or aggression.
  • Cancer – higher than average amounts of cancer in your family tree or a personal history of cancer.
  • Diabetes – several GPX polymorphisms have a strong association with diabetes, insulin resistance, high insulin, and obesity.
  • Heart and cardiovascular issues – cardiomyopathy, troubles with peripheral circulation and vascular tone, atherosclerosis and signs of cardiac inflammation.
  • Overweight – very easy to gain weight even with a healthy, normally-portioned diet. This especially coincides with the blood sugar troubles related to this gene SNP.
  • Brain fog and memory problems – peroxide is especially damaging to your brain and neurological tissues.

How to Help When You Have A GST or GPX Mutation

There are some great ways to help your body compensate for a GST or GPX polymorphism. Here are some of the most important:

  • Avoid Toxins – eliminate as many chemicals from your home and environment as you can. Get rid of the air fresheners, chemical cleaning products, plastics, pesticides and herbicides on your lawn and in your food. Invest in air and water filters.
  • Don’t smoke (!!!) – this is absolutely crucial.
  • Boost your glutathione – you can use some of the methods we’ve already talked about here and here.
  • Take NAC – NAC is the direct precursor to glutathione and it’s best taken on an empty stomach. If you have a hard time tolerating this one, then look for a liposomal glutathione preparation.
  • Make sure you get enough selenium – selenium is crucial to the formation of glutathione and selenium restriction makes the effects of both GPX and GST worse..
  • Balance your methylation – we’ve talked about it before, but for glutathione to be produced, methylation needs to be functioning well. If you don’t know where to start with that, you can start here.
  • Get your riboflavin (or vitamin B2) – riboflavin helps to recycle and regenerate your glutathione for optimal functioning. In great news, it’s also a cofactor for the methylation reactions, so this one is doing double duty.
  • Avoid toxins – I know I mentioned it 20 seconds ago, but it’s the most important thing. Seriously avoid those toxins.
  • Focus on a high fruit and veggie diet – getting lots of good antioxidants, vitamins, and minerals in your diet and helping your body to keep inflammation down is vital, and fruits and veggies are one of the best ways to do that. Just try to go organic whenever possible, especially if you’re buying something in the EWGs “dirty dozen” list.

There is an investigational drug called Ebselen that is an analog to the GPX enzyme and is being investigated for reperfusion injury, stroke, hearing loss, tinnitus, bipolar disorder, and Covid-19. It is not yet approved or clinically available, but may be some time in the future.

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S2E32: Glutathione Review with gene SNPs GGS, and GGT.

We haven’t discussed glutathione in a while, but MTHFR’s effects on glutathione production are of major consequence in the health of all of us MTHFR folks. While a sluggish methylation typically leads to a sluggish glutathione production, there are some particular gene SNPs that have a far greater impact. The most notable are GGS, GGT, GST and GPX.

Glutathione – The Master Antioxidant

Glutathione is an antioxidant just like vitamin C or vitamin E and it helps to scavenge free radicals and stop them from damaging your vital tissues. It is considered your “master antioxidant” because it also recycles other antioxidants, like vitamin C, so they can be used again. Kind of like an antioxidant double-whammy.

In addition to antioxidant function, glutathione is vital for a number of different detoxification reactions, specifically phase II detox reactions called glutathione conjugation. This type of reaction is necessary for some herbicides and pesticides with xenobiotic compounds known as “persistent organic pollutants”, or “POPs.” Mercury detoxification, especially from your brain, is dependent on glutathione.

Also, tylenol which in spite of being a common over the counter drug worldwide, is also the #1 leading cause of fatal overdoses. Tylenol, also called acetaminophen or paracetamol, needs glutathione to be detoxified. Remarkably, the life-saving hospital treatment for tylenol overdose is a glutathione IV, which saves an incredible number of lives but only if it is administered quickly.

If all of that weren’t enough, glutathione is vital for the function of your mitochondria. Your mitochondria power your cells, quite literally supplying the energy required for the rest of the cell to work. Creating this energy, however, leads to an extremely high burden of reactive oxygen species, or free radicals. If the mitochondrial glutathione isn’t enough to keep this in balance, then cellular energy production falters, leaving cells without the proper fuel to function. As you can imagine, this makes for a chronically tired, worn-down body.

Lastly, glutathione is vital to appropriate cellular death. Cellular death may be something that sounds like a thing you don’t want, but let me assure you – appropriate death for cells is actually crucial to your survival. Cells that do not die appropriately, in addition to adding a burden to your body, boosting inflammation, and creating an unhealthy internal environment, lead directly to cancer. Cancer is, quite literally, a cell that won’t die and reproduces without check. Glutathione is one of your body’s internal defenses against such cells.

Gene SNPs that Affect Glutathione Production – GSS and GGT

GSS stands for glutathione synthetase, and this gene encodes for one of the main enzymes involved in the actual manufacture of glutathione. As you might guess, SNPs affecting this gene tend to reduce the amount of glutathione produced by the body and so manifest in a reduced capacity to detoxify mercury and persistent organic pollutants, and has been implicated in some heavy hitting chronic disorders such as COPD and ALS.

Outside of this, however, this SNP has not received much research attention and so there is a lot we don’t know. Information on different SNPs and the level of glutathione impairment isn’t out there yet, so watch for this one in emerging research over the next few years.

GGT stands for gamma-glutamyltransferase and there are a number of different varieties of this gene and enzyme, so we see GGT1 through 7. This enzyme also is not well studied, but is another essential step in the formation of glutathione. There is some evidence that risk of acute pancreatitis is higher in smokers with a polymorphism in GGT1, Outside of that, however, this area is largely unexplored in humans.

I think it is entirely possible that these genes will be found to be consequential in future research, but at the moment that data just does not exist.

Natural Ways to Boost Glutathione

There are some great natural ways to boost glutathione that we covered in more detail in Season 1, Episode 14: Glutathione and MTHFR. That episode also covered known diseases linked to low glultathione. Some of the best ways to boost glutathione include:

  • Whey protein
  • Omega-3 fatty acids
  • Foods high in selenium like brazil nuts
  • Riboflavin
  • Vitamin C
  • Vitamin E
  • Alpha-lipoic acid
  • phytonutrients from fruits and veggies
  • Brassica veggies specifically – including broccoli, cauliflower, kale, cabbage, and brussels sprouts.
  • Herbs including rosemary, turmeric, milk thistle, and ginkgo biloba, green tea
  • Fruits and vegetables that actually contain glutathione including: asparagus, avocado, cucumber, green beans, and spinach.

Thank you so much for listening and next week we’ll talk about two well-explored genes that affect glutathione, called GST and GPX.

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S2E31: COMT Fast

The COMT fast picture, as you can imagine, is the flip-side of COMT slow. This enzyme works too well, eliminating crucial substances before they have the chance to act. The most well researched polymorphism that contributes to this picture is the COMT Val158Met Val/Val pattern, but again total COMT activity is additive across all the COMT polymorphisms and is best determined by symptoms and personality.

Signs and Symptoms of Fast COMT

In terms of neurotransmitters, low dopamine, epinephrine, and norepinephrine looks like:

  • Lack of enthusiasm
  • Relaxed, laid-back personality
  • Low motivation
  • Difficulty remaining focused on one task
  • ADD/ADHD
  • Addictive tendencies.

These neurotransmitters do double-duty as stress hormones and so we also see:

  • Suddenly shine in stressful situations, like they are at their best under pressure.
  • Stimulation-seeking – want lots of noise, lights, chatter in the work environment, and chaos to get their neurotransmitters fired up.
  • Sleep easily
  • Tendency toward restless legs and constipaton
  • Typically better with caffeine or other stimulants.

COMT also affects estrogens – meaning it lowers them – and so people with fast COMT often have:

  • Dry skin
  • More prone to osteoporosis
  • Often started their menses later than their peers
  • Symptoms related to low estrogen such as .moodiness, irregular periods, absent periods,
  • Lower tendency toward hormonal cancers including breast and prostate. 
  • Potentially lower sex drive

Remember that other gene SNPs can affect these same neurotransmitters,  and hormones, but if you have this symptom pictures then addressing the situation is appropriate no matter what your gene report says.

The COMT fast genotype carries with it some superpowers as well. On a surface level, the COMT variants get divided into Warrior and Worrier pictures.  COMT fast, because of the lower level of stress hormones, falls into the warrior category.

We say warrior, because stressful situations truly do make people with the COMT fast genotype shine. While others are overwhelmed or overstimulated, these folks are in the zone, at peak performance, and completely on-point. COMT fast folks are well suited to working in emergency rooms, the trading floor on Wall Street, or possibly on the race track. They also have a gift in terms of shifting between topics or areas of focus quickly. None of us are good at multitasking, but COMT fast folks can switch between tasks and activities with ease. This remarkable skill is called cognitive flexibility.

Managing a Fast COMT

Step 1: Balance Your Methylation.

As we discussed, the COMT enzyme is dependent on healthy methylation, so the first thing you would do in this situation, just like in COMT slow, is to optimize your methylation. Get your basic B vitamins, find the best B12 for you, and add a methylation driver like 5-LMTHF or SAMe. Optimize your doses of those things based on how you actually feel and how your symptoms look on a symptom tracker. If you don’t have one yet, you can get a free symptom tracker by signing up for the newsletter at tohealthwiththat.com.

Keep in mind that with a fast COMT your neurotransmitters are naturally low and pushing methylation drivers in this case can make a huge and immediate difference to your mood and affect. Getting good methylation drivers into the works will help tremendously.

Step 2: Optimize Your Diet

Protein boosts dopamine, which is exactly what you want with fast COMT. In a fast COMT situation eating a high protein diet will keep those flagging neurotransmitters up for a good mood and focus. Focus on a higher protein meal at breakfast, and lunch, and have a moderate protein dinner so the neurotransmitters don’t interfere with sleep.

Adding in high magnesium foods helps as well because magnesium is one of the best nutrients for a fast COMT. Look for dark green leafy veggies, low-fat dairy, nuts, and legumes. The magnesium will also balance the tendency toward constipation, muscle cramps, and restless legs.

Step 3: Stimulate

Such a big part of this picture involves stress hormones, and so balancing the helps to optimize performance. This means:

  • Like the slow COMT counterparts, declutter your home and keep it tidy. A calm, chaos-free environment reduces stress hormones, which is not as crucial for COMT fast folks, but it also makes focus easier.
  • Interrupting work with activities that give your brain a dopamine boost, like video games or a quick burst of exercise. Just make sure you’re keeping it in check because these things can become addictive in low-dopamine brains.

Step 4: Balance the Hormones.

As I said last week, balancing hormones is an entire podcast series in itself. Still there are a few things you can do in low hormone states as well:

  • Seed cycling. It’s too much to get into right here, but here’s a link to a detailed article. It’s a lovely way to help balance and regulate hormones safely.
  • Herbal medicines. Shatavari, black cohosh, and red clover are all known to boost estrogens in a relatively safe way, but it is best to work with a knowledgeable practitioner.
  • Exercise to build muscle mass and reduce fat. Dropping estrogens can decrease lean muscle mass and gaining muscle mass helps to balance and regulate all of your hormones.

Thanks so much for listening today and next week we’ll review glutathione before we talk about some of the SNPs that can affect levels. Please subscribe so you don’t miss any episodes and if you like what we’re doing here, I’d really appreciate it if you’d leave a review. Thanks so much!

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