Mastering Nutrition

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How to manage blood levels of omega-3 and omega-6 fatty acids. | Masterjohn Q&A Files #95 Mar 31, 2020

Show notes

Question: How to manage blood levels of omega-3 and omega-6 fatty acids.

I don't specifically want to look at the omega-3-to-omega-6 ratio. The AA/EPA ratio, I do not believe in wanting to get it low enough to prevent inflammation. I don't believe in using it that way. But I do believe that if it were too low, it could cause problems. I don't know what the cutoff would be. But if you're on the low end of normal, then I would think about cutting back your intake of EPA.

But my main concern would be if you're in the low or even middle end of the normal range for either arachidonic acid or DHA, I think you want to increase your intake of those. Particularly if your intake is already high, look for the cause of low levels. Especially if both of them are low, that could be caused by inflammation or oxidative stress.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/09/06/ask-anything-nutrition-march-8-2019

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Access the show notes, transcript, and comments here.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Can PEMT genetics cause fat malabsorption, mineral deficiencies, and oxalate problems?| Masterjohn Q&A Files #94 Mar 30, 2020

Show notes

Question: Can PEMT genetics cause fat malabsorption, mineral deficiencies, and oxalate problems?

First of all, saponification of minerals, the point here is that if you have malabsorption of fat, the fatty acids are going to bind to any positively charged minerals in your diet. This has been particularly well studied in preterm infants where the poor absorption of fatty acids causes the fatty acids to bind to the calcium that have lower bioavailability. Yeah. If you surpass your ability to absorb the fat, the fatty acids can bind minerals and induce mineral deficiencies. I agree with this.

PEMT polymorphism is a marker of poor synthesis of phosphatidylcholine. That will impair export of fat from the liver. Low phosphatidylcholine synthesis due to PEMT. I was thinking of it as a direct marker. It's not a direct marker, but it could theoretically impact. This is probably especially true if you have a low phosphatidylcholine intake. Probably eating phosphatidylcholine protects against this. But yeah, low phosphatidylcholine levels in the liver partly as an interaction between low activity in the PEMT enzyme and low intake of phosphatidylcholine from food could cause bile acid issues, which could in turn cause fat malabsorption.

If you have fat malabsorption and you have enough digestion of the fat to release the free fatty acids from triglycerides, but you don't have enough absorption of those fatty acids, the fatty acids will bind calcium. They won't bind oxalate, they can't. Binding the calcium will lower the calcium absorption, and it will also prevent the calcium from binding oxalate. Calcium binding oxalate is what prevents oxalate absorption, so yes, I would think that would increase oxalate absorption.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/09/06/ask-anything-nutrition-march-8-2019

Access the show notes, transcript, and comments here.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Could an elevated BUN indicate protein malabsorption and low stomach acid? | Masterjohn Q&A Files #93 Mar 27, 2020

Show notes

Question: Could an elevated BUN indicate protein malabsorption and low stomach acid?

I get the Heidelberg test. That's the only accurate way to assess stomach acid. If you want to do something else, it would be better to use the kitchen techniques, like take half a teaspoon of baking soda and see how long you take to burp, or take HCl with your meal and keep adding capsules and see how many capsules you can take without reflux. That's probably both more accurate than using BUN.

I find it almost certainly the case that a slightly high BUN would never be a useful marker of low stomach acid and would never be a good marker of poor protein digestion. If you want to know if you have poor protein digestion, measure the protein in your stool. Get a GI stool test that looks at what you're not absorbing. That's how you test that.

The reason that this sounds nuts to me is maybe you are allowing the protein to ferment in your gut and generate urea from the microbes that you're absorbing, like maybe. But where does most of the urea come from that's in your blood? It comes from the urea cycle, which is how you get rid of ammonia. How do you get ammonia in your body that goes into the urea cycle? You digest protein into amino acids, you absorb the amino acids, and then you break them down so that you can either burn them for energy or turn them into glucose or turn them into certain neurotransmitters or whatever, and then you lose ammonia that you put into the urea cycle.

Why wouldn't the urea be a marker of having good digestion? I'm not even sure that we could say it could be an equally useful test of good digestion and bad digestion of protein. I don't know if it's as good a marker of bad digestion of protein as it is of good digestion of protein. But even if it were just as good a marker of bad digestion of protein as it is of good digestion of protein, something that's an equally good marker of two opposites is not a good marker of anything.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/09/06/ask-anything-nutrition-march-8-2019

Access the show notes, transcript, and comments here.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Are bilirubin and uric acid useful markers of antioxidant defense and oxidative stress? What are better markers? | Masterjohn Q&A Files #92 Mar 26, 2020

Show notes

Question: Are bilirubin and uric acid useful markers of antioxidant defense and oxidative stress? What are better markers?

I think intracellularly where most of antioxidant support is highly relevant, then they're not that big a deal. In the plasma, they can be a big deal. It's quite possible that uric acid is one of the most important antioxidants in plasma. But I would say it's highly debatable whether we put uric acid into the blood specifically to achieve that versus that happens to be an accidental sort of just incidental to making uric acid during the excretion of purines, which make up the building blocks of DNA and ATP and things like that.

I think the best marker of oxidative stress in plasma is the cysteine to cystine ratio. Cysteine is the reduced form of the amino acid cysteine. Cystine is the oxidized form. There are good studies at a general population level showing that that is the major specific indicator of oxidative stress that takes place in the plasma.

The glutathione couple, glutathione reduced versus oxidized, is probably the best marker in the blood of what's happening with oxidative stress intracellularly. Unfortunately, the only test that looks at this is HDRI. I feel very, very torn about whether we should be working with HDRI because I know a lot about measuring glutathione. I've had some clients who got their glutathione test. What you need to do to accurately measure glutathione to preserve the sample, according to my client who did the test, is not at all part of the instructions or process that they use, so I am very skeptical of using them. No one else offers the reduced to oxidized version of glutathione.

So, what I would recommend to assess oxidative stress would be Genova's Oxidative Stress 2.0 panel. It does give you the cysteine to cystine ratio. I'll put a note to put a link to that in the show notes. I think that's the best marker. They do have glutathione on there, and they do have a bunch of other things that can be useful in assessing oxidative stress. I would use that.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/09/06/ask-anything-nutrition-march-8-2019

Access the show notes, transcript, and comments here.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Does it matter what form of B12 you take? | Masterjohn Q&A Files #91 Mar 25, 2020

Show notes

Question: Does it matter what form of B12 you take?

Cyanocobalamin is cheap and there's not really any clear evidence that it's harmful, but I just don't like the idea that it is cobalamin bound to cyanide. It's not found in the food supply. Forming cyanocobalamin and peeing it out is actually one of the main ways you detoxify cyanide.

Hydroxocobalamin is also relatively inexpensive. It's relatively easy to get as injections. It is not an end product of detoxification. It is found in very high concentrations in the food supply. The normal forms of vitamin B12 that you find in the diet from food are hydroxocobalamin and methylcobalamin in milk, and hydroxocobalamin and adenosylcobalamin in meat. Hydroxocobalamin is the most universal food form of cobalamin, and it is always a substantial part of the food supply. I'm pretty sure it's cheaper than methylcobalamin, so I would use intramuscular injections of hydroxocobalamin.

Most B vitamins start their absorption in the stomach and then mostly absorb in the small intestine. In the case of B12, when you're dealing with food, you're absorbing it in the small intestine almost exclusively with intrinsic factor that's produced in your stomach.

Start with a milligram of oral hydroxocobalamin. Test that against your serum B12. If it's not moving your serum B12, see if 2, 3, 4, 5, 6 milligrams do. Because if they do, then taking that every day is going to be probably easier. Well, I mean, it depends on what you like. But you're probably going to like taking oral B12 more than you're going to like getting intramuscular injections. I would see if raising the dose works first. I'd use oral hydroxocobalamin. Then if you have to use intramuscular, I will use hydroxocobalamin.

I guess you just have to judge it against from a medical perspective they're always worried about compliance, because unlike the people who are showing up to this AMA, the general population has very low motivation compared to us. Injection is preferable from that standpoint because there are fewer things to do. Plus, you have an accountability buddy because someone's got to inject you. You get an accountability buddy to do something once a month versus you have the personal responsibility to do something every day. From a compliance perspective, it's vastly superior, the getting injected. But if you're already taking 15 supplements every morning, then it's probably way easier for you to just add megadose of B12 in with those oral supplements than to get intramuscular injection. I'd prefer it.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/09/06/ask-anything-nutrition-march-8-2019

Access the show notes, transcript, and comments here.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Is it useful to measure urine pH? | Masterjohn Q&A Files #90 Mar 24, 2020

Show notes

Question: Is it useful to measure urine pH?

The urine pH is telling you the acid burden that your body has been subjected to. It's telling you, you can make an inference about the compensations that your body has had to engage in. You can also make an inference about the limitations of your body in compensating for that because even your urine pH should be buffered. It's not the case that you put a little bit of acid in the urine and then boom your pH is going to go down. It's the case that your body has a whole bunch of systems to buffer even the urine pH as you excrete acids from your body.

The system is, like in your blood, the tiniest, tiniest change in your pH is immediately going to set in motion a change in your breathing rate that is going to cause you to either increase or decrease the exhalation of carbon dioxide in order to adjust the pH of the blood. Then there's going to be a longer-term compensation where you're going to take some of those acids and pee them out. When you pee them out, your kidney is going to buffer those acids in the way of preserving the urine pH.

If your urine pH goes down from 6.5 to 5.5, it tells you that your urine pH is like ten times more acidic, but it doesn't tell you that your blood is ten times more acidic. The critics of using urine pH will point that out. But what it does tell you is that your body has been subjected to a rather enormous acid burden, number one; and number two, that you're even starting to overwhelm your kidney's ability to buffer the urine and prevent the pH of the urine from changing. And so it does tell you about the stress put on the system.

A high potassium intake would be the number one thing that would acutely affect it apart from taking the bicarbonate. By the way, always take bicarbonate on an empty stomach away from food.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/09/06/ask-anything-nutrition-march-8-2019

Access the show notes, transcript, and comments here.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Why AGEs and deficient insulin signaling are the main problem in diabetes. | Masterjohn Q&A Files #89 Mar 23, 2020

Show notes

Question: Why AGEs and deficient insulin signaling are the main problem in diabetes.

The reason that methylglyoxal, which I did my doctoral dissertation on, the reason that methylglyoxal, which is quantitatively the most important form of advanced glycation end products in diabetics, the reason that it is elevated is not because of hyperglycemia. It's because of deficient insulin signaling.

That is for two reasons. One is that you can derive methylglyoxal from glycolysis. You can derive methylglyoxal from ketogenesis. You can derive methylglyoxal from protein, specifically from the amino acid threonine. Insulin prevents you from making methylglyoxal in the glycolytic pathway no matter how high the glucose level is. Insulin, what it does in glycolysis is at the step where the intermediates spill out to generate methylglyoxal, insulin stimulates that enzyme that sucks the intermediates down.

Diabetes, you have lower expression of that enzyme, and you have greater spillover out of glycolysis into forming methylglyoxal. In untreated diabetes, you can have blood glucose that goes up five times normal. That will be a factor that is influencing you to make not just five, maybe ten or far more times methylglyoxal on glycolysis. But the reason the glucose is elevated is because of deficient insulin signaling. No matter how much glucose you have or don't have, once the glucose gets into the glycolytic pathway, insulin is protecting against methylglyoxal by clearing the glucose down.

The role of methylglyoxal starts at the first instance of hyperglycemia to cause the development from an acute first ever instance of hyperglycemia through the pathway of developing diabetes. Then in diabetes, methylglyoxal is overwhelmingly responsible for causing the cardiovascular complications, the complications in the eyes, and the neurological complications of diabetes, cataracts, all of these things. And so I think it's a huge mistake to think that the spiking glucose is the thing going on rather than the deficient insulin signaling.

Now, if you want to use a rule of thumb that is not individually tailored to you, then the answer is use the 140 limit. But you follow that up with, is there evidence to support this? No, I think the evidence says that this is a mediocre approximation of how to identify whether there's a problem. But a good way to try to identify whether you're having a problem with glucose spikes is the GlycoMark test.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/09/06/ask-anything-nutrition-march-8-2019

Access the show notes, transcript, and comments here.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Nutritional recommendations for MTR and MTRR polymorphisms. | Masterjohn Q&A Files #88 Mar 20, 2020

Show notes

Question: Nutritional recommendations for MTR and MTRR polymorphisms.

In the methylation cycle, I've talked a lot about MTHFR, which helps finalize the methyl group of methyfolate. But then folate has to donate that methyl group to vitamin B12 in order for vitamin B12 to donate it to homocysteine. In that process, that's how you clear homocysteine primarily in the fasting state rather than the fed state. It's also how you recycle homocysteine to methionine to use for methylation, again, primarily in the fasting state rather than the fed state.

If your MTHFR is working fine, then the creatine is much less relevant, and the glycine really isn't that relevant. Glycine is still important for everyone, but it's not specifically relevant because of the genetic variations. With that said, I do think that because some tissues rely more on folate and B12 than they do on choline that there might be some tissues that would benefit from supplementing creatine, so you could play around with it. I supplement creatine, and I don't have any problems. I mean, there's no harm in trying out the creatine.

In my view, there's no blanket recommendation for someone with MTRR polymorphisms. What I say is because in theory you will be bad at repairing B12 when your B12 gets very damaged, you should thoroughly look at your B12 status at least once. Then every time you enter a new health era, you should monitor your B12 status again.

What I mean by health era is your health changes or your developmental stage changes in a way that could impact your health. So, change in health eras, and I'm making this term up, this is not a medical term, but the change in health eras means you get sick with a sickness you never had before. That's a change in your health era. Or you go through puberty. That's a change in your health era. You go through menopause. That's a change in your health era. Or you go on birth control. That's a change in your health era.

Look, my MTRR, as I said before, looks terrible on paper. I measured everything I could think of about my B12 status, and everything looked fine. I'm not talking about just serum B12. I'm talking about all the functional markers too. They looked just fine. That just reinforced my belief and the observational data that these things are so common.

If these things dramatically impacted your B12 status in a very negative way most of the time, not many people would have the polymorphisms. And yet, they're very common. Those are huge reductions in activity. They're very, very common. So, I think it's ridiculous to make a generalized nutritional protocol around either of those. MTR, it gives you a couple ideas you can experiment with. MTRR, be proactive about monitoring your B12 status.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/09/06/ask-anything-nutrition-march-8-2019

Access the show notes, transcript, and comments here.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Nutrition for children with ADHD. | Masterjohn Q&A Files #87 Mar 19, 2020

Show notes

Question: Nutrition for children with ADHD.

In adults 100 to 800 milligrams per day has been used in a couple studies showing effects in the brain. One of the things that's going wrong in ADHD is that the brain is not getting dopamine's signal that something is valuable enough to keep paying attention to it.

I think the drugs that are used to treat ADHD are increasing the tonic level of dopamine in the frontal cortex, and they're increasing the tonic level of dopamine in the basal ganglia. In the frontal cortex, the increased dopamine is basically making more stable mental states. If you focus on something, you will hold on to that better. In the basal ganglia, increasing the tonic dopamine is making it harder for a new thing to grab your attention, which reinforces the fact that you are more focused. Anything that increases dopamine is going to be good. There's that.

Should we just use the glycine to promote sleep, or should I also use it in the morning? I would say, ultimately, you have to judge it based on the results you get, but you should try it at other times during the day because one of the roles of glycine would be to provide the buffer against excess methylation.

For dopamine to make you pay attention to something that has value, you must have GABA suppressing attention to everything else. Dopamine cannot be a meaningful signal of the value of placing attention on something unless you have adequate GABA to suppress your attention paid to everything else. Because if you're paying attention to your schoolwork while you are also paying attention to your video games and to the mosquito in the corner equally as much, then you're not actually paying attention to your schoolwork. So, I think that anything that would boost GABA would be helpful.

So, yes to the glycine during the day. Yes, you do want to keep choline levels up. But remember that choline is a methyl donor. Choline is a double-edged sword here. First of all, the choline is needed for acetylcholine. When dopamine tells you to pay attention to something, once you're paying attention, you need acetylcholine to sustain your attention on that thing and get results. Dopamine is the signal that that thing has value to pay attention to. Acetylcholine is what you actually use to pay attention to it and get results.

You do want to help his acetylcholine levels, but you have to remember that choline is a methyl donor and that the more choline you have, the more important it becomes that the glycine is kept high enough to buffer excess methylation. Otherwise, choline could act as a double-edged sword and potentially wind up reducing dopamine levels.

The other thing that I would add is the GABA. Maybe start at 100 milligrams a day and work your way up to 800 and just be careful with the low dose. See what results you get. If it seems promising, try increasing the dose.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/09/06/ask-anything-nutrition-march-8-2019

Access the show notes, transcript, and comments here.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Coronavirus: Foods and Supplements Mar 18, 2020

Show notes

Here's what I'm doing about the coronavirus:

chrismasterjohnphd.com/covid19

Here's my 41-page 92-reference guide, The Food and Supplement Guide for the Coronavirus:

chrismasterjohnphd.com/coronavirus

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

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