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Mastering Nutrition

Hi, I'm Chris Masterjohn and I have a PhD in Nutritional Sciences. I am an entrepreneur in all things fitness, health, and nutrition. In this show I combine my scientific expertise with my out-of-the-box thinking to translate complex science into new, practical ideas that you can use to help yourself on your journey to vibrant health. This show will allow you to master the science of nutrition and apply it to your own life like a pro.
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Now displaying: Page 1
Feb 27, 2020

Question: What does it mean when histamine intolerance and blood sugar dysregulation occur together?

Well, if his blood sugar is no longer as stable and he has histamine intolerance, then that drug probably interferes with vitamin B6 metabolism. Let me try to take one minute to see if I can find quick information on this. I can't. I can't find it quickly.

My instinct is to say that the drug is affecting vitamin B6 metabolism on the basis that 80% of the vitamin B6 in the body is used for glycogen metabolism in liver, which is the thing that stabilizes your blood sugar between meals. If your blood sugar is not stable between meals any longer, then yeah, it could be a hormonal thing. What it really probably means is that there's something wrong with the liver's ability to store glycogen or to access the glycogen when it's stored because your blood sugar is stabilized between meals exclusively by the liver's glycogen metabolism.

How does that relate to histamine intolerance? They're both caused by B6 deficiency. That's my take. I'd measure his blood levels of pyridoxal 5’-phosphate. Off the top my head, I believe LabCorp has a test for that. It would be helpful to look at his excretion of xanthurenate, kynurenate, and quinolinate in organic acids test. The Genova ION has all three of those. I don't think the other one is available to have all three. But every urinary organic acids test has some of those. I would go from there.

I mean, if you want to save money, just trial a pyridoxal 5’-phosphate, which is the active form of B6. Trial a supplement of that to see if it helps. I would do that at, maybe start with 10 milligrams, but feel free to work up slowly over a few weeks to 100 milligrams. If a few weeks at 100 milligrams doesn't treat that and he's off the drug, then there's something else going on and I don't know what it is. But that would definitely be first line thinking for me. Thank you, Jennifer, for your question. I'm glad that was helpful.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

Feb 26, 2020

Question: If PTH is mid-normal, do I need a calcium supplement?

I'm assuming that by midrange you mean it's 30. If you mean it's 40, then no, you're deficient or you're probably deficient. You need to test how you respond. But what I would say is, it would still be good for you to try increasing that and see if the PTH goes down anymore. Because my baseline for where I suspect that someone's PTH is maximally suppressed is 30. But the evidence that it's maximally suppressed is that it doesn't get suppressed by more calcium and vitamin D. If it goes down in response to calcium and vitamin D, then it wasn't maximally suppressed. Where you want to be is not 30 to 20. It's the point of maximal suppression.

Then the final thing is magnesium deficiency can compromise your ability to make PTH. I don't think that the average person in our society is deficient enough in magnesium for that to be relevant on the basis that population-wide most people have too much PTH. That contributes osteopenia and osteoporosis. But the big caveat here is if you are magnesium-deficient, then that might invalidate most of what I said if you're deficient enough to affect PTH.
If your PTH is around 30 and not higher than that, you're probably fine. But it's good to know your magnesium status because if it's really bad, that could change that interpretation. It's also good to know if adding more calcium suppresses your PTH further, because if it does, that's probably calcium that you need.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/30/ask-anything-nutrition-march-4-2019

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

Feb 25, 2020

Question: What to do about sky-high pyroglutamate?

Pyroglutamate, its other name is 5-oxoproline. It is something that is primarily produced when you are synthesizing glutathione, but you do not have enough of the second step in glutathione synthesis to keep up with the first step.

Maybe you need more glycine, but your glycine isn't low enough to cause orders of magnitude higher pyroglutamate. It's almost certainly the case that you have a glutathione synthetase deficiency, unless you have extraordinary levels of oxidative stress. I think that would be easy to test for because I just can't imagine that your glutathione levels -- I guess it's not that easy to test for because if you have a glutathione synthetase defect, you're going to have bad glutathione levels. If you have a tremendous amount of oxidative stress, you're also going to have low glutathione levels. If you have low glutathione levels, that's going to cause a tremendous amount of oxidative stress.
I think if it's not a glutathione synthetase defect, then it becomes a lot harder to figure out what it is because it probably means you have massive oxidative stress from somewhere and there's a lot of things that could cause that. That would be a potential Pandora's box of questions that would come out of that. But definitely the first step would be to look at glutathione synthetase.
This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/30/ask-anything-nutrition-march-4-2019

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

Feb 24, 2020

Question: In hemochromatosis, why would ferritin be low but transferrin saturation high?

Ferritin is your long-term iron storage. Transferrin is your short-term iron storage. The problem with hemochromatosis is that usually in a normal functioning system, there is a hormonal regulatory system that prevents you from absorbing iron from food when you have enough iron that when you have too much iron, shuttle the iron into ferritin which is protective both against pathogens eating the iron to grow and against oxidative stress, which free iron causes, which if you don't know the details about can be thought of as wear and tear on your tissues over time.

In hemochromatosis, normally the way you judge how much iron you have is in the circulating transferrin pool, which is your short-term storage. How full is it? The defect in hemochromatosis is that when the short-term storage, transferrin, starts getting fuller than usual, you don't notice it, so you don't stop absorbing iron from food that makes the transferrin saturation go up even further. But you don't shuttle the iron into ferritin. That makes ferritin lower.

What people get confused by is that historically, we have only paid attention to hemochromatosis when it's too late, when the person has been suffering for it from 30 or 40 years and they need organ transplants. What happens at that point is that the ferritin is very, very high. Why is the ferritin high? Not because you had too much iron. The person without hemochromatosis has the ferritin go up when they have too much iron. The defect in hemochromatosis is that you do not stop absorbing from food when you have enough, and you do not put the iron into ferritin when you have too much.

The reason that ferritin is high in someone who's had hemochromatosis for 30 or 40 years is not because they have too much iron. It is because they have oxidative stress and damage caused by that iron. Oxidative stress and damage cause ferritin to go up no matter how much iron you have. So does infection, no matter how much iron you have. Essentially, what you have is ferritin is not the fireman that he should be to put out the fire as it starts, and the smoke detectors go off. Ferritin hemochromatosis is the cleanup crew who got to the fire after the house burned down.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/30/ask-anything-nutrition-march-4-2019

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

Feb 21, 2020

Question: Does folic acid act differently in the body than natural folate? | Masterjohn Q&A Files #68

They don't really. Everything that is said bad about folic acid is sort of true to an extent but has been completely exaggerated in some circles. What happens is you have an enzyme called dihydrofolate reductase, or DHFR. Its purpose is not to metabolize synthetic folic acid obviously because that folic acid molecule doesn't exist in the food supply. Its normal purpose is that every time that you use folate to participate in processes outside of methylation, such as DNA synthesis, you wind up producing dihydrofolate as a byproduct. DHFR recycles that and turns it into tetrahydrofolate, or THF. Tetrahydrofolate is what has the methyl group added to make methylfolate.

The question is, does that synthetic folic acid, we call that unmetabolized folic acid, does that cause harm? There are scientific hypotheses that it might, and it might, but there's no conclusive evidence of that. That's one side of the argument against synthetic folic acid. The other side of the argument is now that you are giving the DHFR enzyme more work, that means that might be detracting from the work that it has in recycling dihydrofolate that came out of the DNA synthesis reactions to make tetrahydrofolate.

People think that they just cut out white flour and therefore they're better off. No. You cut out white flour, now you need to do more work to make sure that you are actually getting your nutrients from whole foods because if you were eating six pieces of white toast that you didn't have to worry about getting nutrients from whole foods and now you do.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/30/ask-anything-nutrition-march-4-2019

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

Feb 20, 2020

Question: Can frozen vegetables be trusted for folate?

You absolutely cannot trust frozen vegetables as a source of folate ever. That's because folate is extremely unstable in the freezer, and you have no idea how old the vegetables are. If they were fresh-frozen yesterday, they'd probably have plenty of folate. But if they were fresh-frozen three months ago, they may seem completely fresh and yet they don't have any folate in them.

I'm not a fan of frozen vegetables mainly on the folate issue, on the basis that many people believe they are getting folate from their vegetables. If they're eating frozen vegetables, they may not be. I'm very worried that there are a lot of people out there who believe that they are doing something good by cutting out refined flour from their diet and starting to eat lots of vegetables. But when they come as frozen vegetables, you may be cutting out a lot of folate from the form of synthetic folic acid added to the enriched flour that you had been eating and cut out of your diet and then not getting anything from the frozen vegetables, and that's a recipe for folate deficiency.

There are a lot of people out there who think folic acid is some kind of toxin. It's not a toxin. It's effective at treating folate deficiency. It is effective at preventing neural tube defects. That's why it's added to flour. It is not the ideal form of folate. There's no question about that. But this is like calcium. People are saying that calcium supplements are bad. Well, not as bad as not getting any calcium. It's the same thing with folic acid. Folic acid is not the ideal form of folate, but it's a lot better than a folate deficiency.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/30/ask-anything-nutrition-march-4-2019

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

Feb 19, 2020

Question: How much spinach, broccoli, and kale is too much?

Cruciferous vegetables have an issue with potential goitrogens. At serving sizes like this, the only issue with cruciferous vegetables is that they increase your iodine requirement. In theory, if you are juicing cruciferous vegetables to have like ten servings a day, in theory, you might get to the point where you cannot overcome the goitrogenic effect with iodine. That is based entirely on animal experiments that were done a long time ago, and we have no human data on where you cross that threshold. But in this case, I think two or three servings of cruciferous vegetables basically just means you need to pay a little bit more attention to your iodine status.

In particular, you want to make sure that you're eating some seafood. If you're eating some seaweed in your diet, you're getting plenty of iodine in most cases. If you're not sure if you're getting enough iodine, then I would say 200 to 400 micrograms of iodine from a kelp powder-based supplement would be fine. Also, as a seasoning, you can get Maine Coast Sea Seasonings where you can just sprinkle seaweed onto your dishes as a flavor. It's like a salt shaker so it's really easy to use. Using that if you don't mind the taste is a great way to get iodine. I think that's really only the main concern there.

The spinach is not a cruciferous vegetable, so it's not really contributing to this problem. It is high in oxalates and so it has its own problem. As long as you're getting calcium with the oxalate, for most people, there are exceptions to this. But if you don't personally have an oxalate issue, meaning a high risk of kidney stones driven by high oxalate levels in your urine or potentially behavioral issues in children some people are tying to oxalates. But if you don't have a specific issue with that, then I think really the only issue with oxalate is you want to make sure that you're consuming calcium in the meal that you're getting it in.

The spinach has calcium, but it's only about 5% bioavailable so you should basically discount the calcium in the spinach. The kale and broccoli have bioavailable calcium. If you're mixing them together, that's probably a great way to do that, but you might not be hitting 300 milligrams of calcium in a meal. I think if you have a lot of oxalate in a meal, you probably really want to make sure you hit 300 milligrams of calcium in that meal.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/30/ask-anything-nutrition-march-4-2019

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

Feb 17, 2020

Question: Can you give any suggestions for increasing delta-6 desaturase activity?

There's a bunch of nutrients involved in that, so many that you basically just need to do a comprehensive nutritional screening for whether something is missing there. You might just have low activity by genetics. It's probably not worth solving that problem.

The big governor though is if you have if you have insulin resistance or you have low insulin levels from chronic carbohydrate restriction, that might increase it. But you also look at your inflammation because you might have some of the higher fatty acids being depleted from inflammation or oxidative stress. I mean, more nutrient-dense diet across the board, more carbohydrate, if that doesn't do it, then just maybe take a supplement or increase the liver and egg yolks to the point where the arachidonic acid is normal. Measure your CRP. If that's high, address inflammation.

In the Testing Nutritional Status: The Ultimate Cheat Sheet, I have a big section on oxidative stress. I go through that testing. A starting point might be Genova's Oxidative Stress 2.0 blood panel. But if inflammation and oxidative stress are the things, work on those. If those aren't issues, then more nutrient density across the board, fix any nutrient deficiencies you find, increase carbohydrate if you're on low-carb. If none of those things work, then just increase your arachidonic acid level in your diet.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

Feb 14, 2020

Question: What are the pros and cons of boosting sulforaphane?

Sulforaphane, the nice thing is it promotes detoxification. The bad thing is it raises the need for iodine. I don't know what ratio to take, but you definitely want to make sure that you're getting some kind of iodine into your diet, whether it's through like 200 micrograms of iodine from a kelp powder supplement or you experiment with milligram amounts from a broken up Iodoral tab or whatever. Because I don't know the dose, I'm just going to say work slowly and work your way up. Certainly, if you have any signs of hypothyroidism or you have any brain fog, increase the iodine or decrease the sulforaphane would be my opinion.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

Feb 13, 2020

Question: Is it true that we can’t absorb more than 1.5 grams of creatine at one time?

I don't think that's true. From what I looked at, it looked like the absorption of creatine was really, really good. I don't know if someone was arguing maybe that we don't retain more than that. But I think the retention of your muscles is going to be best with creatine if you take it post-workout and if you take it with carbohydrate to stimulate insulin. But on the whole, I think that the absorption and retention is good enough that it's more a matter of how fast will you get to peak muscular creatine than it is about where you get in the long-term.

Maybe if you follow all the best procedures to absorb and retain creatine, you'll get to the 30% increase in muscular creatine in two weeks taking 5 grams a day instead of four weeks. Maybe someone who doesn't follow any best practices takes six weeks. But ten weeks later, you're probably going to be at peak effect if you just take 5 grams of creatine at a time without paying attention to all the details around absorption.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

Feb 12, 2020

Question: NMN vs. NR: What’s better? And is TMG necessary?

Yeah. There are no human studies looking at NMN and how it's metabolized. There are studies of NR. No one has showed any positive benefits of supplementing NR in humans yet, but they haven't really done any long-term studies or looked at many things, and they really haven't looked at anything that I would really want to see for NR. They've looked at things like glucose and lipids and other metrics of metabolic health doesn't really do anything for that.

This is what I would say. My strong suspicion is that NMN is not absorbed intact. It's broken down into NR and it's absorbed intact as NR, while NR is just absorbed intact in NR. I believe that both of those supplements are going to lead to NR getting into the liver. I mean, I would use NR because there's more data on NR, and I wouldn't use NMN because there isn't any data on it. But it probably makes no difference at all because they're probably both absorbed as NR.

Maybe if your digestion is weaker, you're going to do better within NR than NMN because you probably almost certainly are not absorbing NMN intact. If you're not digesting it, then you're absorbing less of it. But probably for most people, it makes no difference. I believe that both of these are going to generate NAD levels in the liver much more effectively than nicotinic acid or niacinamide would, the two common niacin supplements that are available on the market now and have been taken for ages. I think it will be better at boosting NAD levels in the liver. I think that will allow the liver to nourish many other tissues in the body to get a better NAD response in those tissues.

My suspicion is that this is going to have a positive effect for anti-aging, for cellular repair. I think it's probably going to have a lot of promise for mental effects in the brain where there's high NAD turnover for neurotransmitter release. I think it's going to have probably really good effects in the gut where there's high NAD turnover because the gut faces so much damage by just being forced to deal with everything that you put into your body, unlike everything after the gut, after absorption, which has really high quality control. I think it's going to be great for skin issues.

I think that in order to get the best NAD response and to tax the methylation system the least, you want to take a smaller dose with every meal rather than taking a higher dose once. I would take like 150 milligrams max at a meal. If you're going to take 450 milligrams, I'd take 150 at each of three meals. If you want to take less than that, you either use the powder or empty half of it out in a capsule. Like take half the capsule, empty it out into your mouth with a meal, 150-milligram capsule to do that. It will give you 75 milligrams. Take that three times a day.

Then there's no good test to really see whether it's doing anything for you. You really have to judge it by your response. Are you getting tangible benefits from it? If so, then I think it's fine to keep it up. But yeah, I would take 100 milligrams of TMG for every 200 milligrams of nicotinamide riboside or nicotinamide mononucleotide. Personally, I wouldn't use the NMN and use the NR because there's more data on it. 

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

Feb 11, 2020

Question: What to do about cataracts.

Carl Rayner says, "Cataract in one eye becoming noticeable. This eye had a posterior detachment about 11 years ago, which is basically healed. I've been on a low-carb diet for over 40 years. Eat raw cream cheese, eggs, meat and liver. In the past few years, adding fasting and more keto diet. Saw your thoughts about glutathione on the cheat sheet and interview with Wendy Myers. Am I on the right track and what else could I do? Grain intolerant. What testing beyond normal tests might be helpful?"

I believe that cataracts in the eye are largely driven by the glycation of lens proteins. The glycation of lens proteins is largely driven by methylglyoxal, which I did my doctoral dissertation on. In direct contradiction to much of the low-carbohydrate literature, glycation is not all driven by carbs. Methylglyoxal is quantitatively the most important source of advanced glycation end products in the body.

Methylglyoxal can be derived from glucose, or it can be derived from ketones, or it can be derived from protein. No one has ever done a very good study to determine whether you have more methylglyoxal on a ketogenic diet versus a high-carb diet. But there was one poorly designed study where they took a small handful of people. They said, "Here's the Atkins diet, new diet," Or what is it called? Atkins New Diet Revolution or whatever that book was called. They said, "Here, read this, go forth and do it." They went home, presumably they read the book or part of it, and they tried to do it. They came back, they lost weight, they had elevated ketones and guess what? They also had significantly higher methylglyoxal.

Also, everything in the pathway that leads from ketones to methylglyoxal was elevated. I would say the data were very strong that in those people, they had higher levels of methylglyoxal because they had higher ketone levels that were generating it. They went on the Atkins diet, and they worsened their glycation risk by making a lot more of the thing that causes most advanced glycation end products and the thing that is probably overwhelmingly driving cataracts. But they didn't show any health consequences, and they certainly didn't measure cataracts in that study because that wasn't the point of it.

They left more questions than answers. For example, what if they had a control group that lost the same amount of weight on a high-carb diet? My suspicion is that methylglyoxal would have gone up during weight loss but just not as much. I also think that if those people stabilized their new weight and then they worked carbs back into their diet, their methylglyoxal would go back down. In fact, I have a consulting client who developed cataracts that corresponded very well with when he started intermittent fasting. He did have poor glutathione status. We were able to improve his glutathione status, but the cataracts didn't go away.

Todd Becker asks, "How do you test methylglyoxal levels?" You don't. You become a guinea pig in a lab because doing a study on it. That's about it. Look, I'm not against keto and I'm not against intermittent fasting. But if you're specifically talking about dealing with cataracts, you're probably not going to get the cataract to go away, but you probably can stop them from getting worse and stop them from forming. I think intermittent fasting and keto is probably going in the wrong direction.

One thing that I do think, I don't think you're going to measure your methylglyoxal levels, but I think you should test your glutathione levels because glutathione is what detoxifies methylglyoxal. If you listen to my riboflavin podcast, we talked about cataracts being a sign of riboflavin deficiency and also being one of the things that's being investigated for whether riboflavin supplementation can help it.

Why does riboflavin supplementation help that? For the exact same reason as when I went on that big, longwinded answer about glucose-6-phosphate dehydrogenase deficiency at the beginning, the riboflavin is there to boost glutathione recycling. I think the whole story, all these pieces knit together to a very, very, very nice story, clean story saying what you want in your eye to avoid cataracts from forming and getting worse, forming in the first place and getting worse, is you want low levels of methylglyoxal in your lenses. How do you get that? You have very good glutathione status.

The keto thing is a maybe. There's no maybe that maybe keto makes that better, but there's a maybe that maybe keto makes that worse. You can't test the glutathione levels in your lens proteins, but you can test the glutathione levels in your blood. I would use the cheat sheet in a very targeted way for everything that's relevant to your glutathione status. I would follow the recommendations in there about how to boost your glutathione status. I would use your blood levels of glutathione as a metric.

Rather than getting them in the normal range, I would try to get them as high within the normal range as you can, and titrate your approaches according to what works. Test it every couple of months, make one very important change. Well, actually, follow all the steps in optimizing glutathione status right now or all the ones you're willing to do. Follow them for eight weeks, test glutathione status, get a baseline glutathione if you can, but eight weeks of all my suggestions or whatever you're willing to do with them. Retest the glutathione, see if it helped. If it helped, then tweak one thing at a time after that. Do that one thing very consistently and stably for four to eight weeks. Retest glutathione.

Whatever I said for glutathione, also consider maybe supplementing with high-dose riboflavin in there. Maybe 100 milligrams of riboflavin at each meal, I would probably revise my glutathione recommendations in the cheat sheet to include that as a possibility. Yeah, optimize against glutathione and consider riboflavin supplementation. Be very open-minded about the carbs, the keto and the fasting because those might be great for many things, but they're definitely not optimal for glutathione and methylglyoxal. Thanks, Carl.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

Feb 11, 2020

Question: What can be done nutritionally to specifically improve antiviral immunity?

Certainly, the fat-soluble vitamins, vitamins A and D, both important. Lauric acid as a fat. Coconut oil might be a good fat choice for the fat in your diet. Monolaurin would be a very good choice for a supplement. Lauricidin is the best monolaurin to take, 3 to 10 grams a day. Be careful of your bowel tolerance, spread it out among your meals, and cut back if it starts to loosen your stool.

Elderberry, which has mostly been studied in the context of flu, that probably has good antiviral properties.

Garlic. Garlic appears to require very high doses if you're just taking a garlic extract. If you're taking stabilized allicin, 180 micrograms a day is good. But you could raise the question what if you're missing on some of the other important compounds in the garlic. I'll debate with some of my friends about that, but what's really been tested is 180 micrograms of stabilized allicin.

Then zinc for sure in the immune response is super important.

Then you get back to nutrient density. Although I'd give special importance to vitamins A and D, arachidonic acid just mentioned, zinc and copper, both, and then those supplements. If you're missing any one particular nutrient, then you're going to wind up with a specific vulnerability that will persist until you fix that one nutrient. Thanks, anonymous.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

Feb 10, 2020

Question: If free T3 looks good, why is TSH still a little high? Why hasn't the T3 brought it down enough?

Your thyroid gland makes thyroid hormone. Thyroid hormone increases your metabolic rate and does a lot of related things. Your hypothalamus is governing that by controlling your pituitary, the master endocrine gland, and its secretion of TSH, which is what controls the thyroid gland and makes it make more thyroid hormone.

The way that the feedback occurs is that the circulating T4 is converted to T3 inside the cells of the pituitary. That is what suppresses the production of TSH, which is basically the pituitary monitoring the thyroid hormone levels to know whether the thyroid has done its job. If the pituitary, the master endocrine gland, decides that the thyroid has done its job, it takes down TSH, the signal to make more thyroid hormone.

You really are not looking at whether the free T3 is suppressing the TSH. Ninety percent of that suppression comes from circulating T4 that's converted to T3 inside the pituitary gland. You really are looking at whether the T4 is on the high end of normal or not. 

If your reverse T3 is on the higher end of normal, then that explains it. You basically have your brain telling your thyroid gland that it needs more thyroid hormone, but you have much of the rest of your body deciding that it's not in the position to carry out the effects on the metabolic rate that the thyroid hormone is demanding. It's converting the thyroid hormone into reverse T3, which is basically a thyroid antagonist.

If your reverse T3 is high, then I think you want to look at things like calorie intake, carb intake, and stress levels because I think those are the main things that might make your body want to resist the signal of thyroid hormone by making the reverse T3. If the reverse T3 is good, meaning it's pretty low, then I think that means that there is something either in your brain, specifically in the hypothalamus or in the pituitary or somewhere in the combination where they're just deciding that your body needs more thyroid hormone than you have.

My suspicion is that that's going to relate to how sensitive your cells are to the thyroid hormone, if your cells are somewhat resistant. Remember in the last AMA, this got brought up, and I talked about zinc deficiency and high free fatty acids being the primary things that are going to reduce sensitivity to thyroid hormone or cellular uptake. There are some indications that high free fatty acids might also decrease cellular uptake, but not much is known about what governs cellular uptake.

In fact, there are some genetic variations in cellular uptake. If the thyroid hormone levels are high in your blood because they're not getting into the cells, then that could easily explain everything. It's just that your problem seems pretty moderate because you're not saying that your thyroid hormones are sky high and your TSH is sky high. You're just saying everything is a little on the high side of normal.

It sounds like there's not a big problem, but that something somewhere your body is determining that you need a little bit more thyroid hormone. If you can address zinc, free fatty acids, and I would address zinc and free fatty acids as the top things, unless the reverse T3 is high, target carbs, calories, and stress.

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019

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Jan 31, 2020

Question: What food supplements and training programs are good for developing muscle mass?

 

Overwhelmingly, what matters for muscle mass is working out, eating enough protein, and eating enough calories. 

 

You want to try and hit 10-20 sets per muscle group per week with eat set hitting within 80% of failure. So, if your doing a set of 8 reps but you could have done 20 reps with your chosen weight, that doesn’t count. You would want to pick a weight that you can lift no more than 10 times. Ideally, you’ll do some sets in the 5-rep range, 10-rep range, and 15-rep range. 

 

For protein, you probably want to be up around 1 gram per pound of body weight or per pound of target body weight. 

 

Then calories, you do need a caloric excess, but you don't want to get fat. If you know how many calories you need to be weight-stable, I recommend titrating the calories up 100 calories a day and then track your progress if you are gaining waist circumference. I know this is a little bit harder when you're a woman because you're going to have more fluctuations in water weight, but in terms of simple things to do to track your progress, waist circumference is valuable, and looking in the mirror is valuable.

 

If you can get an actual Bod Pod or DEXA scan, then that would give you more reliable information. There's a device called Skulpt. It's bioimpedance, I believe, but it's taking it at many different points where you take so much data that it actually becomes pretty accurate, but it's very time-consuming. Anyway, take your choice of what you're going to use to track your progress.

 

If you're not gaining any fat, you can very slowly add your total calories. If you are gaining fat, you need to cut back on the calories. But you need to have a caloric excess to maximize your muscle gains. That right there is probably 90% of it and anything else is probably completely pointless unless you are a very good athlete, in which case you're going to be looking for what's the next.



This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019

 

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Jan 30, 2020

Question: Should I manage my total cholesterol of 305 just for my doctor or should I be doing it for my own sake? If so, how should I do it?

 

You should want to improve your lipid profile for a lot more than to please your doctor.

 

Let's revisit this from a cholesterol skeptic point of view. Uffe Ravnskov, he wrote a book called The Cholesterol Myths. In that book, he shows a graph from the Framingham study where he maps out the people who have heart disease and the people who don't. If you look at that graph, one thing that you see is that everyone who had total cholesterol over 300 had heart disease and no one who didn't have heart disease had cholesterol that high.

 

Look, the only way to have a total cholesterol of 300 or more in most cases is to either have a thyroid disorder or to have a familial hyperlipidemia. We're talking about fasting levels here. You should want to manage your blood lipids for your own sake because people with familial hypercholesterolemia have a dramatically increased risk of having heart disease decades earlier than it becomes normal for the general population. 

 

I'm not saying it's 100% certain that if you have a cholesterol of 300 you will have heart disease, but you are way disproportionate in risk for that reason. You definitely want to address this for the sake of your health.

 

I think that if you have weight to lose, that losing weight should be one of the first things that you do to normalize your blood lipids and your inflammation. Being overweight also contributes to elevated free fatty acids, and elevated free fatty acids do raise your blood lipids. That's, in fact, the entire rationale of using high-dose niacin to lower LDL-C is by suppressing free fatty acid release.

 

It’s also important to address any inflammation in your gut. You might have microbiome issues, and working more high-fiber vegetables into your diet and diversifying across the different plant fibers is a great way to nourish your microbiome, reduce inflammation that comes from the intestines that would negatively affect your blood lipids.

 

If these things that we just talked about aren't enough to get the blood lipids into the normal range, then I think you want to experiment with eating more carbohydrate and a low-fat diet, but selecting those foods to maintain nutrient density. You could add something like psyllium husk fiber , which might be both good for your gut and the inflammation coming from your gut. It will also help reduce your cholesterol by making bile acids go into your feces and making your liver draw cholesterol from the blood.

 

If those natural things don't get your blood lipids into the normal range, then I think that you should consider being open to pharmacological methods. I've gone through all the cholesterol-skeptic literature and I'm against demonizing cholesterol. I do not believe that high cholesterol is the cause of heart disease.

 

But if your lipids are that high, it's overwhelmingly because you are not clearing them from the blood, and not clearing them from the blood is the single most important risk factor for them oxidizing, and them oxidizing does cause heart disease. 

 

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019

 

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Jan 29, 2020

Question: "Do you have any recommendations on how to get enough calcium on a low-carb, no-dairy diet? I've read that vegetables provide calcium, but bioavailability is poor."

 

The bioavailability of calcium from different vegetables is highly dependent on the specific vegetables. 

 

Cruciferous vegetables have very good bioavailability. It's better than from milk. Spinach has like close to zero bioavailability. It's terrible and you shouldn't even count it. Nuts and seeds have about 20% of the calcium being absorbed. If you compare that to milk --- milk is probably going to be like 30% or 40%. Cruciferous vegetables are going to be like 50% or 55%.

 

The real problem is the volume. If you look at broccoli or kale and you look at how much volume of those foods do you need to eat in order to get 1000 to 1500 milligrams of calcium a day, which is the target, it's a ridiculously high volume. 

 

I'm a bit skeptical that you want to eat more than say 200 or 300 grams measured cooked of those foods a day because they're increasing your iodine requirement. At some point, they become a liability for your thyroid gland. I think it's best to eat two or three servings of those cruciferous vegetables a day, and that's basically maxing out the calcium that you can get from them. You're just not going to get anywhere near the 1000- to 1500-milligram target.

 

A low carbohydrate, non dairy containing diet is emulating the traditional diets of the Arctic where plant foods were very limited. How did they get their calcium? They crushed up fish bones. They freeze-dried fish bones, they pulverized them, and they ate the bone powder.

Bone meal is a traditional food. Some consider it as a supplement but it is the historic source of calcium in traditional diets that were low-carb.

 

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019

 

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Jan 28, 2020

Question: What should people with glucose-6-phosphate dehydrogenase deficiency be doing not just about glutathione, but about folate, vitamin K, fatty acids, and neurotransmitters?

 

G6PD, glucose-6-phosphate dehydrogenase deficiency, is an inborn error of metabolism. It's the most common one in the world. About 8% globally have some impairment in this enzyme. The reason that it's important is because glucose-6-phosphate dehydrogenase is the enzyme that allows you to make NADPH, which is a specific derivative of niacin that's involved in antioxidant defense, detoxification, synthesis of neurotransmitters, and synthesis of nucleotides, which are needed for cell division because they're parts of DNA.

 

Someone with G6PD deficiency is vulnerable to hemolysis, or the destruction of red blood cells, because of glutathione deficiency. Glutathione reductase uses energy and NADPH, the thing that you can't make, to recycle glutathione. But it also uses riboflavin. So, one of the adaptations that someone with this impairment has to try to protect themselves is for the glutathione reductase enzyme to hog all the riboflavin so that it says, "I don't have enough of the raw material I need to make this happen, so I'm just going to make myself get way better at using what I do have." That's an adaptation to compensate for not being able to make NADPH is just to get way better at using NADPH to recycle glutathione.

 

Supplementing glutathione is not necessarily a bad idea. You just have to be aware that at a certain point you just can't solve every one of the dozens of problems that are happening. I think that you should measure your glutathione status. Probably the best test available, not because it's the best we could have available but because there's nothing better right now, is LabCorp's test for glutathione. If that looks low, then I would supplement with glutathione to try to bring that up to normal. 

 

For the folate recycling, you have to consider this basically as if you had a really bad MTHFR polymorphism because G6PD is needed to make the NADPH that MTHFR uses, again, with the help of riboflavin to make the methyl group on methylfolate. You can take some methylfolate, but as I've made the point in my MTHFR protocol at chrismasterjohnphd.com/methylation, you have to take 18,000 times the RDA to compensate for the 18,000 times a day that you add a methyl group to the folate molecule using that enzyme. It's not safe to take anywhere near that much folate.

 

What I would do is just very strictly follow the MTHFR protocol that I have at chrismasterjohnphd.com/methylation, and that involves doubling your choline intake because you don't need NADPH to use choline to support methylation. Just as if MTHFR didn't work because of genetics and not enzyme, what you would do is you double your choline utilization for methylation because you're not good at using folate. 

 

On recycling vitamin K, it probably just means that you need a high amount of vitamin K in your diet. I think it's probably similar as if you had a bad VKOR polymorphism. VKOR is the enzyme that recycles vitamin K using NADPH that you got from this pathway that's not working right when you have G6PD deficiency.

 

In terms of all this stuff that you are not good at synthesizing, like cholesterol, fatty acids, nucleotides, and neurotransmitters, I think the only thing that you can do for that is to try to eat a lot of these things preformed. That means eating a diet rich in relatively lean animal foods because they have a lot of preformed stuff, like cholesterol, in them and mainly in the flesh, not the fat. With plants, you want to eat mostly fibrous vegetables because they are highly cellular and rich in nutrients that you can’t make.

 

You don't want to go extremely low-fat, but if you eat a diet fairly rich in animal foods, you're going to get a lot of the specific fatty acids that you can't make. A high-fat diet is mostly giving you just a bunch of fat that you could have made yourself.

 

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019

 

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a



Jan 27, 2020

Question: If my tryptophan is low, and I'm on a low-carb diet, would you recommend 5-HTP supplements or tryptophan supplements or both?

 

There are multiple reasons why tryptophan could be low. It could be that you are not eating enough protein, or it could be that you have a high utilization of the tryptophan. I would look in the test and see if the 5-hydroxyindoleacetate is elevated — because if it is, then that would suggest high serotonin production, and that might explain the low tryptophan.

 

If that is the case, you may want to look into other explanations. In this particular case, we have talked about high estrogen levels and how they might be one of those things. In which case the root cause is the high estrogen levels and you need to address it at that level.

 

Repleting the tryptophan maybe isn't necessarily the goal unless you have symptoms that are related to low tryptophan levels. If you're overproducing serotonin, if anything, you might have symptoms that are more related to high serotonin levels. 

 

You might not have any symptoms that are related to low melatonin levels, which is downstream from serotonin, in which case the main negative effect of depleting the tryptophan would probably be related to niacin because tryptophan is used to synthesize niacin — in which case the goal would probably be best served by supplementing niacin instead of tryptophan. 

 

Something to note: if you're trying to put on lean mass and it's not working, it could theoretically conceivably be possible that serotonin overproduction would be depleting the tryptophan to the point where you didn't have enough tryptophan to put on the lean mass you want.




If the tryptophan is being diverted into serotonin, that's why it's low, again, judgeable by whether 5-hydroxyindoleacetic is elevated, then it makes no sense to put 5-HTP into the system because your problem isn't that you have low serotonin. If anything, it's that you have a high serotonin. 

 

The only other explanation I would say is if you have a low protein intake, you might need to increase your protein intake. But if that were the case, you would probably see other amino acids more across the board that were depleted and not just tryptophan. 

 

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019

 

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Jan 24, 2020

Question: What to do if signs and symptoms of zinc deficiency persist despite taking 75 mg zinc gluconate per day.

 

You should do plasma zinc. 

 

Also you know I kind of wonder whether you're taking that right. So if you're taking 75 milligrams of zinc like at one time then it's not surprising because you're absorbing like seven of those milligrams. The rest you are not. 

 

To maximize absorption take them on an empty stomach in 10-15 mg which is typically the smallest dose available. 

 

If you're doing that and the signs, the deficiency persist they're persisting when you're taking that, then it probably isn’t zinc related.

 

If they're persisting until you take that and it goes away, then either you aren't absorbing the zinc well, or you're not taking it right. Those are the two things. 

 

If you're not absorbing it well it could be a general malabsorption disorder, something causing loss of bile, or a polymorphism or genetic impairment in a zinc transporter, or low methylation which all can affect zinc transporters.

 

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/02/24/ask-anything-nutrition-feb-17-2019/

 

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Jan 23, 2020

Question: Is a high value of arsenic a concern?

 

Yes, arsenic is a toxin. You probably don’t want a lot of it, if it's just a little high it might not cause terrible damage.

 

I would look at methylation if I saw high arsenic, because methylation is needed to get rid of arsenic.

 

Oh actually I should add that methylation supplements have been shown to help arsenic detoxification in areas of the world where arsenic was a serious concern.

 

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/02/24/ask-anything-nutrition-feb-17-2019/

 

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Jan 22, 2020

Question Are low polyunsaturated omega-6 values on the ION test a concern?

 

Not the total, but if the arachidonic acid levels are low I would look at low arachidonic acid intake, or inflammation, or oxidative stress. It would concern me because arachidonic acid is important to a lot of physiological functions, but I don't care about the total omega-6.



This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/02/24/ask-anything-nutrition-feb-17-2019/

 

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Jan 21, 2020

Question: When high selenium does not come down in response dietary efforts and cessation of supplementation, what's going on?

 

Either there's high levels of selenium in the soil where your food is grown, or you have low methylation because methylation is needed to get rid of excess selenium.

 

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/02/24/ask-anything-nutrition-feb-17-2019/

 

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Jan 20, 2020

Question: Creatine, when is it recommend that if you don't have the MTHFR SNP that causes methylation problems?

 

1.)When you want to improve your physique.

 

2.)When you want to improve your athletic performance.

 

3.)When you have a rare creatine synthesis disorder.

 

4.)If you have depression, it might help.

 

5.) If you have any signs that something else is messing with your methylation even though your genetics don't explain it.

 

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/02/24/ask-anything-nutrition-feb-17-2019/

 

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Jan 17, 2020

Question: When should tryptophan be taken on a keto diet? Night, day, both?

 

Presumably you're doing this to try to increase tryptophan getting into the brain. 

 

The best thing to do is to take it two to three hours away from other protein. 

 

The second consideration is if you have an allotment of carbs that you concentrate at one time of day, then it would be best to take the tryptophan then. With the caveat being if you’re eating protein with the carbs. In that case it would be best to take it away from the protein + carb meal. 

 

This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/02/24/ask-anything-nutrition-feb-17-2019/

 

If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a



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