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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: March, 2020
Mar 31, 2020

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

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

Mar 30, 2020

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

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

Mar 27, 2020

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

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

Mar 26, 2020

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

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

Mar 25, 2020

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

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

Mar 24, 2020

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

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

Mar 23, 2020

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

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

Mar 20, 2020

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

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

Mar 19, 2020

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

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

Mar 18, 2020

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

Mar 18, 2020

Question: Nutrients important for neuroregeneration.

Iron, phosphorus, and sulfate are very important for regenerating nerves. Magnesium. Acetylcholine is a major factor in regeneration of nerves, and so choline is important. If you were to use a supplement, alpha-GPC would be the ideal choline supplement to use because it's superior at generating acetylcholine. Vitamin A and zinc are very important for nerve regeneration. DHA, which is one of the omega-3 fatty acids that you find in fish is very important. Vitamin B6. Possibly GABA supplementation can help.

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

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

Mar 17, 2020

Question: Advice for what to do after suffering a transient ischemic attack.

A TIA, a transient ischemic attack, is like a mini stroke, but they all kind of fall into the same category where the development of plaque is a very significant part, is the major thing disposing you to having an event like that.

Nutritionally, the major factors in blood pressure are potassium is the biggest one, the salt-to-potassium ratio, not eating too much. Some people are salt-sensitive, some aren't. But the major factor is really the salt-to-potassium ratio. Some of the other minerals like magnesium and calcium are important. But then stress and physical activity are huge in blood pressure as well. Assuming that's under control, the main nutritional factors that you want to pay attention to are things that get the blood lipids under control and then things that get the process of calcification and inflammation under control.

The reason that the lipids are problematic is because they're getting damaged by free radicals and other damaging molecules, so things like vitamin C and E, glutathione, fruits and vegetables supplying polyphenols, all the minerals like zinc, copper, iron, manganese, selenium, all those things are important.

Figuring out whatever the limiting factor is and managing the details is a really big project. There are some simple rules of thumb like getting regular exercise, provided that the doctor okays it. Obviously, with cardiovascular issues, you have to do that, but whatever is safe for him to engage in. If needed, meditation or stress reduction on the blood pressure. And then just cut the junk food out and include a well-balanced diet.

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

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

Mar 16, 2020

Question: When on a ketogenic diet, it is a problem if ketones are going up to 5 to 6 millimoles per liter?

One of the popular ketogenic advocates was saying that if the ketones are getting above 3, then it's from not eating enough protein. I don't really see it that way. I think that protein will suppress ketogenesis, and so will carbs. Five to 6 millimoles per liter is what you see in therapeutic ketogenic diets.

In terms of how you could bring the ketones down, more carbs or more protein are going to bring them down. Between the two of those, probably protein would be the most important thing to increase as a means of protection against lean mass loss and as a means of keeping neurotransmitters and all the other things that you do with protein healthy. But you could raise the carbs a little bit too. Because remember that your carb demand even on a ketogenic diet is definitely not down to 20 grams of carbs. That's not even feeding your brain on the ketogenic diet.

If you have room to increase carbs, then I think would be great to get the carbs up to at least 30 and then maybe use protein going up to supply the rest of that. Then also pay attention to micronutrients. Do a dietary analysis. If there are certain nutrients that this person is not really getting in that more vegetables would help those micronutrients, then increase the vegetables and the carbs along with them for that purpose. But just on macros alone, I would say go up at least 10 grams on the carbs and go up to, if you can get there, a gram of protein per pound of body weight on the protein, and that will bring the ketones down.

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

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

Mar 13, 2020

Question: Are there any solutions to getting nauseated from zinc supplements even at low doses and even when the zinc comes as oysters?

With the zinc, my general recommendation is to take zinc on an empty stomach. The thing that is not controversial is that phytate is the principal inhibitor of zinc absorption. Phytate is found in whole grains, nuts, seeds, and legumes. I think there's a very broad agreement across the zinc research community that taking zinc not with a meal that contains whole grains, nuts, seeds, and legumes is going to lead to higher zinc absorption.

Then there's some controversy. Does it matter whether the zinc is on an empty stomach compared to a phytate-free meal, which would be a meal that doesn't have any whole grains, nuts, seeds, and legumes? Because there's a gray area there, I say if you can, take it on an empty stomach. If you can't, take it with a phytate-free meal.

Generally, it's the case that if someone takes 15 milligrams of zinc with a full glass of water, they are very unlikely to get nauseated from it. Whereas if almost anyone takes 50 milligrams of zinc with a full glass of water on an empty stomach, they're almost definitely going to get nauseated from it. I would get nauseated from it.

Taking the low dose should allow you to take it on an empty stomach, but for some people, they do get nauseated even taking only 15 milligrams on an empty stomach. Well, you have two options. The ideal thing would be figure out the lowest amount of food that it takes to.

If you eat the oyster at the end of a phytate-free meal, is it still making you sick? If so, I don't think that's the zinc. I think it's something else. And your digestive system might not be up to the task of eating oysters right now at this moment. But if at the end of a phytate-free meal if you can fit in one or two oysters and it doesn't make you nauseated at all, then I think that's great. Oysters are probably the ideal zinc supplement if you can get them in. A couple of oysters a day goes a long way to getting your zinc in.

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

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

Mar 12, 2020

Question: Could low LDL hurt female fertility?

I haven't seen evidence of it, but that would not surprise me at all given that cholesterol is what you make sex hormones from. If you see levels that low, I don't know that it's intrinsically a problem. You kind of want to start looking at what are the reasonable things you could expect to happen from that that affect female fertility? Fat-soluble vitamins could be relevant. Sex hormones could be relevant. I'd start looking at those things.

I doubt that the LDL being that low itself in and of itself is going to be the thing that compromises fertility. This is the thing. Is the LDL low because of really good clearance from the blood, or is it low because of really low production? If it's low because of really low production, then you definitely have problems with fat-soluble vitamin transport. Because if the liver is not making lipoproteins as much, the fat-soluble vitamins are staying trapped in the liver and they're not getting to other tissues that need them.

While there's no evidence for it, it makes perfect sense that dietary cholesterol would help that because dietary cholesterol is very helpful in Smith-Lemli-Opitz syndrome, where the exact same defect is 1,000X to produce a devastating result. It makes total sense that in someone who is a carrier for SLOS, Smith-Lemli-Opitz syndrome, who has defective cholesterol synthesis in their gonadal tissues and therefore has defective sex hormone synthesis, it makes total sense of eating cholesterol would help those people. So, I would try it.

Egg yolks. That's what most people are going to eat for cholesterol. But this all hinges on the question of the LDL is low, so what? Is it because it's being cleared rapidly or because it's not entering the blood due to lack of synthesis? Whether that person is going to have infertility as a result of it and whether that's going to be helped by dietary cholesterol, it's all going to get a hinge on that. But the good news is for both people, it's probably completely harmless to eat some eggs. Eating eggs might just be the thing that helps.

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

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Mar 11, 2020

Question: Is it safe to take creatine when nursing?

If you felt fatigued and you took the creatine and all of a sudden that started reversing, then you either felt fatigued because you had low creatine synthesis, or you felt fatigued because you had a methylation problem. Those aren't mutually exclusive. If you're not methylating well, the most sensitive thing that will happen is you'll synthesize less creatine. But I mean it could have gone beyond creatine. It could have been that you're synthesizing less creatine, and you're not regulating your dopamine properly and things like that.

But certainly, you're addressing a methylation issue/a creatine deficiency issue. I don't know the exact cause and effect scenario that would lead to ovulation, but it makes sense that you ovulate. Think about the regulation of fertility, the whole thought process of the body's regulation of fertility. All of it comes down to energy. It comes down to the fact that when you get pregnant, you're investing -- I don't remember what the numbers are off the top of my head -- something like 50,000 kilocalories in the pregnancy. Then in lactation, you're investing another I think thousand kilocalories a day or something like that. The whole hypothalamic regulation of sex hormones and thyroid hormone is all regulated by leptin and insulin as signals of long-term and short-term energy status.

Insulin and leptin are hormones. Endocrine hormones are between tissues. But what happens at the cellular level is I think it's very plausible that something that's happening at the cellular level and the recognition of what those hormones mean to communicate that energy is present, sufficient for fertility is going to be ATP dependent. If you're missing creatine, then you're going to have a drop in the power of the ATP signal and the recycling of the ATP. This is the basis for why creatine is used for muscular power, but it's also the basis for why creatine is used to use energy in producing stomach acid or to communicate or to transmit light and dark signals through your eye to your brain to make vision. All over the place, creatine is super important to the cellular utilization of energy. My guess is it's correcting a response inside the cell to the leptin and insulin.

In terms of safety in breastfeeding, I don't think there's any evidence one way or another. It's probably safe because you could get this from meat, and there's no evidence of harm. But if you wanted to be hyper careful, I don't think you need to do this, but if you wanted to be like super, super careful, what I would do is divide the 5 grams over three or four meals evenly on the basis that there are very, very trace amounts of byproducts of high-dose creatine. Five grams will cause extraordinarily tiny amounts of toxins that appear in the urine. I mean, not toxins at the level that we're talking about, but I doubt it's a risk. But if you wanted to be hyper careful, divide the dose up evenly. 

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

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Mar 10, 2020

Question: Can you explain plant polyphenols and hormesis?

In brief, our detoxification system didn't evolve to handle the toxins of modern society. Modern society invents a new chemical. Our body knows it's a toxin, but it doesn't know it because we were exposed to it for millions of years. It knows it because it has similarity to other toxins. That similarity may be weaker or stronger depending on the toxin.

Our bodies do evolve to be bad at detoxifying. They evolve to be good at detoxifying. Our system is not designed to get sick when we encounter toxins. It's designed to get healthy when we encounter toxins. The way that works is throughout most of our evolutionary history, the toxins we were exposed to were the toxins in plants. Most of them are polyphenols. Most of them are the things that we ascribe health benefits to. A lot of those health benefits come from the fact that these are the toxins that our bodies are designed to work with.

Xenobiotic defense -- xenobiotic is something foreign -- this defense system is this giant umbrella system that in a very general level assesses the likelihood of how much energy should we invest in keeping that system running based on how much toxins are we exposed to and uses that metric to invest the energy in that entire machinery. We're not investing in getting rid of a specific toxin. We're just taking the collective toxin and investing in the collective detoxification machinery, the collective antioxidant glycation-defense machinery. Because fruit and vegetable polyphenols were the major toxins, our system is designed to be very highly responsive to them, to use them as that metric.

Now, in the modern society, what do we do? We invented new toxins. By the way, the fruit and vegetable polyphenols, what happens if you just take a bunch of them and you dump them on cells? You kill the cells. What happens when we eat them? Ninety-nine percent of them don't get absorbed. Why? Because the intestinal cells have a detoxification pathway that's just like the liver's.

I think where you cross the line is, what you don't want to do is isolate those things into a pill and megadose them. That's why people, when they ask me about sulforaphane and milk thistle, my view of that is that that's what you do when you can't eat a high volume of unrefined plant foods with five to nine fruits and vegetables. But what you don't want to do is say, "Well, if the bottle says one capsule milk thistle a day is good for me, then ten capsules of milk thistle on top of ten servings of fruits and vegetables is good for me." Then you're in the zone of who knows what that's doing to you.

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

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Mar 8, 2020

Question: What to do when serum magnesium is high but RBC magnesium is low?

The magnesium in the blood and the hair is high. When you say blood, I'm assuming this is serum or plasma because the RBC magnesium is low. I'm hoping that's not whole blood magnesium in which case it would be hard to separate from the RBC magnesium. But I mean even for whole blood, if the RBC magnesium is low and the blood magnesium is high, then the magnesium that's in the blood that's high is in the serum or plasma, not in the RBCs obviously.

Clearly this means that you're deficient in magnesium transport. You're not deficient in magnesium. So, the last thing that you should do is start blasting high-dose magnesium at that. Because not only is it not going to help, but you basically have two or three times the risk of harm from supplementing high-dose magnesium, because the harm of high-dose magnesium comes when your serum levels go to double the upper limit of the reference range. If your serum level is high, and your RBC is low, and you start blasting.

B6, even if it's adequate, maybe try 10 milligrams. Work your way slowly up to 100 milligrams of P5P. See if that helps. If it doesn't, you probably have a more serious issue with magnesium transport. You might have a rare genetic defect in a magnesium transporter. Off the top of my head, I'm not sure how to manage that. There's probably things you can't do. It might come down to just maximizing all the different possible ways that you can get magnesium into your system and cells. That might mean that you want a modest hypermagnesemia.

In other words, you want your serum magnesium to be a little over the top of the upper reference range in order to try to drive magnesium into the red blood cells. But you still need to measure it regularly so that you know that you're not anywhere near twice the top of the upper reference range. Then just do what you can to maximize the other factors. Insulin, salt, and B6 is what I think there.

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

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Mar 6, 2020

Question: Is there a potential for adverse effects of 5-10 mg of folate for heterozygous MTHFR?

Is there a potential? Yeah. The tolerable upper intake level for folate was set at 1 milligram on the basis that there are rare hypersensitivity syndromes that have caused reactions to 1 milligram or higher. On the basis that in numerous case reports, supplementation of more folate than that has been the factor that appears to precipitate the neurological degeneration in B12 deficient patients. It seems like if you're B12-deficient and you add a megadose of folate, there might be something causal about adding the folate precipitating the B12 deficiency. That makes sense.

Folate and B12 participate together in methylation. The neurological degeneration specific to B12 deficiency is probably mostly due to the non-methylation functions of B12. That's why it doesn't happen in folate deficiency. If you add folate, you're going to probably redirect some of the B12 into the methylation pathway, rob it from the other pathway, which is metabolizing methylmalonic acid into the citric acid cycle. You do that and you provoke the specific neurological degeneration of B12 deficiency.

The flipside of this is someone could say, well, there's no evidence that outside of these rare things that 50 milligrams of folate causes harm. That's true. There isn't a well-characterized harm from it. But I still think that it's stupid, it's stupid. Why would someone with a heterozygous MTHFR SNP need 10 milligrams of folic acid or methylfolate? That makes no sense biochemically at all. It makes no sense. First of all, are they compound heterozygous or are they just heterozygous for the SNP?

I don't know if it's harmful, but it's irrational to take high-dose methylfolate for this purpose or high-dose folic acid is irrational. It's on the basis that it's not effective. It is five to ten times the Institute of Medicine's tolerable upper intake level. It's not that I know it will cause harm. It's just that it's way into the territory of what has the possibility of harm in some people. Why for no benefit would you take yourself deep into the territory of possible harm?

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

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Mar 5, 2020

Question: Is folate unstable in frozen liver or just in frozen veggies?

The answer is folate is stable in frozen liver. It is not stable in frozen greens. 

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

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Mar 4, 2020

Question: How much vitamin C should I take with collagen?

There's no evidence that you need to take vitamin C with collagen. There is a study by Keith Baar, who showed that 15 grams of gelatin, not collagen, but I suspect the collagen is exactly the same, 15 grams of gelatin but not 5 grams, the dose is important, with 50 milligrams of vitamin C taken before exercise improved collagen synthesis in the tendons. They included 50 milligrams of vitamin C because it's made for collagen synthesis, but they don't show that you needed the vitamin C. They just had the vitamin C in there. I don't know if it even matters in that context whether you need the vitamin C. I also have no reason to think that you need 50 milligrams instead of 10 or that 100 milligrams wouldn't work better because they didn't test the different doses. They tested the different doses of gelatin. I see no reason to think a high dose of collagen is any different in this respect.

Let's assume that it's the same. What that means that I'm very confident that you need 15 grams instead of 5 grams when you take it before exercise to increase synthesis of collagen in tendons if that's what you care about. I have no confidence about how much vitamin C you need if you need any. But if you want to do what they did, then I do feel confident that 50 milligrams is enough to get some effect. I just don't know if it's enough to get maximal effect and I don't know if it's necessary at all or in that dose to get that effect.

If it's for joint health and if it's taken before exercise, the timing is important because what you're trying to do is leverage the exercise to get more blood flow of the nutrients to the joints. That's why the timing matters. In that case, you take the vitamin C with the collagen, 50 milligrams is the dose we know works. We don't know if it's necessary, and we don't know if it's optimal. We just know that it works. If you're not taking it for joint health and you're not taking it specifically before exercise, you still need vitamin C. But the timing doesn't matter and pairing it to the collagen doesn't matter.

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

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Mar 3, 2020

Question: Are liver capsules as good as eating liver?

Liver pills are mainly for people who are not going to eat liver. That's the first thing. The second thing is, there are advantages to taking the dosing schedule of a little bit of liver every day. 

Probably the ideal thing would be to have 10 to 20 grams of fresh liver every day. But the number of people who are going to do that are even smaller than the number of people who are going to eat the fresh liver. What the liver pills do is, number one, they give people who don't eat liver that frequently to get the nutrients that have absorption caps that are better off gotten in small doses at a time to get those every day. It gives people who are not going to eat liver at all a way to get liver in. I don't know. I mean, it's a tradeoff. Probably almost no one is going to eat 10 to 20 grams of liver every day. If you don't, are you better off taking the capsules or are you better off taking liver once a week? You're probably better off taking half and half, like take three capsules every day and still eat liver once a week. It's probably the best thing to do in that case.

I don't recommend anyone who would otherwise eat liver stop eating liver and take the capsules, but I do recommend the people who won't eat liver take the capsules. I think it's a nice thing to do. If you eat liver but take the capsules anyway, then take that in a lower dose because you eat liver. Like I said, eat one serving of liver once a week or twice a month and take two, three, or four of the capsules instead of six; two, three or four capsules every day. I think that's a happy medium that can have best approximates the best thing which is the 10 to 20 grams of liver a day.

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

Mar 2, 2020

Question: Should I take 3 grams of leucine per meal?

Leucine is metabolized into a leucine metabolite that is the signal of protein synthesis. It's the thing that tells your muscles whether they should be synthesizing protein. But do you synthesize more protein when you upregulate all the factors of muscle protein synthesis? Well, that is entirely dependent on the amount of amino acids you have supplied. Think about it this way. Why is leucine used as the marker to determine how much muscle protein to make? Because usually when you get leucine, it's with high-quality protein that has all the other amino acids that you need to make muscle protein.

Now, the question is, is meat better than isolated protein? The research is pointing in the direction that at least some whole foods are just better than protein supplements, number one. Perhaps as a general principle, perhaps whole protein foods are better than protein supplements, number two. Number three, taking leucine or the leucine metabolite that regulates muscle protein synthesis is not going to be better than getting whole proteins even from protein supplements when you get enough protein to provide that leucine because the leucine and its metabolite don't actually achieve peak muscle protein synthesis unless you supply the protein with it. If you supply the protein with it, you do get the leucine.

There probably are questions that can still be worked out about this, but it's probably going to wind up being that it's a waste of time to take the leucine if you're getting enough protein, and it's stupid to take the leucine and not get enough protein. You should just eat a lot of protein is where I think this is going. 

 

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

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