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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 10
Jan 16, 2020

Question: Do you think there are true non-responders to creatine, or do you think that those apparent non-responders have some defects in methylation that makes typical doses of creatine sufficient only for other needs.

 

Alex Leaf would be a great person to ask about this and he's not here right now… 

 

[Alex appears] Alex, so Jen's question is are there true non-responders to creatine or do you just think that non-responders likely have some defect of methylation. It means the typical doses of creatine are only sufficient for their needs.

 

Alex: I don't think that methylation is going to be relevant here. When you look at responders and non-responders, the difference seems to be in their ability to uptake creatine into muscle cells from the serum. So, it's very unlikely be related to methylation and it has to probably do with differences in creatine transporter abilities across cell membranes.

 

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

Jan 15, 2020

Question: How do I bring up low levels of arachidonic acid? Should I supplement with 250 milligrams? What brand is there from well-known company?

 

If you want 250 milligrams of arachidonic acid, eat an egg. I don't know anything about arachidonic acid supplements yet, except that they exist because you can eat eggs and you'll get plenty. Do you want to try the supplement? Well you can, but I don’t think it’s necessary. 

 

You eat two eggs a day already, so eat four. 

 

The oxidative stress and inflammation will consume the arachidonic acid, so look at that too.

 

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



Jan 14, 2020

Question: How to interpret the pattern of high citrate, low cis-aconitate, low glutamate, and high glutamine.

 

The aconitate and citric acid are markers on the citric acid cycle where we metabolize most of our energy. If citric acid is high and isocitric acid is low, (this must be the Great Plains Test which doesn't have isocitrate/cis-aconitate) that would indicate oxidative stress.

 

In terms of the glutamate being low --- if your glutamate is low and your glutamine is on the high side, then you probably have ammonia generation from somewhere that you're mopping up with glutamate. That would be my guess, but that's another can of worms to open.

 

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



Jan 13, 2020

Question: What are the best ways to optimize glutathione status for someone who has a G6PD deficiency?

 

Riboflavin was shown to be of benefit for normalizing oxidative stress in people who have glucose 6-phosphate dehydrogenase deficiency.

 

So for people who don't know what this is G6PD is, glucose 6-phosphate dehydrogenase is an enzyme that you use to take energy from glucose specifically, you can't take it from anything else, and you use it to recycle glutathione which is a master antioxidant of the cell. 

 

You also need this to support the recycling of vitamin K and folate and you need this for synthesis of neurotransmitters among other things.

 

But the big problem with G6PD deficiency is that you can have a lot of things go sideways when you can’t use this pathway. Red blood cells become more vulnerable to hemolysis and that is a result of oxidative stress from poor glutathione recycling in the red blood cell. 

 

One of the adaptive responses to having G6PD deficiency is the glutathione reductase enzyme -- which is the enzyme that uses riboflavin and niacin to recycle glutathione with the energy taken from G6PD. 

 

That enzyme -- glutathione reductase -- it develops a voracious appetite for riboflavin that makes all the riboflavin that won't go anywhere else, get sucked up into that enzyme. So basically you become very dependent on riboflavin support of glutathione reductase because you have lost G6PD, the enzyme that's involved in passing the energy on to riboflavin in glutathione reductase.

 

There's probably no harm to starting at 400 milligrams of riboflavin a day, but if you feel like you want to be more cautious about it, I'd start at 5 or 10 milligrams a day, test the effect on glutathione status.

 

You know in this case I think you want to look at erythrocyte glutathione status, I don't usually recommend that test, but it might be a more relevant test specifically for this condition. 

 

What I would usually recommend for glutathione status would be plasma levels of glutathione. I also think LabCorp does whole blood glutathione. 



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



Jan 10, 2020

Question: Are there diminishing returns in the amount of fish in a weekly diet? I know you mentioned eating fish about twice a week. I've been trying to eat salmon once a day. Is there an ideal ratio of fish to non-fish protein you should aim for?

 

There's not a lot of data backing that up and the data we have is pretty poor quality. But I'm of the mind that the diminishing returns come after one or two servings of fatty fish per week. I think if you're talking about white fish it's different. But I am referring to salmon or mackerel — I think once a week or twice a week is good. 

 

As for white fish — it's not as different from meat as you might think, the real big difference in my view is there are some different, like there's selenium and iodine among other things. The big difference in salmon, mackerel, and other fatty fish, versus lean fish versus meat is the type of fat. 

 

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



Jan 9, 2020

Question: How to deal with the fact that blood tests for nutritional status aren’t adapted to children?

 

There aren't childhood-based ranges that are data-driven. So what if the ranges need to be a little bit different in children?

 

The approach in the Cheat Sheet is not to rely exclusively on ranges, it's also to look at the diet and lifestyle analysis and to look at signs and symptoms. 

 

So what you do is you piece together: does the diet and lifestyle analysis, the blood lab, and the signs and symptoms all say deficiency X, too much Y. Then that's very good information and what you do is you intervene on the basis of what seems probable and you monitor the outcome.

 

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



Jan 8, 2020

Question: I just saw an email from Matt Stone referring to the overly deified nutrient vitamin A. Also, a few Weston A. Price Foundation bloggers are starting to spread the word about being sick on a high vitamin A diet. Any thoughts about this and comments about Vitamin A being toxic?

 

You shouldn't deify any nutrient, right? Any point of view that breaks down the world into good and bad molecules, is a doomed-to-failure point of view because molecules don't have virtues. 

 

Everything is about context. Too much vitamin A cannot be defined outside of context. Not just what your needs are, not just what your genetics are, not just what your turnover rate is, not just whether you are getting pregnant, but also the presence of other things in the diet. For example, vitamins D, E, and K, which will affect the vitamin A requirement because they all regulate each other's breakdown.

 

Some people have too much Vitamin A. Some people take more vitamin A than they should. There's dozens of case reports of vitamin A toxicity, but there's no evidence that people at normal intakes who are not supplementing are getting inflammation from consuming dietary levels of vitamin A.

 

The RDA is 3,000 IU. If you're correcting deficiency, 10,000 IU is highly reasonable over a short period of time. On the other hand, if you have someone who has a very long history of taking vitamin A supplements at 30,000, 40,000, 50,000 IU over 3 years, then, yeah, they might have all kinds of problems from that because they're taking too much. Toxicity is also way more likely if they're not taking vitamin D, vitamin E, or vitamin K.

 

There's nothing remotely controversial about that; no reason to question it. 

 

There are probably a lot of people in Weston A. Price who think that more of a good thing is better, and I know for a fact that many people were taking two or three tablespoons of high-vitamin cod liver oil for many years. That was nuts then and it's nuts now; they’re getting too many fat-soluble vitamins and too many polyunsaturated fatty acids from high levels of cod liver oil like that. 

 

But again, 3 to 10,000 IU, even long-term, there's no evidence of toxicity. Some people are going to be intolerant. I know anecdotes of people who take vitamin A at very low doses and it causes some hypersensitivity reaction. I don't know what causes it. So there will be stories of people who improve when they take the vitamin A out of their diets. It will happen, it makes sense.

 

And on top of that there are epidemic proportions of people with fatty liver. What happens when fatty liver gets bad? The cells that store vitamin A in the liver dump their vitamin A into the bloodstream so they can transform into cells that lay scar tissue down in the liver. So people with fatty liver, which is about three-quarters of people who are obese, right, so about 70 million Americans, maybe more now, have fatty liver disease. Some proportion of them are laying down scar tissue in their livers and they are losing the ability to properly store and metabolize vitamin A.

 

Could taking vitamin A out of the diet for them help? Probably, but it's a very tough place to be in because those people are going to have cellular vitamin A deficiency. So it's like, do you save the liver or do you save everything else? It makes sense to temporarily withdraw vitamin A, but really you need to just fix the obesity and fatty liver disease, then restore vitamin A that is needed.

 

I have no problem saying that some people take too much vitamin A and that it can be toxic, but there are people going around right now saying that vitamin A is intrinsically toxic, and those people are absolutely nuts. That's flat-Earth level thinking that it's just intrinsically toxic and not a vitamin.

 

 

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



Jan 7, 2020

Question: Is it ok to mix carbs and fat? There are a lot of people on the internet that claim the Randle cycle is behind America being fat, since the standard American diet is mixed in fats and carbs. Yet, I feel great on a diet of about 30% protein, 30% fat, and 40% carbs, based on meat, potatoes, fruits, and vegetables. 

 

The randle cycle addresses why you would have elevated fatty acids or hyperglycemia and hyperinsulinemia due to competition. You're more likely to have circulating energy supplies in your blood due to poor tissue uptake when you're consuming carbs and fats together, and you're more likely to be more dependent on a higher insulin response.

 

This doesn't mean that mixing them causes diabetes, it just means that there is more substrate competition and that, all else equal, if someone is on the edge of diabetes eating a mixed diet increases the probability that they're going to go over that edge because of the substrate competition contributing to hyperglycemia and the greater insulin requirement than someone who's on a low-carb or low-fat diet.

 

If you have no evidence of metabolic dysfunction on a mixed diet, then there's no issue.

 

Most Americans are fat because of caloric balance. Thinking that the glycemic or insulin response to eating plays a role in body fat gain is the same erroneous thinking that Taubes makes. There’s an element of truth in Taube’s carb-centric model, in that some people are going to eat more food in response to a high-carb diet if they have blood sugar problems. But that isn’t the norm.

 

To say that the Randle cycle is the cause of obesity is making the same mistake because it’s focusing on the glycemic and insulin responses to eating instead of overall energy balance. What makes you fat is eating too much food. 

 

The only thing that you should change about the calories in calories out (CICO) hypothesis, on a practical level, is to say that it tells you very little about the behavioral modifications that someone needs to make to sustain the caloric deficit over time.

 

So, why do people get fat? I largely endorse Stephan Guyenet's view: it's basically the proliferation of hyperpalatable food. A mixed diet leverages the principle of creating a hyperpalatable diet by mixing carbs and fat, but your diet doesn't sound hyperpalatable.

 

 

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



Jan 6, 2020

Question: Can you explain what parent essential oils are? I was given some articles that seemed to be saying that high-dose cold-water fish oils are damaging to cell membranes and mitochondrial function.

 

"Parent essential oil" is a term invented by Brian Peskin, who looked at some  data that said it's not clear that supplementing with fish oil is good for you because doing so can cause oxidative stress and cause damage to cells.

 

That's true because the highly unsaturated oils found in fish oil, as well as in liver and egg yolks, are highly vulnerable to being damaged. This includes the physiologically essential omega-3 fatty acid, DHA, and omega-6 fatty acid, arachidonic acid. 

 

But that damage comes only when you eat too much. This is where I think Peskin is wrong, because he took that data and concluded that you don’t want to eat any of these oils. Instead, you should eat oils like flaxseed that provide the “parent” fatty acids that your body turns into DHA and arachidonic acid.

 

But the parent oils are prone to being damaged too, just to a lesser extent. On a gram to gram basis, they are safer, but you need to eat a ton of parent oils to get the physiological requirement for DHA and arachidonic acid. So, on a daily requirement basis, the parent essential oils are going to be way more damaging.

 

I recommend simply taking a small amount of arachidonic acid and DHA, since then you fulfill your requirements regardless of genetics or the environment or whatever could impede the transformation of parent oils to these physiologically essential oils. High-dose fish oil is ridiculous, and risky, but that doesn’t mean you shouldn’t consume any. 



Jan 3, 2020

Question: What are your thoughts on monitoring HRV for optimizing performance?

 

Measure your HRV every night and you stop exercising entirely to get a baseline. 

 

You completely stop working out, you don't go “oh no I'm going to lose my muscle mass,” nothing's going to happen for a week or two. And this is the whole foundation of you having good data.

 

This baseline ensures that you have good starting data that isn’t influenced by anything. 

 

Now you start working out. You do one workout that's typical, you keep taking your HRV, you may see your HRV plummet. Then you say, how long does it take me to recover on my current diet and lifestyle?

 

You repeat that, like you don't work out again until it's back up to the plateau level. Then you work out again and you see if you have a repeatable response where there's a certain amount of time on average that's fairly replicable that it takes you to recover your peak HRV after your typical workout. Then when you have that you get on that frequency.

 

You can then start playing around with factors — like does it matter what type of workout I do? Is my recovery level consistently different when I lift weights at 5 reps per set versus 15 reps per set. Is my recovery time consistently different when I do cardio, or when I do cardio and weights on the same day, or when I play soccer. Then you can start to tailor your recovery time around the specific workouts.

 

Maybe it takes you two days to recover from one workout and four days recovering from another. Lower body, upper body, if you have a lower body upper body split, does it take me five days to recover the lower body and does it take me three days to recover from upper body?

 

At that point you can start tweaking diet and lifestyle. Do I recover faster if I eat more carbs? Do I recover faster if I eat food X?  Do it recover faster if I take supplement X? Always testing one thing at a time and making sure it's replicable before you form a conclusion before you do the next test.



Jan 2, 2020

Question: Why did the FDA have a vitamin A requirement during pregnancy at 8,000 IU, which is much higher than the IOM recommendations in the past?

 

I have no idea. I do know that the concerns around vitamin A during pregnancy are that in the first weeks of pregnancy, 10,000 IU and higher has been associated with birth defects. That was one prospective study in 1995, which is higher quality than retrospective studies, but still contradicted all the retrospective studies that came to the opposite conclusion. 

 

So, there's no good consensus on the data, there's just moderately justifiable paranoia about the possibility that you could could cause birth defects. Also, there were like seven or eight letters to the editor about why that study had a bunch of problems with it, like the data just doesn't make sense.

 

So the basis for restricting A in pregnancy is a theoretical concern that doesn't have a lot of data to support it. That said, I see no reason why someone needs 10,000 IU or more going into the first eight weeks of pregnancy.

 

If you eat liver once or twice per week, you're not getting more than that. If you took a half a teaspoon of cod liver oil every day, you're not getting more than that. If you eat eggs and dairy every day, you're not getting more than that.

 

So, I would not supplement with 10,000 IU and higher vitamin A going into pregnancy, not because I'm super paranoid and there is good data justifying the restriction, but because the theoretical concern outweighs the lack of theoretical benefit in most cases for most women.

 

Now if that woman is trying to get pregnant, but her serum retinol is low and her eyes are dry and her night vision is bad and she has hyperkeratosis, then you bend the rules a little bit because you have an obvious justification to get her vitamin A levels up. 

 

It's just speculation versus speculation, so why not pave the middle ground of what you would reasonably get from food?

 

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



Dec 30, 2019

Question: Does mixing carbohydrate with fat cause people to get fat because of the Randle cycle?

 

There's a theory floating around on the internet that mixed diets are more fattening than low-carb or low-fat diets because of the metabolic competition between glucose and fatty acids. 

 

I don't believe this to be true because, in the context of isocaloric diets, mixed diets don’t seem to be more fattening than low-carb or low-fat diets.

 

Isocaloric diets are important for understanding physiological cause and effect, but they interfere with the real-life practical understanding of something. We want to use isocaloric science to study the academic question of, physiologically, are carbs and fat more fattening when combined than not combined. But, in real life, people eat more food on a mixed diet than they eat on a low-fat or low-carb diet.

 

I think someone who says mixed diets are more fattening because of the Randle Cycle is totally misunderstanding this. They are more fattening because of the hyperpalatability factors that Stephan Guyenet has explained. 

 

Also, they probably are more likely to cause metabolic harm because of what Alex Leaf has explained about the Randle Cycle in his post, “Why you may reconsider buttering your potato” at Superhumanradio. He was arguing that you don't want to put butter on your potato because you have substrate competition between glucose and fatty acids, which makes it more difficult to clear the glucose from your blood and causes a compensatory higher insulin response.

 

I'm not so insulin-centric that I believe that you necessarily always want to be minimizing your insulin response, and I definitely know that I have friends and colleagues who disagree with me on that, but I just don't view any disease, including type-2 diabetes, as a problem with hyperinsulinemia.

 

The short of it is that the more you mix carbs and fat in your diet, the more likely you are to overeat. You don't necessarily overeat, but it's way more probable because it's hyperpalatable. The more you mix carbs and fat, the more you don't specialize in one or the other. What's the most efficient thing to do?

 

If you eat a high-carb, low-fat diet your body specializes in burning carbs, you eat a high-fat, low-carb diet your body specializes in burning fat — and you're not going to do either of those as good if you're eating a mixed diet. Can you do them good enough? Often times, but if you have metabolic problems you might want to try a low-carb or a low-fat diet so you can specialize and be more efficient with your metabolism, because if you have metabolic problems whatever you're doing isn't working for you right now.



Dec 27, 2019

Question: What to do if gamma-tocopherol levels are low-normal while taking 100 IU/d of alpha-tocopherol.  

 

My initial impression is that there is nothing wrong because I don't care that much about gamma tocopherol. My doctoral research specialized in gamma tocopherol and there is some evidence that gamma tocopherol does some things that alpha tocopherol doesn't do. It’s likely that people who take high-dose alpha tocopherol supplements are suppressing their gamma tocopherol levels.

 

But you don’t have to be in the middle of the green for gamma tocopherol on the ION test. So if you are taking a 100 IU of alpha tocopherol at the time of test, then stop taking that and replace it with TocoSorb, or take a lower dose. I think a reasonable dose of vitamin E for the average person is 20 IU.



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



Dec 26, 2019

Question: What to do if taking biotin and yet beta-hydroxyisovalerate is elevated.

 

Well in theory that's a marker of biotin deficiency, but you might have a defect in a biotin-dependent enzyme so you can try 5 milligrams, but if you still have high beta hydroxy isovaleric you need to start looking at a metabolic disorder, providing there are symptoms. You might have a 20% decrease in that enzyme activity.

 

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



Dec 24, 2019

Question: For someone who is taking 45 mg of vitamin B6 as P5P but has xanthurenate, kynurenate, and quinolinate high in the urine as markers of vitamin B6 deficiency, and who is a man with high estrogen, what should they do?

 

If you have xanthurenate and kynurenate spilling into your urine, it means that quinolinate would be building up. Quinolinate is usually the last thing to rise in B6 deficiency. 

 

Quinolinate is an excitotoxin: it both can cause neurotoxicity like glutamate does and it can also make you hypersensitive to glutamate, effectively giving you a glutamate sensitivity.

 

You clarified that quinolinate is in the fourth quintile. So you're kind of in the zone quinolinate might be a problem, particularly if you have trouble sleeping, or if you have trouble with anxiety, or you have anything that would be related to glutamate sensitivity, like headaches

 

If you have any of those symptoms, they could be from quinolinate buildup. In that case, I recommend increasing B6. I would titrate it up to 100 mg. I'd be very cautious going higher than that. Don't take any pyridoxine hydrochloride ever.

 

Second course of action is look at iron and riboflavin levels. If there's any things wrong with those fix them, since they are needed to properly convert tryptophan alongside B6.

 

Third course of action is to reduce protein intake, if necessary, or search for low tryptophan proteins and focus on those to meet your protein needs. You need at least a few hundred milligrams of tryptophan in your diet to be okay.



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



Dec 23, 2019

Question: For someone who is homozygous for the H63D allele of the iron- and hemochromatosis-related HFE gene, if ferritin is low but transferrin saturation is high, should they still donate blood?

 

H63D is one of the genes that predisposes to hemochromatosis, a condition of iron overload. Most clinicians who work in this area do not consider the H63D allele to be a concern because it's less severe. With that said, most people who are progressive on the iron research front do believe it's a concern. There is literature showing that people can get clinical hemochromatosis from it and you don't have to get clinically hemochromatosis to be worried about iron overload. 

  

My opinion on this is going to be different than someone who is an expert clinician, but is not immersing themselves deeply in the physiological literature about how this works.

 

I don't have the skills that they have in triaging and filtering who’s ideal for what treatment and looking at large numbers of people that do one or another treatment and knowing intuitively what happens in those — but what I do have is I have immersed myself very deeply in the physiology. 

 

So the way that I look at this is as follows: iron saturation is an estimate of your transferrin saturation. It's a cheaper way to estimate it than to actually measure transferrin saturation, so it's much more common to get iron saturation.

 

But let's assume that we're talking about actual transferrin saturation or that iron saturation is a good metric of it. That's your short-term iron storage. Ferritin is your long-term iron storage. The defect in the H63D allele, same for the C282Y allele of the HFE gene, the two moderate and severe hemochromatosis alleles. Allele is a variant of the gene.

 

In normal physiology what happens is transferrin acts as a gauge of your iron status. The normal physiological levels are between 30 and 40 percent. Now being 41 percent doesn't mean you have a disease, we're not talking about diagnosis here, we're talking about understanding the physiology.

 

Mechanistically this is designed so that as you go from 30 to 40 percent and especially as you go over 40 percent that communicates the signal to a hormonal system that says you have more iron than you need. So you ramp down iron absorption and you ramp up ferritin. Why do you ramp up ferritin? Because you have more than you need in your short-term storage, so that's when you put it into your long-term storage. Also, because ferritin is a protective response that prevents you from having free iron.

 

Free iron is bad because it feeds pathogens and it makes infections worse. Free iron is bad because it causes oxidative stress and causes wear and damage on your tissues. And so to avoid free iron you ramp up ferritin while you take down your absorption from food at the same time.

 

And now is that a problem at all?  You could debate that, but if you're just talking, if you're not talking about diagnosis and you're talking about wellness, and you're talking about health management then… What I would want to do myself in that situation is I would first of all not let the ferritin go under 20, and if it's going near there I

would be getting a CBC to make sure I'm not making myself anemic.

  

And so I would not stop donating blood just because the ferritin is going down 60, 50, 40, I would consider it a gray area, it would be my preference to focus on the transferrin saturation and get it consistently under 40%. You get the pinprick to look at your serum iron levels, they're not going to let you donate blood if you're actually in the danger zone of anemia.

 

So I would get the CBC to be proactive about 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/

 

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



Dec 20, 2019

Question: Thoughts on lowering my resting heart rate. It's often in the high 80s or low 90s once I'm up for the day.

 

I wish I knew the answer to that. I'd use it for my heart rate. I don't even measure my heart rate because my whole life it's been kind of high. I think breathing and meditation are probably the best things that you can do.

 

I've typically had a white coat syndrome response to getting my blood pressure taken, and because as soon as I feel the pressure, I start to get

anxiety and I'm like, “oh no it feels like it's high” and I get an adrenaline rush.

 

A couple of years ago I got rejected from giving blood three times in a year because either my blood pressure, or my pulse was too high when they measured it, both because of the adrenaline surge.

 

I was not able to donate blood until I started using Headspace, the meditation app, in particular the visualizations of the happiness portion.

 

The first time I was able to donate blood was when I went in to get my blood pressure and pulse taken and I imagined that bright light in the middle of my chest I just did the visualization and "boom" my heart rate and my pulse, just went straight into normal zone because I was able to create an association between that visualization and the state that the meditation produced. 

 

So that would be the first thing that I'd try. If I find out that I have a medical condition with a physiological solution I'll let you know, because I have the same thing.



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



Dec 19, 2019

Question:  How to manage the zinc-to-copper ratio and what to do if zinc and copper are both low-normal when supplementing with 15 mg of zinc and 1 mg of copper.

 

I don't recommend looking at the zinc-to-copper ratio. Although there are studies correlating health endpoints with the zinc-to-copper ratio, I do not believe that it is a causal factor in disease. 

 

I believe the zinc-to-copper ratio is often associated with disease because inflammation raises plasma copper and lowers plasma zinc, based on taking zinc up in the cells and mobilizing stored copper out of the liver. You want zinc and copper at the right levels; the ratios are less important. You want both around the middle of the reference range; the bottom of the range is not adequate.

 

If you are taking a supplement, then the simplest thing to do would be to take it twice per day instead of once per day and to make sure you are taking it on an empty stomach. Up to 50 mg of zinc will not cause nausea on an empty stomach in most people if you take it with a full glass of water.

 

Some people do have digestive issues when supplementing on an empty stomach, and if you need to take it with food, do not supplement anywhere near phytate, which is the principal inhibitor of zinc absorption and is found in whole grains, nuts, seeds, and legumes.

 

I recommend Jarrow’s zinc balance, which has the exact ratio that you’re talking about. It’s a convenient way to have the copper in the zinc supplement already. But if you are low in copper, this isn’t an adequate source for two reasons: (1) the amount of copper is too low, and (2) the form of copper isn’t ideal (it has lower bioavailability because it’s not the oxidation state that you get in food).

 

For a copper supplement, I would want to use food first, and liver capsules if you want a supplement. For foods, check out the tiers of copper-rich foods that I recommend, which includes liver, cocoa powder, and certain mushrooms.



Dec 18, 2019

Question: What nutrients are needed to break down old, damaged bone and build new, healthy bone?

 

So you are breaking down bone all the time throughout every second of your life. 

 

We are always breaking down bone, we are always building up new bone, and if you had any kind of defect in the ability to break down old bone, then you would have problems manifesting elsewhere. 

 

Bone breakdown is necessary to maintain your serum calcium levels. You would probably be having severe hypocalcemic attacks if you were not breaking down your old bone — and you probably also would have exercise intolerance and/or poor exercise performance as a result of the undercarboxylated osteocalcin released from bone, which acts as a hormone to improve energy utilization during exercise. 

 

In fact the overwhelming problem in the general population is that people are breaking down too much bone and not building it back up enough. 

 

So if you just look at the course of someone's life over time when we are young we are building more bone than we're breaking down and that, somewhere around 25 years old depending on male and female — we reach peak bone mass and then we spend the entire rest of our lives declining in bone mass.

 

To some degree when you're building bone you need everything. So eating a nutrient-dense diet across the board is important, but things that are extremely important that kind of stand out from building other tissues when you're building bone is collagen.

 

Half your bone is protein — about 95 percent of the protein in your bone is collagen. The limiting factor for collagen synthesis is glycine. Collagen peptides provide glycine and they also are better at stimulating collagen synthesis than just powdered glycine. So collagen peptides, bone broth, edible bones from canned fish or from the ends of small chicken bones, would all probably be helpful. Then clearly calcium and phosphorus are the overwhelming minerals in bones.

 

So you need enough calcium and enough phosphorus — between the two of those in the population most people do not get enough calcium and get too much phosphorus. People get phosphorus from processed foods and from soda, and in addition to the natural phosphorus in meat and other foods. If you are not eating junk food you probably don't get too much phosphorus, but you still probably get enough.

 

If you're not eating junk food, and you're not eating dairy, and you're not eating bones, you probably do not get enough calcium and in particular many people in the natural health community have read a lot of anti-calcium supplementation stuff.

 

I want to emphasize over and over again that it's better to get calcium from food than to get calcium from supplements, but it's better to get calcium from supplements and then not get calcium. 



Dec 17, 2019

Question: What are my thoughts on detoxing heavy metals?

 

My thoughts are first you need to look at how bad the heavy metal is and if it is even at a level that a conventional practitioner would say you have toxicity; for example lead. 

 

If this is your situation then I don’t feel comfortable advising anyone here, but if your levels are slightly high and you would like to reduce them, then my suggestion would be zinc supplementation on the basis that most heavy metals produce a metallothionein increase. 

 

Metallothionein is your endogenous chelatior. 

 

The ability of the heavy metal to provoke that protective response is completely dependent on zinc concentrations inside your cell even across the range of deficiency through normal status through more zinc than you need, and there's no evidence for a threshold or cutoff.

 

So I think if your zinc status is fine and you boost your zinc status a little, without causing any zinc toxicity, or copper deficiency -- I think that's a very gentle and safe way to reduce your load of heavy metals.

 

Unless what you're seeing is arsenic, in which case methylation would be my focus because methylation plays a specific role in addressing arsenic. For anyone who hasn't seen that I have a comprehensive methylation resource at chrismasterjohnphd.com/methylation.

 

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



Dec 16, 2019

Question: What to do about elevated morning blood glucose in the mid 90s.

 

I think usually your morning glucose is primarily impacted by your hormones and very rarely impacted by what you ate the night before, unless you are severely glucose intolerant.

 

So the overwhelming probability is that if your blood glucose is elevated in the morning and mid-90s is not tremendously high; it is most likely cortisol. 

 

If there are other signs of slipping into pre-diabetes then I might come up with another explanation, but I don't think waking up in the morning and often having mid-90s glucose — with everything else being fine, is likely to be a sign other than cortisol levels. 

 

It's not necessarily a bad thing because you're supposed to have a cortisol spike in the morning. You may want to look at your cortisol levels over time. The DUTCH test can do that. It happens to look at a lot of other things that I think are useful so that might be my first go-to. 

 

First you want to know if that's actually the issue. 

 

If cortisol is out of range then you probably want to look at stress reduction as a first step, and there's some evidence for using phosphatidylserine to lower cortisol. 



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Dec 13, 2019

Question: neither my mother nor myself respond to T3 supplementation (cytomel; up to 140 mcg/d). Body temp remains low and reverse T3 stays normal. Could you discuss the factors that might interfere with thermogenesis in response to T3, and offer considerations how to improve this?

 

Having normal levels of reverse T3 tells you that the body isn’t deliberately getting rid of the thyroid hormone. High reverse T3 would be a sign that your body just doesn't want the thyroid hormone around.

 

That doesn't seem to be happening and so that makes me wonder if there could be a problem with taking up the thyroid into the cells. In which case I would expect thyroid hormone levels to be higher in the blood then you would otherwise expect them to be.

 

Or if there's a problem with the thyroid actually carrying out its functions inside the cell to regulate gene expression. This could be a zinc deficiency issue, since zinc is necessary to allow the thyroid receptor to bind to the DNA. In fact, zinc is necessary for everything that has a nuclear receptor that alters gene expression by binding to a nuclear receptor. This includes receptors for vitamin A and vitamin D, receptors for the sex hormones, and for thyroid hormones; all require zinc to act.

 

But, you seem to be saying that your issue is a specific thermogenic response, which makes me ask, are you seeing every other thing that you would expect from thyroid  hormone and not thermogenesis? 

 

If that's the case, I have no idea. But, if you're not seeing any of the effects from thyroid hormone that you would expect, then I would say maybe some kind of resistance to getting into the cell if blood levels are elevated. If blood levels are normal, then maybe it’s not acting on the nuclear receptor, which I'd think zinc deficiency. 

 

I don't know what else you could do with the exception of measuring the free fatty acids, which would be high if you had a zinc deficiency. They might not be if you're taking insulin and you're eating moderate to high carb. Get free fatty acids measured, which would often be called NEFA, for non-esterified fatty acids.

 

You know you can't have everything. I would rather your pancreas just start making all the insulin it needs, but options are limited, right? so I don't know if you can fix the temperature issue. If you can with fixing it at the root problem great, but if you can't then absolutely I would I would manage your temperature with clothing. 

 

This Q&A can also be found as part of a much longer episode, here:https://chrismasterjohnphd.com/podcast/2019/02/09/ask-anything-nutrition-feb-1-2019/ 

 

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



Dec 12, 2019

Question: "What are your top three non-nutrient factors that prevent someone from entering beta-oxidation or ketogenesis? I mean like sleep disruption."

 

Top three non-nutrient factors? Unless you are taking a drug that prevents lipolysis, then they aren't non-nutrient. 

 

The overwhelming things that govern those are carbohydrate and fat intake. You eat more fat, you have more beta-oxidation. You eat less fat, you have less beta-oxidation. You eat less carbohydrate beyond a threshold.

 

==I don't think sleep disruption is going to do that. Sleep disruption is going to increase your stress hormones — so with sleep disruption, your cortisol is going to spike, and it's going to increase your appetite for junk food —  so you're probably more likely to eat things that are anti-ketogenic when you're sleep-deprived because you're eating more junk food, which has more carbs. You probably are not going to have lower beta-oxidation. You're probably going to have higher oxidation because you're going to eat more fat.

 

But most people do not have impairments in beta-oxidation. 

 

If you have a riboflavin deficiency, you can have an impairment in beta-oxidation, but even in disease states, beta-oxidation is higher. If you have a fatty liver, beta-oxidation is increased because your liver is trying to get rid of fat.

 

The overwhelming thing governing beta-oxidation is the relative balance of fat going into your tissues versus out. To the extent carbs displace the fat from being burned, carbohydrate is going to decrease beta-oxidation —  but if you're eating carbohydrate, and you're eating more fat, versus less fat, you're going to have more beta-oxidation when you eat more fat. 

So, yes, sleep disruption will disrupt the appropriate way of handling those things, but I don't think it's going to block ketogenesis or beta-oxidation, except by messing up your appetite.

 

This Q&A can also be found as part of a much longer episode, here:https://chrismasterjohnphd.com/podcast/2019/02/09/ask-anything-nutrition-feb-1-2019/ 

 

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



Dec 11, 2019

Question: "Any recommendations for peripheral neuropathy? Testing vitamin B, lion's mane?"

 

First of all, there is no such thing as vitamin B. I'm not trying to be a nitpick, but there's literally almost a dozen B vitamins, with different tests, that do different things. So, I think it's important to establish a habit of never saying vitamin B because, not to be a grammar nitpick, but I just think it's misleading to think about the concept of vitamin B. 

 

There are quite a few B vitamin deficiencies that can cause peripheral neuropathy. 

 

You can also cause peripheral neuropathy by taking vitamin B6 in too high doses, and that's one of the reasons why you have to separate them out because B6 is unique among the other B vitamins in that respect. 

 

In Testing Nutritional Status: The Ultimate Cheat Sheet; I have an index of signs, and if we go into peripheral neuropathy, I have listed here deficiencies of thiamin, riboflavin, and vitamin E — toxicity of selenium and B6. 

 

This Q&A can also be found as part of a much longer episode, here:https://chrismasterjohnphd.com/podcast/2019/02/09/ask-anything-nutrition-feb-1-2019/ 

 

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



Dec 10, 2019

Question: "If cholesterol, LDL-P, and oxidized LDL are high, the sterol panel is normal, and TGs are great, would you suspect clearance of the particles driven by LDL receptor in the liver is the issue, and what would you recommend to boost LDL-R?"

 

Yes, it sounds like you should target LDL-R. 

 

The big regulators of LDL-R function are thyroid hormone, and the amount of cholesterol in the liver cell, and anything that brings bile acids into the feces, and that's generally a high-fiber diet; psyllium husk would be a fiber you could add.

 

Thyroid hormone is the other piece of that, and that you target with higher carbohydrate intake. Higher carbohydrate intake also acts on PCSK9 to boost LDL receptor activity. 

 

This Q&A can also be found as part of a much longer episode, here:https://chrismasterjohnphd.com/podcast/2019/02/09/ask-anything-nutrition-feb-1-2019/ 

 

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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