Mastering Nutrition

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Alex Leaf answers a question about creatine non-responders and methylation. | Masterjohn Q&A Files #47 Jan 16, 2020

Show notes

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/

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Access the show notes, transcript, and comments here.

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

How to bring up low levels of arachidonic acid. | Masterjohn Q&A Files #46 Jan 15, 2020

Show notes

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/

Access the show notes, transcript, and comments here.

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

How to interpret the pattern of high citrate, low cis-aconitate, low glutamate, and high glutamine. | Masterjohn Q&A Files #45 Jan 14, 2020

Show notes

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/

Access the show notes, transcript, and comments here.

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

Nutritional strategies for glucose 6-phosphate dehydrogenase (G6PDH) deficiency. | Masterjohn Q&A Files #44 Jan 13, 2020

Show notes

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/

Access the show notes, transcript, and comments here.

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

How much fatty fish should you eat? | Masterjohn Q&A Files #43 Jan 10, 2020

Show notes

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/

Access the show notes, transcript, and comments here.

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

How to deal with the fact that blood tests for nutritional status aren't adapted to children. | Masterjohn Q&A Files #42 Jan 09, 2020

Show notes

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/

Access the show notes, transcript, and comments here.

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

Matt stone and the "overdeification" of vitamin A. Or, are there many people who are vitamin A deficient? Hypersensitivity reactions, fatty liver, overzealous use of cod liver oil, and other concerns. | Masterjohn Q&A Files #41 Jan 08, 2020

Show notes

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/

Access the show notes, transcript, and comments here.

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

Is it ok to mix carbs and fat? | Masterjohn Q&A Files #40 Jan 07, 2020

Show notes

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/

Access the show notes, transcript, and comments here.

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

What are "parent essential oils"? Should we get these instead of cold-water fish oils? Response to Brian Peskin's theory. | Masterjohn Q&A Files #39 Jan 06, 2020

Show notes

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.

Access the show notes, transcript, and comments here.

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

How to use an Oura ring to monitor HRV and optimize recovery and performance. | Masterjohn Q&A Files #38 Jan 03, 2020

Show notes

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.

Access the show notes, transcript, and comments here.

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

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