Mastering Nutrition

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Concerns about vitamin A in pregnancy | Masterjohn Q&A Files #37 Jan 02, 2020

Show notes

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/

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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.

Does mixing carbohydrate with fat cause people to get fat because of the Randle cycle? | Masterjohn Q&A Files #36 Dec 30, 2019

Show notes

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.

Access the show notes, transcript, and comments here.

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

What to do if gamma-tocopherol levels are low-normal while taking 100 IU/d of alpha-tocopherol. | Masterjohn Q&A Files #35 Dec 27, 2019

Show notes

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/

Access the show notes, transcript, and comments here.

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

What to do if taking biotin and yet beta-hydroxyisovalerate is elevated. | Masterjohn Q&A Files #34 Dec 26, 2019

Show notes

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/

Access the show notes, transcript, and comments here.

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

B6 deficiency, and who is a man with high estrogen, what should they do? | Masterjohn Q&A Files #33 Dec 24, 2019

Show notes

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/

Access the show notes, transcript, and comments here.

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

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? | Masterjohn Q&A Files #32 Dec 23, 2019

Show notes

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/

Access the show notes, transcript, and comments here.

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

How to lower a resting heart rate in the 80s or 90s. | Masterjohn Q&A Files #31 Dec 20, 2019

Show notes

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/

Access the show notes, transcript, and comments here.

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

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. | Masterjohn Q&A Files #30 Dec 19, 2019

Show notes

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.

Access the show notes, transcript, and comments here.

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

What nutrients are needed to break down old, damaged bone and build new, healthy bone? | Masterjohn Q&A Files #29 Dec 18, 2019

Show notes

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.

Access the show notes, transcript, and comments here.

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

What are my thoughts on detoxing heavy metals? | Masterjohn Q&A Files #28 Dec 17, 2019

Show notes

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/

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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