In this episode we conclude the excellent 3-part series on cholesterol and heart disease with Chris Masterjohn. It’s been a pleasure to have Chris with us throughout the series, as he’s the most knowledgeable person I know about these topics. We’ll certainly have him back in the future!
In this episode, we cover:
2:30 The role of cholesterol in heart disease
11:26 What to do – or not do – about high cholesterol
24:11 The thyroid-LDL connection and why iodine matters
29:36 Are goitrogenic foods inhibiting your thyroid function and raising your cholesterol?
46:01 The telltale sign you need more carbs
Links We Discuss:
- Chris Masterjohn Blog - The Daily Lipid
- Thyroid Toxins Special Report
- Chris Masterjohn article: Bearers of the Cross: Crucifers in Context
- Super Selenium Complex from Life Extension
- Nutrition and Physical Degeneration, By Weston A. Price
Full Text Transcript:
Steve Wright: Hi everyone, and welcome to the Revolution Health Radio Show. I’m Steve Wright from SCDlifestyle.com, and with me today is Chris Kresser, health detective and creator of ChrisKresser.com. How’s it going, Chris?
Chris Kresser: It’s going pretty well, Steve. How are you?
Steve Wright: I’m doing good. The shoulder is healing up, and I’m pretty excited for our special guest today.
Chris Kresser: Yeah, me too. We’ve got Chris Masterjohn back for Part 3 of the Cholesterol Series. Really excited to wrap this up. It’s been a really popular series so far. We’ve gotten a lot of great feedback. People are learning a lot. I’m learning a lot. It’s always a pleasure to have Chris on the show. So, for those of you who don’t know Chris, it’s time for you to crawl out from under that rock you’ve been hiding under! He’s one of my favorite bloggers in the Paleo/Primal food sphere, and he is just super knowledgeable about all this stuff. He is pursuing — well, actually I’ll let him introduce himself. He knows more about what he’s doing right now, but he is pursuing a PhD, and I think those of you who know his work know how much he has to bring to this discussion. So, we’re happy to have you back, Chris. Why don’t you just give a really quick intro for people who don’t already know you, and then we’ll dive in.
Chris Masterjohn: Sure! Thank you so much for having me back, Chris. My website is Cholesterol-and-Health.com. I have a blog there, The Daily Lipid. Right now, I’m just wrapping up my PhD. I’m almost done.
Chris Kresser: Woo-hoo!
Chris Masterjohn: I am getting my PhD in nutritional sciences, and that is studying how diet and nutrition works on a physiological and biochemical level, and I’m currently writing a dissertation on how oxidative stress regulates the production of methylglyoxal and its detoxification, which is a key player in advanced glycation endproducts, which are believed to play a role in diabetes and cardiovascular disease.
Chris Kresser: That’s some light reading for the weekend, maybe.
Chris Masterjohn: Ha-ha, yeah.
Steve Wright: Yeah, that’s a mouthful!
Chris Kresser: Cool. So, we’ve already done Part 1 and Part 2 of this show, and now we’ve got transcripts and you can go back and listen to the original episode. Chris, why don’t we do just, like, a really super-quick recap of what we talked about in the first couple parts, and then we’ll dive into this last part so we have plenty of time to cover that material?
The role cholesterol plays in heart disease
Chris Masterjohn: Absolutely. So, in Part 1 we just outlined my basic ideas about the role of the degeneration of lipids in heart disease, and we talked about the two camps: the cholesterol warriors who are making a war on cholesterol because they see cholesterol as the enemy and, you know, the aggressor in heart disease, and the cholesterol skeptics who basically say, well, blood lipids don’t really have any role in heart disease. And the basic conclusion of Part 1 is that blood lipids do play a role in heart disease, but it’s not that their high concentration is infiltrating the vessel wall; it’s that their degeneration is posing a danger to the blood vessels, and the immune system comes and mops them up to create the atherosclerotic plaque. And that is a positive adaptation to this process of degeneration, but it poses a risk in the long term because that plaque can ultimately break down and cause a heart attack. So, from Part 1, what we concluded was that we don’t want to modify the concentration of lipids in the blood so much as prevent their degeneration.
Chris Kresser: Right, so let me just jump in and summarize there. So, the original theory, the infiltrative theory, is sort of like arteries are like pipes and cholesterol is like gunk, and the pipes get clogged up with cholesterol, and then you have a heart attack. Right? That’s kind of how it was broken down in the mainstream. But, what you’re saying is that what really happens is that the cholesterol — or more accurately, the lipoproteins that are carrying cholesterol and other fats — get damaged by oxidation, and then the immune system’s response to that oxidative process is what causes the buildup of plaque and then ultimately the rupture of plaque and heart attack. Is that accurate?
Chris Masterjohn: Yeah, absolutely. So, what we’re trying to do is protect the vulnerable lipids and get them to go where they need to be. And what we want to do is we want to metabolize the lipids and fat-soluble nutrients and everything that’s in our bloodstream and use them properly. So, for example, cholesterol we want to turn into bile acids for our digestion, sex hormones for our fertility and virility, and we don’t want them left in the blood to be damaged and contribute to atherosclerosis.
Chris Kresser: OK, cool. So, then Part 2 we talked a lot more about testing normal variation of cholesterol markers, particle size, etc. So, take us through that.
Chris Masterjohn: Sure. So, we have to keep in mind that since we’re focused on the degeneration of lipids and protecting those lipids in the blood, when we look at concentrations of lipids, we’re not trying to look at necessarily a cause-and-effect scenario. So, if we’re concerned when total cholesterol goes really high, it’s not because that is causing heart disease, but we’re using this as a metabolic clue. So, in the initial parts of Part 2, what we did was looked at some of the traditional cholesterol levels in populations that have not been through industrial modernization, that have been studied and have been shown to be free of heart disease, to try to see what normal lipid metabolism is like. And we looked at two groups in particular: the Masai and the Kitavans, who have been well studied and shown to be free of heart disease; and we used them to define basically the lower and upper limits of blood cholesterol. And what we see is the Masai have pretty low cholesterol levels, but the Kitavans, who are eating a diet based on fish, coconut, starches, and so on, the men tend to have cholesterol levels around 180, the women tend to have cholesterol levels around 200 to 210, and these tend to increase with age. So, in their 40s and 50s, the women might have cholesterol around 250. In general, the LDL/HDL ratios are between 2 and 4 in these tropical populations. And there are some other populations that have not been studied quite as well but also seem to be free of heart disease, like Tokelau, where the consumption of coconut is much higher, and their cholesterol levels in the case of the men increase from about 180 to 220 with age and in the women tend to increase from about 200 to 245 with age. So, around 250 total cholesterol is where we might set the upper limit of what seems to be normal, according to these traditional populations eating traditional diets that are free of heart disease. That doesn’t mean that a cholesterol level of 251 is gonna kill you. It just means that that might be the point where we might start looking at some other signs and symptoms to see if there is a problem, not necessarily assuming that there is one. And then we went through how do I know when my cholesterol is really increased, because there is a lot of variation that we can normally expect. And we said that if we’re just looking at two measurements — say, we changed our diet, we measured cholesterol once before and once after the diet — if we hadn’t measured our cholesterol very often to get a sense of our own variation, then we should be careful not to assume that it has increased unless we have an increase of at least 35 mg/dL for total cholesterol, about 10 mg/dL increase or decrease for HDL, 30 mg/dL for LDL, and about 40 mg/dL for triglycerides. So, we should be concerned when we see these large increases and they go outside the range of what is considered to be traditional. And the total/HDL cholesterol ratio seems to provide the most information, and particle size and other of these emerging tests probably need to wait on the bench until we can standardize them better and be able to utilize them to provide clearer information than what we have now.
Chris Kresser: Right. Not ready for prime time. There is one interesting test. Maybe in Part 4, eventually when we have that, we’ll talk about it. It’s an oxidized LDL test, which has only been available in the research settings, but there’s a lab in New York that is starting to offer this, and I’ve been corresponding with them. They’re not quite there yet, but hopefully in the near future that will be available. Again, it’s not totally clear how useful that would be yet. I mean, what’s your impression of that from your reading of the literature, Chris, the oxidized LDL marker?
Chris Masterjohn: Well, I think the way that you just summarized it is probably pretty good. It’s not clear how useful it is yet. I do think that it’s probably going to offer some advantages, but there is always gonna be some lack of clarity in interpreting it, because when LDL oxidizes in the blood, it’s cleared very quickly from the bloodstream. So, you have to remember that if you’re looking at oxidized LDL, you’re taking a snapshot of what is in the plasma at an instant, and I think we need to study it more to see how reliably it gauges the actual process of oxidation. We want to try to infer the processes that are going on and not just look at the snapshot as if things are static.
Chris Kresser: Um-hum. OK, so we’ll come back to that maybe when we have some more info on it, but let’s now talk about the meat of Part 3 here, which is the question that’s on a lot of people’s minds, and actually in my practice I still get quite a few of these questions, even people who have read all of your work, Chris, and my work and, you know, they’ve been exposed to these ideas for a long time, but when their cholesterol is somewhere around 250, there are still many, many years of conditioning around the idea that high cholesterol is gonna cause heart disease, and so understandably people, when their cholesterol starts to creep up a little bit like that, their question is — So, you know, they’ve changed to a Paleo Diet or a Weston A. Price / Primal type of diet, and they get their cholesterol checked, and their total cholesterol or LDL cholesterol are out of range, you know, out of the lab range and maybe up towards that 240 or 250 mark that you just mentioned. So, what could be going on here in these cases? This is what we’re gonna talk about today, and what kind of steps can people take to investigate a little further to determine whether that slightly elevated total cholesterol and LDL cholesterol is a problem or whether it’s just part of a natural physiological process.
What to do – and not do – about high cholesterol
Chris Masterjohn: Absolutely. So, the first thing that we need to understand is that there are good reasons and bad reasons for increases in cholesterol in the blood. So, one of the reasons that cholesterol can increase is if we’re clearing lipids from the liver. Let’s say, for example, that a person has nonalcoholic fatty liver disease and they start resolving it. Well, one of the key problems with fatty liver disease is that the lipids get stuck in the liver and they’re not being released into the bloodstream, so once you start clearing that, part of what may happen is you may get an increase in triglycerides, and you may get an increase in cholesterol in the blood. And that is a good thing because nonalcoholic fatty liver disease is not only very dangerous for the liver, but it’s actually a much stronger predictor of cardiovascular disease risk. And this is a currently emerging field, but there is one study that was done in Japanese people, and they just looked at a number of a Japanese population that was apparently healthy, and they looked to see if they had fatty liver or not, and then they followed them over a number of years. And they found that fatty liver disease increased the risk of cardiovascular disease by over fivefold; whereas, LDL cholesterol predicted it somewhat, but the study wasn’t even statistically powerful enough to make that connection to LDL cholesterol statistically significant. And then when they incorporated LDL cholesterol and metabolic syndrome in a statistical analysis, they found that LDL cholesterol and metabolic syndrome, neither of those were even significant, and nonalcoholic fatty liver disease raised the risk of cardiovascular disease by about threefold or fourfold for men and about fourteenfold for women. So, if we’re clearing lipids from the liver, then this is a good thing.
Chris Kresser: Yeah, that’s a pretty phenomenal statistic there, especially in light of some of the estimates that I’ve seen that up to one in three Americans have nonalcoholic fatty liver disease, which would really go a ways to explaining the cardiovascular disease epidemic.
Chris Masterjohn: Absolutely.
Chris Kresser: So, you’ve written about this, Chris, what you were just talking about in terms of switching to a Primal/Paleo type of diet and the lipids going up because the fatty liver is sort of unpacking itself. And you’ve written about this extensively that choline is one of the nutrients that makes that possible, so can you say a little bit more about that?
Chris Masterjohn: Sure. So, the best sources of choline are liver and egg yolks. There are also a number of other nutrients such as folate, for example, that reduces the need for choline. So, it you’re increasing your intake of liver, egg yolks, and leafy green vegetables — you know, a general increase in nutrient density in your diet — it’s very likely that if you do have fatty liver you are going to contribute to its resolution, because choline is the key nutrient that is needed to package the fats in the liver and export them into the bloodstream so they can be metabolized by other tissues. Now, like you said, one in three Americans might have fatty liver, and the best way to diagnose fatty liver, to get certainty, the least invasive way is with an ultrasound. It can also be diagnosable with MRI or biopsy.
Chris Kresser: One of the names for that is FibroSURE.
Chris Masterjohn: For the test?
Chris Kresser: Yeah. Just to let people know, if they want to ask for that test. I mean, in my experience, a lot of doctors won’t order it, but if you want to ask for it, that’s what it’s called.
Chris Masterjohn: Right.
Steve Wright: Are there any blood markers that would, you know, predate that, because you can’t just walk into your doctor’s office and just say, “Hey, can you ultrasound?”
Chris Kresser: You might see a mild elevation in aminotransferases, so like AST and ALT. They’re sometimes called liver enzymes. And ALT is fairly specific to the liver, but AST can reflect tissue breakdown in other organs.
Chris Masterjohn: Yeah, but none of the aminotransferases are very specific to fatty liver, so the best predictor of fatty liver is obesity and insulin resistance. So, among obese Americans, over three-quarters have fatty liver.
Chris Kresser: Wow.
Chris Masterjohn: So, if you are correcting obesity and insulin resistance and you don’t want to have a biopsy or your doctor won’t order an ultrasound, I think you can assume that resolution of fatty liver is a very likely candidate reason for why blood lipids may increase, but they should normalize over time.
Chris Kresser: Yeah, let’s say someone is obese and they go on a low-carb diet and they start eating liver and a lot of coconut oil and, you know, egg yolks and a lot of the foods that are choline-rich and folate-rich, and they experience this change in lipids, do we know from the literature how long we could expect that to take?
Chris Masterjohn: No, I haven’t seen anything good on it, so I think what we need to do is track people’s experiences and start to get some anecdotal evidence on this, and hopefully we’ll see, you know, some guidelines coming out in the scientific literature. But I think if we monitor these things and share some experiences, that might give us some clues sooner.
Steve Wright: Is it a big deal with the egg yolks to cook them or eat them raw?
Chris Masterjohn: I don’t think so. When I eat egg yolks, I usually eat them raw, but I don’t think that that’s going to make a big difference in resolving fatty liver disease. I think providing the choline is the main factor.
Chris Kresser: OK.
Chris Masterjohn: So, clearing lipids from the liver is good. You can have a decreased clearing of lipids into atherosclerotic plaques, and that’s also going to be good. You can have increased weight loss. And weight loss, if you’re clearing lipids from adipose stores, that could elevate your blood lipids, and this could be good or it could have negative effects in some cases. You know, if you have an overweight person, they are a lot more likely to have fatty liver, they are a lot more likely to have insulin resistance, but probably the person who’s probably in the worst-case scenario is the overweight person who is trying to lose weight by restricting calories and is in a sort of chronic starvation mode, where instead of getting a good diet that’s lowering their set-point, they’re always operating underneath their set-point, and that can contribute to a lot of stress and release of free fatty acids and things that can have negative effects on thyroid hormone. But I think if you follow a weight loss strategy that is not leaving you hungry and stressed, I think you can expect a moderate elevation of lipids in some scenarios. And we talked about this in the second episode, so we shouldn’t go into too much detail; but in my opinion, if someone is losing weight and they’re losing it at a healthy pace in a sustainable way and they see fluctuations in their blood lipids, in my personal opinion, they should wait until their weight has been stable for three to six months before trying to interpret it. In other words, if blood lipids go up while you’re losing weight, concentrate on losing the weight and normalizing your metabolism. Then once your weight has been stable, start looking at blood lipids and so on.
Chris Kresser: Yeah, and maybe get a few readings once your weight is stable, given the normal variation that they’ve talked about in the previous show.
Chris Masterjohn: Exactly. So, you always want to get two or three readings to look at that variation. And, you know, while you bring that up, that’s a source of error. I have also seen cases where people go on a diet that seems to be helping, and they say: Why have my blood lipids increased? And it was a simple error like they were fasting one time and they weren’t fasting the other time.
Chris Kresser: Right. Great point.
Chris Masterjohn: So, obviously if it’s due to error, then we can’t say this is good or bad. We need to say, “Correct the error and repeat it once you have the conditions kept the same.” But there are bad cases of increased lipids, and the bad cases are where we are decreasing the clearance of lipids from the blood. And I think that there are basically three reasons that this is likely to happen when someone is switching to a more ancestral diet, which seems to be what most people in this circle are concerned about. Why would these blood lipids increase when we are eating a more Paleo Diet or a more Weston Price type approach, a more ancestral diet? And there are some bad things that can happen, and I think that we should discuss those a little bit. One is that you can have decreased thyroid activity either due to extreme and chronic carbohydrate restriction. The other is that you may have an iodine deficiency if you have increased some of your intake of plant goitrogens and haven’t included enough iodine-rich foods, especially seafoods, in your diet. And I think the other case is in certain cases someone might have familial hypercholesterolemia, and when they switch their diet to a diet that contains more cholesterol and more saturated fat and less polyunsaturated fat, there are reasons why that would increase blood cholesterol that might not be harmful in someone who doesn’t have familial hypercholesterolemia but might actually be harmful in some cases for someone who does have familial hypercholesterolemia.
Chris Kresser: So, just to save us all the breath, because we I think we might talk about this a little bit more, let’s call familial hypercholesterolemia FH. It’s a codeword. I’ve been stumbling over that in previous episodes, so FH from here on out. So, Chris, let’s talk a little bit — I see this actually quite a bit in my practice with iodine and thyroid and activation of the LDL receptors, so let’s talk a little bit more about that.
The Thyroid-LDL connection and why iodine matters
Chris Masterjohn: Sure. OK, so thyroid hormone is the central governor of the LDL receptor, and the LDL receptor is, in turn, the central governor of clearance of LDL cholesterol from the blood. And basically thyroid is a messenger who is communicating that we are in a state of abundance, we have all of the food and nutrients that we need, and it is time to utilize those nutrients for the purposes of reproduction, high physical performance, and other things of that nature. And cholesterol is the precursor to a lot of these key hormones, like the sex steroids, for example, and the bile acids that improve digestion. So, thyroid hormone basically communicates to our cells that all of these nutrients that we need are available, so our cells respond by taking in LDL cholesterol from the blood and making lots of good things out of it, like testosterone, for example. Now, one of the key things that can happen when people start increasing their intake of fruits and vegetables and decreasing their intake of grains, which is a common dietary shift in the Paleo community, for example, is that you can increase your intake of plant goitrogens. Goitrogens are named because they have the ability to cause goiter, which is a problem that occurs as a response to insufficient thyroid hormone, and basically these plant chemicals have the ability to decrease the production or activation of thyroid hormone. Now, in most of the cases, I don’t want to suggest that eating these plants is a bad thing. In most of the cases, all you need to do to compensate is increase your intake of iodine. But in certain cases, if someone is not eating iodized salt, for example, and they’re living in an area where the iodine quality of the soil is poor, and they’re not eating seafood, which is the most reliable source of iodine, they may not be getting the iodine that they need to deal with that level of plant chemicals in the diet. So, it’s not that the plants are intrinsically bad. It’s just that we need to achieve that dietary balance. So, the number of plant chemicals in the plant kingdom that inhibit thyroid function, at least in a sort of test tube assay, is almost innumerable. I mean, there are thousands of plant chemicals. Basically all of the polyphenolics — the flavonoids, for example — they basically all inhibit the enzymes of thyroid hormone. But a lot of these plant chemicals don’t really make it into the system because we detoxify them properly, and sometimes they also even have beneficial effects. So, what we need to do is look at some of the areas where there is really convincing research done either in humans or in laboratory animals showing that certain foods, in the absence of adequate iodine, can contribute to decreased thyroid function.
Chris Kresser: So, I want to jump in here too and just mention that for most people who come to me with thyroid issues, I do a 24-hour urine iodine test, and I would say probably 80% of the people that I test are iodine deficient or have excess bromide levels, which can cause some of the symptoms of iodine deficiency. So, it’s a pretty common problem, and I think that’s partly because a lot of people aren’t eating much seafood these days maybe because of concerns for mercury or just they don’t like it or it’s not available to them in an easy way. And then a switch from iodized salt to natural salt, which has less iodine; that’s pretty common when people are switching to a Paleo or Primal type of diet. So, I don’t think this is a rare problem. I think this is actually something that is fairly common, at least in my patient population.
Steve Wright: When you say “in seafood,” is it everything — shrimp, fish, seaweed — or is it specific to certain types?
Chris Masterjohn: Well, I think seaweed is the most abundant source, but all seafood generally has some iodine in it. The problem with land food isn’t that it doesn’t have iodine. It’s just that it’s so unreliable. You can have, you know, a potato grown in one part of the country and in another part of the country, and their iodine content might vary a hundredfold, but the ocean is rich in iodine, so seafood, in general, tends to be a more reliable source of iodine, but seaweed, of course, is the most abundant.
Chris Kresser: Right. And then, Chris, the other thing I wanted to talk to you about is you’ve written pretty extensively about goitrogens and a great article — I know you had a special report that I read, but also, I think, some articles on your blog about how different methods of preparation can alter the goitrogenic effect of food. So, without going into too much detail about that, can you just give us a little summary?
Are goitrogenic foods inhibiting your thyroid function?
Chris Masterjohn: Yeah, absolutely. So, I went into the most detail, like you said, on my Thyroid Toxins Special Report available on my website, and I think the other article you were thinking of was one that I wrote for Wise Traditions called Bearers of the Cross: Crucifers in Context.
Chris Kresser: Yeah.
Chris Masterjohn: OK, so there are a few different classes of goitrogenic foods, and the way preparation affects them is different depending on the class. The most common that people on an ancestral diet are probably going to be eating is crucifers. So, crucifers, for example, include broccoli, brussels sprouts, cauliflower, cabbage, collard greens, kale, kohlrabi, mustard, rutabaga, turnip, bok choy, arugula, horseradish, wasabi, watercress, maca, and even canola oil is a crucifer.
Chris Kresser: Oh, wow. I didn’t know that.
Chris Masterjohn: It’s a close relative of the turnip.
Chris Kresser: I didn’t know maca was either.
Chris Masterjohn: Yeah.
Chris Kresser: That’s interesting. Yeah. OK.
Chris Masterjohn: So, crucifers have natural pesticides called glucosinolates, and these can be metabolized when we chew the crucifer or when we chop them up and so on. So, whether we’re eating them raw or cooked, we’re gonna get some of these goitrogens. And basically what happens is there’s an enzyme that frees a chemical called isothiocyanate, and then in our bodies we metabolize this to thiocyanate, and thiocyanate decreases the uptake of iodine into the thyroid gland because it basically competes with it. So, if you have a high ratio of isothiocyanate to iodine, then isothiocyanate actually gets into the thyroid gland. It also gets into breast milk, and it crosses the placenta in place of iodine. And then once it’s in the thyroid gland, it will compete for the utilization of the enzyme that makes thyroid hormone.
Chris Kresser: Right.
Chris Masterjohn: Now, thiocyanate, you can completely protect against it simply by getting enough iodine in your diet. Now, a lot of people think that cooking or fermenting cruciferous vegetables is going to get rid of the goitrogens, but that is not true. Fermenting actually activates them. It actually does the conversion to the thiocyanate right in the jar of sauerkraut. So, if you’re eating sauerkraut and kimchi, you are not getting rid of the goitrogens. That doesn’t mean the foods are bad, but it means that you need more iodine when you’re eating those foods. If you steam the vegetables, it decreases the goitrogen yield about 30%, but it leaves about 70% of them there. Not only that, but when you steam the vegetables, the rate of liberation of the true goitrogens in the intestines varies fourfold between different people depending on their intestinal flora, so steaming is not a reliable way of getting rid of them. If you boil them for a half an hour and you keep the water, for example, in a soup, then that gets rid of 65% of the goitrogens, so about two-thirds. And if you get rid of the water, then that gets rid of about 90%, so if you boil them and then you pour the water out. Now, I don’t think that you need to go through all this extensive boiling. I think you just need to increase your iodine. But you have to realize if you have marginal iodine status and then all of a sudden you start eating sauerkraut and kimchi at every meal and then steaming broccoli for dinner, then that may push you over the edge into a frank iodine deficiency if you were on the border.
Chris Kresser: So, Chris, what’s the dose of iodine that’s required to prevent, you know, a moderate intake of goitrogenic foods like we’re talking about now in the context of a Paleo or Primal type of diet from inhibiting thyroid function?
Chris Masterjohn: Unfortunately, that has not been well characterized, but I think if we’re looking at the RDA, we’re looking at about — I think the RDA is still 150 mcg, and there are people out there who are using 50 mg, so I suspect that if you were taking 1 mg, for example, then that should be well more than sufficient to take care of the goitrogens themselves. But again, like you said, with environmental bromine exposure and so many other things, it’s possible that people may need more than that. But I think if we’re just talking about goitrogens, then that should be enough.
Chris Kresser: A minimum, yeah, a minimal dose. OK.
Chris Masterjohn: So some of the other foods are — another common food is cassava, which also goes by tapioca, manioc, yuca; flax; lima beans; and the fruits of all of the Rosaceae family, which includes cherries, almonds, plums, peaches, apricots, pears, raspberries, strawberries — these all contain cyanogenic glycosides, and sweet potatoes also contain a pretty small amount. Now, most of these foods come in different levels of bitterness, and in the more bitter varieties, that’s where you get more of the cyanogenic glycosides, and in the less bitter and more sweet varieties it’s less common. But these are also a source of thiocyanate because they actually release cyanide, and we detoxify the cyanide to thiocyanate, and it has all of the same effects as crucifers. And the most reliable way to detoxify these is to crush the foods and leach them in running water for a few days.
Chris Kresser: Ha-ha!
Steve Wright: Oh, yeah.
Chris Masterjohn: But, seriously, this becomes a key issue when you are consuming massive amounts of these. There are some people, for example, you know, certain populations where they rely on cassava for the main starch.
Chris Kresser: Sure.
Chris Masterjohn: And they actually deliberately breed the bitter varieties because it protects against insects, and they are very vulnerable to goiter unless they process these so extensively.
Chris Kresser: Right.
Chris Masterjohn: So, again, I don’t think that these are going to be a major problem unless you’re adding it on top of the crucifers and on top of the low iodine intake. And the two others are soy and millet. I don’t think that people who are, you know, eating the Weston Price or Paleo ways are really going overboard with soy, but there is a myth out there that fermentation decreases the goitrogens, and it doesn’t. It does the opposite; it increases their bioavailability. So, if you add some fermented soy on top of everything else with low iodine, that can be a problem. And probably the most goitrogenic food in the world is millet, and this could be a problem if people are getting rid of gluten and they start eating a lot of gluten-free bread that’s made from millet, for example. And millet basically inhibits every step of thyroid metabolism, and high iodine intakes cannot overcome the effect of millet. But again, if it’s a minor component of the diet, it’s probably not a problem, but when you’re compounding it with all of these other foods and a low iodine intake, that’s when it can really be an issue. So, I think the solution to all of this is to eat these foods in moderation. Don’t go crazy with them. You know, don’t get the Vitamix out and load it with as many cruciferous vegetables as you can and drink cruciferous vegetable juice all day long. There are people who do that and suffer the consequences. You know, eat these foods in moderation, and make sure that you compensate for their inclusion in the diet with eating more seafood, perhaps some occasional seaweed, and if you need it — you know, you get the iodine test that you do, for example — if you need more iodine, supplement to bring that level up to where it needs to be.
Steve Wright: Hey, Chris or Master J, if I can, because I want to keep you guys straight.
Chris Kresser: Ha-ha!
Chris Masterjohn: Yeah, that’s how I roll.
Steve Wright: OK, that’s what I thought. So, you just touched on it, and I’m glad you brought it up, and that’s the shakes or the juicing because there are a lot of us — and I don’t do it, because I hate cleaning my blender — but a lot of people like to make a shake in the morning, and you’ll see a lot of bloggers telling you to make a green smoothie. Is even doing, like, a cup a day or something in my smoothie, over time is this gonna be a problem?
Chris Masterjohn: I don’t think it’s going to be a problem as long as you have adequate iodine in your diet. I mean, a cup of cruciferous vegetables is not a lot. In all honesty, I sometimes, you know, I’ll eat a whole plateful of kale or something like that, so I don’t think it makes any difference if you just throw it in the juicer. But what I mean is if people are juicing so that they can consume exorbitant quantities of these vegetables compared to what they would be able to eat if they were eating them whole, that’s where you get the problem.
Chris Kresser: And, Chris, you don’t have any thyroid problem that you know of, so maybe someone that does might not necessarily want to eat a plateful of cruciferous vegetables.
Chris Masterjohn: Absolutely. This is the key issue: It’s an individual thing. Like I said, steaming, the goitrogen yield varies, you know, fourfold between different people, and different people have different iodine status. So, I am not saying these foods are bad. I’m saying that if you have symptoms of hypothyroidism when you made a dietary shift towards including more of these foods, then you might suspect those foods and their balance with iodine to be a culprit.
Chris Kresser: Um-hum. Your mileage may vary.
Chris Masterjohn: Right.
Chris Kresser: So, I want to throw in a couple things here just from my clinical practice. One is that I’ve found that for people with elevated LDL and some symptoms of hypothyroidism, even if they’re euthyroid — like, their T4 and T3 are normal and their TSH is fairly normal — that using slightly higher of a dose than we talked about, like 1 mg, more in the range of maybe 2.5 to 6 mg and sometimes even up to 12.5 mg of iodine can have a pretty dramatic effect on total cholesterol and LDL cholesterol, and I’ve been keeping some data, you know, just anecdotally for my practice. Eventually maybe I’ll have enough to do something interesting with, but I have seen that work. One word of caution, though, is that it’s really important that if you do start iodine supplementation that you start at a low dose and you build up slowly over time. And the reason for that is that if you go too quickly, if you just start taking 6.5 mg, for example, or 12 mg, in my experience, that can provoke or exacerbate an autoimmune thyroid response, particularly if you don’t have enough selenium in your diet. And I’ve seen that happen, and I’ve seen people kind of start experiencing hyperthyroid symptoms or symptoms of immune dysregulation or immune attack against the thyroid. So, if you do start to take iodine, I’d recommend starting at a lower dose, like maybe 250 mcg, sticking on that for seven to ten days, maybe doubling it, sticking on that for seven to ten days, and then proceeding to increase from there. The other thing is that — and I just wrote a blog article about this today, the day that we’re recording this show — is that a lot of studies show that selenium can protect against the potentially negative impacts of iodine supplementation for people who have autoimmune thyroid disease. So, if you do have Hashimoto’s or Graves’ or something like that and you’re considering taking iodine, you want to make sure that you’re getting at least 200 mcg of selenium combined from food and supplements each day.
Steve Wright: So, Chris, do you have a preferred form of selenium?
Chris Kresser: I like the Super Selenium Complex from Life Extension, and it has four different forms of selenium in there. It’s got selenomethionine, sodium selenate, selenodiglutathione, and Se-Methyl L-Selenocysteine. Some studies I’ve seen, Chris, and you’re probably familiar with this work — in fact, somebody just sent me a study this morning on type 2 diabetics, the effects of long-term selenium supplementation. They were interested in seeing if selenium could help treat diabetes, but what they found was that 200 mcg a day of selenium actually increased the risk of type 2 diabetes in their study population versus placebo. So, there’s some evidence that certain populations who take too much selenium or too much of one form of selenium, that that can be problematic, which is why I recommend taking multiple forms. What are your thoughts on that, Chris?
Chris Masterjohn: Well, I have a bias that has very little evidence behind it that selenocysteine is probably preferable over selenomethionine because that’s the form that’s incorporated into our proteins. That’s why it’s the form that’s found in animal foods. But I’ve had a similar suspicion as you that in those studies the form might be part of it and interactions with other nutrients might be part of it, but I guess we’ll have to wait and see for some clinical tests of that idea.
Chris Kresser: But, I mean, in general, it’s always the better idea if possible to get as much of your nutrients from food, and that helps avoid this kind of thing, because there’s a lot we still don’t know about nutrient supplementation or augmentation.
Chris Masterjohn: Right. And in a normal diet, you would get that mix because plants have selenomethionine and animal foods have selenocysteine.
Chris Kresser: Right. And Brazil nuts, for those of you that don’t know, are a very rich source of selenium. They’re also very high in omega-6, but I don’t think that’s necessarily a problem because you only really need to eat two or three Brazil nuts, depending on the source, to get 200 mcg of selenium.
Steve Wright: Do either of you take iodine?
Chris Kresser: I’ve experimented with it in the past. I don’t have a thyroid issue, and I eat a lot of seafood and some sea vegetables, so I get it in my diet; but I have experimented with it just because I do that a lot on myself, and if I’m recommending stuff to my patients, I often will do it myself to, you know, just see what it feels like. I’ve gone up to 25 mg of iodine without really noticing any difference personally.
Chris Masterjohn: I don’t supplement iodine right now, but I have plans in the future to see if I can use it to detoxify fluoride that I suspect I have in my system, but I’ll write about that when I get around to it.
Chris Kresser: Yeah, keep us posted.
Steve Wright: Yeah, I’m looking forward!
Chris Masterjohn: OK, so shall we move on to carbohydrate?
Chris Kresser: Yeah, sounds good.
The telltale Thyroid-Cholesterol signs you need more carbs
Chris Masterjohn: All right, so there are a number of studies that have shown that carbohydrate restriction or fasting or calorie restriction can decrease thyroid function, and they tend to show a decrease in T3 in the serum and an increase in reverse T3. T3 is the active hormone, and reverse T3 is kind of an antithyroid hormone. And many of your listeners probably have seen the correspondence between Paul Jaminet’s blog and his guest blogger and Anthony Colpo last year, where these studies were debated quite extensively. And I think when we look at these studies in the context of some of the biochemistry that has been studied regarding insulin’s interaction with thyroid hormone, then I think what we are seeing is a definite effect of the level of carbohydrate in the diet. And I know that there are some confounders in some of these studies, especially when they compared it to fat; a lot of the fat was really low-quality fat, like corn oil. But if we look at what insulin does, we find that there is evidence from humans, from cells, and from rats that insulin cooperates with thyroid-stimulating hormone, or TSH, to increase the production of the enzymes and proteins involved in making thyroid hormone, and we find that it contributes to the enzymes that activate thyroid hormone from T4 into T3, the active form. So, I think what we’re seeing here is when we have insulin operating in its optimal conditions, then insulin is again sort of acting as a messenger that the body is in a state of abundance, and it’s contributing to the production of thyroid hormone and to its activation into T3. And if you prevent the activation into T3, then the T4 — There isn’t very evidence that insulin actively prevents the production of reverse T3, but by promoting the conversion into the active form, that in itself tends to prevent T4 from being converted into the inactive form, reverse T3. So, I think we’re looking at a definite effect of effective carbohydrate here, and I think the best way to test for this is to look for a decreased ratio of T3 to reverse T3. From the clinical studies, that seems to be the most likely marker to look for to see if this is what’s happening, to see if this is why cholesterol has gone up. I think that if you find that T3 or reverse T3 are out of whack, probably the best way to address that is to try increasing the carbohydrate intake — not necessarily meaning you have to go on a high-carbohydrate diet, but, you know, like, Paul Jaminet had sort of concluded at the end of that series that he still advocates a low-carbohydrate diet, but it’s possible to go too low for some people, and that’s when you might get deficiency in thyroid signaling.
Chris Kresser: And I definitely see this, Chris, in my practice, and this is purely anecdotal, but I often get people who come to me who have been on a low-carb Paleo Diet, not for any particular reason, just because that was their understanding of the Paleo Diet, you know, as a low-carb approach. And then they’re suffering from the classic hypothyroid symptoms: Their hair is falling out, and their hands and feet are cold, outer third of the eyebrows thinning, you know, low metabolic symptoms. And then they start eating some more starch and starchy tubers and fruit and increase their carbohydrate intake; and in almost all cases, their symptoms improve significantly. The challenge clinically with that is the patient population who is on a low-carb diet because if they start to reintegrate carbohydrates, their blood sugars go up and they gain weight and they experience all of the metabolic issues that can be associated with that if they have metabolic syndrome, so it’s a little more challenging in those folks to just add the carbohydrates back unless you address the other mechanisms that are causing carbohydrate intolerance, whether they be metabolic issues or gut issues. You know, some people with small bowel bacterial overgrowth can’t really tolerate a lot of carbohydrate. So, it gets a little more complicated, of course, but I think that, at least in my experience, the phenomenon that you’re describing with low-carb diet contributing to hypothyroid and increasing carbohydrate intake improving thyroid function is definitely real.
Chris Masterjohn: Yeah, and I think you highlighted something important there that there are a lot of classic symptoms that go beyond the blood tests, and you know, I think even if you don’t see the changes in T3 and reverse T3, there are other mechanisms. For example, if you have increased liberation of free fatty acids beyond what you’re able to utilize, there is some evidence that the free fatty acids will accumulate in the nucleus of the cell at a high enough concentration to inhibit thyroid binding to its receptor, and that will cause all of these symptoms of the metabolic effects, including the high cholesterol, but it might not show up as changes in thyroid hormones in the blood. So, I think if you see those classics symptoms, if you see high cholesterol and low sex hormones, for example, I think those are good clues in addition to T3 and reverse T3 that might signify that an increase in carbohydrate intake might be needed, but I have an anecdote that I think is pretty interesting to share from Nutrition and Physical Degeneration, Weston Price’s book.
Chris Kresser: Yeah, let’s hear it.
Chris Masterjohn: He says: “For the Indians of the far North this reinforcement” — he’s talking about reinforcement of nutrition for pregnancy — “was accomplished by supplying special feedings of organs of animals. Among the Indians in the moose country near the Arctic circle a larger percentage of the children were born in June than in any other month. This was accomplished, I was told, by both parents eating liberally of the thyroid glands of the male moose as they came down from the high mountain areas for the mating season, at which time the large protuberances carrying the thyroids under the throat were greatly enlarged.” So, what he’s saying is when the moose were about to reproduce, they naturally went into a kind of hyperthyroid state where their thyroids were enlarged, and the people there would harvest the thyroid glands so that they could reproduce, and as a consequence, most of their children were born nine months after the moose mating season.
Chris Kresser: Wow.
Chris Masterjohn: And what the indicates to me is — I mean, it’s difficult to interpret it because he doesn’t go into great detail, but I think what we might be seeing here is up in the Arctic circle — and these are the inland people, they’re not seacoast, so they probably don’t have a lot of iodine in the diet, they certainly don’t have a lot of carbohydrate in the diet. It seems like they, as part of their natural adaptation to their environment, they supplemented with thyroid hormone so that they could convert their cholesterol to sex hormones so that they could increase their fertility, and I think what we’re witnessing is perhaps a natural acknowledgement that under those certain conditions where you have an extremely carbohydrate-restricted diet, you may need supplemental thyroid hormone in order to maintain that fertility.
Chris Kresser: Yeah, I mean, that’s so fascinating. In The Healthy Baby Code, of course, I talk a lot about anecdotes like that and traditional populations and their approaches, like in the Masai culture in Africa. And maybe you can correct me if I’m wrong on this, Chris, because I know you’ve studied them a lot, but something I read a while back where when people are trying to get pregnant or thinking about doing that, then they’ll consume dairy from cows that have been grazing on grass during the particularly lush seasons of the year to increase their fertility.
Chris Masterjohn: Yeah, well, the Masai definitely have an association between animal fat and fertility not only in the diet but in many of their rituals. Animal fat is always associated in that way. And they also have very strong associations between lactation in the cow and sort of the principle of female fertility, so I don’t remember the specifics of their fertility diets in great detail, but that definitely sounds characteristic of the Masai.
Chris Kresser: OK, so we gotta wrap it up. We could go on, and we probably will. I think we’ll have to have you back, Chris. We’ll make it a regular thing, because this is an issue that’s on a lot of people’s minds, and even with all that we’ve learned about it and, you know, a lot of people, like I said before, have been exposed to the idea that cholesterol isn’t necessarily bad and we don’t need to do everything we can to just lower it indiscriminately. I think, just speaking personally from the comments I get on my blog and the people I see in my practice, there’s still quite a bit of concern about it, and in some cases rightfully so, as we’ve learned in this 3-part series. So, I want to thank you, Chris, for coming back, and like I said, we’ll have you back. Maybe we’ll do some case studies. I’m actually speaking at the PaleoFX conference in Austin, and the topic of my talk is gonna be what to do, if anything, about high cholesterol, and I’m gonna present a practical framework in kind of a flowchart format for what you do if, let’s say, you get a cholesterol reading that comes back above 250 and kind of a step-by-step process for how you can investigate that. And I imagine those presentations will be available after the conference is over, so if anyone is interested in some more kind of really down and dirty, practical info on how to deal with this stuff, you can check that out. And, Chris, when are we gonna meet? Are you gonna be at AHS this year?
Chris Masterjohn: Yes, I will be at AHS this year.
Chris Kresser: Cool. So, I’ll see you there if not before and then, I’m sure, at the Weston A. Price Conference in November, as well.
Chris Masterjohn: Yeah, I look forward to it!
Chris Kresser: Yeah. So, Steve, thanks for shepherding us through this again, and we’ll see everybody a couple weeks from now.
Steve Wright: Yeah. It was a great show. Thanks again, Master J, for being on, and it sounds like we’ll hear again soon from you.
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