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Chris Masterjohn on Cholesterol and Heart Disease (Part 3)


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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 case you missed them, here are links to Part 1 and Part 2.

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:

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.

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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.

If you’re confused about what to eat, check out the Personal Paleo Code.  It’s a 3-step process designed to help you discover your own ideal diet and create highly customized meal plans with a few clicks of a button.  Visit PersonalPaleoCode.com to learn more.  And if you’re trying to get pregnant or are already pregnant or nursing, don’t miss The Healthy Baby Code.  It guides you through the essential steps to naturally boost fertility and promote lifelong health for you and your baby.  Find out more at HealthyBabyCode.com.
Please keep sending us your questions at ChrisKresser.com using the podcast submission link.  And if you enjoyed listening to the show, head over to iTunes and leave us a review.  Thanks.

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Join the conversation

  1. Chris M. mentioned that nutrient content of the same (or “same”) food grown in different regions can vary quite drastically. I’m curious how much of this information is available and how frequently standard nutrition information is verified by the authorities that establish it. I’m also curious if the fluctuations can vary as widely (or even more) in animal products as they do in plant products.

    Also, I’m under the impression that as years go by, the soil on a farm tends to become more and more degraded. I know that proper farming practices can prevent this, but doesn’t 99% of the food supply come from massive farming operations that likely do not practice methods to maintain soil integrity? I guess a more simple question that doesn’t necessarily rely on my assumption would be: Do you think that brazil nuts consistently have as much selenium as the established nutritional values indicate and therefore as great an effect as the studies that have been cited?

    • Dylan,

      It varies for each nutrient, and iodine is particularly vulnerable to differences according to region, but it is true to some degree for all nutrients and all foods. Animals are only as nutritious as the plants they ate, which are only as nutritious as the soil they were grown in. In fact there is at least one recorded epidemic of goiter that was tied to the consumption of milk from cows grazing on crucifers. The thiocyanate displaced iodine in the milk, so that the milk was poor in iodine and rich in thiocyanate.


  2. Chris M or Chris K,
    Awsome series!!! I do hope there will be another.
    My question concerns the accuracy of Lipid testing. I know you covered some of how each of these values may fluctuate over a given period. I recently had blood drawn for a yearly physical. I have been low carb paleo for about 2 years now. Don’t ask me how but I managed to get a VAP and a regular lipid panel done at the same time. Blood came from the same vein! The results were a bit confusing and I would’nt know which test to believe.
    Regular Lipid panel was: TC= 238, HDL=60, TG=47 and LDL (calc)=168 If using Iranian Eq LDL = 132
    The VAP came back; TC=258, HDL=59, TG-62 and LDL-C (direct)=183 All pattern A 🙂 Plus a bunch of other numbers.
    My question boils down to the large differences between the TC and TG. Would this be the typical range of error for testing at different labs? Or difference in Methods? Any thoughts on which number to go by?
    Thanks…Really enjoy both of your work!!!

    • Hi Evan,

      There is some error introduced by using different tests even from the same sample, and this could be amplified if they are handled in different labs, if there is any difference in handling of the samples. Your results seem to support the typical method of calculating LDL-C, in which case 168 is not terribly different from 183. Published estimates suggest varying methods should agree about 80%, which is substantial error, but nowhere near the error seen with particle size testing by different methods.


  3. Chris K or M…I jumped in with both feet with supplementation per the Perfect Health Diet recommendations and right off the bat started taking 12.5g of iodine in the form of Optimox Iodoral. It’s been 2.5 months on this dosage. I now realize that I went up too quickly but what’s done is done. I’m wondering if I should just continue at this dosage or perhaps slowly go down and then back up again in a controlled fashion? I’m trying supplementation and higher carbs to address TC of 300+. My doc wants me on statins but I want to control with diet. I was low-carb paleo for and also dropped 65 pounds so I”m hoping that it was a temporary increase that I can bring down the the 200-230 range. What an awesome series. Thank you!

    • Cheryl,

      I can’t address your iodine question, but as I said in the podcast I think you need to keep your weight stable for several months before reading too much into the blood lipids. I would consider the thyroid explanation in the context of other signs and symptoms.


  4. So for a statin-intolerant individual with FH who is thin, has normal T3, T4, TSH, cortisol and leptin and eats a grain-free, legume-free, dairy-free, sugar-free “paleo” diet, you both seem to say: avoid saturated fat and wait for the PCSK9 injections to come out?

    • Hi Jonathan,

      I’ll copy and paste a response I gave to a similar question on my blog:

      My opinions on treating FH are still under formation. I think whatever is done, you need to cooperate with a knowledgeable practitioner. Heterozygous FH is not a death sentence, but it’s dangerous not to treat it. I think you should periodically monitor atherosclerosis directly though, say, carotid ultrasound or calcium score, to verify that it is under control. I think since you are much more able to affect things not directly related to your lipid clearance, you should put the most effort into targeting them. For example, focus on minimizing oxidative stress and inflammation, and providing nutritional support for collagen synthesis (e.g. adequate vitamin C and copper). Thoroughly investigate all aspects of thyroid metabolism and optimize if warranted, as thyroid hormone stimulates LDL clearance even in heterozygous FH. I do think that, if it effectively brings blood lipids into a more normal range, a diet that is restricted in fat and cholesterol may be called for. But I would not use PUFAs, because these would likely promote oxidative stress. I would consider a Kitavan-style diet, where the total fat content is low (~20%) but most of it is saturated because virtually all of it comes from coconut. Naturally you have to consider how you feel on this diet and your other indicators of health, and all of this should be done under the guidance of a health care practitioner.

      • More answers beget more questions: Doesn’t eliminating PUFA mean eliminating omega 3 from walnuts, sardines, fish oil, etc.? Also isn’t Kitavan closer to the Ornish style diet I was on before paleo (www.tripleyourhdl.com)? Perhaps eliminating grains, sugar and dairy are the keys to health for FH individuals like me more than increasing meat and fat and reducing carbs? Last question: can you have normal thyroid numbers – yet lose eyebrow hair?
        BTW: my calcium score = 0 as of age 45 a few years ago.

        • Jonathon-Did you every get an answer to this question…”Can you have normal thyroid numbers – yet lose eyebrow hair?”

  5. Great info in this post.
    I am very interested in Selenium. There are several forms some beneficial, some semi toxic. I have a cnacer family issue. There is extensive research published that indicates that Selenium type Methylene Selenocyate (P-XSC) is a very potent cancer medication, far better than other forms of Se.
    Can you comment on your views PLUS where can this be obtained???
    Thanks, Willis

    • Willis,

      If it is a cancer medication, I would suggest using it only if you have cancer, and under the guidance of an oncologist. If you are looking for a selenium supplement, I prefer selenocysteine, though Chris K recommends a mixed form, which we talked about in the show.


      • Thanks Chris. Yes I am dealing with a family Cancer issue. I would expect to take many years finding
        an oncologist who would stray off the reservation.
        Thanks, you are adding to my knowledge base, which needs to expand rapidly.


  6. Might I suggest now cross-referencing the links, so each part has the links to the other two parts in this series?

  7. I just had my cholesterol tested (I will listen to the podcasts soon) and my TC is over 300. I just had a baby 7 weeks ago (baby was 4 weeks when we tested). I try to eat a WAP diet (not 100%, though). Does cholesterol tend to be high during pregnancy and lactation or is mine a concern?


    • Cholesterol can rise substantially in third trimester pregnancy. For example according to one study Masai women, who ordinarily have very low cholesterol, have cholesterol >200 during the third trimester of pregnancy. I would treat pregnancy like weight loss, and disregard transient fluctuations that seem to result from it. If something seems of moderate concern I would revisit it after you regain your pre-pregnancy weight and keep it stable for several months.


  8. Hi Chris,

    Great podcast but like always it brings up more questions!
    I am interested in this low iodine issue but I am kind of confused where to start. i don’t really want to ask the doctor right now about an iodine test due to the fact that he will badger me about statins. All my ratios are good and my inflammatory markers seem to be in the correct ranges. Without a test should i try supplementing iodine. My cholesterol is 254 and has risen over the past 8 months on paleo and the doc is concerned. I would like to try and lower it a little even though I am not really concerned about it. I have lost almost 60lbs and still probably have 20 to go so it may still be the fatty liver issue also.

    Any thoughts!

  9. So what if you have Hashimotos? Should you still take iodine? I painted with iodine per my holistic drs orders a few years ago and I think that made me hyper for a while and may have even caused my Hashis. Even a multi-vitamin with iodine makes me tired. Should I try to just get it from food? (seaweed?)

  10. just curious, what are you guys’ opinions on Stephan’s idea that saturated fat doesn’t affect blood cholesterol in the long-term, that it’s only a short term effect? The data seems to support it. Also, when I started eating a higher-fat diet, my cholesterol shot up to over 400, then 6 months later it came down to just over 300. This may have been due to eating too few carbs in the first measurement, but who knows. Anyway, do you guys believe that saturated fat has a significant impact on total cholesterol in the long-term? Or does it just have an effect on LDL and HDL individually or what?

    • I think what Stephan showed is that people who eat more saturated fat do not necessarily have higher cholesterol. But replacing saturated fat with PUFAs has been shown to decrease cholesterol over the span of eight years. Shorter-term RCTs show it also raises cholesterol relative to carbohydrate, particularly palmitate, myristate, and laurate. This effect applies when you keep all other factors constant, which doesn’t necessarily apply in the majority of real-world scenarios, where a dietary change involves many factors at once. It also increases HDL-C and not just LDL-C. The purpose here was to address why someone’s cholesterol might go out of the range seen among populations eating diets rich in saturated fat and low in PUFA. It seems in these cases that eating more saturated fat would be a pretty poor explanation. Someone who eats 20 or 30% of their calories as saturated fat would have a tough time explaining this as the reason for their high cholesterol when their cholesterol is a lot higher than what is seen on Tokelau, where people eat 50% saturated fat.


  11. I have a question after listening to the podcast. I recently asked my doctor for an NMR LIPOPROFILE test from Health Diagnostic Lab, Inc. Total CHL= 260, LDL-C Direct= 158, Trigs=63, HDL-C=73,
    non-HDL-C=187. There is also information on the lipoprotein particles and apolipoproteins on here (I can provide if necessary)

    All I know that there are RED marks indicating “high risk” all over this thing. As far as I know there is no history of heart disease in my family. With these numbers in mind should I be concerned? Of course my doctor wants me to take statins, she didn’t indicate how many mg’s/day. Your thoughts…also can you suggest anything I can take if I should be concerned. I pretty much eat a WAP way of eating 90% of the time. Or can you provide the information that you mentioned for the PaleoFX conference for those who’s CHL is over 250. Thx!

    • I would get at least one and preferably two more tests of your cholesterol. They need not be NMR – just standard total cholesterol, LDL and HDL. Possibly a CRP as well. Your current total cholesterol/HDL cholesterol (TC:HDL) ratio is about 3.5. After your next two tests, calculate your TC:HDL ratios from them and then add those three ratios together and divide by 3 to get an average. If it’s pretty close to 3, you’re in good shape. If it’s getting closer to 4 or above, you might want to seek out some help investigating mechanisms that might be involved.

      • Interesting – these numbers are nearly identical to mine, although I had a CRP test conducted. It came back at a lower value than they measure (under 0.5). Would this make you lean towards investigating the thyroid next? Cause you to lose concern?

        I wil be testing my cholesterol again in a week.

  12. Wow this was LONG. A lot of talk about cholesterol measurements, and cardiovascular health. I thought it was determined all across the alternative health scene that there is no proven connection between cholesterol measurements and cardiovascular problems. Hasn’t that already been debunked? Isn’t that just something traditional MD’s talk about to sell people on accepting statins? Why do people keep talking about this?

    Chris’s Kresser’s suggestion about the “oxidized LDL test” is interesting though, as I’ve been given the impression recently that though LDL is not a problem by itself, when it, as an ester, transports oxidized fatty acids, as the omega-6 fatty acids that are ruined by heat or converted to trans fats, then that ester definitely causes damage to the lining of blood vessels and bring about the injury that then attracts plaque. So I would be very interested to see the results of the oxidized LDL tests that Chris mentions. If this, finally, correlates with cardiovascular problems, then maybe, finally, we have something in the cholesterol area to pay attention to.

    As to the importance of iodine. I can’t agree more. I think it went on way too long though as to how some vegetables can cause a problem IF we are low in Iodine. Gosh, the way people read things, you may have people starting to cut back on vegetables. All that is needed is to step up and say we need more iodine.

    From what I’ve read, it’s not just selenium, but also chromium, zinc, iron, progesterone, cortisol and glutathione that are needed in sufficient quantities in order for the body to make T3 from T4. Any deficiency in any of these will result in the production of RT3 instead of T3. And RT3 does nothing for you except block what T3 could have done, so you want to absolutely minimize your production of RT3 by having enough of that whole list of elements and hormones. So to what Masterjohn said on slowly increasing the dosage of iodine, I would add that one should insure they have good levels of the elements, progesterone, cortisol and glutathione in their system. If they do, or if they are willing to just TRY a good strong dose of iodine, as in Logol’s or Iodora, and if they don’t have any hypothyroid symptom manifest, then they can consider they are safe to continue the heavier dose of iodine. You really have little to lose. Personally I’ve taken 12.5 mg of iodine over a 3 month period with no ill effects. I’ve know people to take 50 mg of iodine for 2 years with no ill effect. If the only possible problem with taking iodine is that you suffer an immediate, hypothyroid symptom or two, but you haven’t damaged your system or your thyroid. why not just give it a try. Being short on iodine and then taking weeks to “work up” to the indicated dosage seems to be a little bit ultra-conservative to me. Is there some risk I don’t understand here? Can the thyroid or the body be damaged by a short term hypothyroid condition caused by some reaction to iodine?

    • Hi Glenn,

      Listening to the first two episodes, linked to above, would go a long way to help clarify this. We are looking at these measures as metabolic markers, not causes of heart disease.


      • To use another example, if you have elevated malonyl CoA, this would indicate B12 deficiency. This doesn’t mean that malonyl CoA “causes” anemia or nervous system degeneration, but B12 deficiency does, and malonyl CoA is an important metabolic clue to help diagnose this condition.


    • Glenn: the point of our series was that the “alt med” idea that cholesterol has absolutely nothing to do with heart disease is false and can’t be supported by the current scientific literature. Go back and read/listen to parts 1 & 2 for a very thorough discussion of this. It’s pretty clear that degeneration of the LDL particle does contribute to heart disease, and that poor LDL receptor function is a primary factor in that degenerative process. I think it’s a mistake to ignore cholesterol levels >250/275.

  13. Great podcast as usual.

    @ Steve Wright – a group of us on PaleoHacks and Highbrow Paleo call him Chris Masterhack, though Grandmaster J is pretty cool too.

  14. Fred,

    I don’t believe everyone should take bio-identical thyroid hormone. Some actually do better on synthetics, because they’re either sensitive to the fillers in the bio-identicals or in rare cases, they produce antibodies to thyroid hormone itself.

    All of my patients get the fatty cuts of meat/not too much lean protein talk.

  15. What is recommended for those with FH? I have it, my TC is 360 (family history of individuals with TC from 300-600s) and I’ve been paleo for a year. Do u recommend traditional cholesterol-lowering drugs for ppl like me? I really don’t want to take meds or start a low-fat, whole grain diet as my doctor recommends.

    • Optimizing thyroid hormone and leptin status and natural approaches to lower cholesterol to start. This is the only population I think you can make an argument for the use of statins with, in those cases where the strategies I just outlined don’t work.

      • I concur, and I think that targeting thyroid optimization and minimization of inflammation and oxidative stress should take priority because they are the most modifiable. But I think in this population one might also want to experiment with reducing fat and cholesterol intake, if it proves effective without interfering with other aspects of health. In other words if eating a Kitavan-style diet based on starch with moderate amounts of fish, fruit and coconut brings TC under 300 without causing digestive or blood glucose issues, then I think this would be superior to using a statin. I say this because FH makes a human more similar to herbivorous animals where the metabolism of lipids is intrinsically backed up so that dietary lipids may contribute to an accumulation and oxidation of lipids in the blood under conditions where they might contribute to health in most other people. But I think the totality of health has to be monitored to verify the success of any regimen.


  16. Chris –

    I thought you and others have said that if one needs to take supplemental thyroid hormones, it needs to be bio-identical. I don’t think moose thyroid fits the bill here.

    I know a lot of my clients go paleo/low carb and many of those who complain of thyroid related health issues adopted a low fat, paleo approach which we both know is unhealthy.

    How many of your patients have you grilled to make sure their hair loss and other symptoms were not an outcome of too much lean protein and not enough vegetables eaten with fats?


    • Hi Fred,

      The other Chris stepping in for a moment. It is very difficult to determine a definitive cause of a patient’s n=1 experience, but I think the point here is not to determine the definitive cause but rather to increase awareness of possible causes and identify possible solutions that are likely to offer the most targeted benefit with the least cost. The activation of thyroid hormone by insulin is opposed by glucagon. Neither proteins nor vegetables nor fats will increase the insulin-to-glucagon ratio, but carbohydrate will. In a person who does not have SIBO or unresolved glucose intolerance, a sharp increase in LDL-C following extreme carbohydrate restriction has a high likelihood of being safely resolved by titrating carbohydrates up to an optimal amount, regardless of whether other approaches may have worked if only the patient were grilled intensively enough for further details of their behavior.

      The anecdote about moose thyroid is, like I said, difficult to interpret because of the lack of detail, but it offers a vivid illustration of the well established physiological relationship between thyroid health and fertility. It is certainly interesting, even though proving cause-and-effect is impossible, that this anecdote originates from a population with likely very low intakes of carbohydrate and iodine, the two factors we discussed most extensively in the podcast. I don’t think anyone would recommend moose thyroid as an optimal solution, but the point was to highlight an anecdote that was illustrative of the principle.


      • What puzzles me is “the enlarged thyroid”. Wouldn’t that most often point to goiter and lack of iodine? I also ponder “down from the mountains” – I thought mountains most often where iodine depleted. Of course moose thyroid may well be sufficient for humans even though not enough for the animal… May be the moose thyroid only was safe when the moose was hypo?

        Anyway – if bovine thyroid and pig thyroid is compatible with humans I would believe that moose thyroid is as well.

        • Hi smgj,

          Unfortunately I don’t know very much about the ecology or mating habits of arctic moose, and Price gives little detail, so I can’t give a definitive interpretation to the story. However, I do not think an enlarged thyroid necessarily indicates hypothyroidism. The thyroid enlarges in response to elevated TSH. TSH is a messenger telling the thyroid that more thyroid hormone is needed. The thyroid responds by enlarging and producing more thyroid hormone — or if the TSH is at equilibrium the thyroid responds by maintaining its current weight and its current production of thyroid hormone. TSH will increase whenever the body decides it needs more thyroid hormone. This could be because of decreased thyroid hormone secondary to iodine deficiency, as in the example you give, or it could be because the need increases (e.g. for mating, perhaps). In goiter, the thyroid gland is constantly increasing in response to a need for more thyroid hormone that is never adequately met, so the growth is abnormal. But you can have normal fluctuation of thyroid weight according to need for thyroid hormone, and this is apparently part of some animal’s mating habits. The moose may not have had enough iodine in their diet, I don’t know, but I think if the enlargement consistently happened during mating season, then at least part of the explanation is that during mating season their bodies orchestrated a state of increased thyroid output in order to maintain high fertility.


  17. What are your opinions on a C reactive protein test for measuring heart disease risk? Does it provide information that is helpful in understanding heart disease risk with or without elevated cholesterol levels?

    • Hi Casey,

      Not sure if you are asking Chris K or me, but in my opinion CRP, if measured at least twice and if proper account is made for acute infection, can be a valuable index of inflammation, but there is currently some conflicting evidence about whether it is an independent predictor of heart disease risk. But if you have chronic inflammation, this could affect cholesterol levels one way or another depending on the source of inflammation.


      • Thanks so much for a great podcast! You touched on it being complex for people to increase carbs when dealing with insulin resistance, but can you give any more details on how they can map a path forward? My RT3 is high, LDL is high, but triglycerides are very low. I only just recently started natural thyroid (had been on synthetic for 15+ years with no benefits).

        I stay very low carb because I find that I gain weight nearly instantly when my carb intake goes over 50 gm/day. I don’t eat any grains, sugar, processed foods, even fruits of any kind. I’ve been eating this way for over a year now and hoping the carb intolerance would resolve, but no luck yet. I’m not overweight, but I assume I have insulin resistance though I’ve never had any tests done. Any suggestions on figuring out how to resolve this? Specific tests I should ask for? I certainly don’t want to damage or even decrease my thyroid activity.

        I’d appreciate any suggestions! Thanks!

        • Hi Marisa,

          Chris K is the one with clinical experience and may be able to answer this question better than I can, but I could make a few points that might be helpful. First, eating carbohydrates requires a couple weeks of “carbohydrate adaptation” just like eating fat requires a similar period of “fat adaptation,” so you need to ease very gently into the increase. Second, an immediate gain in weight could be deceptive. If you switch from very low-carb to a higher-carb approach you will likely immediately gain several pounds in glycogen and water, and there’s nothing wrong with this. Third, unless you have fructose malabsorption or an addictive reaction to fruits, there is no reason to restrict them relative to other carbohydrates, and you might handle them better than starches when used in small amounts.

          If you are truly carbohydrate intolerant, I think more testing is required to get at the source, and that could be complicated. Nutrient deficiencies, fatty liver, poor metabolism, iron overload, digestive health, and other causes could be at play.


          • We moved web hosts yesterday, so may be having some lingering issues. But this one obviously came through!

            • Ah, they did! Before when I would comment, my information would be automatically present in the box, and my comment would show up immediately. Now I have to type my ID info in manually and the comments took a delay, so I had thought they weren’t making it through. Are they moderated? If so that would explain it! I just assumed they weren’t because they were appearing immediately the other day.


  18. Thanks for this fascinating and informative post. Perhaps I missed them in the post, but could you include the links to Parts I and II of this series with Chris Masterjohn?

  19. Great interview, thanks………
    What about cholesterol that is too low? I have hashimoto’s and did low-carb for a couple of years, but have recently added back in some rice and buckwheat and starchy veggies. Can’t say I notice much difference in terms of how I feel either way, although I agree that the insulin resistance piece makes it tricky. But, how can I get my cholesterol up despite eating lots of healthy fats?

    • Hi Marleen,

      Cholesterol can be low for good reasons or bad reasons. In my opinion, if you have no evidence of hormonal problems or digestive problems, it may be low because of efficient metabolism, which is good. However, if you don’t feel well, have psychological or emotional problems, have evidence of endocrine problems, or poor digestion, it may be too low because you are not making enough. I would address this by eating a diet very high in cholesterol and medium-chain saturated fats. Lots of eggs and coconut oil. I would also suggest getting a genetic test for Smith-Lemli-Optiz syndrome, as you could be a carrier.