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RHR: 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:

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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.

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.

148 Comments

Join the conversation

  1. Hey guys – great series. Definitely the most informative and easiest for the layperson to understand that I’ve come across.

    I’m abt 30 years old and my cholesterol just got measured (twice) above 300, with LDL of 235. This is much much higher than a year ago, when my LDL was 130. I work out nearly every day – for the last few months I’ve actually been gaining weight and muscle mass – and stick pretty closely to a whole-food diet. Really if it weren’t for this test result I’d be considered to be in superb health. My doc is stumped – all my other blood tests came back normal – do you have any thoughts on my situation?

  2. Oh and I forgot to ask:

    Should we avoid all fermented veggies?

    And does fermenting in any equipment even the Pickl-it jar (which has been said to not increase histamine levels compared to other methods of fermenting) activate goitrogens?

    Thanks

  3. Hi Chris,

    Can thiocynate and goitrogens be reduced significantly by boiling and removing the water of tapioca (pearls/balls/flour)?

    And can sprouting flax reduce its thiocynate and goitrogens significantly?

    Thanks!

  4. thanks for the 3 part information .. I have printed the complete transcript and will be giving it to my VA nutation specialist soon. They do not like my mantra of “NO STARCH, NO SUGAR, NO DAIRY” They are currently handing out information printed in 2007, titled “Take Charge of Your Diabetes” 4th edition. The sad part of this story is that they can not teach anything that is not part of the food plate dogma. And do not like my question why do you want me to consume large amounts of high GI food to control my T2 diabetes? More people need to ask the question. They still promulgate the ‘calories in and more exercise.

    Thanks
    Richard

  5. Hi. Just found your website and it is very informative. I do have a question though. I have been low carb for a couple of years now and love it! When I first tried it, went from 266 lbs. to 228 lbs. I also was able to do this with no exercise. I realize that I do need to exercise however have a really bad left shoulder which limits most any upper body exercising. I used to be a fitness trainer and have worked out most of my life however, have not for many years now.

    Unfortunately I fell off of the low carb wagon and gained most of it back. However, I am committed now to sticking to it and follow a diet somewhere in between atkins (low carb) and paleo (more carbs)
    I am having a real hard time this go around losing the weight and can’t figure out why. My optimal weight should be anywhere between 200 −210. Currently weigh about 255 lbs. I also just had a blood panel done and this is where I am at:

    Cholesterol: 227
    Triglycerides: 277
    HDL: 29
    Cholest/HDL Ratio: 7.83
    LDL (Calculated): 143
    Non-HDL Cholesterol: 198

    I also have atrial fibrilation with a 25% blockage in one of the arteries of my heart. I am 49.

    I am a little confused about how I need to go about getting these numbers down. I have listened to the podcast about cholesterol but need some help understanding what needs to be done. Any help would be appreciated. Thank you

    • Hi Mark,
      There are still a number of things you can do. One is to eat to increase insulin sensitivity. generally supplements of chromium, biotin, and niacin are helpful for this as is adding cinnamon. Eating apples, grapes and some other fruit was shown to increase insulin sensitivity. Limit intake of fructose and replace saturated fats with mono unsaturated or Omega 3 fats.

      If you have a high calcium load in your arteries, taking the MK4 form of Vitamin K2 is known to reverse this and its used to treat heart disease and bone loss in Japan. Be sure to read the panel as the MK7 form of vitamin K2 is known to cause sleeplessness and lumpy fast heart beats in those sensitive to it. Typical MK4 doses are 1.5 mg once or twice a day, ranging up to 15 mg three times a day used for treatment and research in Japan and the Netherlands research by Dr Vermeer.

  6. [Marked as spam by Antispam Bee | Spam reason: Server IP]
    Hi There

    Thanks for these three postings, and the audios which I intend to listen through as I drive. I have been on a ketogenic diet (with some ignorant aberrations) since October last year and have lost about 6 kgs, gone down 2 sizes in trousers and am feeling pretty good all round. However my lipid panel has some really high readings (apo-A1 = 1.56 and apo-B = 1.66). I have been searching the web for what to do next but most of what I have found is based on the low fat dieting and the food pyramid. it is good to hear that this could be part of the process but this is lipid world is complex so I am under no illusions – I just want to get some facts before searching out a local fat-friendly doctor.

  7. I’m just now reading this… I have a low thyroid (actually just “low-normal”, but had all the symptoms and improved greatly with meds from the endocrinologist). Since that time I’ve started following a traditional Weston Price diet (raw milk, cod liver oil, grass-fed meats, etc..). I’m just getting into fermentation and that’s where I came across the link to this article. Now I’m concerned about my low thyroid + sauerkraut plans. I’m planning to look into adding more iodine to my diet thanks to your suggestions, but I do have a question.

    I would really like to go off of my synthetic thyroid meds. Is there anything I could be eating to increase my thyroid function? Iodine?

  8. It seems like the Green Pastures Fermented Cod Liver Oil and High Vitamin Butter Oil would have selenium and iodine. Unfortunately, there’s appears to be no way to know just how much is in them. So confusing!

  9. I do moderate, resistance training prior to the refeeds, so that should be taking into considering. Also, depending on how my current weight and weight goals are at the moment, that influences my intake. Anyways, I usually do approximately 100-150 grams of Carbs.

    Did you mean cream, not butter? Since you are not consuming much dairy (and do not have overt autoimmune reactions) than pasteurization should not be a concern.

    I am also in making my own kefir, but thought about first doing it with a tiny bit of yogurt as a starter and whole milk (both organic, grass-fed, but not raw– not sure which would be more important to consider raw).

    I eat lower fat on refeed afternoons/evenings (more in line with Carb Back Loading protocols of having almost all carbs in post-work out windows and in the evenings), but probably not as low as fat-phobic people shoot for. Leangains.com has some good ratios, for some looking to be ultra jacked and ultra lean. However, you may be coming from a completely different background and have completely different goals…

    best,

    Henry Duran

    • Nope, I actually put butter and coco oil in my coffee! Yes! I follow Leangains but more specifically, Jason Ferruggia’s version of carb backloading. I aim for around 50-60 G fat on workout days instead of 100+ but it’s a little hard…I also don’t get enough calories that way. Umm I’m [email protected] if you want to take this convo to email?

  10. Between oxalates, FODMAPs, nightshades, and goiterogens, I am now confused about what vegetables are safe to eat. I am on GAPs and avoid potatoes, is winter squash and occasional blueberries, rotated with a few lower carb days with just carrots or summer squash adequate enough to avoid glucose depletion/thyroid problems? I suffer from acne/gut issues if I go much above 100 G carbs (I tried a few small servings of yam this past week and got breakouts). It would be very helpful if you could provide a sort of vegetable “meal plan” outlining a few days of ideal vegetable intake, or how to rotate types of vegetables when you have a limited diet to avoid negative effects.

    • Elyse,

      I am also cautious of these offenders, some more than others in my circumstance. However, I am more concerned in optimizing thyroid and paleo foods that irritate me or have unfavorable ratios of fructose for weight management. If you breakout from all of the categories you listed, I would recommend trying turnips, boiling goitregenic foods like broccoli past fork-firm and drain the water (a la Masterjohn).

      I have read Jaminet say he doesn’t believe nightshades need to avoided by practically anyone, even those with hashimotos. Or at least that eating a small amounts of nightshades should be fine. Although he wasn’t absolutely positive. I personally eat tomatoes and other nightshades in moderation, but can’t tolerate a lot of spice.

      This might simply a gut-skin axis issue and you might need some digestive support like probiotics or digestive enzymes to begin tolerating other foods. I read Loren Cordain’s “Dietary Cure for Acne” long ago, and recommend you consider checking it out. It’s basically a shorter version of his original Paleo Diet, but has plenty of personal testimonials and tracking down particular foods that worsened their skin conditions.

      http://blog.katescarlata.com/fodmaps-basics/fodmaps-checklist/

      Henry

      • Thanks for the response Henry. I do always cook my cauliflower/broccoli/cabbage, otherwise I get stomach pain, but I eat about a cup of those vegs almost every day. I basically cycle carbs based on weight training days (around 50-100 off days just lettuce, a cruciferous veg mentioned above, try to also get carrots, tomatoes, bell peppers, asparagus, or summer squash, 100-150 training days about 3 times a week with winter squash or pumpkin, occasional blueberries-I think I’m turning orange hehe) but am concerned about not getting enough starches. I eat fermented veggies (dairy intolerant) at least once if not twice a day, meat broth, have lemon water before my big dinner, and I have biokult but only take it once in awhile, maybe I should be more stringent with that or start taking HCL? Thank you I will check out that book!

        • Hi Elyse,

          I think your carb intake is in the right appropriate amounts. Why do you feel you’re not getting enough starch? I personally like to make things simple and eat 3-6 yams/sweet potatoes at a time, but I’m sure others want more variety. (Btw, are both yams and sweet potatoes nightshades?) Chris Kresser posted a piece on skin conditions. It was all old info to me, but what I took away from it was how essential Vit A plays in skin health. Yams have the highest amounts of Vit A, I believe. Also, are having fat with every food?

          I like fermented foods and I also don’t tolerate MOST forms of dairy. I like grass-fed ghee, full fat, unsweetened yogurt and hard cheeses (in that order). I tried to keep good saurkraut around, but I noticed it simply wasn’t worth the price for the tiny bit of digestive support I was getting. I really like New Chapter’s probiotic (soy and dairy free).

          In regards to the meat broth I think almost all of the potential benefits of broths come from bone broths, not meat broths.

          Do you include rice? Haiga rice is more nutritious, but more expensive. Melissa Mcewen has some good posts. I include rice on occasion when I feel my digestion is going great, and seem to do fine on it.

          http://huntgatherlove.com/content/cooking-resiliency

          http://huntgatherlove.com/category/tags/rice

          I have seen improvement in digestion FODMAPS, particularly fructose, when my digestion has been compromised (and thought I was hypothyroid or had Hashimoto’s autoimmunity for a while).

          You may want to take out biokult.

          Have you tried digestive enzymes like Now Foods Super Enzymes? Robb Wolf loves the stuff and talks about how to take it. I also got the New Chapter tip from him for those looking for a solid non-dairy probiotic supplement.

          Henry

          • It’s possible that I just havn’t allowed enough time for healing. I have read and tried a lot of things concerning acne. I started GAPs in March. I have lost my period, was having low energy before upping my carbs (was only about 30G/day for a few months), and started getting these weird heat related hives (certain things make them worse, like garlic powder). However, since adding winter squash, and a few yams/sweet potatoes/blueberries (no rice) my acne is getting worse again. I have always had irregular bowel movements. I’ll try dropping the potatoes and see how I do with just squash.

            I am pretty active and have to lift heavy stuff at work, which is why I believe my energy was so low and starches not high enough. I also was not seeing the gains I wanted doing strength training, and I’ve been reading more and more that, women in particular, need at least 50-100 G starchy carbs a day not including veggies, which I don’t really want to do. I eat roughly 100-120G protein a day, then cycle carbs and fat depending on weight training (100+C, 70G F w/o, or 50-100G C, 100+ rest days). I eat my biggest meal and majority of my carbs at night.

            I do eat grassfed butter, my only dairy, coco oil, olive oil, eggs, grassfed lamb, lots of fish, salmon, sardines, etc. I have not tried digestive enzymes for fear of becoming dependent, but I might give it a go. Thanks again for all the resources I am so frustrated it’s nice to talk about this with someone!

            • Yeah definitely want to be cautious with going too LC for too long. I like to stay on the lower side since I’m not that active, but will do a carb refeed at least once a week. No problem. I hope to hear what you experiment with. Also, you might want to try replacing the butter for ghee.

              Henry

              • Ohh how many carbs do you eat on refeed days? I actually made ghee for the first time last week out of my kerrygold butter, super tasty. I really only use butter in my coffee, which is why I havn’t purchased raw butter-seems like it would be a waste. I’m considering getting raw milk to try my own kefir, though.

  11. Glenn – here is a link to an excellent forum for men I am a member of that has a thread all about Dr. Kane whose work I am somewhat familiar with:
    http://www.musclechatroom.com/forum/showthread.php?20061-Dr.-Patricia-Kane&highlight=patricia+kane

    Speaking of the O6/O3 ratio of 4:1, this is something new, as several other opinions have it as 1:1. I am just the OPPOSITE! My O3/O6 ratio is like 6:1, way too much O3. I have since been taking more of Kane’s Body Bio Balance oil to help correct this. We’ve been brainwashed by the fish oil makers for years that we are deficient in O3, me included!

    As to the link on the coumadin, thanks, I did see that one before. What it says is that you end up having lower TC which is not in my case, so it I surmise it is perhaps indirectly affecting lipids via destruction of the procoagulant protein. I still haven’t made the link from this to increased lipids.

      • Wout, please see my comment to Mark today, which addresses some of these issues.
        Your first link is spot on regarding marine-oil supplements. The krill oil advocates claim that the astaxanthin will help protect from oxidation and that may be true, but I agree to stay away from the supplements when there are so many other sources of omega-3 in our lives. I would only counsel to steam or otherwise carefully control the heating of the fish, as we can spoil in our own kitchens the fragile omega-3’s we are trying to get, if we heat to high or for too long!
        Your second link is ambiguous because it consistently confuses the omega-6 issue with the processed oils we ingest. These oils are primarily omega-6, but many have an omega-3 component. But they are all termed “omega-6” when they should be called, and considered, just TOXINS and not to be ingested. So of course, someone ingesting these poisons is going to have elevated rates of cardiovascular disease, insulin resistance and cancer. But it is playing into the fish-oil salesman’s hand to call these poisons “omega-6” oils. Lets not do that. What the typical, gullible, though ostensibly “health conscious” reader will assume is that “all omega-6 is bad” and one must absolutely minimize their intake of “all omega-6”. This is going to cause the next health problem. Everyone is going to be as omega-3 conscious as possible, is going to be dumb as an ax-handle regarding the essential nature of omega-6, and they are going to experience all kinds of problems still, even though they are dosing heavily on omega-3 supplements.
        You can see several examples of this right in the reader comments to the article! On April 3, 2011, Darrin naively asks: “Are there any good omega-6 fats?” Now why would he ask this if the whole truth had been explained in the article, instead of just statements like “minimize omega-6”?
        So now the author, Paul Jaminet has to explain the truth:
        “I would just eat natural foods, get omega-6 and omega-3 in the proportions they are found in real foods, and let my body control which fatty acids are converted into which.”
        Now finally he’s talking about “real foods” (in other words what he had been calling “omega-6” and was related statistically to problems like heart disease, was not really “real food”!) This is a great example of typical, alternative health sensationalism. You find it everywhere. They find a bad guy and throw rocks at him, even though he is actually an essential nutrient. Then when someone says, “But isn’t there are good side to this guy?” They have to admit there is. I wish we didn’t have the sensationalism, but it’s the way people get you started into an article. To make you think your life is threatened by something you eat every day. There’s some truth, but a lot of distortion until the Q/A brings out some more detail.

        So, read Mark’s link. And my earlier link on toxins and how you need, need, need, omega-6 derivatives (Arachidonic acid and prostaglandin one) if you have any heavy-metal detox going on, and you just (single) need them in all cases to stay healthy. Prostaglandin one (PGE1) is the strongest anti-inflammatory agent that comes out of the omega’s. But fish-oil articles don’t mention it is from omega-6. They keep calling omega-6 “inflammatory” don’t they? It turns out that inflammation can be caused by lots of things, and ruined commercial oils is one of those things. But those oils shouldn’t any longer be considered omega-6, because they have no health benefits to your body whatsoever, but cause damage to your blood vessels, take up a spot in your 70 trillion cell membranes that SHOULD have been occupied by omega-6 that is needed to transport oxygen into your cells, so you lose oxygen in every cell where this takes place. I say, “if it can’t function as omega-6, it’s a crime to call it omega-6”. But that’s fish-oil sales.
        Then read this:
        http://www.brianpeskin.com/BP.com/reports/CAMB-Fish-Oil-Fallacies-Report.pdf
        Best of health!

    • Mark, yes the Dr. Patricia-Kane cite is refreshing. She has it right and has all the omega-3 salesmen pegged as just that, salesmen.
      I notice she also mentions butyrate in her supplement recommendations!
      If you scroll down and find her chart of the typical body compositions of wild animals, you see that there is usually a O6:O3 ratio of from 4:1 to 6:1. I think using the 4:1 ratio for humans is a bare minimum, since most of our organs or systems have parent O6 in at least a 4:1 ratio to O3, but it varies as high as 6.5:1 in muscle, to 100:1 in the brain and nerves, and you can say it’s 1000:1 in skin and in the lining of our circulatory system because there is almost no O3 there at all!
      And Wout, you need to look at this too (in addition to the other links Mark and I have been providing). What your sources confuse is the issue of ruined “vegetable” oils with healthy omega-6. There is no way I am going to call an oxidized fat, such as commercial corn/soybean/safflower oil, let alone that same oil that has been in a deep-fry vat for 3 hours, preparing the “average American’s” next order o
      f fries, “omega-6” oil. Lets get real here. That is what the fish-oil business has been doing, but it isn’t right, and it is misleading the public into over-consumption of both the ruined oils AND omega-3 supplements.
      A ratio of 4:1 is a bare minimum for O6:O3 if you are looking at healthy oils. Please read the links Mark and I have been providing. There are 2 veins of thought in alternative health. One is influenced by the marine-oil salesmen and aims, with no scientific justification, at a 1:1 ratio in spite of all tests on animals to show that no animal maintains that percentage in any of their tissues. The other is the much smaller in terms of web-site patronage and representation, but based on scientific research. This is what you should look at before you follow the alternative “crowd”. Please take a look and let us know what you think!

  12. Thanks for the insight, Glenn.
    Any chance you have that link that explains that warfarin increases hepatic LDL levels?

    As to why I’m on it – I was dx’d with a DVT (clot) in my left leg 3 mos. back and began the standard 6-month anticoagulant prohylaxis protocol (warfarin). I have less than 2 mos. left. Still, I wonder how warfarin may have directly or indirectly affected my lipid levels in just this short time. My LDL has never been this elevated. If it’s not resolution of fatty liver as Chris M explains above, then my next guess would be the warfarin, as I have not increased sat. fats or carbs whatsoever. Despite the spike in lipids, I have also lost weight and gotten a little leaner in the last 3 mos since going hardcore LC Paleo and doing Martin’s leangains program. I, too, had the so-called perfect profile a couple years back (low TC, LDL, TRIGS), yet I was overweight and had more bodyfat than I do now. Go figure.

    Perhaps as Chris M explains above, “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. ”

    Just hoping that is the case (and when I get off the warfarin).

    • Ah, finally found what you asked for. Took forever!!

      “Coumadin binds to bile acids in the intestine leading to increased excretion of bile acid in the feces leading to increased oxidation of cholesterol to bile acids resulting in increased numbers of low density lipoprotein receptors with increased hepatic uptake of LDL and lower serum cholesterol levels ”

      This statement I found in: http://www.flash-med.com/Side_Effects_Coumadin.asp

      Could find nothing else on this LDL effect anywhere though.

      While I was searching, I found this interest thing, slightly related to our diets, which I thought I would pass on though:

      http://articles.mercola.com/sites/articles/archive/2003/08/09/detoxification-biotoxins.aspx

      I’m fascinated by the relationship of diet, toxins, and excessive coagulation and also the fact that coagulation is not just in the plasma, but is very important as a blocking of the respiration of endothelial cells of the veins (walls), called here a “membrane disturbing event”, which both blocks the vital flow of fluids in and out of the circulatory system, but also allows toxins to penetrate through the walls. Just another reason to work to detoxify our systems and then eat as pure foods as possible.

      If you read this whole article, notice also the extreme importance the polyunsaturated fats, omega-6 and omega-3, are given. The recommended ratio is 4:1, respectively, and the derivative fats from these parents, such as arachidonic acid and the prostaglandins are described as essential to our health, though threatened on a cell by cell basis by toxins in our systems.

      I have to thank your request for my even discovering this article! I’m keeping it on file for future reference.

      Happy 4th!

  13. @ Glenn – Nope, I have cut my fructose intake to 15g or less and only on workout days (EOD). Yes, I agree Martin is wrong here on the poisons (especially the die soda of all things). I was eating a diet with a moderate amount of fruit prior to my dx of fatty liver. So, my mini carb refeeds are safe starch paleo carbs (wild rice, starchy tubers, quinoa) and no more than 75g.

    Again, that aside, I am hoping the spike in LDL and Trigs are a result of resolution of fatty liver by having been on LC Paleo/IF for the last few months.

    • Thanks for the info. on your amounts and types of carbs, Mark. Other than that mention of Martin’s allowance for low-carb sweeteners, I like his methods, and actually follow his plan amazingly closely, considering I never read about it before your post!

      I would have never called the 16 hr. periods that I usually go without significant intake a “fast”, but if that’s what he calls it, fine enough. I always think of a “fast” as something difficult you must commit to, and diligently stick to. I find going without food from 8 PM until Noon the next day as very natural and hunger/pain free. But I am slim, and have, I’m sure, low leptin levels.

      My main problem, not doing this whole thing for any kind of “training”, is that I will run low on sufficient exercise occasionally. At that time I experience a bit of depression or at least a feeling of low energy, which I believe is a normal low-leptin reaction that is necessary, paleo-wise, to further conserve energy. And the solution for me is merely to get up and run, or exercise strenuously in any way. Endorphins kick in, or whatever, but the depression is gone. It would have been a normal paleolithic occurrence to get sustenance. Food would have been obtained to satisfy the hunger/low-leptin level, and all would be well, or else there would have been another period of low-leptin lethargy to help conserve energy.

      Sometimes when I feel lethargic, I begin to think “I must be low on protein”, or “I must be short on essential enzymes”, etc. But every time, the solution is always exercise. The food has been fine, but the missing ingredient to energy is merely the exercise. That is what I find life like on a low-leptin diet, in a low-fat body.

      It’s all so natural. Only the fact that we can work for money, save it, then use it to buy food that we haven’t physically worked for confounds modern man. We have to go back and re-create the healthy “must-work(out)-for-it” relationship between man and man’s food in order to be healthy again.

      Thanks again for Martin’s “LeanGains” site. I find it very helpful, in that it supports a very healthy lifestyle.

    • Mark, I forgot to say, I’m sorry I don’t have any great advice on why your tests are giving you some confounding results!

      I did also read that Warfarin increases hepatic LDL levels, but not necessarily the levels in the plasma. I don’t know why you are on Warfarin but usually it’s for reducing blood clotting. You might talk to your Dr. about the benefits of using grounding (earthing) instead of the Warfarin. Read up on it. It has an almost immediate (within minutes) effect on the clumping tendencies of red blood cells.

      I have no idea why your LDL and Trigs spiked. I’d guess it’s more a result of drugs though than diet. I believe our bodies put the lipid levels where they need to be, and I don’t try to mess with levels. There are people who die of old age at 90 who have way-wrong cholesterol, and those who have heart attacks with a very fine set of statistics.

      I tend to have different ideas than Masterjohn on fats as foods and on cholesterol as a threat to my health, so I won’t get into that here, but I would say I am very careful about the degree of refinement of all polyunsaturated fats I take in. The least refined the better. Ideal is from minimally cooked (say boiled only, or near raw) organic, free-range animals or eggs. You work downward from there, by accepting foods that are not organic, or not fresh, or cold-pressed, or manufactured from fish that has been mashed into fish meal with oils as a bi-product. Lowest levels are the cheap vegetable oils, or foods deep-friend in them.

      Since I accept only the highest quality of foods, especially as regards oil content, I don’t worry at all about cholesterol. I last had cholesterol tested over 15 years ago and it was OK and I’ll never have it checked again. For me it’s just a hook a Dr. is asking me to accept so I can stay on his program. I won’t do that. As I understand it, it’s a combination of sugars and ruined fats that cause vascular damage and inflexibility. Hopefully you’ll soon get your statistics to where you also can break away and never return to the flock. Best of luck.

  14. FACTS:
    Male, white, 52
    5-7
    170lbs
    approx. 130lbs fat-free mass
    Bodyfat: approx. 19%

    GOAL: <10% bf using a LC PaIeo diet combined with Intermittent Fasting which means I must lose at least 17lbs of bf, both subcutaneous and visceral.

    Resistance train 4xs/week
    Cardio interval train 2-3xs/week

    I was dx'd via ultrasound with non-alcoholic fatty liver disease (NAFLD) two years ago. It is indeterminate how long I've had it. Liver enzymes continue to remain within normal range and I notice no symptoms

    I am hypothyroid and have been taking 75mcg of sustained-release T3. My latest thyroid numbers are posted in the link below [p2, 3, 10].

    TSH has improvement over last labs. Both T4 and T3 show depressed, however, I was fasting for nearly 20 hours on the first day. rT3 is less this time, which is a good thing.

    Have been on LC Paleo diet for last three months and doing between a Lean Gains [ http://www.leangains.com/2010/04/leangains-guide.html ] 16/8 IF protocol to as much as 20/4 IF protocol. I do mini-carb refeeds (about 50-60g) on my workout days only. If I increase carbs more than this, my post-prandial BG will exceed 125.

    What's freaking me out are my latest lipid tests. I had the top three done in a matter of two consecutive days [p2, 5, 11-14].

    LATEST LABS: http://s57.photobucket.com/albums/g207/CS2006/LABCORP%2006-19-12%20and%2006-20-12%20LABS/

    If we’re clearing lipids from the liver, then this is a good thing, but HOW CAN I DETERMINE THAT IT'S THIS AND NOT FROM THE DIET ITSELF?

    In other words, is the increase due to CREATION or CLEARANCE (resolution of NAFLD)?

    I have not changed any macros in my diet, maybe slightly more lean grass-fed animal protein, but saturated fat intake has remained constant throughout. And most of the saturated fat is drained because I steam all my meats, so how can it be CREATION?

    The only other fats I eat with frequency are O3s (2-4g), coconut, flax, macadamia and olive oil.

    What evidence supports this unconventional theory?

    I understand that 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.

    How could this be the case when taking liver support supplements like milk thistle, dessicated liver, choline, lecithin, etc.? Why wouldn't such intervention spur on the purge also?

    Why wouldn't free fatty acids (FFAs) from stored subcutaneous fat be released into the bloodstream as well?

    Could this explanation be the mechanism behind the clearance of FFAs: During fasting or starvation, free-fatty-acids are released during lipolysis into the liver and muscles to be burned as energy, this is called fat-oxidation. During the fed-state and especially while eating a starch-based-diet, fat-oxidation is inhibited and replaced with carbohydrate-oxidation, insulin is what mediates this shift. When carbohydrate-oxidation is taking place, fatty-acids are shuttled back and "locked away" in adipose-tissue… where they belong.

    In addition to LC Paleo/IF, I also began taking 1g of choline nearly a month before the labs + 3mg methylfolate/day to help with a genetic methylation defect.

    Could the above combination have created a mega-purge?

    Could the answer be that the best predictor of fatty liver is obesity and insulin resistance?

    Another thing:
    I have been on warfarin for 3 months and must remain on it for another 3 months. This was the only thing I could find on warfarin and its effects on blood lipids:

    Coumadin binds to bile acids in the intestine leading to increased excretion of bile acid in the feces leading to increased oxidation of cholesterol to bile acids resulting in increased numbers of low density lipoprotein receptors with increased hepatic uptake of LDL and lower serum cholesterol levels
    source: http://www.flash-med.com/Side_Effects_Coumadin.asp

    Anomalies to purge theory:

    Why the decreased HDL when I was making nice progress before?

    Lastly, I had been fasting for 18-20 hrs prior to my blood being drawn. My fasting insulin was only 5.2. Then why an elevation in HbA1c (5.8) and FBG (95)? Should've been in the low 80s, especially when fasting for LONGER periods AND on LC Paleo.

    This even when on a broad range of BG-lowering natural agents including corosilic acid, chromium, cinammon, etc.

    So, why is my insulin sensitivity is taking a nosedive during this so-called healing crisis as well [see Insulin Resistance Score – p12, 14]?

    Can someone please interpret my lipid profiles, especially the NMR LipoProfile and tell me what is going on?

    • Mark,

      I don’t have the answer for you, but the focus of this article, and seemingly of your post, is on fats.

      Non-alcoholic fatty liver disease is more due to excessive toxins and just plain old fructose in the diet than anything more exotic. People eat typical foods, heavy in toxins (not organic for the most part) and heavy in sugars. You didn’t mention what your “mini-carb re-feeds” consist of. Quality is important here. Are you taking in fructose?

      And as you said “Could the answer be that the best predictor of fatty liver is obesity and insulin resistance?”. You hit it. And the way to get it cleared simply seems to be to get off carbs and get exercising. So I still wonder why you wonder. Are you just confused by your test results?

      Martin Berkhan’s protocol says things like “No calories are to be ingested during the fasted phase, though coffee, calorie free sweeteners, diet soda and sugar free gum are ok (even though they might contain trace amount of calories).”

      To be curt, he’s talking poisons here. I think you should look elsewhere for a way to health.

      Best of health to you.

  15. Hi Chris,
    Great recent series with Chris Masterjohn. I took in all three parts. It seems to me that the degenerative theory does not let cholesterol concentration off of the hook. Just as more cholesterol gives a higher chance of infiltration in that theory, so would more cholesterol equate to more substrate for degeneration in the degeneration theory. Therefore; I don’t believe that the blood cholesterol level is unrelated to frequency and size of plaque formation. I do accept that there would be additional remedies under the degenerative theory like the prevention of oxidation.

    I don’t like statins, and hope to find more alternatives to using them. I plan to read some of the cholesterol articles by you on your website. Sincerely, Tom K.

  16. Hello Chris and Chris.

    What are your opinions on proteolytic enzyme supplements such as bromelain, papain, pancreatin, or serrapeptase for fighting inflammation?

  17. Recently, a CT scan showed that I have a fatty liver. My guess is that it would be more from lack of sleep, and a history of alcohol abuse, than dietary, since I have been “paleo” for over a year now. I’ve been trying to piece a lot together, as what to do. Obviously, no more booze. What I am unclear on is if there is a difference between AFLD and NAFLD, and what foods to eat/avoid during an attempt to get my liver as back to normal as possible. On the positive side, all of my other blood work and scans check out fine.

  18. What are your thoughts on using proteolytic enzymes to manage high cholesterol, assuming that all other diet and lifestyle factors are addressed? Could this be an effective way to decrease inflammation and dissolve arterial plaque?

    • Hello Lightcan, if you are still around, can I ask you some questions? In regard to your high lipid issues back in ’09. I’m having similar problems and would like to pick your brain.

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