RHR: Chris Masterjohn on Cholesterol and Heart Disease (Part 3) | Chris Kresser
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RHR: Chris Masterjohn on Cholesterol and Heart Disease (Part 3)

by Chris Kresser

Last updated on

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.

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.


Join the conversation

  1. hello all,

    I’m coming in late to this conversation, but I found it after researching for alternatives to statins for high TC and high LDL (my trig’s are ok).

    I’ve tried two versions of bergamot, it did nothing for me.

    Chris Kesser: in this podcast, you had said “…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.”

    — did this ever get uploaded somewhere ?

    thanks 🙂

  2. Suzanne, you and I have VERY similar profiles. You have familial hypercholesterolemia type II. It is much more common among Jews and Syrian Christians than among the general population. 1 in 72 people.

    I tried a “Dean Ornish” low fat diet for 10 years without success at changing my risk profile. Then, I tried every cholesterol medication, but all had near immediate life altering side effects, so I quit them all in 2008. My search for another solution led me to the Paleo diet in 2008. Within months, my blood tests started to show unexplained, large HDL increases without medication that caught the attention of my doctor. Continued efforts to optimize HDL and bile acid led to me eliminating nearly all symptoms of poor digestion and IBS. Today, I stick to a paleo diet that seems different than how many others define paleo. I keep a diet high in vegetables, low in animal fat, medium in protein, while I eats tons of raw macadamia nuts, olive oil and avocados. I avoid butter, dairy, and anything fried. I also add lots of psyllium and guar gum fiber to water twice a day and take curcumin, taurine, selenium, digestive enzymes, Benecol chews, and a red rice yeast pill once a week (with lots of side affects). Soon enough, you and I may be eligible for the PCSK9 based treatments now in testing.

    • Jonathan: Thank you for the insight. Totally fascinating. Looks like we’re taking a similar modified Paleo style approach to our address our specific needs. In addition I’m concerned about my thyroid function. And will need to address this too. Supplementally I use Resources to maintain a healthy digestive system, Replenish my gut bacteria And assist and optimizing thyroid and adrenal function. Not sure that any of this plays into my cholesterol levels but I finding the need to support my G.I. function as priority.
      I am hoping this is the right path.

      • Suzanne,

        I am banking on my hypothesis that digestive function is key in people like us. Guar gum, Saccharomyces Boulardii, and silymarin have radically changed my life as much as much as paleo, if not more. The last 6 years of optimizing gi have had to have a positive impact. I just feel better and no longer need sudden, emergency restroom visits. There are studies of the relation in bile/digestion function that trump cholesterol measurements as a predictor of heart disease. Do a search and find ones like this: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3105622/

    • You are going to take an experimental drug that has no long term data yet and cost 100,000 per month but you put down statin’s for the side effects? How does that make any sense?

  3. Hi Chris & Chris,

    I was wondering if I could get your take on some lab results.
    Here’s a quick background:
    Diet: Paleo with the occasional white rice or potato (I live in Idaho). My carb intake reflects my activity level & fluctuates.
    Age: 41
    Gender: Female
    Activity: Sorry, but I’m an avid runner, cyclist, DH & XC skier. I take care to rest & recover with much less volume outside of Summer. CrossFit or strength train in the off season, yoga & regular massage
    Sleep: 8-9 PM- 5-7 AM rested most nights.

    My cholesterol has always been high but consistent. Unfortunately, I’ve only been tracking my labs since going Paleo in May 2011.

    My Paleo-friendly GP says I should be a case study. Great! Yeah for me….

    Here’s my most recent labs through Health Diagnostic
    TC: 354
    LDL-C direct: 92
    LDL-c: 189
    Tri: 50
    Non-HDL-C: 165
    Apo B: 83
    LDL-P: 2139
    sdLDL-C: 37
    Apo A-1: 368
    HDL-p: 53
    HDL2-C 108
    Apo B: Apo A-1 ratio: .22
    Lp (a): 8
    Fibinogen: 327
    hs-CRP: <.3
    Lp-PLA2 213
    Myeloperocidase 179
    Mycardial function: optimal range
    Genetics: Apolipoprotein E 3/4
    Insulin: 3
    Free Fatty Acid: .49
    HbA1c: 5.3
    Average Glucose: 105.4
    25-Vit D: 40
    Uric Acid 4.5
    TSH: 3.99
    Homocysteine: 7
    Sterol Absorption markers:
    campesterol 3.7
    campesterol ratio: 101
    Sitosterol 4.34
    Sitosterol ratio: 114
    Cholestanol 3.7
    Cholestanol Ratio: 104
    Demosterol 2.39
    Demosterol ratio 66

    Liver, Renal, Electrolytes are all optimal

    TSH: 3.99
    T4, free .71
    T3 2.1
    Reverse T3 6
    Anti-thyroglobulin antibody 14
    anti-thyroid Peroxidase antibody 17

    I am about to do a diurnal adrenal test to check my cortisol levels.
    What's a girl to do? I feel pretty solid on a Paleo style diet. My doc suggests that I remove some of the saturated fats. UGH!
    I am a bit concerned about my genetics & the fact that my particle size is small and dense….

    Any suggests or insight would be fantastic.

    Thanks again for all the wonderful work that you both do.

    Warm regards,

  4. I remember reading in native american populations if they were having problems with fertility they would eat bear meat until the problem was resolved.

  5. 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?

  6. 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?


  7. 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?


  8. 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.


  9. 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.

  10. [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.

  11. 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?

  12. 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!

  13. 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…


    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?

  14. 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.



      • 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.



          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.


          • 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.


              • 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.

  15. 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:

    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:
        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!

  16. 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:


      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!

  17. @ 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.

  18. FACTS:
    Male, white, 52
    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.

  19. 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.

  20. Hello Chris and Chris.

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

  21. 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.

  22. 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.

  23. oh yeah, i forgot to mention that dr. glueck always writes me a prescription for crestor every time i see him, but i tear it up when i leave his office. i’m pretty pleased with my last lipid profile but i’m still wondering about the hc.. didn’t know that was so serious until i listened to your interview. 🙂

  24. hey chris and chris – i just listened to all 3 parts, and i think it was in part 2 in which you talked about how genetic hypercholesterolemia really needs to be dealt with and addressed. i go to see dr. charles glueck at the cholesterol center in cincinnati (don’t know if you’ve heard of him). he’s more of a mainstream doc but he also does a lot of cholesterol research, and he tested to see if i had hc, and i have the MTHFR C677T homozygous gene. in my last lipid profile (11/11), my total was 270, triglycerides 52, HDL 112, VLDL 10, and LDL 148. however, in the past, my total has been as high as almost 400, and LDL over 200. i feel that i don’t have anything to worry about – but what are your thoughts? also, do you ever use niacin therapy to lower total and LDL? i attribute my lower levels to niacin – i take 500 mg whenever i go in my far infrared sauna, about once or twice a week. my diet is sort of paleo, sort of weston price. however, i’m trying to eat more starchy carbs for sleep and energy. mostly i just eat non processed whole real food. and i’ve exercised regularly for 3 decades. thanks for any info or advice on my lipid situation.

  25. Haha, oh man, I just realized you were talking to Chris K. I’m disappointed I no longer have a baby girl promised to me but you and Chris are still awesome. But please, call us Master J and Special K — we have nicknames for a very practical reason! 😉


    • My bad!!! Sorry to get your hopes up – no baby girl for you, at least not yet!
      I’ve got the nicknames down now – I get it!!
      Our local hospital is doing another blood draw for the health fair in two weeks so we will go get another round of cholesterol measurements. I’m concerned about Jeff’s status. Looking over all the thyroid symptoms we can’t come up with even one that applies! That’s great news of course. and, ah, no problems in the hormone department – know what I mean? No metabolic problems that are apparent. What other endorcrine signs might we look for that might indicate a problem there? Its a head scratcher. I am anxious to get another round of testing done! Perhaps he is just a wide swinger.
      Thank you! Valerie

  26. Your awesome Chris and I really appreciate the time you take to provide this information for free. I realize you can’t get to every question and appreciate the insights and answers you able to provided.

    Please keep up the good work and don’t let the negative comments get you down!! Now go play with your baby girl and have a great day!! 🙂

      • Haha, oh man, now I realize you were talking to Chris K. I’m disappointed I no longer have a baby girl promised to me, but you and Chris are still awesome. But please, call us Master J and Special K — we have nicknames for a very practical reason! 😉


  27. Hi Chris and Chris,

    On the intake of crucifers and iodine: I’ve recently had symptoms of hypothyroid (cold hands and feet, taking libido) and I’m 23 years old. I had been taking half a tab of Iodoral (6mg/day) for over a year and recently upped that to a full tab when these symptoms came about. I also eat around a pound or more of a variety of crucifiers (always well-cooked in the microwave) 5 days a week. I still don’t know the cause of these symptoms (iodine or goitrogens) but have decided to drop the iodine for a month to see how I feel.

    For those of us whom crucifers are a staple food, is a 1mg/day iodine intake enough?

    Secondarily, will the iodine/supplement be effective if taken at the same time as crucifers?

    Many thanks for your valuable information and incessant research.

    • Hi John,

      I speculated that 1 mg is enough to take care of the goitrogens, but a) this was speculation, and b) there are many other reasons some people might need higher intake. So no, I don’t think we can assume it is enough and Chris’s clinical experience supports that it often isn’t because he said he sometimes needs to use up to 6.5 mg/dL to bring down LDL-C in people with other symptoms of hypothyroidism. It doesn’t matter when you take the iodine supplement. It might even be more effective if taken with crucifers, if it makes any difference at all.


    • Hi John,

      I’m also 23 years old and seem to be hypothyroid. I just started Lalonde’s autoimmune protocol from Robb Wolf’s episode 68 and hope to see benefit in the future.

      Have you seen improvement?

      As a young guy with a similar condition it would cool to talk to someone who can relate.

      Feel free to e-mail:

      [email protected]


  28. Someone a little ways up asked the same question I had but no responses, so I’ll ask too: what if you have Hashimoto’s? As far as I can make out (and my endocrinologist has been ZERO help here), I’m not really supposed to be having iodine in the first place. I love making my own sauerkraut and other ferments, and I can switch it out to more carrots and beets and less cabbage (or just make sure I’m only using lightly-cooked crucifers instead of raw or fermented), so that’s not a huge deal-breaker for me, but it would be nice to have some more definitive guidance on iodine, crucifers, the whole package, in terms of Hashimoto’s.

    Been pretty much Paleo/Primal for several months now, gone gluten-free a couple months ago, and actually been OFF my thyroid replacement (synthetic T4) for over a year since it was giving me BP spikes and migraines, and my endo isn’t terribly supportive of that either; pharmacological intervention is her answer for everything, which leaves me short of resources. 🙁

    Would love some comments from you, or maybe its own post? Thanks! 🙂

    • Iodine is safe for most people with Hashi’s, with two conditions: 1) they start at a small dose (200-400 mcg) and build up very slowly over time, and 2) they get adequate amounts of selenium (200 mcg/day). Unfortunately there’s no one-size-fits all approach with crucifers or iodine. Different patients with Hashi’s have different levels of tolerance.

  29. Something’s wrong with the comments section. I can see my comment now after a long delay but it’s been cut short at the start. This is sort of what I said:

    What I said was that I originally found out about my high cholesterol last summer after having been eating LC (100g carbs per day) and eating some of Paul’s recommended supps, I got this down to reasonable levels:

    TC: 280
    LDL: 155
    HDL: 81
    TG: 60

    At this time, I stopped worrying about lipids. End of last year, I started out on ‘Leangains’ (Martin Berkhan’s 16/8 IF protocol incorporating carb/calorie cycling on Workout and Rest Days). I initially kept carb intake around 200-250g on WO days (3x a week, hypercaloric), eventually raising it to 400-450g. For Rest Days, it stayed around 50g (hypocaloric).

    After about 10 weeks of doing this, I got lipids retested:

    TC: 396
    LDL: 275
    HDL: 73
    TG: 89

    This was alarming and I went back to Paul for advice. He told me to make sure I got in >100g of carbs even on Rest Days and never went below. Also, he asked me to check if I may be deficient in some micros. I stuck to this advice for 2 weeks (while having to take time off from the gym because of back spasms) and basically ate around 100-150g carbs everyday with lower total calories to account for the lower activity level.

    From here on, you can read my first comment as it continues the ‘story’.

  30. Hello Chris K and Chris M,

    Thank you for the extremely informative discussion. I developed high TC and LDL last year while eating quite LC (100g carbs everyday for 2 weeks before getting retested:

    TC: 360
    LDL: 243
    HDL: 66

    I reduced my caloric consumption to account for my lower activity level during these two weeks. Lipids improved slightly, but I guess it was too early to see a big difference.

    Also got Free T3 and Free Testosterone results:

    Free T3: 1.96 pg/ml
    Free Test: 16.5 pg/ml

    Even though my lab’s reference range shows them as being ok, I’m thinking these values are quite low. Do I have hypothyroidism induced high LDL and TC?

    Also, I get only 150mcg Iodine from my multi, not much else. I do eat cauliflower and turnips cooked with my beef, alongwith a plate of cucumbers, tomatoes and green bell peppers quite regularly. Can I benefit from further Iodine supplementation? What dose would you recommend?

    As of now, I am unsure if I have FH because I did get my TC down to about 250-ish last year, even though LDL was still high then. The best numbers I had were TC of 280 with LDL 155 and HDL 81. I don’t think those numbers wouldn’t be possible no matter what I ate if I had FH.

    It seems more likely that the high again cholesterol is a case of carbohydrate restriction combined with insufficient Iodine. I would really appreciate your answers and comments!


  31. Ok here we go! Two Paleo-ish/WAPFer’s (4 yrs in). My husband and I TODAY, picked up our health fair blood tests. and guess what ….

    (we both had screening for cmp/tsh/lip-d ldl/fer)
    Me: 47, healthy weight, active, all other blood markers are normal. TSH is 1.14 (is that lowish?)
    Jeff: 40, healthy weight, very active, all other blood markers are normal. TSH is 2.63

    me: TC 256 trig 70 hdl 60 ldl direct 199 TC:HDL ratio 4.2
    jeff: TC 265 trig 98 hdl 57 ldl dierct 198 TC:HDL ratio 4.6

    One item of note in the results was jeffs 25-oh D3 was low at 26, mine was moderately low at 37 (I supplement with liquid d3, he takes just FCLO). All of our other blood markers are all well within normal ranges.

    NOW WHAT??? Our ratios indicate we need to look into a problem??!!
    So … Ok, so I have ruled out your other “reasons” for an increase in our lipids (no fatty liver, obesity, or thyroid malfunctions) Mine TSH seems a tad sluggish?

    We eat a serving or two of saurkraut or kimchi each day with meals, and some seaweed also take small iodine/iodide supplement occassionally. Never eat out, all food from scratch, we eat liberally of meat dairy eggs and organs organic/pastured/grassfed or wild, We eat a high animal fat diet, all fats from animals are rendered at home. We do eat starchy veggies, and sourdough white bread, but otherwise very little refined carbs. Seed PUFAs come from whole nuts. WOW! What a purified diet. We are healthy and vibrant! Jeff is an iron man! And Im no slouch. We sleep well, have low stress (more or less) outdoor exercise, have strong sex drives. There is nothing to indicate trouble in our paradise – until NOW!??!??!!

    As per this discussion my plan is we will get tested again 2 more times to get an aveage TC:HDL ratio. Should I space the testing over a two week period? Than if our average ratios are still above 4 we can begin to panic??? Your thoughts please??

    • Space the tests over the next 4-6 weeks and take an average. Even if your ratios are above 4 for both of those tests, it’s not time to panic. You both sound like you’re healthy and taking good care of yourselves. Remember these are just one set of markers in an overall picture.

      • Thanks for the super fast reply. I settled down a little. I’m on board, I know we are healthy! I just want to be sure that we are safely in range of the ratio recommended. This stuff is CRAZY. I don’t think I would have paniced if not for the range from masai to katavins, and highish ratio. I will follow your suggestion, and thanks again!! I really admire what you guys are doing for the discussion on fats. It is invaluable information and a source of comfort to be able to tune in and learn this obscure stuff in terms I can understand. Keep it coming…. 🙂

      • Chris, I listened to an older interview today with Sean Croxton from 09 today. In it Chris mentions that a tc:hdl ratio of 4 is fine, but when it up near 7, that is cause for concern. Has Chris changed his stance on that? He also mentions in the interview particle size pattern a/b testing IS useful but here he states … not so much. Can you help clarify these two things for me? Thank you!

        In addition to iodines’ role, can you suggest foods & herbs, cooking methods, and supplements which will enhance or impair a robust ldl reception process? 🙂

        • I can’t speak for Chris, but I know my own knowledge on this topic continues to evolve. I need to go back and edit/update some of my previous articles/videos because of that, but I’m struggling to find the time. I am hoping that continuing to get the word out on my radio show and new articles will help.

        • Hi Valerie,

          I would go by my more recent information, as my understanding continues to involve, and, I hope, improve. I do not have much to say about LDL receptor activity except improving thyroid status, although any of the traditional digestive remedies that stimulate bile production will also help, as will any soluble fibers that cause excretion of bile acids, though with the latter you have to keep in mind how your digestive system tolerates them.


    • Hi Valerie,

      I agree with Chris, I would get them tested several times, spaced out over a few months, and not panic. I have a few more comments to add.

      First, the elevations are moderate, but they are stronger for your husband than you. I say this because in native populations women’s cholesterol is consistently higher than men’s, and when I say 220-250 is roughly the upper limit for what we see in these populations this is based on men from Tokelau and middle aged women from Tokelau or Kitava. Cholesterol is around 180 for Kitavan men and may increase with age to about 220 in men from Tokelau where they eat 50% of their calories as saturated fat. Based on your age and sex, your total cholesterol is unremarkable even when compared to a Kitavan woman, where the diet is low in fat, or a Tokelauan woman, where it is high in fat. Based on Jeff’s age and sex, his total cholesterol is substantially higher even than that on Tokelau, where they eat perhaps the most saturated fat in the world.

      I would still consider your husband’s elevation modest, and of more concern if his total-to-HDL-C ratio is high. It is modestly high, but it is not, say, 7 or 8 as occurs in some very concerning cases. Keep in mind that in many people the total cholesterol will swing up or down some 35 mg/dL, and this is an average, which means that some people swing a lot more than that! So if this is his only test, it means nothing at all without several more. What if by random chance you got unlucky and caught him on the high end of a swing? His “real” average total cholesterol could theoretically be 200 and his “real” average ratio could be, say, 3.5 for all we know.

      The ratio in and of itself can be affected by genetics as well, so it has to be considered in the big picture. It’s a non-specific marker. If total is high and the ratio is high, and this is consistent, it is time to integrate this into the big picture of total health, looking especially at endocrine health (thyroid and sex hormones).

      If you find that it is not stable but actually rising over time, then I would consider it higher priority to examine total health more thoroughly because this can indicate the beginning of an endocrine problem you could nip in the bud before it gets worse. But you are not there yet. I think if you get a few more tests this will help clarify things.


  32. So much info ….. really gets confusing though ….. what to do,what not to do? …… I’ve recently been following a “higher fat” diet, i.e. more olive oil, coconut oil, etc., not too much animal fat …. but have started to increase my “red” meat (3 or 4 oz., once/twice per wk.) a little and also calves liver twice a month or so. I used to eat mostly chick, turkey, fish and only eat “red” once a month or so. I’ve increased my consumption of vegetables considerably also, rarely eat bread/cereal anymore (1/3 c. dry oatmeal/day). I’m trying to control my diabetes w/o meds. Just had bloodwork done and my A1C came down to 6 – 3 mos. ago was 6.7, before that was over 8. Have lost about 25 lbs. in 4 mos. But I’m still confused about the cholesterol issues, T256, HDL, 57, LDL, 176, VLDL, 23. My iron was a little low (that’s why I decided to start eating liver/beef). When I heard that too many veggies might reduce thyroid function? (although I don’t think I am “overdoing” it, I’m eating a healthy amount) I got to wondering about if I am getting enough iodine. I hardly ever use salt (I usually don’t use “processed foods”). My bloodwork shows my “sodium” is 141.4 …. does this have any reference to iodine? Thanks for your wealth of information.

    • Jean: your total and LDL cholesterol are still in the range of what we see in hunger-gatherer populations following their traditional diets who are completely free of heart disease. I don’t see anything to be concerned about there.

      • Than you Chris, I guess I got carried away with my questions, but could you answer my question about the iodine? (last question above)

        • No, not related to iodine. If you’re not eating much salt, and don’t eat seafood or seaweed, you’re probably iodine deficient.

          • Please what do you do if yeast has increased greatly and you are well on in the GAPS Or SCD diet and you are forced to go back to no fruit – basically meat and veg but that gives one dry eyes and mouth though. I had that until I started eating the fruit and got rid of it by eating it! Thanks ever so much, Clodagh

  33. It think it was briefly discussed in part 2 of the podcast about a leptin / thyroid connection, but it would be great if a future episode to go into more detail.

    Can leptin be measured directly or is it only via thyroid markers? How do the 2 interact?

  34. Chris K,
    How does your blood chemistry panel services, work? I’m interested in having blood tests done, especially since I haven’t had one since as long as I can remember, but not sure if any the labs you are affiliated with are in my humble small town!

    • colleen,

      i take a brown seaweed extract called modifilan. it’s used for detoxing heavy metals and radiation, but it has lots of natural iodine in it. you might want to look into it. btw, i have no connections in any way with the company, i’m just a consumer. it was on sale on a website that i order food/supplements from, so i bought a bunch.

  35. Hi! I was recently diagnosed with metabolic syndrome and leaky gut. Dr. put me on L-glutamine and zinc-carnosine to fix. Do you think this will work?

  36. My understanding was that the thyroid adapts to whatever iodine dosage you are chronically taking in. So when you give the recommendation to increase iodine to 1mg, it seems rather empty if you’re always taking in 1 mg. Or am i misunderstanding, and your true suggestion is to increase your iodine dosage by 1mg on days when you are taking in crucifers, compared to days when you are not?

    • Hi Lenny,

      This isn’t about the thyroid’s adaptation to iodine. It is about the ratio of iodine to thiocyanate reaching the thyroid. For any given number of receptors expressed by the thyroid gland, an decreased ratio would lead to these receptors incorporating thiocyanate instead of iodine. Even if the thyroid adapted to this by increasing the expression of receptors, this would lead to a greater increase in thiocyanate than in iodine. So regardless of the thyroid’s adaptation, it is necessary to maintain a high ratio of iodine to thiocyanate.


  37. I am sorry you did not discuss LDL particles and the large discordance that appears for many between LDL cholesterol and the carriers, the particles. One could have a normal LDL reading, but an abnormally high level of LDL particles. Thyroid can be normal in this population as well as weight, insulin and
    BG. Interestingly enough there are many out there that exhibit these characteristics; perhaps it is genetics particularly with family history of heart disease and may have to do with the liver and how it packages the cholesterol, and strength of LDL receptor activity. If lifestyle changes cannot change the profile the only treatment i am aware of is Statins

    • Steve,

      As we discussed in the second part, it is unclear whether particle size/count is an independent risk factor for heart disease that adds additional information to the classical blood lipid risk factors, and it is unclear how much this is due to the intrinsic amount and type of information provided or two inaccuracies in the testing, but we didn’t deal with this question in more detail precisely because there is no hard science on it.


  38. Hi all,

    What do you think of Dr. Kharrazian’s (author of Why Do I Still Have Thyroid Symptoms? When My Lab Tests Are Normal: A Revolutionary Breakthrough In Understanding Hashimoto’s Disease and Hypothyroidism) contention that the “goitrigen model” is outdate. In other words, that goitregenic foods cause thyroid issues. This is, of course, an oversimplification, but am very curious what both Masterjohn and Kresser think about Dr. Kharrazian and this claim.

    I heard him say this on the Underground Wellness podcast.


  39. 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.


  40. 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.


  41. 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.


  42. 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.

  43. 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.


  44. 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.


  45. 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!

  46. 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?)

  47. 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.


  48. 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.

  49. 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.

  50. 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.

  51. 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.

  52. 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.


  53. 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.


  54. 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.


            • 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.


  55. 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?

  56. 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.


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