Chris Masterjohn on Cholesterol and Heart Disease (Part 3)
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.
In Episode 6 of “Jimmy Moore Presents: Ask The Low-Carb Experts,” we have Chris Masterjohn from Cholesterol-And-Health.com who is a blogger and doctoral candidate in Nutritional Sciences at the University of Connecticut where he will be graduating this Spring. 
