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:

• Chris Masterjohn Blog - The Daily Lipid
• Thyroid Toxins Special Report
• Chris Masterjohn article: Bearers of the Cross:  Crucifers in Context
• Super Selenium Complex from Life Extension
• Nutrition and Physical Degeneration, By Weston A. Price

Full Text Transcript:

Steve Wright:  Hi everyone, and welcome to the Revolution Health Radio Show.  I’m Steve Wright from SCDlifestyle.com, and with me today is Chris Kresser, health detective and creator of ChrisKresser.com.  How’s it going, Chris?

Chris Kresser:  It’s going pretty well, Steve.  How are you?

Steve Wright:  I’m doing good.  The shoulder is healing up, and I’m pretty excited for our special guest today.

Chris Kresser:  Yeah, me too.  We’ve got Chris Masterjohn back for Part 3 of the Cholesterol Series.  Really excited to wrap this up.  It’s been a really popular series so far.  We’ve gotten a lot of great feedback.  People are learning a lot.  I’m learning a lot.  It’s always a pleasure to have Chris on the show.  So, for those of you who don’t know Chris, it’s time for you to crawl out from under that rock you’ve been hiding under!  He’s one of my favorite bloggers in the Paleo/Primal food sphere, and he is just super knowledgeable about all this stuff.  He is pursuing — well, actually I’ll let him introduce himself.  He knows more about what he’s doing right now, but he is pursuing a PhD, and I think those of you who know his work know how much he has to bring to this discussion.  So, we’re happy to have you back, Chris.  Why don’t you just give a really quick intro for people who don’t already know you, and then we’ll dive in. 

Chris Masterjohn:  Sure!  Thank you so much for having me back, Chris.  My website is Cholesterol-and-Health.com.  I have a blog there, The Daily Lipid.  Right now, I’m just wrapping up my PhD.  I’m almost done.

Chris Kresser:  Woo-hoo!

Chris Masterjohn:  I am getting my PhD in nutritional sciences, and that is studying how diet and nutrition works on a physiological and biochemical level, and I’m currently writing a dissertation on how oxidative stress regulates the production of methylglyoxal and its detoxification, which is a key player in advanced glycation endproducts, which are believed to play a role in diabetes and cardiovascular disease. 

Chris Kresser:  That’s some light reading for the weekend, maybe.

Chris Masterjohn:  Ha-ha, yeah.

Steve Wright:  Yeah, that’s a mouthful! 

Chris Kresser:  Cool.  So, we’ve already done Part 1 and Part 2 of this show, and now we’ve got transcripts and you can go back and listen to the original episode.  Chris, why don’t we do just, like, a really super-quick recap of what we talked about in the first couple parts, and then we’ll dive into this last part so we have plenty of time to cover that material?

The role cholesterol plays in heart disease

Chris Masterjohn:  Absolutely.  So, in Part 1 we just outlined my basic ideas about the role of the degeneration of lipids in heart disease, and we talked about the two camps:  the cholesterol warriors who are making a war on cholesterol because they see cholesterol as the enemy and, you know, the aggressor in heart disease, and the cholesterol skeptics who basically say, well, blood lipids don’t really have any role in heart disease.  And the basic conclusion of Part 1 is that blood lipids do play a role in heart disease, but it’s not that their high concentration is infiltrating the vessel wall; it’s that their degeneration is posing a danger to the blood vessels, and the immune system comes and mops them up to create the atherosclerotic plaque.  And that is a positive adaptation to this process of degeneration, but it poses a risk in the long term because that plaque can ultimately break down and cause a heart attack.  So, from Part 1, what we concluded was that we don’t want to modify the concentration of lipids in the blood so much as prevent their degeneration.

Chris Kresser:  Right, so let me just jump in and summarize there.  So, the original theory, the infiltrative theory, is sort of like arteries are like pipes and cholesterol is like gunk, and the pipes get clogged up with cholesterol, and then you have a heart attack.  Right?  That’s kind of how it was broken down in the mainstream.  But, what you’re saying is that what really happens is that the cholesterol — or more accurately, the lipoproteins that are carrying cholesterol and other fats — get damaged by oxidation, and then the immune system’s response to that oxidative process is what causes the buildup of plaque and then ultimately the rupture of plaque and heart attack.  Is that accurate?

Chris Masterjohn:  Yeah, absolutely.  So, what we’re trying to do is protect the vulnerable lipids and get them to go where they need to be.  And what we want to do is we want to metabolize the lipids and fat-soluble nutrients and everything that’s in our bloodstream and use them properly.  So, for example, cholesterol we want to turn into bile acids for our digestion, sex hormones for our fertility and virility, and we don’t want them left in the blood to be damaged and contribute to atherosclerosis. 

Chris Kresser:  OK, cool.  So, then Part 2 we talked a lot more about testing normal variation of cholesterol markers, particle size, etc.  So, take us through that.

Chris Masterjohn:  Sure.  So, we have to keep in mind that since we’re focused on the degeneration of lipids and protecting those lipids in the blood, when we look at concentrations of lipids, we’re not trying to look at necessarily a cause-and-effect scenario.  So, if we’re concerned when total cholesterol goes really high, it’s not because that is causing heart disease, but we’re using this as a metabolic clue.  So, in the initial parts of Part 2, what we did was looked at some of the traditional cholesterol levels in populations that have not been through industrial modernization, that have been studied and have been shown to be free of heart disease, to try to see what normal lipid metabolism is like.  And we looked at two groups in particular:  the Masai and the Kitavans, who have been well studied and shown to be free of heart disease; and we used them to define basically the lower and upper limits of blood cholesterol.  And what we see is the Masai have pretty low cholesterol levels, but the Kitavans, who are eating a diet based on fish, coconut, starches, and so on, the men tend to have cholesterol levels around 180, the women tend to have cholesterol levels around 200 to 210, and these tend to increase with age.  So, in their 40s and 50s, the women might have cholesterol around 250.  In general, the LDL/HDL ratios are between 2 and 4 in these tropical populations.  And there are some other populations that have not been studied quite as well but also seem to be free of heart disease, like Tokelau, where the consumption of coconut is much higher, and their cholesterol levels in the case of the men increase from about 180 to 220 with age and in the women tend to increase from about 200 to 245 with age.  So, around 250 total cholesterol is where we might set the upper limit of what seems to be normal, according to these traditional populations eating traditional diets that are free of heart disease.  That doesn’t mean that a cholesterol level of 251 is gonna kill you.  It just means that that might be the point where we might start looking at some other signs and symptoms to see if there is a problem, not necessarily assuming that there is one.  And then we went through how do I know when my cholesterol is really increased, because there is a lot of variation that we can normally expect.  And we said that if we’re just looking at two measurements — say, we changed our diet, we measured cholesterol once before and once after the diet — if we hadn’t measured our cholesterol very often to get a sense of our own variation, then we should be careful not to assume that it has increased unless we have an increase of at least 35 mg/dL for total cholesterol, about 10 mg/dL increase or decrease for HDL, 30 mg/dL for LDL, and about 40 mg/dL for triglycerides.  So, we should be concerned when we see these large increases and they go outside the range of what is considered to be traditional.  And the total/HDL cholesterol ratio seems to provide the most information, and particle size and other of these emerging tests probably need to wait on the bench until we can standardize them better and be able to utilize them to provide clearer information than what we have now.

Chris Kresser:  Right.  Not ready for prime time.  There is one interesting test.  Maybe in Part 4, eventually when we have that, we’ll talk about it.  It’s an oxidized LDL test, which has only been available in the research settings, but there’s a lab in New York that is starting to offer this, and I’ve been corresponding with them.  They’re not quite there yet, but hopefully in the near future that will be available.  Again, it’s not totally clear how useful that would be yet.  I mean, what’s your impression of that from your reading of the literature, Chris, the oxidized LDL marker?

Chris Masterjohn:  Well, I think the way that you just summarized it is probably pretty good.  It’s not clear how useful it is yet.  I do think that it’s probably going to offer some advantages, but there is always gonna be some lack of clarity in interpreting it, because when LDL oxidizes in the blood, it’s cleared very quickly from the bloodstream.  So, you have to remember that if you’re looking at oxidized LDL, you’re taking a snapshot of what is in the plasma at an instant, and I think we need to study it more to see how reliably it gauges the actual process of oxidation.  We want to try to infer the processes that are going on and not just look at the snapshot as if things are static. 

Chris Kresser:  Um-hum.  OK, so we’ll come back to that maybe when we have some more info on it, but let’s now talk about the meat of Part 3 here, which is the question that’s on a lot of people’s minds, and actually in my practice I still get quite a few of these questions, even people who have read all of your work, Chris, and my work and, you know, they’ve been exposed to these ideas for a long time, but when their cholesterol is somewhere around 250, there are still many, many years of conditioning around the idea that high cholesterol is gonna cause heart disease, and so understandably people, when their cholesterol starts to creep up a little bit like that, their question is — So, you know, they’ve changed to a Paleo Diet or a Weston A. Price / Primal type of diet, and they get their cholesterol checked, and their total cholesterol or LDL cholesterol are out of range, you know, out of the lab range and maybe up towards that 240 or 250 mark that you just mentioned.  So, what could be going on here in these cases?  This is what we’re gonna talk about today, and what kind of steps can people take to investigate a little further to determine whether that slightly elevated total cholesterol and LDL cholesterol is a problem or whether it’s just part of a natural physiological process.

What to do – and not do – about high cholesterol

Chris Masterjohn:  Absolutely.  So, the first thing that we need to understand is that there are good reasons and bad reasons for increases in cholesterol in the blood.  So, one of the reasons that cholesterol can increase is if we’re clearing lipids from the liver.  Let’s say, for example, that a person has nonalcoholic fatty liver disease and they start resolving it.  Well, one of the key problems with fatty liver disease is that the lipids get stuck in the liver and they’re not being released into the bloodstream, so once you start clearing that, part of what may happen is you may get an increase in triglycerides, and you may get an increase in cholesterol in the blood.  And that is a good thing because nonalcoholic fatty liver disease is not only very dangerous for the liver, but it’s actually a much stronger predictor of cardiovascular disease risk.  And this is a currently emerging field, but there is one study that was done in Japanese people, and they just looked at a number of a Japanese population that was apparently healthy, and they looked to see if they had fatty liver or not, and then they followed them over a number of years.  And they found that fatty liver disease increased the risk of cardiovascular disease by over fivefold; whereas, LDL cholesterol predicted it somewhat, but the study wasn’t even statistically powerful enough to make that connection to LDL cholesterol statistically significant.  And then when they incorporated LDL cholesterol and metabolic syndrome in a statistical analysis, they found that LDL cholesterol and metabolic syndrome, neither of those were even significant, and nonalcoholic fatty liver disease raised the risk of cardiovascular disease by about threefold or fourfold for men and about fourteenfold for women.  So, if we’re clearing lipids from the liver, then this is a good thing.

Chris Kresser:  Yeah, that’s a pretty phenomenal statistic there, especially in light of some of the estimates that I’ve seen that up to one in three Americans have nonalcoholic fatty liver disease, which would really go a ways to explaining the cardiovascular disease epidemic.

Chris Masterjohn:  Absolutely.

Chris Kresser:  So, you’ve written about this, Chris, what you were just talking about in terms of switching to a Primal/Paleo type of diet and the lipids going up because the fatty liver is sort of unpacking itself.  And you’ve written about this extensively that choline is one of the nutrients that makes that possible, so can you say a little bit more about that?

Chris Masterjohn:  Sure.  So, the best sources of choline are liver and egg yolks.  There are also a number of other nutrients such as folate, for example, that reduces the need for choline.  So, it you’re increasing your intake of liver, egg yolks, and leafy green vegetables — you know, a general increase in nutrient density in your diet — it’s very likely that if you do have fatty liver you are going to contribute to its resolution, because choline is the key nutrient that is needed to package the fats in the liver and export them into the bloodstream so they can be metabolized by other tissues.  Now, like you said, one in three Americans might have fatty liver, and the best way to diagnose fatty liver, to get certainty, the least invasive way is with an ultrasound.  It can also be diagnosable with MRI or biopsy.

Chris Kresser:  One of the names for that is FibroSURE.

Chris Masterjohn:  For the test?

Chris Kresser:  Yeah.  Just to let people know, if they want to ask for that test.  I mean, in my experience, a lot of doctors won’t order it, but if you want to ask for it, that’s what it’s called.

Chris Masterjohn:  Right.

Steve Wright:  Are there any blood markers that would, you know, predate that, because you can’t just walk into your doctor’s office and just say, “Hey, can you ultrasound?”

Chris Kresser:  You might see a mild elevation in aminotransferases, so like AST and ALT.  They’re sometimes called liver enzymes.  And ALT is fairly specific to the liver, but AST can reflect tissue breakdown in other organs.

Chris Masterjohn:  Yeah, but none of the aminotransferases are very specific to fatty liver, so the best predictor of fatty liver is obesity and insulin resistance.  So, among obese Americans, over three-quarters have fatty liver. 

Chris Kresser:  Wow.

Chris Masterjohn:  So, if you are correcting obesity and insulin resistance and you don’t want to have a biopsy or your doctor won’t order an ultrasound, I think you can assume that resolution of fatty liver is a very likely candidate reason for why blood lipids may increase, but they should normalize over time. 

Chris Kresser:  Yeah, let’s say someone is obese and they go on a low-carb diet and they start eating liver and a lot of coconut oil and, you know, egg yolks and a lot of the foods that are choline-rich and folate-rich, and they experience this change in lipids, do we know from the literature how long we could expect that to take? 

Chris Masterjohn:  No, I haven’t seen anything good on it, so I think what we need to do is track people’s experiences and start to get some anecdotal evidence on this, and hopefully we’ll see, you know, some guidelines coming out in the scientific literature.  But I think if we monitor these things and share some experiences, that might give us some clues sooner. 

Steve Wright:  Is it a big deal with the egg yolks to cook them or eat them raw?

Chris Masterjohn:  I don’t think so.  When I eat egg yolks, I usually eat them raw, but I don’t think that that’s going to make a big difference in resolving fatty liver disease.  I think providing the choline is the main factor.

Chris Kresser:  OK.

Chris Masterjohn:  So, clearing lipids from the liver is good.  You can have a decreased clearing of lipids into atherosclerotic plaques, and that’s also going to be good.  You can have increased weight loss.  And weight loss, if you’re clearing lipids from adipose stores, that could elevate your blood lipids, and this could be good or it could have negative effects in some cases.  You know, if you have an overweight person, they are a lot more likely to have fatty liver, they are a lot more likely to have insulin resistance, but probably the person who’s probably in the worst-case scenario is the overweight person who is trying to lose weight by restricting calories and is in a sort of chronic starvation mode, where instead of getting a good diet that’s lowering their set-point, they’re always operating underneath their set-point, and that can contribute to a lot of stress and release of free fatty acids and things that can have negative effects on thyroid hormone.  But I think if you follow a weight loss strategy that is not leaving you hungry and stressed, I think you can expect a moderate elevation of lipids in some scenarios.  And we talked about this in the second episode, so we shouldn’t go into too much detail; but in my opinion, if someone is losing weight and they’re losing it at a healthy pace in a sustainable way and they see fluctuations in their blood lipids, in my personal opinion, they should wait until their weight has been stable for three to six months before trying to interpret it.  In other words, if blood lipids go up while you’re losing weight, concentrate on losing the weight and normalizing your metabolism.  Then once your weight has been stable, start looking at blood lipids and so on. 

Chris Kresser:  Yeah, and maybe get a few readings once your weight is stable, given the normal variation that they’ve talked about in the previous show.

Chris Masterjohn:  Exactly.  So, you always want to get two or three readings to look at that variation.  And, you know, while you bring that up, that’s a source of error.  I have also seen cases where people go on a diet that seems to be helping, and they say:  Why have my blood lipids increased?  And it was a simple error like they were fasting one time and they weren’t fasting the other time.

Chris Kresser:  Right.  Great point.

Chris Masterjohn:  So, obviously if it’s due to error, then we can’t say this is good or bad.  We need to say, “Correct the error and repeat it once you have the conditions kept the same.”  But there are bad cases of increased lipids, and the bad cases are where we are decreasing the clearance of lipids from the blood.  And I think that there are basically three reasons that this is likely to happen when someone is switching to a more ancestral diet, which seems to be what most people in this circle are concerned about.  Why would these blood lipids increase when we are eating a more Paleo Diet or a more Weston Price type approach, a more ancestral diet?  And there are some bad things that can happen, and I think that we should discuss those a little bit.  One is that you can have decreased thyroid activity either due to extreme and chronic carbohydrate restriction.  The other is that you may have an iodine deficiency if you have increased some of your intake of plant goitrogens and haven’t included enough iodine-rich foods, especially seafoods, in your diet.  And I think the other case is in certain cases someone might have familial hypercholesterolemia, and when they switch their diet to a diet that contains more cholesterol and more saturated fat and less polyunsaturated fat, there are reasons why that would increase blood cholesterol that might not be harmful in someone who doesn’t have familial hypercholesterolemia but might actually be harmful in some cases for someone who does have familial hypercholesterolemia. 

Chris Kresser:  So, just to save us all the breath, because we I think we might talk about this a little bit more, let’s call familial hypercholesterolemia FH.  It’s a codeword.  I’ve been stumbling over that in previous episodes, so FH from here on out.  So, Chris, let’s talk a little bit — I see this actually quite a bit in my practice with iodine and thyroid and activation of the LDL receptors, so let’s talk a little bit more about that.

The Thyroid-LDL connection and why iodine matters

Chris Masterjohn:  Sure.  OK, so thyroid hormone is the central governor of the LDL receptor, and the LDL receptor is, in turn, the central governor of clearance of LDL cholesterol from the blood.  And basically thyroid is a messenger who is communicating that we are in a state of abundance, we have all of the food and nutrients that we need, and it is time to utilize those nutrients for the purposes of reproduction, high physical performance, and other things of that nature.  And cholesterol is the precursor to a lot of these key hormones, like the sex steroids, for example, and the bile acids that improve digestion.  So, thyroid hormone basically communicates to our cells that all of these nutrients that we need are available, so our cells respond by taking in LDL cholesterol from the blood and making lots of good things out of it, like testosterone, for example.  Now, one of the key things that can happen when people start increasing their intake of fruits and vegetables and decreasing their intake of grains, which is a common dietary shift in the Paleo community, for example, is that you can increase your intake of plant goitrogens.  Goitrogens are named because they have the ability to cause goiter, which is a problem that occurs as a response to insufficient thyroid hormone, and basically these plant chemicals have the ability to decrease the production or activation of thyroid hormone.  Now, in most of the cases, I don’t want to suggest that eating these plants is a bad thing.  In most of the cases, all you need to do to compensate is increase your intake of iodine.  But in certain cases, if someone is not eating iodized salt, for example, and they’re living in an area where the iodine quality of the soil is poor, and they’re not eating seafood, which is the most reliable source of iodine, they may not be getting the iodine that they need to deal with that level of plant chemicals in the diet.  So, it’s not that the plants are intrinsically bad.  It’s just that we need to achieve that dietary balance.  So, the number of plant chemicals in the plant kingdom that inhibit thyroid function, at least in a sort of test tube assay, is almost innumerable.  I mean, there are thousands of plant chemicals.  Basically all of the polyphenolics — the flavonoids, for example — they basically all inhibit the enzymes of thyroid hormone.  But a lot of these plant chemicals don’t really make it into the system because we detoxify them properly, and sometimes they also even have beneficial effects.  So, what we need to do is look at some of the areas where there is really convincing research done either in humans or in laboratory animals showing that certain foods, in the absence of adequate iodine, can contribute to decreased thyroid function.

Chris Kresser:  So, I want to jump in here too and just mention that for most people who come to me with thyroid issues, I do a 24-hour urine iodine test, and I would say probably 80% of the people that I test are iodine deficient or have excess bromide levels, which can cause some of the symptoms of iodine deficiency.  So, it’s a pretty common problem, and I think that’s partly because a lot of people aren’t eating much seafood these days maybe because of concerns for mercury or just they don’t like it or it’s not available to them in an easy way.  And then a switch from iodized salt to natural salt, which has less iodine; that’s pretty common when people are switching to a Paleo or Primal type of diet.  So, I don’t think this is a rare problem.  I think this is actually something that is fairly common, at least in my patient population.

Steve Wright:  When you say “in seafood,” is it everything — shrimp, fish, seaweed — or is it specific to certain types?

Chris Masterjohn:  Well, I think seaweed is the most abundant source, but all seafood generally has some iodine in it.  The problem with land food isn’t that it doesn’t have iodine.  It’s just that it’s so unreliable.  You can have, you know, a potato grown in one part of the country and in another part of the country, and their iodine content might vary a hundredfold, but the ocean is rich in iodine, so seafood, in general, tends to be a more reliable source of iodine, but seaweed, of course, is the most abundant.

Chris Kresser:  Right.  And then, Chris, the other thing I wanted to talk to you about is you’ve written pretty extensively about goitrogens and a great article — I know you had a special report that I read, but also, I think, some articles on your blog about how different methods of preparation can alter the goitrogenic effect of food.  So, without going into too much detail about that, can you just give us a little summary?

Are goitrogenic foods inhibiting your thyroid function?

Chris Masterjohn:  Yeah, absolutely.  So, I went into the most detail, like you said, on my Thyroid Toxins Special Report available on my website, and I think the other article you were thinking of was one that I wrote for Wise Traditions called Bearers of the Cross:  Crucifers in Context.

Chris Kresser:  Yeah.

Chris Masterjohn:  OK, so there are a few different classes of goitrogenic foods, and the way preparation affects them is different depending on the class.  The most common that people on an ancestral diet are probably going to be eating is crucifers.  So, crucifers, for example, include broccoli, brussels sprouts, cauliflower, cabbage, collard greens, kale, kohlrabi, mustard, rutabaga, turnip, bok choy, arugula, horseradish, wasabi, watercress, maca, and even canola oil is a crucifer.

Chris Kresser:  Oh, wow.  I didn’t know that. 

Chris Masterjohn:  It’s a close relative of the turnip.

Chris Kresser:  I didn’t know maca was either.

Chris Masterjohn:  Yeah.

Chris Kresser:  That’s interesting.  Yeah.  OK. 

Chris Masterjohn:  So, crucifers have natural pesticides called glucosinolates, and these can be metabolized when we chew the crucifer or when we chop them up and so on.  So, whether we’re eating them raw or cooked, we’re gonna get some of these goitrogens.  And basically what happens is there’s an enzyme that frees a chemical called isothiocyanate, and then in our bodies we metabolize this to thiocyanate, and thiocyanate decreases the uptake of iodine into the thyroid gland because it basically competes with it.  So, if you have a high ratio of isothiocyanate to iodine, then isothiocyanate actually gets into the thyroid gland.  It also gets into breast milk, and it crosses the placenta in place of iodine.  And then once it’s in the thyroid gland, it will compete for the utilization of the enzyme that makes thyroid hormone.

Chris Kresser:  Right.

Chris Masterjohn:  Now, thiocyanate, you can completely protect against it simply by getting enough iodine in your diet.  Now, a lot of people think that cooking or fermenting cruciferous vegetables is going to get rid of the goitrogens, but that is not true.  Fermenting actually activates them.  It actually does the conversion to the thiocyanate right in the jar of sauerkraut.  So, if you’re eating sauerkraut and kimchi, you are not getting rid of the goitrogens.  That doesn’t mean the foods are bad, but it means that you need more iodine when you’re eating those foods.  If you steam the vegetables, it decreases the goitrogen yield about 30%, but it leaves about 70% of them there.  Not only that, but when you steam the vegetables, the rate of liberation of the true goitrogens in the intestines varies fourfold between different people depending on their intestinal flora, so steaming is not a reliable way of getting rid of them.  If you boil them for a half an hour and you keep the water, for example, in a soup, then that gets rid of 65% of the goitrogens, so about two-thirds.  And if you get rid of the water, then that gets rid of about 90%, so if you boil them and then you pour the water out.  Now, I don’t think that you need to go through all this extensive boiling.  I think you just need to increase your iodine.  But you have to realize if you have marginal iodine status and then all of a sudden you start eating sauerkraut and kimchi at every meal and then steaming broccoli for dinner, then that may push you over the edge into a frank iodine deficiency if you were on the border.

Chris Kresser:  So, Chris, what’s the dose of iodine that’s required to prevent, you know, a moderate intake of goitrogenic foods like we’re talking about now in the context of a Paleo or Primal type of diet from inhibiting thyroid function?

Chris Masterjohn:  Unfortunately, that has not been well characterized, but I think if we’re looking at the RDA, we’re looking at about — I think the RDA is still 150 mcg, and there are people out there who are using 50 mg, so I suspect that if you were taking 1 mg, for example, then that should be well more than sufficient to take care of the goitrogens themselves.  But again, like you said, with environmental bromine exposure and so many other things, it’s possible that people may need more than that.  But I think if we’re just talking about goitrogens, then that should be enough.

Chris Kresser:  A minimum, yeah, a minimal dose.  OK.

Chris Masterjohn:  So some of the other foods are — another common food is cassava, which also goes by tapioca, manioc, yuca; flax; lima beans; and the fruits of all of the Rosaceae family, which includes cherries, almonds, plums, peaches, apricots, pears, raspberries, strawberries — these all contain cyanogenic glycosides, and sweet potatoes also contain a pretty small amount.  Now, most of these foods come in different levels of bitterness, and in the more bitter varieties, that’s where you get more of the cyanogenic glycosides, and in the less bitter and more sweet varieties it’s less common.  But these are also a source of thiocyanate because they actually release cyanide, and we detoxify the cyanide to thiocyanate, and it has all of the same effects as crucifers.  And the most reliable way to detoxify these is to crush the foods and leach them in running water for a few days.

Chris Kresser:  Ha-ha!

Steve Wright:  Oh, yeah.

Chris Masterjohn:  But, seriously, this becomes a key issue when you are consuming massive amounts of these.  There are some people, for example, you know, certain populations where they rely on cassava for the main starch.

Chris Kresser:  Sure.

Chris Masterjohn:  And they actually deliberately breed the bitter varieties because it protects against insects, and they are very vulnerable to goiter unless they process these so extensively.

Chris Kresser:  Right.

Chris Masterjohn:  So, again, I don’t think that these are going to be a major problem unless you’re adding it on top of the crucifers and on top of the low iodine intake.  And the two others are soy and millet.  I don’t think that people who are, you know, eating the Weston Price or Paleo ways are really going overboard with soy, but there is a myth out there that fermentation decreases the goitrogens, and it doesn’t.  It does the opposite; it increases their bioavailability.  So, if you add some fermented soy on top of everything else with low iodine, that can be a problem.  And probably the most goitrogenic food in the world is millet, and this could be a problem if people are getting rid of gluten and they start eating a lot of gluten-free bread that’s made from millet, for example.  And millet basically inhibits every step of thyroid metabolism, and high iodine intakes cannot overcome the effect of millet.  But again, if it’s a minor component of the diet, it’s probably not a problem, but when you’re compounding it with all of these other foods and a low iodine intake, that’s when it can really be an issue.  So, I think the solution to all of this is to eat these foods in moderation.  Don’t go crazy with them.  You know, don’t get the Vitamix out and load it with as many cruciferous vegetables as you can and drink cruciferous vegetable juice all day long.  There are people who do that and suffer the consequences.  You know, eat these foods in moderation, and make sure that you compensate for their inclusion in the diet with eating more seafood, perhaps some occasional seaweed, and if you need it — you know, you get the iodine test that you do, for example — if you need more iodine, supplement to bring that level up to where it needs to be. 

Steve Wright:  Hey, Chris or Master J, if I can, because I want to keep you guys straight.

Chris Kresser:  Ha-ha!

Chris Masterjohn:  Yeah, that’s how I roll.

Steve Wright:  OK, that’s what I thought.  So, you just touched on it, and I’m glad you brought it up, and that’s the shakes or the juicing because there are a lot of us — and I don’t do it, because I hate cleaning my blender — but a lot of people like to make a shake in the morning, and you’ll see a lot of bloggers telling you to make a green smoothie.  Is even doing, like, a cup a day or something in my smoothie, over time is this gonna be a problem? 

Chris Masterjohn:  I don’t think it’s going to be a problem as long as you have adequate iodine in your diet.  I mean, a cup of cruciferous vegetables is not a lot.  In all honesty, I sometimes, you know, I’ll eat a whole plateful of kale or something like that, so I don’t think it makes any difference if you just throw it in the juicer.  But what I mean is if people are juicing so that they can consume exorbitant quantities of these vegetables compared to what they would be able to eat if they were eating them whole, that’s where you get the problem. 

Chris Kresser:  And, Chris, you don’t have any thyroid problem that you know of, so maybe someone that does might not necessarily want to eat a plateful of cruciferous vegetables.

Chris Masterjohn:  Absolutely.  This is the key issue:  It’s an individual thing.  Like I said, steaming, the goitrogen yield varies, you know, fourfold between different people, and different people have different iodine status.  So, I am not saying these foods are bad.  I’m saying that if you have symptoms of hypothyroidism when you made a dietary shift towards including more of these foods, then you might suspect those foods and their balance with iodine to be a culprit.

Chris Kresser:  Um-hum.  Your mileage may vary.

Chris Masterjohn:  Right.

Chris Kresser:  So, I want to throw in a couple things here just from my clinical practice.  One is that I’ve found that for people with elevated LDL and some symptoms of hypothyroidism, even if they’re euthyroid — like, their T4 and T3 are normal and their TSH is fairly normal — that using slightly higher of a dose than we talked about, like 1 mg, more in the range of maybe 2.5 to 6 mg and sometimes even up to 12.5 mg of iodine can have a pretty dramatic effect on total cholesterol and LDL cholesterol, and I’ve been keeping some data, you know, just anecdotally for my practice.  Eventually maybe I’ll have enough to do something interesting with, but I have seen that work.  One word of caution, though, is that it’s really important that if you do start iodine supplementation that you start at a low dose and you build up slowly over time.  And the reason for that is that if you go too quickly, if you just start taking 6.5 mg, for example, or 12 mg, in my experience, that can provoke or exacerbate an autoimmune thyroid response, particularly if you don’t have enough selenium in your diet.  And I’ve seen that happen, and I’ve seen people kind of start experiencing hyperthyroid symptoms or symptoms of immune dysregulation or immune attack against the thyroid.  So, if you do start to take iodine, I’d recommend starting at a lower dose, like maybe 250 mcg, sticking on that for seven to ten days, maybe doubling it, sticking on that for seven to ten days, and then proceeding to increase from there.  The other thing is that — and I just wrote a blog article about this today, the day that we’re recording this show — is that a lot of studies show that selenium can protect against the potentially negative impacts of iodine supplementation for people who have autoimmune thyroid disease.  So, if you do have Hashimoto’s or Graves’ or something like that and you’re considering taking iodine, you want to make sure that you’re getting at least 200 mcg of selenium combined from food and supplements each day.

Steve Wright:  So, Chris, do you have a preferred form of selenium?

Chris Kresser:  I like the Super Selenium Complex from Life Extension, and it has four different forms of selenium in there.  It’s got selenomethionine, sodium selenate, selenodiglutathione, and Se-Methyl L-Selenocysteine.  Some studies I’ve seen, Chris, and you’re probably familiar with this work — in fact, somebody just sent me a study this morning on type 2 diabetics, the effects of long-term selenium supplementation.  They were interested in seeing if selenium could help treat diabetes, but what they found was that 200 mcg a day of selenium actually increased the risk of type 2 diabetes in their study population versus placebo.  So, there’s some evidence that certain populations who take too much selenium or too much of one form of selenium, that that can be problematic, which is why I recommend taking multiple forms.  What are your thoughts on that, Chris?

Chris Masterjohn:  Well, I have a bias that has very little evidence behind it that selenocysteine is probably preferable over selenomethionine because that’s the form that’s incorporated into our proteins.  That’s why it’s the form that’s found in animal foods.  But I’ve had a similar suspicion as you that in those studies the form might be part of it and interactions with other nutrients might be part of it, but I guess we’ll have to wait and see for some clinical tests of that idea.

Chris Kresser:  But, I mean, in general, it’s always the better idea if possible to get as much of your nutrients from food, and that helps avoid this kind of thing, because there’s a lot we still don’t know about nutrient supplementation or augmentation. 

Chris Masterjohn:  Right.  And in a normal diet, you would get that mix because plants have selenomethionine and animal foods have selenocysteine. 

Chris Kresser:  Right.  And Brazil nuts, for those of you that don’t know, are a very rich source of selenium.  They’re also very high in omega-6, but I don’t think that’s necessarily a problem because you only really need to eat two or three Brazil nuts, depending on the source, to get 200 mcg of selenium.

Steve Wright:  Do either of you take iodine?

Chris Kresser:  I’ve experimented with it in the past.  I don’t have a thyroid issue, and I eat a lot of seafood and some sea vegetables, so I get it in my diet; but I have experimented with it just because I do that a lot on myself, and if I’m recommending stuff to my patients, I often will do it myself to, you know, just see what it feels like.  I’ve gone up to 25 mg of iodine without really noticing any difference personally. 

Chris Masterjohn:  I don’t supplement iodine right now, but I have plans in the future to see if I can use it to detoxify fluoride that I suspect I have in my system, but I’ll write about that when I get around to it.

Chris Kresser:  Yeah, keep us posted.

Steve Wright:  Yeah, I’m looking forward!

Chris Masterjohn:  OK, so shall we move on to carbohydrate?

Chris Kresser:  Yeah, sounds good.

The telltale Thyroid-Cholesterol signs you need more carbs

Chris Masterjohn:  All right, so there are a number of studies that have shown that carbohydrate restriction or fasting or calorie restriction can decrease thyroid function, and they tend to show a decrease in T3 in the serum and an increase in reverse T3.  T3 is the active hormone, and reverse T3 is kind of an antithyroid hormone.  And many of your listeners probably have seen the correspondence between Paul Jaminet’s blog and his guest blogger and Anthony Colpo last year, where these studies were debated quite extensively.  And I think when we look at these studies in the context of some of the biochemistry that has been studied regarding insulin’s interaction with thyroid hormone, then I think what we are seeing is a definite effect of the level of carbohydrate in the diet.  And I know that there are some confounders in some of these studies, especially when they compared it to fat; a lot of the fat was really low-quality fat, like corn oil.  But if we look at what insulin does, we find that there is evidence from humans, from cells, and from rats that insulin cooperates with thyroid-stimulating hormone, or TSH, to increase the production of the enzymes and proteins involved in making thyroid hormone, and we find that it contributes to the enzymes that activate thyroid hormone from T4 into T3, the active form.  So, I think what we’re seeing here is when we have insulin operating in its optimal conditions, then insulin is again sort of acting as a messenger that the body is in a state of abundance, and it’s contributing to the production of thyroid hormone and to its activation into T3.  And if you prevent the activation into T3, then the T4 — There isn’t very evidence that insulin actively prevents the production of reverse T3, but by promoting the conversion into the active form, that in itself tends to prevent T4 from being converted into the inactive form, reverse T3.  So, I think we’re looking at a definite effect of effective carbohydrate here, and I think the best way to test for this is to look for a decreased ratio of T3 to reverse T3.  From the clinical studies, that seems to be the most likely marker to look for to see if this is what’s happening, to see if this is why cholesterol has gone up.  I think that if you find that T3 or reverse T3 are out of whack, probably the best way to address that is to try increasing the carbohydrate intake — not necessarily meaning you have to go on a high-carbohydrate diet, but, you know, like, Paul Jaminet had sort of concluded at the end of that series that he still advocates a low-carbohydrate diet, but it’s possible to go too low for some people, and that’s when you might get deficiency in thyroid signaling.

Chris Kresser:  And I definitely see this, Chris, in my practice, and this is purely anecdotal, but I often get people who come to me who have been on a low-carb Paleo Diet, not for any particular reason, just because that was their understanding of the Paleo Diet, you know, as a low-carb approach.  And then they’re suffering from the classic hypothyroid symptoms:  Their hair is falling out, and their hands and feet are cold, outer third of the eyebrows thinning, you know, low metabolic symptoms.  And then they start eating some more starch and starchy tubers and fruit and increase their carbohydrate intake; and in almost all cases, their symptoms improve significantly.  The challenge clinically with that is the patient population who is on a low-carb diet because if they start to reintegrate carbohydrates, their blood sugars go up and they gain weight and they experience all of the metabolic issues that can be associated with that if they have metabolic syndrome, so it’s a little more challenging in those folks to just add the carbohydrates back unless you address the other mechanisms that are causing carbohydrate intolerance, whether they be metabolic issues or gut issues.  You know, some people with small bowel bacterial overgrowth can’t really tolerate a lot of carbohydrate.  So, it gets a little more complicated, of course, but I think that, at least in my experience, the phenomenon that you’re describing with low-carb diet contributing to hypothyroid and increasing carbohydrate intake improving thyroid function is definitely real.

Chris Masterjohn:  Yeah, and I think you highlighted something important there that there are a lot of classic symptoms that go beyond the blood tests, and you know, I think even if you don’t see the changes in T3 and reverse T3, there are other mechanisms.  For example, if you have increased liberation of free fatty acids beyond what you’re able to utilize, there is some evidence that the free fatty acids will accumulate in the nucleus of the cell at a high enough concentration to inhibit thyroid binding to its receptor, and that will cause all of these symptoms of the metabolic effects, including the high cholesterol, but it might not show up as changes in thyroid hormones in the blood.  So, I think if you see those classics symptoms, if you see high cholesterol and low sex hormones, for example, I think those are good clues in addition to T3 and reverse T3 that might signify that an increase in carbohydrate intake might be needed, but I have an anecdote that I think is pretty interesting to share from Nutrition and Physical Degeneration, Weston Price’s book.

Chris Kresser:  Yeah, let’s hear it.

Chris Masterjohn:  He says:  “For the Indians of the far North this reinforcement” — he’s talking about reinforcement of nutrition for pregnancy — “was accomplished by supplying special feedings of organs of animals.  Among the Indians in the moose country near the Arctic circle a larger percentage of the children were born in June than in any other month.  This was accomplished, I was told, by both parents eating liberally of the thyroid glands of the male moose as they came down from the high mountain areas for the mating season, at which time the large protuberances carrying the thyroids under the throat were greatly enlarged.”  So, what he’s saying is when the moose were about to reproduce, they naturally went into a kind of hyperthyroid state where their thyroids were enlarged, and the people there would harvest the thyroid glands so that they could reproduce, and as a consequence, most of their children were born nine months after the moose mating season.

Chris Kresser:  Wow.

Chris Masterjohn:  And what the indicates to me is — I mean, it’s difficult to interpret it because he doesn’t go into great detail, but I think what we might be seeing here is up in the Arctic circle — and these are the inland people, they’re not seacoast, so they probably don’t have a lot of iodine in the diet, they certainly don’t have a lot of carbohydrate in the diet.  It seems like they, as part of their natural adaptation to their environment, they supplemented with thyroid hormone so that they could convert their cholesterol to sex hormones so that they could increase their fertility, and I think what we’re witnessing is perhaps a natural acknowledgement that under those certain conditions where you have an extremely carbohydrate-restricted diet, you may need supplemental thyroid hormone in order to maintain that fertility. 

Chris Kresser:  Yeah, I mean, that’s so fascinating.  In The Healthy Baby Code, of course, I talk a lot about anecdotes like that and traditional populations and their approaches, like in the Masai culture in Africa.  And maybe you can correct me if I’m wrong on this, Chris, because I know you’ve studied them a lot, but something I read a while back where when people are trying to get pregnant or thinking about doing that, then they’ll consume dairy from cows that have been grazing on grass during the particularly lush seasons of the year to increase their fertility.

Chris Masterjohn:  Yeah, well, the Masai definitely have an association between animal fat and fertility not only in the diet but in many of their rituals.  Animal fat is always associated in that way.  And they also have very strong associations between lactation in the cow and sort of the principle of female fertility, so I don’t remember the specifics of their fertility diets in great detail, but that definitely sounds characteristic of the Masai. 

Chris Kresser:  OK, so we gotta wrap it up.  We could go on, and we probably will.  I think we’ll have to have you back, Chris.  We’ll make it a regular thing, because this is an issue that’s on a lot of people’s minds, and even with all that we’ve learned about it and, you know, a lot of people, like I said before, have been exposed to the idea that cholesterol isn’t necessarily bad and we don’t need to do everything we can to just lower it indiscriminately.  I think, just speaking personally from the comments I get on my blog and the people I see in my practice, there’s still quite a bit of concern about it, and in some cases rightfully so, as we’ve learned in this 3-part series.  So, I want to thank you, Chris, for coming back, and like I said, we’ll have you back.  Maybe we’ll do some case studies.  I’m actually speaking at the PaleoFX conference in Austin, and the topic of my talk is gonna be what to do, if anything, about high cholesterol, and I’m gonna present a practical framework in kind of a flowchart format for what you do if, let’s say, you get a cholesterol reading that comes back above 250 and kind of a step-by-step process for how you can investigate that.  And I imagine those presentations will be available after the conference is over, so if anyone is interested in some more kind of really down and dirty, practical info on how to deal with this stuff, you can check that out.  And, Chris, when are we gonna meet?  Are you gonna be at AHS this year? 

Chris Masterjohn:  Yes, I will be at AHS this year.

Chris Kresser:  Cool.  So, I’ll see you there if not before and then, I’m sure, at the Weston A. Price Conference in November, as well.

Chris Masterjohn:  Yeah, I look forward to it!

Chris Kresser:  Yeah.  So, Steve, thanks for shepherding us through this again, and we’ll see everybody a couple weeks from now.

Steve Wright:  Yeah.  It was a great show.  Thanks again, Master J, for being on, and it sounds like we’ll hear again soon from you.  

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 this episode we discuss the following topics:

• A recent study demonstrating that low cholesterol is associated with higher risk of death in women
• What truly normal blood sugar levels during pregnancy are, and cut-offs for pre-diabetic and diabetic women during pregnancy
• Whether there’s any science behind breaking weight loss plateaus by adding carbs back in the diet
• Best practices for people with Hashimoto’s
• Why there has been such an explosion in food sensitivities, celiac disease and leaky gut
• The connection between diet and body odor
• Recommendations for moderate to severe ulcerative colitis

Please note that in the next few weeks, the name of the show will be changing. It will be called “Revolution Health Radio”, with Chris Kresser. There’s nothing you need to do. You’ll just notice that the graphic and show name are different at some point.

This week we’re glad to welcome Chris Masterjohn back to the show. Chris joined us on Episode 11 to discuss the role of cholesterol in heart disease, and to dispel the many myths associated with those subjects. There was so much to cover, we had to have Chris back for part 2 (and in fact, we still didn’t cover all of the material so he’s going to come back for part 3 in the future!)

In this episode, we discuss (among other things):

• what is a “normal” cholesterol? what can anthropological studies tell us about this?
• are lipoprotein particle size tests accurate? what’s the best way of determining particle size?
• why do some people have high cholesterol (TC & LDL) after adopting a Paleo/WAPF diet? is this something to be concerned about?

Enjoy the show!

This week we’re glad to welcome Chris Masterjohn to the show. Chris is currently pursuing a PhD in Nutritional Sciences with a concentration in Biochemical and Molecular Nutrition at the University of Connecticut. He writes a blog called The Daily Lipid and is also a frequent contributor on the Weston A. Price Foundation’s blog.

I consider Chris to be one of the foremost experts on the topic of cholesterol and its relationship to heart disease. In this episode, we discuss (among other things):

• the history of the cholesterol-heart disease connection
• misconceptions around diet vs. lipid hypothesis
• finding middle ground between cholesterol skeptics and proponents of the lipid hypothesis
• the LDL receptor and familial hypercholesterolemia and what they can tell us about cholesterol and CHD in normal populations

We didn’t get to any questions this time around, but Chris has graciously offered to come back and do an entire episode devoted to Q&A in the future – so look out for that!

Chris Masterjohn from The Daily Lipid is going to join us on the podcast to summarize a new paradigm of understanding cholesterol and it’s role in health and disease. As you know, there’s perhaps no issue in health & nutrition that is more characterized by controversy, propaganda and misinformation.

We’ll be taking a 30,000 foot view of “an evolutionary perspective of cholesterol in the 21st century”. By that I mean summarizing what we know about cholesterol and its relationship to heart disease from the perspective of the most reliable modern evidence and anthropological evidence.

We’ll see how both conventional doctors and researchers, who claim that cholesterol is the cause of heart disease, and cholesterol skeptics, who claim that cholesterol numbers are completely irrelevant, are both wrong.

The episode will be recorded next Friday the 20th, but due to scheduling issues won’t air until June 21st. We probably won’t have much time for questions, but if you have a burning one on this topic, leave it here before Thursday, May 19th and we’ll try to get to it.

I do a lot of public speaking. As you might suspect, regardless of the specific topic I’m presenting the dietary recommendations I make are always essentially the same: high-fat, nutrient-dense and low in toxins. Since omega-6 vegetable oils are toxins, when I say high fat I’m talking about saturated and monounsaturated fat. You know this.

But a lot of people I speak to don’t. They fully steeped in 50 years of mainstream propaganda perpetuating the idea that saturated fats cause heart disease – primarily by raising blood cholesterol. So, inevitably, when I stand up in front of a group of people and tell them all to eat lots of saturated fat, I get a question that goes something like this:

But won’t that raise my cholesterol? And won’t high cholesterol give me a heart attack?

I haven’t yet perfected an answer that can dismantle a half century of cultural brainwashing about fat and cholesterol in less than 3 minutes. But I’m working on it.

In the meantime, I usually explain some variation of the following:

Point #1: Eating saturated fat doesn’t raise cholesterol levels in the blood

There’s no convincing evidence that eating saturated fat raises blood cholesterol. Stephan Guyenet spanked that old yarn to the curb in this recent blog post. In short, of all of the studies examining the relationship between saturated fat intake and serum cholesterol, only one found a clear relationship between the two and even that association was weak. The rest found no association at all.

Point #2: Eating cholesterol doesn’t (usually) raise cholesterol levels in the blood

Nor is there evidence that eating cholesterol in the diet raises cholesterol levels in your blood. A recent review of the scientific literature published in Current Opinion in Clinical Nutrition and Metabolic Care clearly indicates that egg consumption has no discernible impact on blood cholesterol levels in 70% of the population. In the other 30% of the population (termed “hyperresponders”), eggs do increase both circulating LDL and HDL cholesterol.

An increase of HDL is a good thing. And as it turns out, so is a boost of the type of LDL that eating saturated fat and cholesterol increases. We now know there are two different types of LDL: small, dense LDL, and large, buoyant LDL. Small, dense LDL is a significant risk factor for heart disease because it’s more likely to oxidize and cause inflammation. Large, buoyant LDL is not a risk factor for heart disease. And guess what? Eating eggs not only increases the benign large, buoyant LDL, but it also decreases the harmful small, dense LDL by 20%. I’ve written more about this here and here, and you can also watch some videos on this topic here.

Point #3: Even if eating saturated fat and cholesterol did raise cholesterol levels in your blood, it wouldn’t matter because “high cholesterol” isn’t a strong risk factor for heart disease.

This is the one that really spins people out. Even if they follow me on the first two points, their eyes tend to glaze over when I mention this one. As Mark Twain used to say:

The history of our race, and each individual’s experience, are sown thick with evidence that a truth is not hard to kill and that a lie told well is immortal.

Nowhere is that more true than with the lie that high cholesterol causes heart disease. It’s so deeply ingrained in our collective consciousness that it’s become an almost unassailable article of faith. That’s why people are so surprised to learn that there’s very little evidence to support the idea.

This point is the current bottleneck in my “3-minute” explanation, because it takes a while to explain why it’s not true. I’ve written about it extensively here, here and here. For the purposes of this brief article, we’ll have to leave it at this: both total and LDL cholesterol – which are the numbers your doctor, the media and everyone else seems to be concerned with – are only weakly associated with heart disease.

If “high cholesterol” were the cause of heart disease, you’d expect it to be a risk factor in:

1. All populations around the world.
2. In both men and women.
3. In people of all ages.

And you’d also expect that lowering cholesterol should prevent heart disease.

Makes sense, right?

Unfortunately for the lipophobes, the cholesterol hypothesis fails on all fronts.

1. High cholesterol is not a risk factor in all populations. The French have among the highest cholesterol levels in the world, and among the lowest rates of heart disease of any industrialized nation. The Austrians and other European nations are similar.
2. Women on average have 300% lower rates of heart disease than men, despite higher average cholesterol levels.
3. The rate of heart disease in 65 year-old men is 10 times that of 45-year old men. Yet high cholesterol is not a risk factor in men over 65. (In fact, men over 65 with low cholesterol (<150 mg/dL) are twice as likely to die from heart disease as those with normal or even "high" cholesterol.)

Finally, more than 40 trials have been performed to see if lowering cholesterol prevents heart disease. In some trials more people got heart disease, in others fewer. But when all the results were taken together, just as many people died in the treatment groups (those who took cholesterol-lowering drugs) as the control groups (those who did not).

Point #4: If you want to worry about your cholesterol numbers, forget about total cholesterol and LDL and pay attention to the ratio of triglycerides to HDL.

In general I’m not a fan of people worrying about their lipid panel numbers at all. Like Dr. Kurt Harris, I think this compulsive testing and re-testing of lipids that has become common in the Paleo community not only isn’t necessary, but may even be harmful. There’s still a lot we don’t know about how these numbers change on a day-to-day basis. What’s more, it’s not always easy to distinguish between cause and effect. Researchers made the mistake of assuming high cholesterol was the cause of heart disease, when in reality it’s much more likely that high cholesterol is a consequence of it.

But for crying out loud, if you’re going to get your lipds tested at least pay attention to the right numbers. And the most important number on a conventional lipid panel is the relationship between triglycerides and HDL. (Divide triglyercids by HDL to get it.) If that number is less than 2, this suggests you have mostly large, buoyant LDL – which is not a risk factor for heart disease. If that number is higher than 3, it suggests you have mostly small, dense LDL – which most certainly is a risk factor for heart disease.

Point #5: Eat good food and don’t worry about the numbers.

But in the end, even that ratio doesn’t matter so much. Why? Because the treatment is always the same! If your TG:HDL ratio is high (bad), what should you do? Eat a high-fat (saturated, of course) diet. This will reduce your triglycerides and small, dense LDL, and increase your HDL. Triple win. And if your TG:HDL ratio is low (good), what should you do? The exact same thing: eat a high-fat diet.

Conversely, replacing saturated fat with carbs, as we’ve been told to do for 50 years to protect ourselves from heart disease, actually contributes to it in three ways: it increases triglycerides and small, dense LDL, and decreases HDL.

Finally, I often get emails from people who’ve switched to a high-fat / Paleo-type diet expressing concern that their LDL and total cholesterol levels have gone up. My response usually has three parts: 1) don’t worry about it, because high total and LDL cholesterol do not cause heart disease; 2) the increase is usually temporary, and may be the result of the body curing itself of fatty liver (a good thing!); 3) don’t worry about it. Doesn’t hurt to remind them.

**Note: if your total cholesterol levels are very high (i.e. above 300 mg/dL), this may be an indicator of a metabolic abnormality or inflammatory process that needs to be addressed. Cholesterol is a repair substance in the body, and persistent elevations beyond a certain threshold may point to an underlying problem that hasn’t been identified.

You’ve probably noticed that I haven’t been able to write as much lately for the blog. I’ve been incredibly busy with my private practice, launching the Paleo Detox program, preparing and delivering talks locally, developing new content like ongoing class series and an eBook, and of course continuing my research on various topics.

I’ve got one more article to write for the series on diabesity. I’ll discuss what I believe to be the most effective form of exercise for restoring glucose tolerance and insulin sensitivity. I hope to get to that this weekend.

After that, I’ll be sending out a survey to get your input on the next series, as well as several other topics related to the blog and various projects I’ve got in the works.

I hope to get back to a more regular writing schedule at some point, but with everything going on it may take a while. In the meantime, I may try out some new formats, like posting a brief summary of articles from around the web that I’ve found interesting during the week.

Here are a few from this week.

Why Is My Cholesterol So High On This Diet?

In this article, Chris Masterjohn explains why some people see their cholesterol go up (often temporarily) when they switch to a nutrient-dense, whole-foods based diet. His theory, which is plausible from a physiological standpoint, is that the temporary cholesterol elevation is occurs because these folks are curing themselves of fatty liver disease.

In any event, we know that total and LDL cholesterol are weakly correlated with heart disease, so I’m never concerned when I see people’s cholesterol go up on a paleo or nutrient-dense diet. It’s expected. Especially when their HDL goes up and their triglycerides go down, which is the typical response.

Huge Metastudy: “Non Diabetic” Blood Sugars Cause “Diabetic” Retionopathy

Throughout my series on diabesity, I’ve presented evidence that blood sugar levels considered to be “normal” by mainstream standards are anything but, and that they can lead to complications like retinopathy and peripheral neuropathy.

Jenny Ruhl blogged today about a recently published meta-analysis that confirms this once again. In the study, blood sugar levels of 117 mg/dL or above, and an A1c of 6.3 or above (both below current limits) significantly increased the risk of retinopathy. But, as Jenny points out, the safe limits are lower still, because retinopathy is one of the last complications of diabetes to appear. Heart disease risk increases as post-meal blood sugars rise above 155 mg/dL, and increases in a straight line with A1c above 4.7, becoming quite significant as it rises above 6.

Grasse Based Health: Food For Thought

In this video, Peter Ballerstedt argues that animal protein and animal fat are not only superior to grains for human health, but also more sustainable from an agricultural and ecological perspective.

The presentation is quite dry, but the information is solid and it’s definitely worth watching.

Statins are the most popular drugs in history. Drug companies made $26 billion selling statins alone in 2008. 25 million Americans take them, and the number is growing each year.

One reason why statins are the best-selling drug category by far is that 92% of people taking them are healthy. The FDA has approved the prescription of statins to people at low risk for heart disease and stroke, who don’t even have high cholesterol. Two years ago the American Academy of Pediatricians recommended that statins be prescribed for kids as young as eight years old.

With sales statistics like this, you’d think statins are wonder drugs. But when you look closely at the research, a different story emerges. Statins have never been shown to be effective for women of any age, men over 65, or men without pre-existing heart disease. Early studies did suggest that statins are effective for men under 65 with pre-existing heart disease, but later, more rigorous clinical trials has not confirmed this benefit.

In addition, statins have been shown to have serious side effects and complications in up to 30% of people who take them. Studies have also shown that the majority of these adverse events go unreported, because doctors are largely unaware of the risks of statins.

Watch the two videos below to learn the whole story. Or, you can read this article for a concise summary of the evidence.

Video Presentation

Handouts

• Statin research summary: lists the eight statin studies performed in 2008 – 2009, including the drugs and populations studied and the results. If you’re currently taking a statin, you might consider printing this out and taking it to your doctor as a springboard for a conversation about whether statins are right for you.

References

ENHANCE
KasteleinJJ, AkdimF, StroesES, for ENHANCE investigators. Simvastatin with or without ezetimibe in familial hypercholesterolemia. N Engl J Med 2008;358:1431-43

CASHMERE
O’Riordan M. CASHMERE: no IMT effect with atorvastatin over 12 months. (link)

ACHIEVE
O’Riordan M. ACHIEVE stopped: IMT study with Niacin/Laropiprant halted by Merck & Co. (link)

SEAS
Rossebø AB, Pedersen TR, Boman K, et al. Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis. N Engl J Med 2008;359:1343-56

GISSI-HF
GISSI-HF Investigators, Tavazzi L, Maggioni AP, Marchioli R, et al. Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomized, double-blind, placebo-controlled trial. Lancet 2008;372:1231-9

CORONA
Kjekshus J, Apetrei E, Barrios V, et al. Rosuvastatin in older patients with systolic heart failure. N Engl J Med 2007;357:2248-61

AURORA
Fellström BC, Jardine AG, Schmieder ME, et al for the AURORA study group. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med 2009;360:1395-407

JUPITER
Ridker PM, Danielson E, Fonseca FA, et al, for the JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-Reactive protein. N Engl J Med 2008;359:2195-207

Still think saturated fat is bad for you? Still think eating eggs raises cholesterol? Still think high cholesterol causes heart disease?

If you answered yes to any of those questions, you really need to watch these videos. (But hey, you might learn something even if you answered “no”.)

In this presentation I:

• debunk the myth that eating saturated fat and cholesterol causes heart disease.
• explain why LDL and total cholesterol are not useful markers for heart disease.
• present three markers that are useful markers for heart disease.
• demonstrate that low-fat, high carb diets promote – rather than protect against – heart disease.
• show you how eating saturated fat and cholesterol can prevent heart attacks
• tell you how to order a test that more accurately predicts your risk of heart disease

At the end of these two videos, you’ll be heading to the fridge for some extra butter or cheese on those veggies or a little extra cream in your coffee!

Summary:

• The simplified view of cholesterol as “good” (HDL) or “bad” (LDL) has contributed to the continuing heart disease epidemic
• Not all LDL cholesterol is created equal. Only small, dense LDL particles are associated with heart disease, whereas large, buoyant LDL are either benign or may protect against heart disease.
• Replacing saturated fats with carbohydrates – which has been recommended by the American Heart Association for decades – reduces HDL and increases small, dense LDL, both of which are associated with increased risk of heart disease.
• Dietary cholesterol has a negligible effect on total blood LDL cholesterol levels. However, eating eggs every day reduces small, dense LDL, which in turn reduces risk of heart disease.
• The best way to lower small, dense LDL and protect yourself from heart disease is to eat fewer carbs (not fat and cholesterol), exercise and lose weight.

Not all cholesterol is created equal

By now most people have been exposed to the idea of “good” and “bad” cholesterol. It’s yet another deeply ingrained cultural belief, such as the one I wrote about last week, that has been relentlessly driven into our heads for several decades.

But once we’ve put on our Healthy Skeptic goggles, which I know all of you fair readers have, we no longer simply believe what we’re told by the medical establishment or mainstream media. Nor are we impressed or in any way swayed by the number of people that tell us something is true. After all, as Anatole France said, “Even if fifty million people say a foolish thing, it is still a foolish thing.”

Words to live by.

The oversimplified view of HDL cholesterol as “good” and LDL cholesterol as “bad” is not only incomplete, it has also directly contributed to the continuing heart disease epidemic worldwide.

But before we discover why, we first have to address another common misconception. LDL and HDL are not cholesterol. We refer to them as cholesterol, but they aren’t. LDL (low density lipoprotein) and HDL (high density lipoprotein) are proteins that transport cholesterol through the blood. Cholesterol, like all fats, doesn’t dissolve in water (or blood) so it must be transported through the blood by these lipoproteins. The names LDL and HDL refer to the different types of lipoproteins that transport cholesterol.

In addition to cholesterol, lipoproteins carry three fat molecules (polyunsaturated, monounsaturated, saturated – otherwise known as a triglyceride). Cholesterol is a waxy fat particle that almost every cell in the body synthesizes, which should give you some clue about its importance for physiological function.

You do not have a cholesterol level in your blood, because there is no cholesterol in the blood. When we speak of our “cholesterol levels”, what is actually being measured is the level of various lipoproteins (like LDL and HDL).

Which brings us back to the subject at hand. The consensus belief, as I’m sure you’re aware, is that LDL is “bad” cholesterol and HDL is “good” cholesterol. High levels of LDL put us at risk for heart disease, and low levels of LDL protect us from it. Likewise, low levels of HDL are a risk factor for heart disease, and high levels are protective.

It such a simple explanation, and it helps drug companies to sell more than $14 billion dollars worth of “bad” cholesterol-lowering medications to more than 24 million American each year.

The only problem (for people who actually take the drugs, rather than sell them, that is) is the idea that all LDL cholesterol is “bad” is simply not true.

In order for cholesterol-carrying lipoproteins to cause disease, they have to damage the wall of an artery. The smaller an LDL particle is, the more likely it is to do this. In fact, a 1988 study showed that small, dense LDL are three times more likely to cause heart disease than normal LDL.

On the other hand, large LDL are buoyant and easily move through the circulatory system without damaging the arteries.

Think of it this way. Small, dense LDL are like BBs. Large, buoyant LDL are like beach balls. If you throw a beach ball at a window, nothing happens. But if you shoot that window with a BB gun, it breaks.

Another problem with small LDL is that they are more susceptible to oxidation. Oxidized LDL, or oxLDL, is formed when the fats in LDL particles react with oxidation and break down.

Researchers have shown that the smaller and denser LDL gets, the more quickly it oxidizes when they subject it to oxidants in a test tube.

Why does this matter? oxLDL is a far greater risk factor for heart disease than normal LDL. A large prospective study by Meisinger et al. showed that participants with high oxLDL had more than four times the risk of a heart attack than patients with lower oxLDL.

I hope it’s clear by now that the notion of “good” and “bad” cholesterol is misleading and incomplete. Not all LDL cholesterol is the same. Large, buoyant LDL are benign or protect against heart disease, whereas small, dense LDL are a significant risk factor. If there is truly a “bad” cholesterol, it is small LDL. But calling all LDL “bad” is a dangerous mistake.

Low-fat, high-carb diets raise “bad” cholesterol and lower “good” cholesterol

Here’s where the story gets even more interesting. And tragic.

Researchers working in this area have defined what they call Pattern A and Pattern B. Pattern A is when small, dense LDL is low, large, buoyant LDL is high, and HDL is high. Pattern B is when small, dense LDL is high, HDL is low, and triglycerides are high. Pattern B is strongly associated with increased risk of heart disease, whereas Pattern A is not.

It is not saturated fat or cholesterol that increases the amount of small, dense LDL we have in our blood. It’s carbohydrate.

Dr. Ronald Krauss has shown that reducing saturated fat and increasing carbohydrate intake shifts Pattern A to Pattern B – and in the process significantly increases your risk of heart disease. Ironically, this is exactly what the American Heart Association and other similar organizations have been recommending for decades.

In Dr. Krauss’s study, participants who ate the most saturated fat had the largest LDL, and vice versa.

Krauss also tested the effect of his dietary intervention on HDL (so-called “good” cholesterol). Studies have found that the largest HDL particles, HDL2b, provide the greatest protective effect against heart disease.

Guess what? Compared to diets high in both total and saturated fat, low-fat, high-carbohydrate diets decreased HDL2b levels. In yet another blow to the American Heart Association’s recommendations, Berglund et al. showed that using their suggested low-fat diet reduced HDL2b in men and women of diverse racial backgrounds.

Here’s what the authors said about their results:

Translation: following the advice of the American Heart Association is hazardous to your health.

Eating cholesterol reduces small LDL

The amount of cholesterol in the diet is only weakly correlated with blood cholesterol levels. A recent review of the scientific literature published in Current Opinion in Clinical Nutrition and Metabolic Care clearly indicates that egg consumption has no discernible impact on blood cholesterol levels in 70% of the population. In the other 30% of the population (termed “hyperresponders”), eggs do increase both circulating LDL and HDL cholesterol.

Why is this? Cholesterol is such an important substance that its production is tightly regulated by the body. When you eat more, the body produces less, and vice versa. This is why the amount of cholesterol you eat has little – if any – impact on the cholesterol levels in your blood.

Eating cholesterol is not only harmless, it’s beneficial. In fact, one of the best ways to lower small, dense LDL is to eat eggs every day! Yes, you read that correctly. University of Connecticut researchers recently found that people who ate three whole eggs a day for 12 weeks dropped their small-LDL levels by an average of 18 percent.

If you’re confused right now I certainly don’t blame you.

Let’s review what we’ve been told for more than 50 years:

1. Eating saturated fat and cholesterol in the diet raises “bad” cholesterol in the blood and increases the risk of heart disease.
2. Reducing intake or saturated fat and cholesterol protects us against heart disease.

Now, let’s examine what credible scientific research published in major peer-reviewed journals in the last decade tells us:

1. Eating saturated fat and cholesterol reduces the type of cholesterol associated with heart disease.
2. Replacing saturated fat and cholesterol with carbohydrates lowers “good” (HDL) cholesterol, raises triglyceride levels, and increases our risk of heart disease.

Dr. Krauss, the author of one of the studies I mentioned above, recently said in an interview published in Men’s Health, “Everybody I know in the field — everybody — recognized that a simple low-fat message was a mistake.”

In other words, the advice we’ve been given by medical “authorities” over the past half century on how to prevent heart disease is actually causing it.

I don’t know about you, but that makes me very angry. Heart disease is the #1 cause of death in the US. Almost 4 in 10 people who die each year die of heart disease. It directly affects over 80 million Americans each year, and indirectly affects millions more.

We spend almost half a trillion dollars treating heart disease each year. To put this in perspective, the United Nations has estimated that ending world hunger would cost just $195 billion.

Yet in spite of all this money spent, the best medical authorities can do is tell us the exact opposite of what we should be doing? And they continue to give us the wrong information even though researchers have known that it’s wrong for at least the past fifteen years?

Really?

Sometimes it seems like everything is backwards.

How to reduce small LDL

Eating fewer carbs is perhaps the best place to start. Reducing carbs has several cardio-protective effects. It reduces levels of small, dense LDL, reduces triglycerides, and increases HDL levels. A triple whammy.

Exercise and losing weight also reduce small, dense LDL. In fact, weight loss has been shown to reverse the evil Pattern B all by itself.

As we saw above, eating three eggs a day can reduce our small LDL by almost 20%. Interestingly, alcohol has also been shown to reduce small LDL by 20%.

In other words, if you want to reduce your risk of heart disease, do the opposite of the American Heart Association (and probably your doctor) tells you to do. Eat butter. Eat eggs. Eat traditional animal fats. Reduce your intake of carbs, vegetable oils and processed foods, and stay active and within a healthy weight range.

Testing your small LDL level

I’m not a fan of arbitrary testing. Our medical system is obsessed with testing. But where has testing has brought us with cholesterol and heart disease? Has it improved outcomes? On the contrary, we test for a number (total LDL) that tells us very little, and then medicate it downwards recklessly and expensively.

If you’re worried about your small LDL level, my advice would be to eat fewer carbohydrates, eat plenty of saturated fat and cholesterol (instead of vegetable oils), exercise, lose weight if you need to, and have a drink every now and then! Since this is the same advice I’d give you if you took a test that actually showed high levels of small LDL, I don’t see much value in doing the test.

However, if you need to see the test results to get motivated to make the changes I suggested above, by all means do the test. There are a few ways to go about it.

First, keep in mind that a regular cholesterol test at your doctor won’t tell you anything about your small LDL level. The standard tests measure your total cholesterol, LDL and HDL. But they don’t distinguish between the dangerous small LDL and benign or protective large LDL.

The fastest and cheapest, albeit most indirect, route is to test your blood sugar both before and then 60 minutes after a meal (this is called a “post-prandial” glucose test). The reason a post-prandial blood glucose test can be a rough indicator for small LDL is the same foods that trigger a rise in blood sugar also increase small LDL. Namely, carbohydrates.

Blood glucose monitors are readily available at places like Walgreens and cost about $10. You’ll also need lancets and test strips, which aren’t expensive either. If your post-prandial glucose is higher than 120 mg/dl, that may be suggestive of a higher than desired small LDL level. This test is not a perfect approximation of small LDL, but it’s the cheapest and and easiest way to get a sense of it.

If you want to get more specific, there are two tests I recommend for small LDL that use slightly different methodology:

1. LDL-S3 GGE Test. Proteins from your blood are spread across a gel palette. As the molecules move from one end to the other, the gel becomes progressively denser. Large particles of LDL cholesterol can’t travel as far as the small, dense particles can, Dr. Ziajka says. After staining the gel, scientists determine the average size of your LDL cholesterol particles. Berkeley Heart Lab. About $15 with insurance.
2. The VAP Test. Your sample is mixed into a solution designed to separate lipoproteins by density. Small, dense particles sink, and large, fluffy particles stay at the top. The liquid is stained and then analyzed to reveal 21 different lipoprotein subfractions, including dominant LDL size. The Vap Test. Direct cost is $40.

I recently came across two articles that I think you should read.

The first is over on Dr. William Davis’s blog, The Heart Scan. Dr. Davis reviews a study demonstrating that consumption of excess carbohydrate can raise cholesterol.

Now, if you’ve been reading my blog for a while you know that normal LDL cholesterol isn’t a risk factor for heart disease, right? So I am generally not concerned with what does or doesn’t raise cholesterol. However, there is a type of cholesterol that is a significant risk factor for heart disease: small, dense LDL cholesterol.

Small, dense LDL particles are more likely to become oxidized, and as I have explained in How to Increase Your Risk of Heart Disease, oxidized LDL is one of the strongest risk factors for heart disease we know of.

Dr. Davis clearly explains how eating too many carbs can increase your levels of small, dense LDL and he also explains why so many doctors and researchers don’t make this crucial connection. Check out the full article here.

The second article is on Dr. Barry Groves’ Second Opinions blog. He reviews a study which links consumption of linoleic acid to Inflammatory Bowel Disease (such as Crohn’s and Ulcerative Colitis) and Irritable Bowel Syndrome (IBS).

Linoleic acid is an omega-6 (n-6) essential fatty acid. “Essential” in this context means that humans can’t make it internally and need to eat it in the diet. However, we only need a tiny amount – about a teaspoonful per day – and eating too much of it can cause serious problems. Eating too much linoleic acid dramatically increases oxidized LDL cholesterol levels, which as I just explained in the last section significantly elevates our risk of heart disease. Linoleic acid is also pro-inflammatory, and inflammation is a major contributor to modern diseases like cancer, diabetes, heart disease and, you guessed it, Inflammatory Bowel Disease and Irritable Bowel Syndrome.

Tragically, linoleic acid has become one of the primary sources of calories in the American diet. Vegetable oils containing linoleic acid (such as soybean, corn, safflower, sunflower, cottonseed) are found in nearly all packaged and processed foods and all foods cooked in a restaurant. Almost all fried foods are extremely high in linoleic acid.

Is it any wonder, then, that Irritable Bowel Syndrome has reached such epidemic proportions? It is now the #2 leading cause for people missing work, behind only the common cold. It affects millions of people in the U.S. and abroad. There is no known “cure”, and the medications prescribed for it are largely ineffective.

This is yet another example of how toxic and harmful our modern diets are. If you want to avoid these conditions, eat traditional, saturated fats like butter, lard and coconut oil instead of industrially-processed vegetable oils. You’ll feel better, and you’ll enjoy your food a lot more too!

Dr. John Briffa wrote a post worth reading on his blog today about the significant side effects of statin drugs, and the considerable effort pharmaceutical companies and the medical establishment spend trying to convince people that these drugs are safe.

Sadly, they’ve been largely successful. Some time ago a physician in the UK by the name of Dr. John Reckless (you can’t make this stuff up) suggested that statins are so safe that they should be put in the water supply!

That’s ridiculous, of course. Statins are dangerous drugs. What’s more, they don’t reduce the risk of total mortality (death from any cause) for 95% of the population. See my articles The Truth About Statin Drugs and More Statin Shenanigans for more on this.

If you’re wondering why you haven’t heard more about the danger of statin drugs, check out another great post Dr. Briffa wrote a couple of weeks ago called Adverse effects of drugs are “neglected, restricted, distorted or silenced”.

There’s big money in the drug business, folks. The total pharmaceutical industry is worth hundreds of billions, and drug companies make $25 billion on statin sales alone. Do you think they’re going to go out of their way to tell everyone about the side effects and risks of these drugs? They’re legally obligated to maximize profits for their shareholders, as are all corporations, and maximizing profits means selling as many pills as they can.

That’s just the way it works. Unfortunately, people like you and I and our families are the victims of this profit-driven health care system.

For the last 50 years mainstream medical “authorities” have been hammering it into our heads that high cholesterol levels are dangerous and low cholesterol levels are desirable; that eating saturated fat is bad for us; and that a low-fat, high carbohydrate diet is healthy and helps people lose weight.

If you’re a new reader, you might be surprised to learn that there’s very little evidence to support these recommendations and plenty of evidence that contradicts them. Long ago I learned that if I wanted to live a long, healthy life it was in my best interest to ignore the dietary advice of the medical mainstream. And of course that’s why I started this blog – to share this information with all of you so you can make educated, and informed choices about your health.

Lately I’ve been encouraged by the number of studies being published that undermine the anti-fat, anti-cholesterol dogma we’ve been brainwashed with for so long. This is good news.

The bad news is that paradigm shifts do not happen overnight. It took half a century for researchers and doctors to convince people that eating toxic, highly processed, nasty-tasting vegetable oils was somehow better for them than eating traditional animal fats like butter and lard; that eating dry bagels, boneless-skinless chicken breast and salad with fat-free dressing was a path to good health; and that the best way to lose weight was to eat a highly unnatural diet high in processed, refined carbohydrates and low in fat.

So I don’t expect these ideas to disappear anytime soon, in spite of the solid evidence being published that contradicts them. It’s going to take time. But my sense is that it will take less time to convince people that eating traditional, nutrient-dense, whole foods that have been minimally processed is better for them than eating what the industrial food conglomerates have been selling us.

Here are the three studies.

The first is yet another study that associates low cholesterol with an increase in the risk of death (total mortality). It showed increased death rates in hospitalized patients with low cholesterol levels.

This shouldn’t be a surprise. There’s already plenty of evidence suggesting low cholesterol increases the risk of death – as well as contributing to other conditions such as cancer and depression. For more on this see my previous article Cholesterol Doesn’t Cause Heart Disease.

The second study shows (once again) that cutting carbs is the best way to lose weight and fight obesity.

No surprise here either. Countless studies, trials and reviews have demonstrated that low-carb diets are superior for weight loss, managing diabetes and preventing many of the other modern diseases which plague us. How long will it take until doctors and the media get the message? For more on one such recent review, see Low-carb Diet Best for Weight Loss.

The last study I want to share with you was performed by a Swedish PhD student. It demonstrates that children who eat saturated fat and full-cream dairy products are healthier than those who do not.

If you’re surprised by this, read my recent post Have Some Butter with Your Veggies as well as Whole Fat Milk: Benefits for Moms and Kids.

Research by an Iowa State University scientist due to be published this month in the journal Proceedings of the National Academy of Sciences indicates that cholesterol-lowering drugs (statins) may lessen brain function.

The results of the study show that drugs that inhibit the liver from making cholesterol may also keep the brain from making cholesterol, which is vital to efficient brain function.

“If you deprive cholesterol from the brain, then you directly affect the machinery that triggers the release of neurotransmitters,”, said Yeon-Kyun Shin, the lead researcher. “Neurotransmitters affect the data-processing and memory functions. In other words – how smart you are and how well you remember things.”

Cholesterol is abundant in the tissue of the brain and nervous system. Myelin, which covers nerve axons to help conduct the electrical impulses that make movement, sensation, thinking, learning, and remembering possible, is over one fifth cholesterol by weight. Even though the brain only makes up 2% of the body’s weight, it contains 25% of its cholesterol.

We now know that the formation of synapses, or connections between neurons, is directly dependent on the availability of cholesterol.

The formation of these synapses are what give us the ability to remember and learn. The benefits of sleep for memory formation and learning are in part a result of increased cholesterol synthesis during sleep.

“If you try to lower the cholesterol by taking medicine that is attacking the machinery of cholesterol synthesis in the liver, that medicine goes to the brain too. And then it reduces the synthesis of cholesterol which is necessary in the brain,” said Shin.

This study is yet another strike against statin drugs, which have numerous side effects and are not effective in reducing mortality for the vast majority of the population. Please see my recent article, The Truth About Statin Drugs, for more on why statins are probably not a good idea for you and your loved ones.