After reading my recent articles about red meat, I hope none of you are concerned that eating it will negatively impact your health. But I realize that nutrition is only one of the factors that motivate people to limit or eliminate red meat consumption; one of the primary reasons many go vegetarian is their concern about environmental impact.

We’ve all heard the claims that red meat production is harmful to the environment, so in this two-part series, I’d like to address some of those concerns. In many ways, the environment is as complex as the human body, so measuring the impact of meat production isn’t clear-cut. But at the very least, I hope to shed some light on the topic, dispel some common myths, and put the issue in perspective.

Is eating red meat really more harmful to the environment than eating a vegetarian diet?

Greenhouse Gases

A commonly cited statistic is that cows produce more greenhouse gases than all the world’s transportation combined, or 18% of all greenhouse gases. This statistic originated from a report by the UN Food and Agriculture Association called Livestock’s Long Shadow, and has since been cited frequently in the media and elsewhere as a reason to stop eating red meat. If you think that figure sounds unbelievable, you’re right; it turns out that the researchers were quite biased in their calculations, resulting in numbers that were skewed. One of the authors of the report even admitted later that it wasn’t a fair comparison. A more accurate analysis of the data resulted in a much more respectable estimate: that cattle contribute less than 3% of global greenhouse gas emissions. (1)

However, even the revised figure doesn’t take into account that grazing livestock can actually help remove carbon from the atmosphere. (2) Grasslands are capable of sequestering more carbon than any other ecosystem, and livestock can enhance the incorporation of carbon into the plants and soil. (3) One study showed that grazing cattle can also reduce the land’s natural emissions of nitrous oxide, a greenhouse gas that environmentalists agree is more damaging than carbon dioxide. (4) Some research shows that when cattle are raised on natural pasture with no additional fertilizer or supplemental feed, their ability to enhance carbon sequestration actually outweighs their greenhouse gas emissions. In other words, under the right circumstances, cows are carbon negative!

Water Use

Another common argument against red meat production is that it supposedly uses way more than its fair share of water. Graphics like this are often used to display how water-intensive red meat is compared with other foods. But are these figures accurate? Consider that previous studies have come up with water usage figures anywhere from 209 L/kg of beef to 105,400 L/kg of beef. (5) That’s a huge difference! When there’s that much variation, it usually pays to look a little deeper into the research to see what’s going on.

One reason for this variation is simply location. Water usage is going to be very different, say, for a feedlot in the US than for a pastoralist in Australia. But another reason is that researchers don’t always agree on how to classify ‘water use,’ and this creates some serious methodological inconsistencies in the literature.

Feed production is the most water-intensive part of raising livestock for red meat, whether the feed is grain, soy, or forage-based. (6) Some of this water comes from natural rainfall, while some is supplied through various irrigation methods. The problem is that many researchers don’t distinguish between rainfall and other forms of water use. This means that a large portion of the water attributed to red meat production is simply rain that falls on the fields or pasture used to feed the livestock.

Although measuring in this way does give an accurate depiction of the sheer amount of water that’s necessary to produce red meat, it gives little to no indication of how environmentally friendly red meat production is. It doesn’t make sense to say that raising cows on non-irrigated pasture drains water resources, when the only water being used is natural rainfall. Even feed crops often receive much of their water through rainfall, and it just isn’t logical to classify that in the same way as, say, drawing water from a nearby reservoir for irrigation.

Luckily, some researchers from Australia thought the same thing, so they did their own analysis. (7) They measured the actual water usage of three different production systems in southern Australia over the course of two years. They classified ‘water use’ as water that was “removed from the course it would take in the absence of production or degraded in quality by the production system.” Thus, under their calculations, things like rainfall and evaporation weren’t counted towards the total ‘water footprint’ of beef unless the water quality was somehow reduced when it reentered the water cycle. To me, this approach gives a much more accurate picture of the impact red meat production has on water resources.

The researchers analyzed a small organic beef supplier, a larger supplier where the animals spend part of their time in a feedlot, and a mid-sized sheep meat supplier. For the systems without a feedlot, they came up with a range of 18-214 L/kg of meat, depending on the year and whether they were measuring water use based on input amount or output quality. For the feedlot system, they came up with a range of 34-540 L/kg. Compared to earlier estimates of 15,000 L/kg and beyond, these new estimates are tiny! However, these results can only be generalized to southern Australian production systems, and systems in the US tend to be more irrigation-intensive.

For a US-specific estimate, we can look at an older study on the average water required for beef production in the US. (8) This study was based on national government statistics as opposed to actual water usage measurements from individual production systems, but they classified ‘water use’ in a similar manner to the previous study by excluding rain and only counting the water needed for irrigation, drinking, and processing. They came up with 3,682 L/kg of meat, which is significantly higher than the Australian estimate. This reflects the higher use of concentrate-based feeding in the US, which usually requires more irrigation than natural pasture. However, this estimate is still much lower than some of the most commonly cited numbers, and demonstrates that red meat isn’t singlehandedly draining the world’s freshwater resources.

In the second article of this two-part series, I’ll discuss the claim that grazing livestock leads to soil erosion and desertification, as well as the different environmental impacts of grass-fed versus grain-fed meat.

In this episode I review new research on vitamin D that has led me to slightly modify my recommendations, and we discuss how multitasking and the internet are literally rewiring our brains.

It’s also the first episode with our super-duper new sound dampening equipment. I think we’ve finally reached audio quality nirvana. Let us know what you think!

In this episode, we cover:

3:16 A surprising update on new vitamin D research (and Chris’s revised recommendation)
26:53 The myth of multitasking – and what you really need to know
36:39 How the internet is rewiring our brains

Links We Discuss

• Multitasking May Not Mean Higher Productivity
• Zaradic And Pergams “Videophilia” – The Journal of Developmental Processes
• The Shallows: What the Internet Is Doing to Our Brains

Full Text Transcript:

Steve Wright:  Hi, everyone.  Welcome to another episode of the Revolution Health Radio Show.  This show is brought to you by ChrisKresser.com, and I’m your host, Steve Wright from SCDLifestyle.com.  With me is integrative medical practitioner and healthy skeptic Chris Kresser.  Chris, how has your day been going?

Chris Kresser:  It’s fantastic.  It’s so beautiful lately here.  It’s been in the high 70s and 80s.  I’ve been outside every day getting some sunlight and vitamin D, which actually we’re going to talk about today, and doing lots of hiking with Sylvie and Elanne.  It’s one of these times where I’m just so grateful to live in California and particularly this part of California where I live, so couldn’t be better.  How about you, Steve?

Steve Wright:  Well, you’re making me a little jealous, but I am riding an avocado high right now.  I just had this massive avocado, so I have a belly full of fat, and I’m interested to hear about this new vitamin D stuff because I’ve actually been doing my own tinkering.  I cut off all vitamin D supplementation in February and just ran my numbers, and I’m back down to 30 without anything except for one or two teaspoons of fermented cod liver oil a week.  So I’m curious to see what the new stuff is, and I think it’s going to be a good show.

Chris Kresser:  Yeah, we’ll get into it.  My other update is that I’m not in the closet again, but I have this fancy new audio-dampening equipment.  There are these two heavy screens with some kind of material; I’m not even sure what it is.  There are two screens, and each of them has two panels, and then they have hinges so you can kind of position them any way you want.  And so I’m sitting in a chair, and I’m basically wrapped around by these panels, and I think it’s going to make a big difference, but we’ll have to hear from all of you to tell us if it does or not.

Steve Wright:  Yeah.  Leave a comment.  If you’re in iTunes, go over to ChrisKresser.com and let us know about the sound quality.  So, Chris, before we get into this week’s show, go ahead and fidget with your new sweet screens, maybe reach outside of them and get a drink of water, and I want to tell everybody about Beyond Paleo.  So if you’re new to this podcast, or if you’re new to the paleo diet, or maybe you’re just interested in optimizing your health, you’re going to want to check out what over 30,000 other people have already signed up for.  It’s Chris’ free 13-part email series called Beyond Paleo.  Now, this email series goes over Chris’ best tips and tricks for burning fat, boosting energy, and preventing and reversing disease without drugs.  To sign up, go over to ChrisKresser.com, and look for the big red box.

OK, Chris, did you get in and out of your box?

Chris Kresser:  I’m in my cocoon.

Steve Wright:  OK.

Chris Kresser:  It’s amazing.  It totally blocks out the sound even from my own office.

A surprising update on new vitamin D research (and Chris’s revised recommendation)

So I want to talk about a couple different things today, and we’re going to start with vitamin D.  There’s a lot of new research coming out that is pretty surprising, I think, to many of us who’ve been following this issue for a while, perhaps more surprising to people who’ve been recommending really high levels of vitamin D.  For the last several years I’ve been warning against excessively high levels of vitamin D for some of the reasons we’re going to talk about today, but there’s a lot of controversy about this.  The science is definitely mixed and inconsistent, and the jury is certainly not out.  But I want to talk about some of the newer findings and go into some detail about what that might mean in terms of optimal vitamin D levels and vitamin D supplementation and sunlight versus supplements and things like that.  And then if we have time, I want to talk about multitasking, electronic media, and how the Internet is rewiring our brains.  It’s a topic that I’m really fascinated by, and I heard an interview with a neurologist on NPR Science Friday last week about it that really just kind of got my juices flowing about it again, and so I gathered together some of the research that I’ve done on this over the years, and I’ve been doing additional research about it for my book, which is coming up soon.  I’ll have an exciting announcement about that, I think, probably by the next show.  So consider this a preannouncement.

Steve Wright:  Dun dun duunnn.

Chris Kresser:  So let’s get into it, and we’ll see how far we get, and we can pick it up on the next show if we run out of time.

The stimulus for this vitamin D conversation, the most recent one at least, was a new prospective cohort study with over 1.2 million participants, so a pretty big sample size.  And this study showed that the lowest mortality or risk of death from all different causes and the lowest rates of cardiovascular disease were observed at vitamin 25D levels between 20 ng/mL and 36 ng/mL.  That may surprise some of you because as you probably know, in the US the lower end of the lab reference range is 30 ng/mL, so a big chunk of that range where the researchers found that the risk of death and heart disease was the lowest is actually in a range that would be considered deficient by current standards.  This isn’t the only study that reached this conclusion.  There are actually several other fairly large epidemiological studies that have been done in the past few years that have suggested that the optimal vitamin D level might be much lower than is currently recommended, especially by some of the vitamin D advocacy organizations, like the Vitamin D Council.  Some of the other studies, the range was 20 to 30.  I think there was one that was 20 to 35, and then one went up to, I think, as high as 40, so it’s all basically in the same range.

Now, as I’m sure many of know who have been listening to this show now for a while or have been following my blog, you understand that observational research, epidemiological data like this always has to be taken with a big grain of salt because there’s a lot of potential for confounding factors.  You know, something that we might consider right off the top of our head is that vitamin A and vitamin K2, as Chris Masterjohn has pointed out in several really great articles on his blog and in the Weston A. Price journal and that I’ve written about as well, vitamin A and K2 protect against vitamin D toxicity.  So one reason that people with higher vitamin D levels in these studies might be experiencing a higher risk of death and a higher chance of cardiovascular disease is that they’re also deficient in vitamin A and vitamin K2, which would lower the threshold for vitamin D toxicity.  And unfortunately, we have no way of knowing whether that’s the case because in these big studies of vitamin D levels, they never measure vitamin A or vitamin K2 status.  And there’s even controversy about how to accurately do that, so I don’t think that’s, unfortunately, going to happen anytime soon.  We’re left to just kind of speculate based on the biochemical mechanisms that we understand and some other studies that have shown that vitamin A protects against vitamin D toxicity and vice versa.

And then just understanding the mechanism of K2, one of the main roles of K2 is to make sure that calcium gets into the bones and the teeth and the hard tissues where it belongs and stays out of the soft tissues where it doesn’t belong.  And vitamin D, of course, regulates calcium metabolism, too.  So if you have really high levels of vitamin D, which could increase soft tissue calcification, and then you have low levels of vitamin K2, which would also contribute to soft tissue calcification, that’s kind of a double whammy.  And a lot of people probably do have vitamin K2 deficiency.  Vitamin K is plentiful in green vegetables and can be converted into vitamin K2, but the conversion is pretty inefficient.  And vitamin K2 is only found in certain foods, like organ meats and natto, which is a fermented soy product, and cheeses, particularly grass-fed dairy and grass-fed cheese because, as I just mentioned, vitamin K is found in green vegetables or in grass that the cows eat.

So with all those caveats in mind, let’s just talk a little bit about some of the problems with the idea that a vitamin D level of 50 or above, which I think the target for the Vitamin D Council is 50, and their suggested range is 40 ng/mL to 80 ng/mL with a target of 50, but when you look at the actual research that was done to determine the reference range for vitamin D, you’ll find that it’s pretty thin and sloppy in a lot of cases.  The earlier justification for the reference range of 30 and above, which is the one we use in the US, was looking at what level of vitamin D led to the maximum suppression of parathyroid hormone, and this was based on looking at parathyroid hormone levels in cross-sectional analysis of large populations, and there is a point where the average parathyroid hormone level bottoms out, but the range is really enormous.  There’s tons of variation in these studies.  So it’s really difficult to say this level of vitamin D is optimal for suppressing parathyroid hormone in everybody because the variation was so big.  And then the Vitamin D Council, I think, based their recommendation of 50 ng/mL on a similar type of evidence, but in this case, as Chris Masterjohn pointed out to me in a discussion we were having about this, the endpoint was the inferred storage of vitamin D in body fat and then saturation of an enzyme called 25-hydroxylase, I think that’s involved in converting 25D to the active form of vitamin D, which is 1,25D.  So there were never any obvious connections to serum vitamin D levels and any clinically significant endpoint in the Vitamin D Council’s recommendation.  And then they took two of the older studies on this issue and used one of the studies that later was found to have unreliable methods of reporting 25D levels.  I know that’s probably pretty technical and complicated, but the gist of it all is that the studies that were used to determine these ranges, 30 and above and then 50 ng/mL for the Vitamin D Council, are problematic and have been criticized by a number of different commentators in the scientific literature.

Steve Wright:  Hey, Chris, you mentioned 1,25D as well as 25D.  Which one’s the active form, and do we know much about the ratio between the two?

Chris Kresser:  Yeah.  The inactive form is 25D, and that is converted into 1,25D, which is the active form.  A lot of the effects of vitamin D toxicity that we’re talking about now happen when there’s too much of the active form in the body.  Something else that’s pretty interesting about that is that there are variations in how much of the active form, 1,25D, will be produced from a given amount of 25D, the inactive form.  And there are actually genetic polymorphisms that have been identified at this point that vary geographically that affect that conversion.  For example, we know that among Indians the level of vitamin 25D that’s required to produce a given level of 1,25D is higher than among the Inuit.  That suggests that the optimal vitamin D exposure for Indians in Southeast Asia, those living in equatorial regions, is higher than for people living at northern latitudes.  And this is a fairly new finding, but it really means that one person’s optimal vitamin D level is different than another person’s, and unfortunately we’re not at the point where we can easily identify that and where you can go in and just get a test and get a piece of paper that says this is your optimal vitamin D based on your genetics and skin color and latitude and all of that stuff.  It probably isn’t that far away, but we’re not there yet.

Steve Wright:  Why is all the research done on the inactive form, though, and not on the active form?

Chris Kresser:  Well, that’s a very good question.  Actually in this conversation I was having with Chris Masterjohn, one of the things that he brought up is that 25D has been long used as the main marker for vitamin D status, and it’s been assumed that it’s an accurate marker of active vitamin D status, but it turns out it’s possible to have kind of a disconnect between your 25D levels and your 1,25D levels.  They’re not always what you would expect them to be, in part because of these polymorphisms and in part possibly because of disease states that cause an over-conversion of 25D to 1,25D, the active form, that happens in some autoimmune diseases.  So 25D turns out to not be a very good indicator of vitamin D status, and I believe Chris said he’s going to be writing a blog series about this in the future, which I look forward to reading, and he’s going to take on that topic specifically.

The other thing about this, too, that makes me think that the optimal level might not be as high as we thought is that in most indigenous populations that have been studies, their levels of 25D are typically lower than 50 ng/mL.  I think the highest level in any indigenous population that has been measured was 46, and that was in the Maasai.  But as Chris pointed out, that was done with modern Maasai who no longer paint themselves for war and are living a different lifestyle than their predecessors would have been, so we can’t really know necessarily that that historically would have been the typical vitamin D level in the Maasai population.  But even if it is, that’s still the highest that’s ever been identified in any traditional population.  Usually it’s significantly lower, and that’s still lower than the 50 ng/mL recommendation from the Vitamin D Council.

So when all of this is taken together, it does make me wonder what the optimal level for vitamin D is as a general recommendation, given that we can’t really identify all the individual differences yet.  Up until today I’ve been recommending a range of 35 to 50 or 60 and ensuring that vitamin A and vitamin K2 levels are adequate, and I don’t think that that’s far off, even considering everything that we’ve been talking about today.  I’m thinking about lowering the lower end of that to maybe 30 or 25, targeting 35 ng/mL as a kind of optimal number with an upper limit of maybe 50, and I think that range of 25 to 50 is pretty well supported by the current evidence, and I don’t think there’s much of a risk of toxicity at 50 if you’re getting enough vitamin A and vitamin K2.  And considering that bone density peaks usually between 20 ng/mL and something like 35 in people over 50 — in some populations it continues to increase up to 45, like in Mexican-Americans, I think — I think that’s probably a pretty good range to shoot for, 25 to 50 with a target of 35.

Steve Wright:  So is there also a target range or a number that people should start tracking for the active form, the 1,25D?  You know, for a long time, the push was always to only get the inactive form tested.  Now with all this new research, those of us who are testing freaks and just like to monitor this stuff on a regular basis, is it worthwhile to start getting the active form tested, too?

Chris Kresser:  It may be, but I don’t know enough about it yet to make a recommendation.  I mean, there’s far less literature on that topic just because 25D has been the recognized marker for vitamin D status for so long, so that’s what’s usually used.  Some studies do measure 1,25D along with 25D, but a lot don’t.  So there’s just less data to draw any conclusions from.  The data on 25D on already so unclear, so it’s going to take some time for me to dig into that a little further, but of course, as always, I’ll keep everyone posted.

There are a couple other things to point out about this.  Generally, sunlight is considered to be a safer way of meeting your vitamin D needs if you can.  I mean, obviously that’s not possible for everybody, depending on where you live and your lifestyle, etc., and your skin tone, because full exposure to sunlight, midday sun exposure 15 to 20 minutes in a light-skinned person produces about 10,000 IU of vitamin D, but in a darker-skinned person, it could take up to 2 hours to produce that same amount of vitamin D.  But one reason why sunlight might be better than supplements is that the body does have some ability to put the breaks on the conversion of ultraviolet light into vitamin D when it’s had enough.  So there’s a little bit more of an inherent regulatory mechanism there, whereas when you eat vitamin D in the form of supplements of foods, although there aren’t many foods that have much vitamin D, there isn’t really a regulatory mechanism there.  You’ll just keep absorbing more and more vitamin D from the gut even when you have more than you need.

The other reason is that sunlight has been shown to have several other benefits aside from vitamin D production.  You don’t need a degree in science to know this!  People feel good when they go outside and they get sun.  But it is interesting to see some of the research.  For example, sunlight has been shown to increase nitric oxide production, and nitric oxide is a vasodilator, and that means it will lower blood pressure.  And blood pressure is one of the single strongest independent risk factors for heart disease.  In fact, I think I remember seeing a study that a drop in 20 mm Hg of systolic blood pressure — which is the number on the top of the equation.  When they say 120/80, the 120 refers to systolic. — A drop in only 20 mm Hg cuts heart disease in half in people who are 20 to 49 years of age, so it’s a really, really significant risk factor, and anything that lowers blood pressure will have a really big impact on heart disease risk.  And sunlight increases the amounts of nitric oxide, which in turn lowers blood pressure.

There are also a lot of other studies that suggest that the incidence of autoimmune diseases is correlated with sunlight and ultraviolet light exposure.  It’s been observed for some time that MS flares happen more in the winter than they do in the summer.  People are more likely to have MS that are born in northern latitudes without much sun exposure and less likely to have it in equatorial regions.  And of course, you could say:  Oh, well, we don’t know where the chain of causality lies there.  But interestingly enough, when people move from one place to another, they assume the risk of the new place, so that suggests that there is a causal relationship and it’s not just something to do with the genetics of people living at those different latitudes.  That said, it is still possible to experience vitamin D toxicity from only sun exposure.  There was a study done on Israeli lifeguards, and their vitamin D levels were between 50 and 60 ng/mL just from sun exposure.  They weren’t supplementing at all.  And their rate of kidney stones was 20-fold higher than that of the general population, which is a pretty significant difference, and that’s probably caused by an increase of calcium.

There’s definitely a lot more to this story than is typically reported in the media.  There’s no doubt that vitamin D is crucial.  It affects over 3000 genes.  It plays a really important role in a lot of different processes.  Vitamin D deficiency is associated with numerous different diseases, so yes, we absolutely need to ensure adequate levels of vitamin D.  But as is the case with many other nutrients, perhaps all nutrients, there is a U-shaped curve for vitamin D, which means too little of it is not good, but too much of it is also not good.  And I think now we’re starting to see more research on the other end of that spectrum, whereas for a while it was almost exclusively dedicated towards the effects of deficiency.

Steve Wright:  You know, just more anecdotal ideas, but interestingly enough, last week I asked on our SCDLifestyle Facebook page how many people have flare-ups of their digestive issues in the summertime, and the overwhelming feedback was that people always seem to be healthier in the summertime.  And I think you hit on a great point there, Chris, that science doesn’t even understand how beneficial the sun is, but it seems like from every possible angle being out in the sun and getting adequate exposure on a daily basis seems to really help everyone.

Chris Kresser:  Well, yeah, and this is once again where the evolutionary lens can be helpful.  I mean, we evolved in an environment with a lot of sunlight, in the equatorial region, and it makes sense that we would be genetically and biologically adapted to that kind of environment.  And yes, it’s true that genetic change didn’t stop in the Paleolithic, and a lot of genetic changes have occurred since that time, which we’ve discussed a lot on this show, but it doesn’t mean that our entire genetic makeup has changed.  And so we’re still kind of hardwired to have some sun exposure, and there’s definitely a lot of modern evidence that supports that as well.

OK, so we’ll come back to that.  Let us know what your questions are.  This is an ongoing investigation, and it’s something that I continually discuss with Chris Masterjohn, Stephan Guyenet, and Robb Wolf, and we have a kind of little email group.  We trade studies when they come out, and we talk about them, so I’ll be curious to see how the research evolves over the next few years.

Steve Wright:  Great, well, that’s like part 2 or 3 for you, so stay tuned until parts 4, 5, and 6.

Chris Kresser:  Exactly.  It’s a work in progress.

The myth of multitasking – and what you really need to know 

All right, so we may not have time to finish this.  We’ll probably come back to it, and it’ll probably be a multipart series because it’s an issue I’m really interested in and I think it’s important, and it’s one that I don’t think gets enough airplay, and there’s actually a lot of resistance to it, even among my audience, I’ve noticed, whenever I post something about it, which I’ll come back to in a minute.

So the other day I was driving the car and I was listening to a program on Science Friday, and Ira was interviewing a neuroscientist… I believe he’s a neuroscientist.  He’s a professor at Stanford, his name is Clifford Nass, and the topic was multitasking, or rather the myth of multitasking.  And that was Nass’ contention, that it is a myth, and of course, there’s a ton of other studies that back that up and that basically say that multitasking, at least in the case of computers and electronic media, is a misnomer and that we should really be calling it multi-switching because the human brain doesn’t have the capacity to focus on several tasks at once.  And if you are multitasking, what you’re doing is just switching really quickly back and forth between tasks.  He did a study of 262 college students to complete experiments that involve switching among tasks, number one; and then filtering irrelevant information, number two; and then using working memory.  Working memory is the part of our memory that we’re consciously aware of.  We have short-term memory, working memory, and long-term memory.  And working memory is the part that calls stuff out of long-term memory, and it’s what we’re kind of, like I said, consciously aware of at any given moment.

The researchers thought that effective multitaskers would outperform the people that were just focusing on single tasks, and they turned out to be completely wrong.  The multitaskers were terrible at all three of the tasks, and the scariest part was that only one experiment actually involved multitasking.   The others were just single activities, which of course suggests that frequent multitaskers use their brains less effectively, even when they’re focused on a single task.  And it also suggests that multitasking might actually rewire our brains in a way that isn’t beneficial.  Other research out of other labs has shown that when people focus on two tasks at the same time, each side of the brain tackles a different task, and that suggests that we might have a two-task limit.  So again, this idea that we can focus on four or five different things at once is really a myth.  But that doesn’t stop most of us from trying, right?!  Another study at Stanford, I think by Nass as well, found that 25% of students at Stanford use four or more media devices when they’re using one.  So if they’re watching TV, they might have their phone, their tablet, and perhaps a computer or something else going.  They’re writing a paper, they’re on Facebook, they’re tweeting, and they have music playing.  This, of course, is increasingly common.  It’s not just limited to students at Stanford.

And younger kids are increasingly using media and multitasking with media.  For a long time, the American Academy of Pediatrics has been recommending that kids under 2 years of age have no screen time at all.  And this is based on a large body of evidence showing that screen time for kids that young may have harmful effects, and yet, according to a Kaiser Foundation report, 90% of parents report that their kids under 2 years of age are using electronic media, 68% of kids under 2 years of age use electronic media for more than 2 hours, and 26% of kids under 2 have TVs in their room.  This is less true for kids under 2 who can’t probably turn on the TV themselves, but for older kids when TV is in the bedroom, viewing increases by 1 or 2 hours per day, and the risk of being overweight increases by 31%, and the likelihood of smoking doubles.

Steve Wright:  This is staggering.  Twenty-six percent of kids under 2 have a TV?!

Chris Kresser:  Yeah, and almost 70% are using electronic media more than 2 hours a day.  Getting a little older, the average American child now spends more than 7 hours a day in front of an electronic screen.  The only other activity that the average kid does more than planting himself or herself in front of a screen is sleeping, and that’s actually reducing.  We’ve talked before about the decline in average amount of sleep, so they’re probably getting closer.

Screen time in many ways also is replacing green time.  Recent studies have shown that people living in the US, Japan, and Spain are spending between 18% and 25% less time in wilderness or natural environments today than they were just 30 years ago.  This is, of course, a concern because nature has been shown to have numerous health benefits.  For example, in preschool children, time spent outdoors in nature is the single most predictive factor in how physically active they’ll be.  Other studies have shown that contact with nature reduces stress, reduces loneliness and depression, helps with stress tolerance, improves mood, etc.

Steve Wright:  Up-regulates the immune system.

Chris Kresser:  Yep, up-regulates the immune system.  And there are a lot of theories on why this might be.  One of them was created by E.O. Wilson, who coined the term ‘biophilia’ and the biophilia hypothesis.  This is basically a fancy way of saying that humans are inherently drawn to natural environments, and it’s based on a lot of studies that demonstrate how strongly people respond to open grassy landscapes, scattered stands of trees and meadows, water, winding trails, and elevated views, which is exactly the environment that humans evolved in.  The biophilia hypothesis is not universally accepted.  It’s somewhat controversial, but it certainly, to me, makes sense from an evolutionary perspective.

I recently came across, while researching for my book, a study by a couple of other researchers named Zaradic and Pergams, and they coined a new term, in kind of a play on biophilia, called ‘videophilia.’  And videophilia is the love of playing video games, surfing the Internet, and watching movies and TV.  And in contrast to biophilia, it’s been shown to have harmful impacts on our health.  It can increase the risk of obesity, contribute to a lack of socialization, possibly to attention disorders and poor academic performance.  The evidence on screen time and ADHD, for example, is somewhat controversial and mixed.  There are certain studies that suggest a connection between screen time and ADHD and others that don’t, and even in the ones that do suggest a connection, it’s not always clear where the causality lies.  But on the Science Friday program I was listening to, Clifford Nass made a good point, which was that ADHD is actually a misnomer.  It’s not a deficit of attention.  We all have the same amount of attention, essentially.  ADHD is problem where the attention that we have to devote to any particular thing is spread over too many things.  And if you think about it, that’s exactly what multitasking does, right?  It spreads our attention over an increasing number of things.  If you’re writing a paper and then you have Facebook and Twitter open and your email and your phone and music, that’s dividing your attention among multiple different inputs.  And it’s not at all hard to see how doing that kind of thing on a regular basis could lead to behavior that would be labeled as ADHD.  There are about seven studies documenting the possibility of language delays in kids that are exposed to excessive electronic media under 2 years of age, and there’s not a single study showing that electronic media contributes positively to infant development.  There’s a lot of research showing that unstructured play time in the real physical world is far more important to the development of creativity, problem solving, reasoning skills, and motor skills than electronic media.

How the internet is rewiring our brains

And the most disturbing thing, I think, about all of this is research that suggests that using electronic media, playing video games, computers, and the Internet is not only changing our behavior, but it’s actually rewiring our brains… and not in a good way.  I’m reading this book right now called The Shallows: What the Internet Is Doing to Our Brains.  Maybe some of you have read it or heard of it.  It’s by a Pulitzer Prize finalist, Nicholas Carr, and the whole subject of the book is how the Internet is actually physiologically changing our brain.  It’s been long thought up until, I don’t know, maybe the past few decades that the mainstream theory was that the brain was static and it didn’t really change much in our adult lives.  There were, as far back as the ’50s, I think, a few heretics that were challenging that idea and maybe even further back, but really the dominant paradigm was that once you’re born and you go through the main developmental period, once you’re an adult, your brain is just set, and you can change your behavior, but it’s not going to have any impact on any real physical connections in your brain.  But now there’s overwhelming evidence that that’s not true and that the brain is actually quite plastic.  This means that the way that we think and behave can form new connections and really literally rewire our brains.  There’s a saying in neurology that neurons that fire together, wire together.  And that just reinforces what I just said.  There’s a great quote in the book where Nicholas Carr says: “If, knowing what we know today about the brain’s plasticity, you were to set out to invent a medium that would rewire our mental circuits as quickly and thoroughly as possible, you would probably end up designing something that looks and works a lot like the Internet.”  What he means is that the online environment involves a certain kind of stimuli that is exactly what would be likely to rewire the brain.  The online environment “promotes cursory reading, hurried and distracted thinking, and superficial learning,” and a state of mind which the poet T.S. Eliot called “distracted from distraction by distraction.”

I just want to take a pause here for a second and give everyone a little bit of a breather and let you know that I’m not suggesting we don’t use the Internet.  I mean, you wouldn’t even be listening to me if it wasn’t for the Internet.  I wouldn’t have my blog.  I wouldn’t be able to do the work that I do.  Of course, the Internet is here to stay.  I’m not a Luddite in any way.  I am suggesting that some of these new technologies have consequences, and as much as we love them and use them and benefit from them, that we should at least be open to considering what the science says about the consequences and possibly adjusting our behavior based on that.

So getting back into this, there’s another neuroscientist named Michael Merzenich, and I think he’s at UC San Diego.  And he’s repeatedly warned that our brains are “massively remodeled” by exposure to technologies like the Internet.  He said: “When culture drives changes in the ways that we engage our brains, it creates different brains.”  And he goes on to say that the use of the Internet and other electronic media has significant “neurological consequences.”  He did a great study to illustrate this.  He took two groups of people, one that was really experienced with the web and using Google, and the other group was people who were complete novices and hadn’t used the web or Google much.  I don’t even know where he found these people!  It just seems so ubiquitous now.  So he scanned their brains as these two different groups used the Internet, and the people with experience using the Internet had much higher levels of activity in an area of the brain called the dorsolateral prefrontal cortex, and the people with very little experience or no experience using the Internet and Google had almost no activity in that brain region.  And as a control, he had both groups read just linear text from a book, and they had not identical, but very similar levels of brain activity.  So that suggests there wasn’t any fundamental difference in the brains of these people.

Steve Wright:  Well, I hope he age-matched them because I think the only people he could have found that were novices were probably a little bit older.

Chris Kresser:  Yeah.  So then the remarkable thing about this study was that he repeated the test six days later, but in the interim the researchers had the people who were previously novices spend about an hour a day online, you know, using ‘the Google machine,’ and when they measured again, the novices’ prefrontal cortex that had been largely dormant before now showed extensive activity at a level almost equivalent to the prefrontal cortex of the people that were experienced.  So, just 5 hours over 5 days of Internet use completely changed levels of activity in the brain.  And he asked the question, “If our brains are so sensitive to just an hour a day [for 5 days] of computer exposure, what happens when we spend more time [online]?”

The intro, the whole kind of premise of this book that I’m reading, The Shallows: What the Internet Is Doing to Our Brains, is that Nicholas Carr, who is a writer and a journalist, an author, and someone who has spent his life reading books and writing books, was noticing over time that he was less and less able to focus on a book, to actually read a book from start to finish, because as he increasingly used electronic media and online technologies, his attention became more and more fragmented.  He found it more and more difficult to focus on any one thing for any significant length of time without wanting to get up and go check his email or take a call that was coming in or check his Facebook feed or whatever.  And he went around and he interviewed a bunch of other people and found that he wasn’t alone, that a lot of people were reporting a similar kind of experience, and people had mixed feelings about it.  Some people felt like:  I don’t need to read books.  I can get everything I need.  All the books are indexed on Google.  If I want to look something up, I can just type it into a search engine and it’s right there.  The Internet has unquestionably vastly expanded the amount of information that’s available to us.  I mean, I couldn’t even imagine how I could do the work that I do without the Internet and PubMed.  The kind of research that I do to write a blog post would probably have taken weeks or monthly to do before.  I mean, it’s really profound, and it’s incredible, the benefits that have come from it.  But there’s another side to the coin, as it turns out, and I’ve certainly noticed it in my own life.  If I have a day where I’m spending a lot of time online or on a computer, my mind feels different.  I definitely have a different experience of thinking.  My body feels differently, too, although that’s a slightly different topic.

My point in bringing this up is that, like I said before, I’m not suggesting we stop using computers or stop spending time online.  That’s pretty ridiculous for most of us.  I am suggesting there may be consequences to this new technology, and the consequences that we’re beginning to understand are not necessarily all beneficial.  And the hardest part about this is that it’s a problem without a solution.  Not all problems do have solutions.  It’s not always so easy and black and white.  And maybe a better label to use for this would be a predicament, because with a predicament you can respond to it in any number of ways, and that doesn’t necessarily make it go away, but it’s just a way that we are in relationship with it.

Quite a while prior to reading this book, I kind of recognized this on my own, and I had also read some other studies.  And then actually, I think, a while back when Tim Ferriss released his first book, I read a review about it where he talked about batching email.  And so I started doing things, like I turned off all notifications on my phone, and even the ringer off and I don’t leave it on unless I am available to take calls.  But I’ve turned off any email notifications, so if an email comes in, it doesn’t beep or show a badge or anything like that on my phone.  I’ve turned that off for my email program.  I keep my email program off except for distinct periods throughout the day.  And this is actually recommended by Clifford Nass, the neuroscientist at Stanford.  He suggests when you use email that you do it in distinct periods of at least 20 minutes.  Most people just check email periodically through the day.  They leave their email open.  If they’re working on something and an email comes in, they feel obligated to kind of go over and get it.  And as an interesting kind of side note, part of that is because that is rewarding.  We’ve talked about the food reward concept with Stephan Guyenet and the concept of reward as a psychological term.  Something that is rewarding makes us want to do more of it.  Email and all these kinds of notifications of something popping up on your feed or a tweet, that’s all rewarding from a psychological perspective.  It satisfies something for us, and it makes us want more.  The vast majority of people will just leave their email open, and any time something comes in, they go over and they check it, and that ends up distracting them, it dilutes their focus, makes them less effective in whatever else it is that they’re doing.  Tim Ferriss recommended just checking email two or three times a day and leaving it closed the rest of the time.  Clifford Nass’ recommendation isn’t a specific number of times that you check email but that when you do it, you devote at least 20 minutes to it as an activity, and then when you’re finished, you stop and don’t come back to it again until you’re ready to devote another 20 minutes.

You know, if I’m writing my book, for example, I have everything else closed.  There’s no Facebook, there’s no Twitter, no email.  Even for me, I’ve never really liked having music on when I write or read.  I prefer just to focus on what I’m doing.  And I’m still a big fan of books.  I actually read a lot of books.  I read them from start to finish.  And I don’t know why that is, and there’s no better or worse, it’s just that I’ve always been a book lover, and for whatever reason, that hasn’t stopped even in spite of how much I use computers and electronic media.

So I think there are little, small things that can be done like I just mentioned that can significantly mitigate the potentially harmful consequences of all this stuff.  And I think the added benefit there is that there aren’t that many opportunities for solitude anymore in our culture.  It used to be that if you were walking or maybe you were taking public transportation or riding a bike or you were in a car, there were moments where you just naturally had the opportunity to be alone with yourself and your thoughts, and I think that that’s really important for psychological and emotional and spiritual health and actually for creativity and deep thinking and just being a healthy person in this world.  But these days, the opportunities for that seem fewer and fewer if we have phones with us at all times, and I regularly see people checking their email and stuff walking down the street.  I’ve done that a few times myself, so I’m not perfect!  You know, we have access to all kinds of different programming in the car now.  If we’re on the BART, we have an iPad with us or a phone.  It just seems like there’s a lot less time now for those spontaneous moments of solitude and quietness and just being in our own little world, and I just wonder about the effects of that.  I think this is an unprecedented time.  There’s never been a time in human history where we’ve had that kind of disconnection from self and as much exposure to this kind of stuff as we have now.  And my idea is that it’s having a significant effect, and I think there’s a lot of research to support that, but that’s also just a hunch that I would have even if there wasn’t a lot of research to support it.

One thing that I find really interesting about this is how much of a backlash there often is.  The AAP, each year they update their guidelines, the American Association of Pediatricians.  They’re the ones who recommend no screen time under 2 years of age.  There are actually a lot of other groups that recommend that, too.  But each year when they publish them, there’s a huge, huge backlash.  I mean, there are articles on The Huffington Post and in women’s magazines, etc., from people saying this is ridiculous, it’s unrealistic, how can we be expected to parent without electronic media?  There are a lot of people who chime in and say that they don’t think that technology is harmful.  People are, of course, entitled to their opinions, but my question for them is, what is your opinion based on?  It’s one thing having an opinion, it’s another thing having an informed opinion, and there’s a lot of research, only a fraction of which we’ve gone over today, that suggests that there is harm to these technologies, especially when they’re used by kids under 2 years of age.  And there’s even a documented phenomenon, which I came across in one of the studies, that I thought was pretty fascinating called the third-person effect, which means that teenagers and adults often think that media influences everybody except themselves or their kids.  So when they interview people in these studies, they’ll acknowledge that media probably does influence people in these ways, but they think it doesn’t apply to them or their kids.  And again, all the research suggests that none of us are immune to these effects.

So I think that’s all I have to say about this.  Based on the reaction to things that I’ve posted along these lines in the past on Facebook, I imagine people will have some strong thoughts about this, so let’s open up a discussion on the comments thread of this podcast at my website, and I really do want to hear your thoughts about it, and I’m curious to see also any research that people want to share that might support a different viewpoint than the one that I presented here.  But yeah, let’s talk about it a little bit and talk about what the effects of this stuff are, maybe what your reactions to this are, what comes up for you when you listen to it.  Do you feel like there’s no way that you could change things, that multitasking is a fact of life for you and it’s just nonnegotiable?  Do you feel like it’s just impossible not to use electronic media for kids under 2?  I’m just curious.  I’d love to hear everyone’s thoughts, so let’s open up the discussion.

Steve Wright:  Aww, shoot.  Chris, what were you talking about?  I got lost in YouTube and my phone… sorry.  No!  I thought you hit a really good point there about how it’s almost a need now to schedule alone time.  I’m not good at it, for sure, but I know that when I have those days where I do have no screen time and alone time… and trust me, I’m kind of like you probably, where I have a queue of things I want to listen to on my phone, so even when I might have alone time, I’m too busy listening to some history podcast or health podcast or something.

Chris Kresser:  Yeah.  One of the biggest gifts of meditation for me is just the regular opportunity to just sit there and do absolutely nothing, just be completely alone with my sensations and thoughts and feelings and breath.  Earlier before we had Sylvie, I used to go on regular retreats, and that was even better because I got to do that for 10 days or even as much as 30 days.  Of course, that sounds like absolute torture to some people!  But it’s an incredible gift and opportunity for me, and I’m looking forward to it.  I think now that Sylvie’s getting a little older, both Elanne and I might be able to start going on retreats again.  That’s been a big part of Elanne’s life as well.  So yeah, I think that people do recognize this, of course, and know it in their own lives.  I mean, outdoor sports are really popular, and if you go rock climbing or hiking, things like that, of course, those are all opportunities to be in this kind of state that we’re talking about.  But given the reduction in the amount of time that people are spending in nature and the kind of perpetual increase in screen time, I just think it’s something that we need to bring our awareness to, and I think it’s actually probably a significant contributor to some modern diseases, and it’s just that it hasn’t really been talked about all that much in the public.

Steve Wright:  Well, I will say that I think that since we’re airing some of our dirty laundry about our habits, I think it’s rewired my ability to read books because when I was a kid, I would read a Hardy Boys book from start to finish and get that thing done in a few days, but I can tell you right now I’m in the middle of, like, six books, so I’m an ADD book reader right now.

Chris Kresser:  Yeah, and you’re not alone.  Like I said, Nicholas Carr was interviewing people who do that for a living, they read and write books for a living, and a lot of these folks are finding it really hard to finish books or even start books.  So I think you’re a step ahead of the game as far as that goes!

Yeah, so again, no judgment here, just questions.  I think there’s no downside to being aware, keeping our eyes and ears open, learning about this research and thinking about how we might make changes in our life that aren’t drastic, necessarily, or dramatic, but that do maybe mitigate some of the impact of this stuff in our own lives and in our kids’ lives.  Sylvie is almost 2 now.  She’s 21 months, and she really has had almost no exposure to screens.  That’s just the decision we made early on, and the exceptions to that are that we will occasionally do a video Skype with my parents or with Elanne’s parents, so of course, there’s a little bit of screen time there, but outside of that, she doesn’t have any screen time.  And I’ll tell you, there have definitely been times where we’ve been like:  Let’s just put her in front of the TV!  Where we’re going nuts or we’re at the end of our rope and we just wish we could plop her in front of the TV and turn it on and have it babysit her, but always in the back of my mind there was that kind of nagging voice that had read all the research that I’ve read about that.  And surely doing that a few times isn’t going to make a big difference, but I felt like it was kind of a slippery slope, and if we did it a couple of times, we might get pretty addicted to it, so we’ve just avoided it.  You know, this is the sample size of n=1, we have nothing to compare it to, and I wouldn’t even begin to try because it’s ridiculous, but I at least know that it’s possible.  And of course it’s possible because we were all raised and there were lots of generations that came before us that were raised without any access to screens.

Steve Wright:  Well, I commend you on that because I know a lot of people who would have a really hard time doing that.  And I don’t have any experience with kids, but I can tell you that that would definitely be difficult.

Chris Kresser:  Yeah, 90%, so I’m in the minority for sure, and once again, it’s not a value judgment.  It’s just something to continue to be aware of.  I think that’s it.  We’re coming up to an hour here.  Like I said, I’d like to hear your comments on both the vitamin D issue and the electronic media and rewiring our brain issue, and next time, I know we have a lot of questions.  Steve asked me to let you know that we have over a hundred questions in the backlog, and we’ll try to get through them.  It’s hard because I only do this twice a month and occasionally I have things I want to talk about like this, so I realize we don’t make as much progress as some other Q&A-oriented shows that are going four times a month.  So thanks for your patience and thanks for continuing to send in your questions.  At the very least, even if I’m not able to answer them, it tells me what all of you are thinking about, what’s important to you, and that actually helps me craft the show, so please do keep them coming.

Steve Wright:  Yeah, and thanks for listening.  I think it’s been a great show, Chris.  Thanks for broadening my horizons both on what the Internet is doing to me and furthering this vitamin D thing because I think everyone is so quick to jump on the black or the white side on all these health issues, so just keeping an open mind and remembering that it’s such a gray scale on all these issues, I think, is really important.

Chris Kresser:  Yeah, I think so, too.  And let us know what you think of the audio quality, too.  We’d love to hear from you about that.

Steve Wright:  Awesome.  Well, thanks, everyone, for listening to this show.  Again, as Chris mentioned, please keep sending us the questions.  We get them; we read them all.  You can send us more questions at ChrisKresser.com using the podcast submission link.  And if you enjoyed listening to the show, especially if you’re doing this on iTunes right now, please head over to the iTunes Store and leave us a review.  It helps boost our rankings in iTunes, and lets other people listen to the show, kind of spreads the word about it.

Note: I earn a small commission if you use the links in this article to purchase the products I mentioned. I only recommend products I would use myself or that I use with patients in my practice. Your purchase helps support this site and my ongoing research.

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This is the final article in the Diet-Heart Myth series I’ve been writing over the past several weeks. If you missed the previous articles, you can find them on the special report page for heart disease.

Ben Franklin said, “An ounce of prevention is worth a pound of cure.” Heart disease is no exception. According to the INTERHEART study, which examined cardiovascular risk factors in 51 countries, 9 out of the 10 strongest risk factors for heart disease are modifiable by changes in diet and lifestyle. (1)

While taking action now does not guarantee that you’ll never get heart disease (as age is perhaps the strongest risk factor), it does vastly improve your chances of avoiding it or at least delaying it significantly. In this article, I’ll teach you how to do that in three simple steps: Eat a Heart-Healthy Diet, Live a Heart-Healthy Lifestyle, and Boost Your Heart-Healthy Nutrients.

3 simple steps to living a heart healthy lifestyle that your doctor has never told you about.

Eat a Heart-Healthy Diet

When most people hear the phrase “heart-healthy diet”, they think of egg-white omelettes, a salad with no dressing or similar low-fat, low-cholesterol fare. But if you’ve been reading this series, or my blog in general, you know better. The “Paleo Template” approach I’ve written about here is an excellent starting place. It includes all of the necessary micronutrients in their most bioavailable form, emphasizes an optimal balance of fats, eliminates highly processed and refined foods, and reduces other food toxins that interfere with nutrient absorption. On the other hand, the American Heart Association’s “heart healthy” diet emphasizes nutrient-poor foods such as whole grains and vegetable oil, and unnecessarily restricts nutrient-dense foods like red meat, animal fat and cholesterol.

But which version of the “Paleo Template” is best for preventing heart disease? In this series we’ve been focusing on LDL particle number as one of the primary drivers of atherosclerosis. We also discussed the five main causes of elevated LDL-P, including insulin/leptin resistance, genetics, poor thyroid function, infections and leaky gut. If you have elevated LDL-P while on a Paleo diet, the key is to first discover what’s causing it and then tailor your diet accordingly. In this article, I’m going to focus on insulin/leptin resistance and genetics, since those are the two most common causes of elevated LDL-P that I see in my practice.

Insulin/leptin resistance

In this case, the best approach is often a low-carb Paleo diet. When I say low carb, I generally mean between 50–100 grams of carbohydrate per day in the form of fruit and starchy vegetables like sweet potatoes, potatoes, plantain, yuca and taro. I do not count non-starchy vegetables toward the carbohydrate intake, because I don’t believe they make a significant enough contribution to matter. The purpose of this approach is to improve insulin and leptin sensitivity and promote weight loss, which will in turn decrease LDL-P.

Genetics

If you have high LDL-P, but normal triglycerides, HDL, small LDL-P and your lipoprotein insulin resistance (LP-IR) score on the NMR LipoProfile is normal, and you’ve ruled out thyroid problems, infections and leaky gut, than it’s very likely that you have one of the many genetic variants that can lead to increased LDL particle number. In this case, a low-carb Paleo diet will often increase—rather than decrease—LDL-P. In my practice I will often recommend what I call a “Mediterranean Paleo diet” in these cases. This means following the basic Paleo approach, but reducing intake of fat and increasing intake of fruit and starchy vegetables. You can still eat fat as it naturally occurs in food, but try not adding as much additional fat to meals, and using more monounsaturated fat than saturated fat. In many cases this will decrease LDL-P quite significantly.

The trickiest situation is when someone has both insulin and leptin resistance and a genetic issue. A low-carb diet will usually drive up LDL-P in that situation, but it will improve many other markers that are also risk factors for heart disease, including triglycerides, HDL, fasting insulin, fasting glucose, etc. So I will usually recommend a low-carb diet for these patients, and if their LDL-P goes up, try to use natural therapies to bring it down.

Live a Heart-Healthy Lifestyle

Physical activity

Exercise has been shown to reduce LDL particle concentration even independently of diet. (1) Regular exercise prevents the development and progression of atherosclerosis, improves lipids, and reduces vascular symptoms in patients that already have heart disease. The benefits of exercise are related to maintenance of body weight or weight loss, blood pressure control, return of insulin sensitivity, and beneficial changes in lipids, all of which in turn promote endothelial stabilization and vascular health.

In addition to distinct periods of exercise, it’s also important to sit less and stand and walk more. In fact, some research suggests that this “non-exercise” physical activity may have a greater impact on our cardiovascular health than exercise. Dan’s Plan has some fantastic recommendations for physical activity, as well as a great software and hardware-based tracking system.

Sleep

I have come to believe that chronic sleep deprivation is one of the most pernicious—yet under-recognized—contributors to the modern disease epidemic. Sleep deprivation has been associated with weight gain, insulin resistance, increased appetite and caloric intake, overconsumption of highly palatable and rewarding food, decreased energy expenditure and a reduced likelihood of sticking with healthy lifestyle behaviors. Sleep duration and quality are inversely associated with blood pressure in epidemiological studies, and high blood pressure is one of the strongest independent risk factors for cardiovascular disease (CVD). (2) Finally, the Nurses Health Study found that those who reported fewer than 5 hours of sleep at night had a 38% greater risk of coronary heart disease (CHD) than those reporting 8 hours of sleep. (3)

For tips on how to improve your sleep, see my article “Sleep More Deeply“.

Stress management

Stress increases the risk of cardiovascular disease in numerous ways. It increases intestinal permeability, impairs blood sugar control, depresses immunity (which increases the risk of infection), contributes to fat storage in the liver, and promotes consumption of comfort and junk foods. But perhaps the most significant contribution stress makes to CVD is that it promotes inflammation. Stress has been shown to increase circulating inflammatory markers like C-reactive protein (CRP) and interleukin-6 (IL-6), both of which are associated with heart disease (4). On the other hand, stress management can have a profound impact on heart disease risk. One recent randomized trial showed that regular meditation decreased the risk of death from heart attack, stroke and all causes by 48%—a much greater reduction than what is observed with statins even in the highest risk population. (5)

Boost Your Heart-Healthy Nutrients

In addition to the basic heart-healthy versions of the Paleo template I mentioned above, there are several specific foods/nutrients that have been shown to improve cardiovascular health.

Cold-water, fatty fish

Cold-water, fatty fish are an excellent source of EPA and DHA, long-chain omega-3 fats with several cardiovascular benefits. An analysis of randomized trials since 2003 suggests that regular fish consumption or consumption of fish oil would reduce total mortality or deaths from all cause by 17%. (6) This is remarkable when you consider the fact that statin drugs only reduce total mortality by 15%, and even then, only in certain populations.

Monounsaturated fat

Monounsaturated fats have been shown to reduce LDL and triglycerides and increase HDL. They also decrease oxidized LDL, reduce oxidation and inflammation in general, lower blood pressure, decrease thrombosis, and they may reduce the incidence of heart disease. (7) The best sources of monounsaturated fat are olives, olive oil, macadamia nuts, and avocados.

Antioxidant-rich foods

Antioxidant-rich foods protect against heart disease in a number of important ways. Our antioxidant defense system is what protects us from oxidative damage, which as you now know is a major risk factor for heart disease. Strengthening this system has two sides: reducing our exposure to oxidative stress and increasing our intake of antioxidant-rich foods. When most people think of antioxidants, they think of fruits and vegetables like dark, leafy greens and fruits like berries. But while it’s true that these foods are rich in antioxidants, what a lot of people don’t know is that red meat and organ meats are also very rich in important antioxidants that aren’t found in significant amounts in plant foods, like CoQ10 and retinol, which is preformed vitamin A. A good rule of thumb is to eat the rainbow, choosing a variety of colors of fruits and vegetables, as well as organ meats, meats, eggs, and grass-fed dairy.

Polyphenol-rich foods

Polyphenols are a diverse class of molecules made by plants, certain fungi, and a few animals. They serve a lot of purposes including defense against predators and infections, defense against sunlight damage, chemical oxidation, and coloration. The color, in fact, of many fruits and vegetables like blueberries, eggplants, red potatoes, and apples comes from polyphenols. Some of the best studied polyphenol-rich foods are tea, especially green tea; blueberries; extra-virgin olive oil; red wine; citrus fruits; hibiscus tea; dark chocolate; coffee; turmeric; and other herbs and spices. Polyphenol-rich foods have been shown to have a number of beneficial health effects. For example, dark chocolate has been shown to lower blood pressure and LDL cholesterol and improve insulin sensitivity, red wine has been shown to prevent the increase in oxidized fats that occur after consuming a meal high in oxidized and potentially oxidizable fats, several studies have shown that hibiscus tea lowers blood pressure in people with hypertension, and blueberries have been shown to lower blood pressure and oxidized LDL in men and women with metabolic syndrome. (8)

Nuts

Some studies have shown that nut consumption may reduce the risk of cardiovascular disease. In a recent analysis of NHANES data from 1999 to 2004, investigators found that nut consumption was associated with a decrease in a wide range of cardiovascular disease risk markers, including body mass index, waist circumference, and systolic blood pressure, compared to non-consumers of nuts. (9) This is observational data so we can’t be sure that it was the nuts, rather than some other factor that wasn’t adequately controlled for, that led to the improvements. That said, a review of five large prospective studies (including NHANES) as well as clinical trials examining the effects of nut consumption on lipid parameters found similar results. (10) I favor macadamia nuts, almonds and hazelnuts because they are lower in omega-6 linoleic acid, which research suggests may contribute to CVD when consumed in excess.

Soluble fiber

In the NHANES study, subjects followed for more than 19 years with the highest quartile of dietary soluble fiber intake had a 15% lower risk of heart disease and had a 10% lower risk of cardiovascular events. (11) Soluble fiber binds bile acids or cholesterol; upregulates LDL receptors in the liver; increases clearance of LDL; inhibits fatty acid synthesis by producing short-chain fatty acids like acetate, butyrate, and propionate; improves insulin sensitivity; and increases satiety with lower overall energy intake. (12)

Summary

I hope you’ve enjoyed the Diet-Heart Myth series, and that the information I’ve presented will help protect you and those you love against heart disease. I’ve done my best to cover the most important steps you can take, both in terms of diagnosis and treatment. That said, cardiovascular disease is a complex, multifactorial process and it’s difficult to give it the attention it deserves in a blog series. That’s why I created the High Cholesterol Action Plan. It’s a 9-week, digital course that goes into much more depth on these topics than I was able to go into here, including additional tests that help determine your risk, natural alternatives to statins, and a step-by-step framework that helps you determine your own, customized “action plan”. Click here to learn more about it and sign up.

Here is The Roundup, Edition 5, bringing you the best from around the web from the past two weeks!

Blast from the Past

Last May (2012), I wrote an entire series on salt, including the history of salt in the human diet, the dangers of salt restriction, and my recommendations for a healthy salt intake. There’s no evidence that adding salt to taste to a whole foods, Paleo diet is unhealthy, and salt restriction to the level recommended by the American Heart Association (AHA) is not only completely unnecessary, it’s potentially harmful. There are far more effective ways to reduce blood pressure and the risk for heart disease and stroke than salt restriction, such as increasing dietary intake of potassium, magnesium, and calcium.

Now, a New York Times article explains how a new expert committee, commissioned by the Institute of Medicine (IOM) at the request of the CDC, confirmed that there’s no rationale restricting sodium intake to 2,300 milligrams a day—let alone the AHA target of 1,500 mg per day. The IOM committee also agrees that a sodium intake this low could increase rates of heart attacks and the risk of death in certain populations. It’s incredible to me that this is still considered a controversial topic and that there is so much disagreement between various health organizations on how much salt is “too much” for the general population. It’s perfectly reasonable for most people to consume between 3-4 grams per day, which is right around the world average for salt intake (3,400 mg/day or ~1.5 tsp salt).

Hopefully this (non) issue will be settled soon, and we can focus our attention on the dietary components that really do make a difference in the general population’s health.

Research Report

• New evidence suggests that gluten intolerance may drive at least some cases of IBS.
• Research finds that sunlight prolongs lifespan by lowering blood pressure, demonstrating how the benefits of sun exposure outweigh the risks.
• A new study suggests lowest risk of death occurs at vitamin D levels between 20-36 ng/mL. (Note that 20-30 ng/mL is deficiency according to current standards. I will discuss this on my next podcast.)
• A hospital survey found that kids living in the U.S. who were born elsewhere are 59 percent less likely to have allergic diseases, but their risk increases with time spent in the country.

Worth A Look

• Nourished Kitchen: Jenny explains why she drinks full fat, local, raw milk.
• Mark’s Daily Apple: The top 8 most common reactions to your grain-free diet, and how to respond.
• Forbes.com: A new app allows you to easily boycott Monsanto products—not just food.
• SexyBack Summit: Sean Croxton hosts another great summit, this time focused on all aspects of sexual health.

For the Foodies

• Against All Grain: Watermelon Mint Lemonade
• Food Renegade: Cilantro Lime Chicken Salad on Avocado
• Homemade Mommy: Ghee Mayonnaise
• PaleOMG: Honey Mustard Crunchy Chicken Plantain Salad
• Rubies and Radishes: Chorizo Mashed Yams
• Health-Bent: Italian Sweet & Sour Pork Tenderloin with French Pork & Beans

To read more about heart disease and cholesterol, check out the special report page.

Cardiovascular disease is one of the most misdiagnosed and mistreated conditions in medicine. In the first article in this series, I explained the evidence suggesting that eating cholesterol and saturated fat does not increase the risk of heart disease. In the second article, I explained it’s not the amount of cholesterol in your blood that drives heart disease risk, but the number of LDL particles. In the third article, I discussed the five primary causes of elevated LDL particle number.

In this article, I will debunk the myth that statin drugs save lives in healthy people without heart disease, and discuss some of the little known side effects and risks associated with these drugs.

Myth #3: Statins save lives in healthy people without heart disease

Statins have been hailed by many in the conventional medical establishment as wonder drugs, with some physicians going as far as suggesting they should be added to the water supply. (The doctor that made that particular suggestion is named John Reckless – I kid you not.) But are statins really the wonder drugs they’ve been made out to be?

Are statins really the wonder drugs they’ve been made out to be?

Before we dive into the statistics on statins, I need to briefly explain the difference between relative and absolute risk reduction. Researchers and pharmaceutical companies often use relative risk statistics to report the results of drug studies. For example, they might say “in this trial, statins reduced the risk of a heart attack by 30%”. But what they may not tell you is that the actual risk of having a heart attack went from 0.5% to 0.35%. In other words, before you took the drug you had a 1 in 200 chance of having a heart attack; after taking the drug you have a 1 in 285 chance of having a heart attack. That’s not nearly as impressive as using the 30% relative risk number, but it provides a more accurate picture of what the actual, or “absolute” risk reduction is.

With that in mind, let’s take a closer look at the efficacy of statins in two broad groups of people: those with pre-existing heart disease, and those without pre-existing heart disease. In the medical literature, these groups are referred to as “secondary prevention” and “primary prevention”, respectively.

Secondary prevention (those with pre-existing heart disease)

There’s little doubt that statins are effective in reducing heart attacks and deaths from heart disease in people who already have heart disease. Several large controlled trials including 4S, CARE, LIPID, HPS, TNT, MIRACL, PROV-IT and A to Z have shown relative risk reductions between 7% on the low end in MIRACL and 32% on the high end in 4S, with an average risk reduction of about 20%.

However, absolute risk reductions are much more modest. They range from 0.8% in MIRACL on the low end to 9% in 4S on the high end, with an average of 3%.

An analysis by Dr. David Newman in 2010 which drew on large meta-analyses of statins found that among those with pre-existing heart disease that took statins for 5 years (1):

• 96% saw no benefit at all
• 1.2% (1 in 83) had their lifespan extended (were saved from a fatal heart attack)
• 2.6% (1 in 39) were helped by preventing a repeat heart attack
• 0.8% (1 in 125) were helped by preventing a stroke
• 0.6% (1 in 167) were harmed by developing diabetes
• 10% (1 in 10) were harmed by muscle damage

A heart attack or stroke can have a significant negative impact on quality of life, so any intervention that can decrease the risk of such an event should be given serious consideration. But even in the population for which statins are most effective—those with pre-existing heart disease—83 people have to be treated to extend one life, and 39 people have to be treated to prevent a repeat heart attack.

Moreover, these results do not apply to all populations across the board. Most studies have shown that while statins do reduce cardiovascular disease (CVD) events and deaths from CVD in women, they do not reduce the risk of death from all causes (“total mortality”). (2)

Nor do these results apply to men or women over the age of 80. Statins do reduce the risk of heart attack and other CVD events in men over the age of 80, and especially at this age, these events can have a significant negative impact on quality of life. However, the bulk of the evidence suggests that statins don’t extend life in people over 80 years of age, regardless of whether they have heart disease, and the highest death rates in people over 80 are associated with the lowest cholesterol levels. (3), (4)

Primary prevention (those without pre-existing heart disease)

Statins do reduce the risk of cardiovascular events in people without pre-existing heart disease. However, this effect is more modest than most people assume. Dr. Newman also analyzed the effect of statins given to people with no known heart disease for 5 years (5):

• 98% saw no benefit at all
• 1.6% (1 in 60) were helped by preventing a heart attack
• 0.4% (1 in 268) were helped by preventing a stroke
• 1.5% (1 in 67) were harmed by developing diabetes
• 10% (1 in 10) were harmed by muscle damage

These statistics present a more sobering view on the efficacy of statins in people without pre-existing heart disease. They suggest that you’d need to treat 60 people for 5 years to prevent a single heart attack, or 268 people for 5 years to prevent a single stroke. These somewhat unimpressive benefits must also be weighed against the downsides of therapy, such as side effects and cost. During that hypothetical 5 year period, 1 in 67 patients would have developed diabetes and 1 in 10 patients would have developed muscle damage (which can be permanent in some cases, as we’ll see later in this section).

In addition, while statins do moderately reduce cardiovascular events such as heart attack in people without heart disease, they’ve never been shown to extend lifespan in this population. This is true even when the risk of heart disease is high. In a large meta-analysis of 11 randomized controlled trials by Kausik Ray, MD and colleagues published in the Archives of Internal Medicine, statins were not associated with a significant reduction in the risk of death from all causes. (6)

This trial included 65,000 people without pre-existing heart disease but with intermediate to high risk of heart disease. It was important because it was the first review that only included participants without known heart disease. Previous studies suggesting that statins are effective in reducing death in people without pre-existing heart disease included some people that did have heart disease, which would have skewed the results.

The lack of significant effect on mortality is even more interesting in light of the fact that LDL cholesterol levels did decrease significantly in the statin group; the average LDL level in those taking placebo was 134 mg/dL and the average in the statin-treated patients was 94 mg/dL—roughly 30% lower. Yet in spite of this marked reduction in LDL cholesterol in the statin group, there was no difference in lifespan between the two groups. This is yet another line of evidence suggesting that the amount of cholesterol in LDL particles is not the driving factor in heart disease.

A meta-analysis of statin trials in people without heart disease by the prestigious Cochrane Collaboration came to a similar conclusion. (7) They also observed that all but one of the clinical trials providing evidence on this issue were sponsored by the pharmaceutical industry. This is significant because research clearly indicates that industry-sponsored trials are more likely than non-industry-sponsored trials to report favorable results for drugs because of biased reporting, biased interpretation, or both. (8)

Adverse effects of statins

If statins were harmless and free, then it wouldn’t matter how many people need to be treated to prevent a heart attack or extend someone’s lifespan. But statins are not free, nor are they harmless. Statin use has been associated with a wide range of side effects, including myopathy (muscle pain), liver damage, cataracts, kidney failure, cognitive impairment, impotence and diabetes.

Unfortunately, studies show that physicians are more likely to deny than affirm the possibility of statin side effects, even for symptoms with strong evidence in the scientific literature. (9) Assuming that physicians would likely not report the adverse reaction in these circumstances, it’s probable that the incidence of statin side effects is much higher than the reported rates.

One of the most troubling side effects of statins that has only recently become apparent is their potential to increase the risk of diabetes, especially in women. A study by Dr. Naveed Sattar and colleagues published in The Lancet in 2010 examined 13 randomized clinical trials involving over 90,000 patients taking statins. They found that statin use was associated with a 9% increased risk in developing diabetes. Note that this is a relative risk, so the absolute risk of developing diabetes while taking a statin is very low. That said, observational data from the Women’s Health Initiative found a 48% increased risk of diabetes in healthy women taking statins after adjusting for other risk factors. (10)

To summarize:

• The only population that statins extend life in are men under 80 years of age with pre-existing heart disease.
• In men under 80 without pre-existing heart disease, men over 80 with or without heart disease, and women of any age with or without heart disease, statins have not been shown to extend lifespan.
• Statins do reduce the risk of cardiovascular events in all populations. A heart attack or stroke can have a significant, negative impact on quality of life—particularly in the elderly—so this benefit should not be discounted.
• However, the reductions in cardiovascular events are often more modest than most assume; 60 people with high cholesterol but no heart disease would need to be treated for 5 years to prevent a single heart attack, and 268 people would need to be treated for 5 years to prevent a single stroke.
• Statins have been shown to cause a number of side effects, such as muscle pain and cognitive problems, and they are probably more common than currently estimated due to under-reporting.

My intention here is not to suggest that statins have no place in the treatment of heart disease, but rather to give you the objective information you need to decide (along with your doctor) whether they are appropriate for you. The decision whether to take them should be based on whether you have pre-existing heart disease, what your overall risk of a heart attack is, how healthy your diet and lifestyle is, what other treatments you’ve already tried, and your own risk tolerance and worldview. It’s clear that statins reduce heart disease as well as the risk of death in those that have already had a heart attack, so if you’re in this group and you’ve already tried diet and lifestyle interventions without much impact on your lipid or inflammatory markers, you are more likely to benefit.

In the next and final article of this series, I’ll discuss three steps to preventing and reversing heart disease naturally, without drugs.

Are you suffering from low libido? Has your sex drive gradually drifted away? Are you looking for ways to connect more deeply with your partner, and cultivate a more rewarding and satisfying sex life?

If you answered yes to any of these questions, you should definitely check out Sean Croxton’s upcoming SexyBack Summit. He’s assembled a group of experts in all aspects of sexual health, including balancing hormones, supercharging sex drive, cultivating intimacy and connection, optimizing nutrition and fitness, and boosting fertility.

The summit will consist of 24 video slideshow presentations, including talks by Dr. Sara Gottfried, Paul Check, Jane Bennett, Elliot Hulse, Dr. Jen Landa and yours truly. The title of my talk is “How Stress Sabotages Your Sex Drive—And What to Do About It.” I’ll discuss the intricate connections between the thyroid, adrenals and ovaries/gonads in both men and women, and how imbalances in one system can lead to dysfunction in the others. Here’s a sampling of other presentations that will be available:

• Get in the Mood, Stay in the Mood by Dan Kalish
• Low T: Causes, Symptoms and Solutions by Reed Davis
• 50 Shades of Better Sex: Secrets of a Harvard Gynecologist by Dr. Sara Gottfried
• Natural Birth Control Alternatives by Jane Bennett
• Chasing the Big O: Overcoming the Inability to Orgasm by Cynthia Pasquella

In case you’re not familiar with the online summit format, here’s how it works. The summit startstakes place over six days, beginning on May 19th and concluding on May 26th. Each day will feature three to four presentations, which can be watched for FREE during a 24-hour period (9am to 9am Pacific). At 9am each morning, the previous day’s presentations are taken down and the next day’s go up. This means you can watch the entire event free of charge. Pretty cool, huh?

Sean is kicking the SexyBack Summit off with some cool free videos covering the top 5 ways to supercharge your sex drive. There’s a video for men (with functional medicine expert Reed Davis), and another for women (with celebrity nutritionist Cynthia Pasquella). To watch the videos and register (for free) for the Summit, just CLICK HERE.

If you’re subscribed to my email list, I’ll send out an email the day before my talk (which is happening on Day 6). I’ll also post reminders on Facebook and Twitter.

I hope you enjoy the Summit!

Note: I may earn a commission if you use the links in this article to purchase any products or programs I mentioned. I only recommend products I would use myself or that I use with patients in my practice. Your purchase helps support this site and my ongoing research.

In this episode I discuss a couple of interesting recent studies, and answer some questions. Enjoy!

In this episode, we cover:

1:35 What Chris ate for breakfast
6:27 Early evidence for meat consumption
18:33 Solving the cholesterol controversy
38:22 More details from Chris’s daily routine (and more treadmill desk)
44:00 Additional sources of magnesium
48:35 When should I stop breastfeeding?
52:49 What to do about anxiety during pregnancy

Links We Discuss:

• Oldowan hunting behaviors at Kanjera South – John Hawks Blog
• Lipids and lipoproteins and risk of different vascular events in the MRC/BHF Heart Protection Study

Full Text Transcript:

Steve Wright:  Hey everyone, welcome to another episode of the Revolution Health Radio Show.  This show is brought to you by ChrisKresser.com, and I’m your host, Steve Wright from SCDLifestyle.com.  With me is integrative medical practitioner and healthy skeptic Chris Kresser.  Chris, how are you doing today?

Chris Kresser:  I’m great, Steve.  It’s absolutely gorgeous today.  It’s been gorgeous the last several days, like in the high 70s, low 80s.  I’ve just been spending a lot of time outside with Sylvie, going on walks in the woods near my house.  Having grown up in Southern California and being used to 300 days of sunshine a year, I have to say this is happy weather for me!

Steve Wright:  Yeah, I actually just got back from a little vacation to Colorado, and even though while I was there it was everything from 25 degrees all the way to 80, it was sun shining every day, and it was the most sun I have seen in the last six months.

Chris Kresser:  Yeah, that’s the thing about Colorado, huh?  It’s very sunny there even when it’s freezing cold a lot of the time in the winter.

Steve Wright:  Yeah, it was beautiful.

Chris Kresser:  Great.  So I think it’s going to be another Q&A show today, but I have a couple studies we’re going to talk about first.

What Chris ate for breakfast

Steve Wright:  OK, well, before we get into the studies, did you have anything special for breakfast today?

Chris Kresser:  Well, I don’t know if it’s special.  I liked it.  I had two duck crépinettes.

Steve Wright:  A what?

Chris Kresser:  A crépinette.

Steve Wright:  Oh.

Chris Kresser:  This is from the charcuterie that I frequent at the farmers’ market.  It’s called The Fifth Quarter.  This guy Scott makes fantastic sausages and salamis and duck and liver pâtes and all kinds of artisanal meats.  And I may get this wrong in terms of the precise description, but a crépinette is like a patty of meat and spices that’s then wrapped in pork fat.  So I just cooked them in a pan.  These ones were duck.  He also makes some lamb crépinettes and, I think, pork crépinettes as well.  They’re really tasty.  They’re amazing.  And then I had some taro sliced really thin with a mandolin and roasted in a little bit of duck fat.  And I had some steamed broccoli with a little bit of olive oil and then a little bit of beet kvass to wash it all down.

Steve Wright:  Sounds pretty gourmet.

Chris Kresser:  It was good.  I’m doing my two-meal-a-day thing today.  It just seems to be the pattern I’m in right now, and it’s working for me.

Steve Wright:  Awesome.  Well, whenever you want to invite me over for breakfast, I’ll try one of these crépinettes.

Chris Kresser:  Anytime.  I think you’d like it.

Steve Wright:  Well, anything wrapped in pork fat, I think, is a hit for myself or anyone listening to this show.

Chris Kresser:  It’s hard to argue with, huh?

Steve Wright:  Yeah.  OK, well, before we get rolling into the studies, I want to tell everybody about Beyond Paleo, Chris.  So I don’t know if you need to… We’re not in the closet today, right?

Chris Kresser:  That’s right.  We’re out of the closet.  I’m committed to making the audio as good as I possibly can, but I discovered there’s a limit to that commitment.  However, I will say that one of our listeners, Mike, stepped up.  He has a lot of audio experience, and he generously donated a lot of his time to explaining several different ideas.  First of all, he said the audio for our show is great, and that’s a testament to you and Jordan and all the help you guys have given me in making this a fantastic show already.  But he said there were a few things we could do just to reduce the echo, which is kind of the main problem that some people have noticed.  So I bit the bullet, bought some extra sound-dampening equipment that I can set up.  I don’t have it yet.  It’s going to be here in time for the next show.  And I think once we get that set up, the audio is just going to be perfect, so I’m excited about that.  And I’m excited to be back in my office overlooking the redwood trees.  It’s much more picturesque than the closet, I’ll tell you.

Steve Wright:  Than a t-shirt?

Chris Kresser:  Yeah.

Steve Wright:  OK, awesome.  Well, huge thanks to Mike, and we’re doing our best to make this the best sounding as well as the best content on the web.  Chris, go ahead and take a break here.  I want to tell everyone about Beyond Paleo.  So if you’re new to this podcast, if you’re new to the paleo diet, or maybe you’re just someone who’s interested in optimizing your health, you’re going to want to check out what over 30,000 other people have already signed up for and started to read.  It’s called Beyond Paleo, and it’s a free 13-part email series on burning fat, boosting energy, and preventing and reversing disease without drugs.  To sign up, head over to ChrisKresser.com, and look for the big red box.  In that box, go ahead and enter your name and your email address, and Chris will go ahead and ship off the first email to your right away.  It’s pretty awesome.  I would highly recommend you start reading this series right away.

Chris, if people want more info from you in between podcasts, they can head over to Facebook and Twitter, right?

Chris Kresser:  That’s right.  Yeah, Facebook, I have a really vibrant community there, lots of great discussion.  I post a lot of studies and just things I’m thinking about throughout the week that don’t make it to my blog, and I do the same thing on Twitter.  So definitely join us there if you’re on Facebook and Twitter.

Steve Wright:  And to get there, if you’re just listening to this on iTunes, go to Facebook.com/ChrisKresserLAc or Twitter.com/ChrisKresser.

Chris Kresser:  All right.

Steve Wright:  Let’s do some studies!

Early evidence for meat consumption

Chris Kresser:  Yeah.  Those of you who follow me on Facebook and Twitter may have already seen my link to these studies, but there was one anthropological study I want to talk about that John Hawks, an anthropologist whose blog I follow and some of you may, reported on earlier in the week.  The earliest evidence of humans butchering animals for meat with stone tools is about 2.6 million years old, and that’s kind of the background for this study.  But the issue with that is that a lot of that could have been scavenging kills from other animals.  So instead of humans purposefully hunting the animals themselves and then eating them, they came across a carcass from an animal that had been hunted by some other prey animal, like a lion, for example.  That in a lot of ways, as John Hawks pointed out, is no less impressive because presumably humans were having to, in many cases, compete with these other animals for the carcass, whether the animals were there at the time or they came back, so it’s still a pretty amazing testament to the collective intelligence and teamwork of our distant ancestors.  But there were a lot of questions still then about whether we were hunting animals ourselves versus just encountering the carcasses that had already been killed.

The first really good evidence for actual hunting is about 1.8 million years old, and that was found at the Olduvai Gorge in Tanzania.  This new study that John Hawks talked about has made a big contribution to our understanding in this area because it analyzed fossil remains from Kenya, from Kandera South, which is an assemblage of artifacts and animal bones from about 2 million years ago.  And this was during what’s referred to as the Oldowan period, which is the earliest stone tool industry, which lasted from about 2.6 million years ago to about 1.7 million years ago.  Now, what was different about this study compared to some of the other ones that have been done before is that the researchers used some pretty smart methods to determine that the animal bones that were found at the site were from animals that were actually hunted and killed by humans rather than scavenged.  And they did this by looking at tooth and cut marks on the bones.  Carnivores who get to chew on bones for a while once they kill an animal, they tend to leave the middle of the bones covered in tooth marks, but if humans get access to the carcass early, they strip off the meat from the midshafts, and then they break those shafts into bits, which leaves different marks on the bones.  So in this study, they compared the tooth and cut marks on the bones that they found, and at this particular site they found marks that were much more consistent with what happens when humans get access to the carcass first, which, of course, suggested that humans had hunted and killed these animals.

Another interesting finding in this study is how our ancestors ate the animals that they killed.  A lot of these animals were really too large to carry in their entirety back to a central place like a cave, campsite, living area where they could all share it.  So what they did is they dismembered the animals on-site where they were hunted, and they only carried back certain parts of the animals, which would, of course, been the parts that were favored and easier to transport.  The parts that they brought back were the legs and the heads, and then they left the rest of the body behind.  So the legs are pretty obvious.  Those of us who eat meat often eat the legs of animals, and they’re some of the best parts there.  But the heads may not be as obvious at least at first glance, but I’ll read from a quote from the paper to explain why they did this, so it says:

But why acquire, transport, and process an abundance of medium-sized heads?  In living animals, these remains contain a wealth of fatty, calorie-packed, nutrient-rich tissues: a rare and valuable food resource in a grassland setting where alternate high-value foodstuffs (fruits, nuts, etc.) are often unavailable.

So essentially the heads contain brains, and brains are very rich in fatty acids, and in particular, the long-chain omega-3 fat DHA, which increasing evidence suggests is essential, meaning not only very important, but the technical definition of essential here from a dietary perspective means a nutrient that we need for proper functioning but cannot synthesize in our body.  Now, historically the shorter chained omega-3, primarily plant-based fat has been considered essential.  That’s alpha-linolenic acid, and it’s found in flaxseeds and walnuts, mostly nuts and seeds.  And it’s true that some alpha-linolenic acid can be converted into DHA, but that conversion is extremely poor in most people.  In fact, in the average person, less than 0.5%, or one-half of 1%, of alpha-linolenic acid gets converted into DHA.  And that’s in relatively healthy people.  That conversion is dependent on enzymes that in turn require adequate amounts of certain nutrients, like B6 and zinc, and a lot of Americans — I think up to about one-third of Americans — are deficient in the nutrients that are involved in that enzymatic conversion.  And especially vegans and vegetarians tend to have higher levels of deficiency of those nutrients.  So that one-half of 1% is kind of a best-case figure.  In reality, it’s probably a lot less than that.  And the problem there is that alpha-linolenic acid has not been shown to have the same benefits as the long-chain omega-3 fats, like EPA and particularly DHA.  So you have a situation where we need DHA, and yet even though in theory we can convert some of the shorter chained fats into DHA, in practice, especially amongst people with chronic illness or any nutrient deficiencies at all, which are really common, very little gets converted into DHA.  So what this suggests is that DHA is really, rather than alpha-linolenic acid, the real essential omega-3 fat.

This research in some way contributes to our understanding of why this might be.  I mean, we might wonder, why is that conversion so poor?  Well, if our ancestors were eating a lot more DHA, preformed DHA, like from the brains of animals that they hunted or from fish, for example, then the need to make that conversion from the short-chain omega-3 fat into DHA would have been a lot less.  And in fact, most studies do suggest that this is true.  Historically speaking, our ancestors’ intake of DHA — and for that matter, the long-chain omega-6 fat, which is arachidonic acid — our ancestors’ intake of those longer chained polyunsaturated fats was much higher than our average intake today, so it’s very likely that they didn’t really have a need to make those conversions.

This is an interesting study for me for a number of different reasons, both the evidence that we were hunting and not just scavenging animals as long ago as 2 million years ago and that we were eating the brains, which implies that we had a significant source of long-chain omega-3 fats, which could explain some of the problems we see in the conversion and adds some data to the idea that DHA rather than alpha-linolenic acid is essential.  Now, of all of the reasons that I think vegan and vegetarian diets aren’t optimal for many people for long-term health, this is probably one of the biggest because DHA is so important to the function of the brain and our vision and the growth and development of the fetus, and it just plays so many important roles that a diet that doesn’t have any preformed DHA, which a vegetarian and vegan diet would not, is really kind of difficult to support from a nutritional perspective.  This doesn’t, of course, address the various ethical and perhaps social reasons or religious reasons that people might choose to do a vegetarian or vegan diet, but I’m just speaking right now in terms of a nutritional perspective.  Vegans and vegetarians, I highly recommend taking an algae supplement.  Algae is where fish get DHA from, so it does contain preformed DHA, certain types of microalgae.  It has to specifically be for DHA.  There are a few out there.  Unfortunately, they’re quite expensive, and you have to take a lot of it to get the recommended amount of DHA, but it’s better than not taking any at all.

Let’s see if I have anything else to say about that study… Yeah, I don’t think so.  That’s it for that.

Steve Wright:  It think it’s an awesome new piece of research to definitely add to, I guess, our stack of research that supports all the recommendations we always make on this show.  I really appreciate you just going through that study, so thanks, Chris.

Solving the cholesterol controversy

Chris Kresser:  Yeah.  I’m fascinated by medical anthropology, and if I could go back to college now, I would probably study medical anthropology.  It’s a really interesting subject to me, and I think it has a lot to teach us as well.

The second study I wanted to talk about is actually a paper published in the journal Circulation, and it made kind of a big splash, at least within the research community, so some of you might have seen it already.  But this paper, what they were trying to do is determine which measures of cholesterol and lipoproteins are most predictive for a future risk of heart attack in a very high-risk population.  I’ve actually been writing a series on the blog the last couple of weeks about this, about cholesterol and lipoproteins and the difference between the two and which tests are best in terms of predicting your heart disease risk.  And there’s a fair amount of controversy still in this area, and some studies, for example, in the past have shown that the ratio of total cholesterol/HDL is just as good as a marker as LDL particle number, which is the number of LDL particles that are actually moving around in the bloodstream.  And then there have been a lot of other studies that have shown that LDL particle number or ApoB, which is a kind of proxy marker for LDL particular number, are much better predictors of risk.  So that’s what this study was setting out to look at, that question.

What made this a little bit different than some previous studies that have been done in this area is that the previous studies were observational in nature, so they were looking at observational or epidemiological data, and this study looked at data from a randomized clinical trial that was done.  This particular trial was the Medical Research Council/British Heart Foundation Heart Protection Study, and it was 20,000 high-risk men and women, and they followed them for an average of five years.  And the original trial was actually looking at the effect of a statin drug versus an antioxidant, but they measured a whole bunch of stuff, as they often do in randomized clinical trials, so in this paper the researchers just harvested some of that data.  They looked at levels of total cholesterol, LDL cholesterol, HDL, total cholesterol/HDL ratio, and then all of the different lipid subfractions like LDL particle number.  They looked at LDL particle size, you know, small LDL versus large LDL.  They looked at HDL particle number, HDL size, so they had a lot of information to work with.  And what they found in this study was that all of the LDL measurements were equally predictive for a heart attack in this high-risk population, so LDL cholesterol, LDL particle number, and ApoB, which again is a kind of proxy for measuring LDL particle number, were all relatively similar in terms of their ability to predict a heart attack in the future.

They also found that HDL was a lot less predictive, particularly in those that had pre-existing heart disease, and this is interesting, this has come up before in other studies, and what it suggests — and what some other research also suggests — is that the function of HDL decreases in people with heart disease, so there’s kind of a reverse causality there.  And one of the reasons we might see low HDL or low HDL particle number or even a normal HDL particle number but increased risk of heart disease or higher incidence of heart attack in people that have already had heart disease is that the heart disease itself actually weakens the function of HDL so it can’t carry out its protective function as well as it does in someone that doesn’t have heart disease.  So that was interesting.

And in this study there was a much stronger correlation between LDL cholesterol and LDL particle number.  As I wrote in a recent article on my website, LDL cholesterol and LDL particle number are sometimes related.  They’re often related, but not always.  And in fact, in people with metabolic syndrome, insulin resistance, they can have normal or even low levels of total and LDL cholesterol and high LDL particle number, in which case they’ll be at increased risk.  So this study showed a correlation of about 0.79, which is quite strong.  It’s certainly not perfectly correlated, but it’s stronger than the correlation that has been observed in previous studies, which was closer to 0.6.  It was 0.62 or 0.63, I think.  So the data in this is a little bit different in terms of the relationship between LDL cholesterol and LDL particle number.

There was an accompanying editorial in the journal about this study, and it was written by a doctor, and his main point is that we don’t need these extra fancy tests for estimating heart disease risk because this study shows that the standard markers are just fine in terms of predictive value.  And the other point he makes is that most people who have a heart attack have at least one risk factor.  It doesn’t just happen out of the blue.  He points to a study that looked at 21,000 deaths from fatal heart attacks, and exposure to at least one clinically elevated major risk factor was present in 87% to 100% of the people who died from a heart attack, and ‘risk factor’ in this study was defined as total cholesterol of at least 240 mg/dL, systolic blood pressure of 140, diastolic blood pressure of at least 90, cigarette smoking, and clinical diabetes.  So one of those was present in 87% to 100% of people who had a fatal heart attack, the point being that we kind of know already what the risk factors are for heart disease.  The basic lipid markers that we have are sufficient, so we don’t really need to do any more advanced testing.

I definitely agree with parts of that analysis.  I do think, as I’ve argued many times, that heart disease is a complex, multifactorial process and that it’s heavily influenced by lifestyle factors.  There was the famous INTERHEART study that looked at heart disease in over 50 countries around the world, and they found that 9 out of 10 heart attacks could have been prevented by modifiable diet and lifestyle factors, which, similar to the statistics here, it suggests that maybe 1 in 10 heart attacks are due primarily to genetics or maybe some other lifestyle or diet factor that wasn’t measured, like perhaps chronic stress or maybe gut dysbiosis or some kind of emerging factor that we don’t fully understand yet how it contributes and that isn’t often easy to measure and isn’t often measured in these studies.  So I definitely agree with that.

Also, as I pointed out in the High Cholesterol Action Plan, the ratio of total cholesterol/HDL is often in a general sense, or we should say on average, it’s just as predictive as LDL particle number, but the problem is we don’t treat averages in the clinic.  I mean, any clinician knows this.  We treat individual patients.  So studies are really good at determining trends and average effects.  They take a whole bunch of people, they measure what happened, and they average out the results and come up with a basic finding that then can be applied to clinical settings, and that’s how research is used to make treatment decisions and determine what the standard of care is.  And I’m not suggesting that I have a better way to do it, necessarily, but what I am saying is that there are always outliers on either side of the equation.  And in fact, in the editorial he says:  “It is useful to seek better discrimination of risk in those at the margins, but it is not where our greatest effort should be focused.”  And again, it’s true.  In most cases, most people just need to clean up their diet, clean up their lifestyle, get their blood pressure down, lose weight, improve their insulin sensitivity and glucose tolerance, and stop smoking.  You know, they need to take care of the basics.  That’s absolutely true.  But in the population of people that I work with, I’m hard-pressed to think of any of my patients, maybe two, that smoke cigarettes.  And many of my patients are not overweight significantly, they don’t have high blood pressure, they don’t have diabetes, they don’t fit this normal risk profile.  And yet some of them have very high LDL particle number with normal total cholesterol.  Some have high LDL particle number with high cholesterol.  Some have high cholesterol with normal LDL particle number.  So all of these situations are outside of what most doctors are seeing in their average clinical practice, and they deserve a different approach than those situations because a lot of the data that we have on the relationship between these lipid markers and heart disease doesn’t really necessarily apply to people that are on the margins, so to speak.

So I think this study adds some really important information in terms of determining a kind of general approach in standard practice, but I don’t think it invalidates the use of LDL particle number or some of the more advanced markers in one-on-one patient care, especially when someone has a more specialized practice and is treating people who are already pretty healthy, at least from a cardiovascular perspective, and are mostly interested in optimizing their health.

I will say, though, that one thing that has been really consistent in these studies is that LDL particle size does not add any predictive value once LDL particle number is known.  I think the confusion in the past where we did see these relationships between LDL particle size and heart disease is that at that time, LDL particle number was often not being measured, and so it appeared that the particle size was significant in terms of predictive value, but now when you adjust for LDL particle number, when you know the particle number, adding particle size doesn’t add any additional value.  Part of what helped us figure this out is the observation that people with familial hypercholesterolemia, which is a genetic condition that leads to very high LDL particle number and cholesterol levels, they often have large, buoyant, fluffy LDL, and yet they’re still at three times greater risk of death from heart disease than people without familial hypercholesterolemia.  So I think we can safely not worry too much about particle size as long as we know particle number, and as always, like most other diseases, heart disease is, as I said, complex and multifactorial.  There are a number of different things to consider when we’re determining the overall picture of risk.  I still think LDL particle number is a better lipid marker than LDL or total cholesterol or even the total/HDL cholesterol ratio, but total/HDL ratio for most people is a good surrogate for LDL particle number, and if you can’t afford to get or don’t have access to ApoB or LDL particle number, that can be a good substitute for many people.

Steve Wright:  Hey, Chris, let’s bring it really home for our listeners, if you can.  We just talked about total cholesterol, we talked about the ratio total/HDL, we talked about LDL-P.  Can you just give us your numbers that we should be trying to hit?  People are going to listen to this.  They’re probably going to get these things checked.  Our listeners are like your population, most likely, so can you give us some of your functional numbers for people to go after?

Chris Kresser:  Well, it’s quite complex.  I wish I could answer that question really simply.  Now, that’s part of the reason I ended up doing the High Cholesterol Action Plan, is that I realized that there was no simple way I can answer the question.  The course ended up being nine weeks long because it is really quite an involved process to determine your heart disease risk, and the reason I’ve been hesitant to just throw out a certain number is that it really varies in the sense that you have to consider the rest of the context.  Let’s say, for example, that I said you want your total cholesterol/HDL ratio to be under 4 — and that is a standard target — so if you divide your total cholesterol by HDL, it should be less than 4.  Some say less than 3 is much better and more optimal.  But let’s take two hypothetical people.  Let’s say one person has a total cholesterol/HDL ratio over 4, but they have no other risk factors for heart disease.  They’re in excellent shape, they’re fit, they exercise regularly, they’re physically active, they don’t sit a lot, they eat a really healthy diet, they manage their stress, they sleep well, etc.  They’re like the poster child for health except they have this ratio that’s above 4.  Maybe it’s 4.1 or 4.2.  And then you have another person who has the same exact total/HDL ratio, but they have high blood pressure, they’re obese, they’re not exercising, they’re not managing their stress, and they’re eating a standard American diet, and they’re 20 years older than the other people.  Obviously those two people are going to have really different heart disease risk, and even though their total/HDL ratio is the same, they’re not at all in the same boat.  And one person might need a lot of treatment, a crash course in diet changes, everything else.  The other person may not need any treatment at all, depending on the situation, maybe their family history and things like that.  So that’s kind of my hesitation, but the general target for total/HDL ratio is less than 4.

LDL particle number is really contextual, in my opinion.  I mean, the National Lipid Association and folks like Dr. Dayspring, who has written a lot about LDL particle number, and the NLA has been really responsible, to a large degree, for getting the word out there about LDL-P.  They want to see it below 1000, which is below the 20% percentile.  It’s separated into quintiles.  So if you’re below 1000, you’re in the zero to 20th percentile.  If you’re 1000 to 1299, I think, you’re in the 20th to 40th percentile.  If you’re 1300 to 1599, I think, you’re in the 40th to 60th.  1600 to — I may be getting this slightly wrong because I think I just missed — 1600 or 1700 to 1999, you’re in the 60th to 80th.  And then above 2000, you’re in the 80th to 100th percentile.  The NLA wants to see people below 1000, and they will medicate anybody with statins regardless of their other risk factors or their ‘picture.’  They’ll medicate anyone with a statin to get their LDL-P below 1000.  I’m not so sure that that’s necessary.  I think context does matter.  So if somebody comes to see me and they have an LDL-P of 1300, which puts them still in the sort of low moderate risk, maybe moderate risk group, if they have no other risk factors, I think it’s hard to justify medication in that situation, given the current evidence and what we know about the multifactorial nature of heart disease.  And as I just said, in people who had fatal heart attacks in the study that we talked about in the editorial, 87% to 100% of them had a major risk factor.  So I’m a little less aggressive as far as that goes and a lot more likely to look at the other factors.

Steve Wright:  OK, well, thanks for taking a shot at that.

Chris Kresser:  Sure.  So I think that’s it for that study.  We have time for a few questions now before we finish.

More details of Chris’s daily routine (and more treadmill desk)

Steve Wright:  OK, let’s transition.  The first question that we have here comes from Laura, and she wants to know more about your standing desk, Chris.  She says that she has transitioned to a standing desk while at the corporate office and has the opportunity to use a treadmill desk as well.  “What are your thoughts on decompressing the spine after long periods of standing?  I’ve learned that in order to help improve recovery after endurance events that you should spend time upside down or with your feet up against a wall.  What are your thoughts on this related to long periods of standing?  If I work standing for 8 hours, should I end my day with 8 minutes of time lying on the ground with my legs vertically against the wall?  Is there anything that you would recommend doing to balance out the body after standing all day?”

Chris Kresser:  Yeah, that’s a good question.  Truthfully, this isn’t an area of expertise for me.  This might be something I would defer to my wife on.  She has a lot more advanced understanding of biomechanics and has spent a lifetime studying that.  She had a treadmill desk, right?  Not just the standing desk?

Steve Wright:  I think she says she has both.

Chris Kresser:  Um-hum.  So one thing I mentioned, I think, when we first started talking about treadmill desks is there’s actually some research that suggests that standing for long periods is not that beneficial and possibly harmful.  I’m not sure that standing for 8 hours is an improvement from a health… I think it probably is an improvement over sitting for 8 hours, but I think if your choice is standing desk or sitting desk, maybe a mixture of both, actually, throughout the day is a better idea than just standing for the entire day at the desk, based on what some of the research about standing for too long suggests.  I myself actually switch back and forth between several different postures and positions.  I have a standing desk, of course, and then I have the treadmill desk, and then I have a sitting desk with a really nice chair, a Herman Miller chair that I will often sit on the edge of so that my back is still straight.  And then I have a balance disc, or a sitting disc they’re called, and I can put that on my chair, and when I’m sitting on it, I have to continually kind of adjust my posture.  It scoots me forward on my sits bones, so it’s really hard to slouch while I’m sitting on it.  And then I have a yoga ball as well.  So I alternate back and forth between all of those different positions throughout the day, and I find that I feel best when I do that.  If I walk for too long, that actually can start tightening the hamstrings, and I feel a little bit too sore at the end of the day or just stiff, and it doesn’t feel good.  If I stand for too long, certainly I have that issue, and of course, if I sit for too long, I don’t feel good.  So for me, a mixture back and forth is ideal.  But if you do stand or even walk or some combination of both for the entire day, then something like what you described is probably helpful, and I can’t see how it would be harmful, so by all means, give that a shot.

Steve Wright:  So also has a follow-up question that I think is appropriate to address.  She also wanted to know if you had any thoughts or preferences about the shoes that you wear during the day and using an anti-fatigue mat for the standing desk.

Chris Kresser:  I do have an anti-fatigue mat, but unfortunately it’s now under the treadmill!  The treadmill is resting on it.  The reality is, along with what I just said, I stand comparatively little to walking.  I probably walk most, then I sit on the yoga ball and the chair and the sitting disc a distant second, and then third would probably be standing.  And that’s in part because the way my desk is set up now, the treadmill is under the desk.  So if I’m standing, I’m standing on the treadmill, which isn’t actually ideal from a biomechanical perspective, the way that it’s set up, and then the anti-fatigue mat is under the treadmill, so I’m not standing on that.  In terms of footwear, I’m barefoot.  If I’m in my home office, I’m barefoot whether on the treadmill or sitting or whatever.  Occasionally I’ll be wearing very thin-soled… I have some Patagonia shoes that are really kind of more barefoot than any other barefoot shoes I’ve tried except for Vibrams and maybe a few others.  And so sometimes I’ll wear those if I’ve been outside and I’ve just come back or something like that.  But I think minimalist footwear is always a good idea for this kind of thing.

Additional sources of magnesium

Steve Wright:  All right, awesome.  I think this next question is very appropriate for this podcast.  Eden wants to know, “Where did humans traditionally get magnesium in their diet?”

Chris Kresser:  Yeah, this is a question that often comes up, and I’m not entirely sure.  One thing that I’ve heard and read about quite a few times and I’ve been searching around in the scientific literature for something to corroborate this, but I’ve found general references to nutrient depletion in the soil that would include magnesium, but I haven’t found any specific comparisons between soil from preindustrial times or maybe a place that hasn’t been developed with monocropping and industrialized agriculture in a more rural place, but there’s this idea that the diversity and the quality of nutrients in soil has changed quite a bit since the industrialization of agriculture.  And it’s not just an idea.  I mean, there is data to support this.  So there was probably more magnesium in nuts and seeds and even some vegetables and fruits and starches like plantains than there is now, so there was just more magnesium in the diet due to better soil quality.

But in terms of the diet now and historically, nuts and seeds have been one of the highest sources of magnesium.  One of the issues there, though, is traditional cultures almost always prepared nuts and seeds by soaking them and then drying them.  And we know that nuts and seeds have phytate, phytic acid, which inhibits the absorption of magnesium and that these traditional preparation methods, like soaking and drying, break down the phytate so that more of the nutrients and minerals in the food can be absorbed.  So it’s possible that they got most of their magnesium from nuts and seeds.  Today in the sort of modern diet, pumpkin seeds and Brazil nuts are relatively high in magnesium.  Like 6-8 Brazil nuts have about 107 mg of magnesium.  A half ounce of pumpkin seeds has about 75 mg.  Buckwheat is actually a seed.  It’s not related to wheat at all, in spite of its name, and a cup of buckwheat flour has about 300 mg of magnesium.  And actually plantains are a good source of magnesium.  One medium plantain has about 65 mg of magnesium.

But I generally would recommend that people get 400 to 500 mg of magnesium, if not more if they’re dealing with constipation or muscle pain or some other symptoms, and that, in my experience, it’s just really difficult to get from the diet, so that’s one of the reasons I recommend it as one of the few nutrients that most people benefit from supplementing with.

Steve Wright:  Do you do anything special in your daily life to ensure that you get magnesium, like supplement?  Or do you do it all through food?

Chris Kresser:  I take a magnesium supplement.  Magnesium and fermented cod liver oil are the only two supplements that I take.  I have tried to get magnesium from food, and I notice a difference when I’m not supplementing with magnesium, so as I said, along with fermented cod liver oil, it’s the only one I take on a regular basis.

When should I stop breastfeeding?

Steve Wright:  Awesome.  All right, let’s move on to the next question.  This question comes from Christina, and Christina has a little bit of a paragraph here, so bear with me.  She has a soon-to-be 1-year-old son, and she has yet to have her first period.  She’s still nursing him two to three times a day plus pumping once at night.  She works part time, so the pumping at night is for during the next day.  Her pediatrician said that she should ditch the pump when he turns 1, despite knowing all the benefits of breastfeeding.  “I have to say that I’m ‘pumped’ to get rid of it.  Bad pun, but anyway, I’m wondering how normal this is.  He’s my first son, and I have a history of irregular periods.  Do some people have amenorrhea until they completely wean their child?  Is there any risk involved with not having a period?  My biggest concern is that my husband and I would like to start trying again, and knowing that I am getting my period would help me a lot.  Would you recommend acupuncture treatments to help me get things started again?  Thanks for all your help.”

Chris Kresser:  OK, so I just want to take a step back and throw in my plug for complementary nursing until at least 22 months.  I know she’s pumped to stop pumping, and I completely understand that.  I’ve worked with a lot of women who have had to pump a lot, and I know it can be difficult, but there’s a considerable amount of research that suggests that along with exclusive breastfeeding to 6 months that there’s a real and measurable benefit to continuing to do supplemental breastfeeding up to 22 months.  And the recommendation is to just do it on demand, meaning you offer it when baby wants it.  Of course, that’s not necessarily practical in this situation, given the work schedule and the pumping and things like that.  But I would encourage you to at least consider biting the bullet and continuing for up to 22 months or as close to that as you can get because I think the research suggests that there’s some significant benefit there.  The benefit seems to stop from a health perspective at around 22 months.  I mean, of course, that’s an estimate.  It’s going to vary from baby to baby, but that’s a general guideline.  The decision to nurse beyond 22 months really depends more on parenting philosophy and questions of attachment and development and things like that.  It’s not really related to nutrition in most cases.

In terms of the amenorrhea, it’s not unusual to be amenorrheic at one year if you’re nursing.  And different women have a different ‘normal’ here.  Some women start menstruating really relatively quickly even if they’re still nursing.  Other women take quite a while to get back to menstruation when they’re nursing.  And it doesn’t necessarily indicate any kind of pathology or problem; different women just have a different rhythm and pattern there.  In some cases, it can indicate a problem, a hormone imbalance, something that’s not clicking back into place after the birth, but I wouldn’t suspect that at 1 year, especially given the history of irregular menstrual cycles before.  And someone who has a history of irregular menstrual cycles is more likely, in my experience, to be a little bit slower getting back into their normal rhythm since their rhythm wasn’t really normal in the first place.  It sounds to me like there isn’t anything to be concerned about, but of course, that’s something you should also double-check with your OB/GYN or midwife or whoever’s care you’re under.

What to do about anxiety during pregnancy

Steve Wright:  All right, so let’s move on to the next question.  “What are your thoughts on supplemental support with PharmaGABA and/or L-theanine during pregnancy?  What about certain adaptogens, like ashwagandha, during pregnancy?  This would be in regards to anxiety during pregnancy.  Thanks for your consideration.  Ben”

Chris Kresser:  GABA is the major inhibitory neurotransmitter, for anyone who doesn’t know what GABA is.  It’s kind of like the off-switch in the brain and elsewhere.  It leads to feelings of calmness and relaxation, and so the idea, of course, is supplementing with GABA would reduce anxiety.  But GABA is a very large molecule, and it shouldn’t actually cross the blood-brain barrier, is my understanding.  And so if you take GABA and you have a response, some practitioners kind of actually use that as a way of diagnosing leaky brain.  We’ve talked a lot about leaky gut, I’ve even written a bit about leaky skin, but the blood-brain barrier is another barrier system in the body that’s designed to keep certain things out and let certain things in, and large molecules are not supposed to pass through the blood-brain barrier.  There’s one school of thought that says that supplementing with GABA shouldn’t work, and if it does work, it’s actually indicative of a leaky blood-brain barrier and that’s what should be investigated and treated.

But as far as this question goes, supplements during pregnancy are always a tricky thing because we don’t have a lot of data on the safety of supplements during pregnancy, and we never will because those studies are unethical to do.  Imagine a trial where you take two groups of pregnant women and you give one group a supplement and give the other a placebo and then you watch what happens to them and their babies.  I mean, obviously no one is going to sign up for that study and they shouldn’t.  It’s completely unethical.  So we’re left kind of wondering a lot about the effect of various supplements, and the only way to really know is to, in some cases, look at the history of safe use of those supplements by herbalists and other types of health care practitioners throughout history.  You can consider the mechanism of how the substance works and whether it’s likely to shift anything around in pregnancy, although it’s pretty sketchy to do it that way because we just don’t know.  I mean, there are so many profound changes in pregnancy that it’s really difficult to predict how something might impact the developing baby or the mother.

So my general philosophy on supplementation during pregnancy is to be extra cautious, to do as much as possible with lifestyle-based interventions and diet, and when using supplements, to use only the ones that have the longest record of safe use and that are the least likely to cause any harm or difficulty.  For anxiety during pregnancy, I will tend to recommend acupuncture.  It seems to really take the edge off for a lot of women.  The only side effects are typically feeling better, for the most part, and it’s pretty affordable these days if you find a community acupuncture clinic.  Mindfulness-based stress reduction, which we’ve talked about numerous times on the show, and the Rest Assured program are two ways of inducing the parasympathetic nervous system, and mindfulness-based stress reduction, particularly, is clinically proven to reduce anxiety in several different studies, and that you can search online for a class nearby or you can even download some free audio programs.  The body scan is one way of doing MBSR, mindfulness-based stress reduction.  You can download some of those for free from the Internet to learn how to do it.

Then there are some botanicals, like skullcap — Chinese skullcap, not American skullcap.  There are two different varieties.  It’s really important.  Chinese skullcap is generally considered by most herbalists to be safe during pregnancy, particularly when taken as a tea.  Lemon balm and chamomile are two other botanicals that are generally considered to be safe.  And if you use one of the over-the-counter teas that have them in it or you combine those together, they’re generally, again, considered to be safe.  Now, if you search for some of these on the Internet, you might see some mixed views, and that’s in part because of what I just said before.  We don’t have randomized clinical trials that give us this type of information, and different people have a different take, but the vast majority of even mainstream sources consider chamomile and Chinese skullcap and lemon balm to be safe.  American skullcap is not considered to be safe.

5-HTP, which is an intermediate between tryptophan and serotonin and is often used for depression and anxiety in non-pregnant people, is questionable.  There are mixed opinions, again, about that.  And I would be hesitant myself to prescribe it during pregnancy because we just don’t know.  On the other hand, a lot of doctors do prescribe SSRIs, prescription antidepressants that, I think, have probably an even greater impact on serotonin metabolism than taking 5-HTP, and a lot of women take SSRIs during pregnancy.  I’m not arguing for that, and two wrongs don’t make a right, of course, but I guess it depends on the extent of the anxiety and depression because that can be harmful for the baby as well, especially if it leads to harmful behavior in the mother.

So if you’re going to explore any of those more, 5-HTP or anything like that, absolutely do it in conversation with your healthcare provider or under the supervision of whomever you’re working with.  Otherwise, the lifestyle interventions, like acupuncture and mindfulness-based stress reduction, spending time outdoors, making sure to get plenty of sleep if possible — I know that’s sometimes challenging when you’re pregnant, especially in the later stages — and then considering using some of those teas, when you add all of those kind of smaller interventions up, they can actually equal a larger intervention.

Steve Wright:  Awesome.  Well we’ve covered a lot of different topics today from science on why we should be eating what we’re eating and pregnancy to standing desks to all kinds of things.

Chris Kresser:  Yeah, and it was a lot more enjoyable than being in the closet.

Steve Wright:  You just like the window!

Chris Kresser:  Hopefully the sound is good, and next time it’ll be even better because I’ll have my fancy new sound-dampening equipment, which I’m excited about.

Steve Wright:  Awesome.  Well, as always, Chris, thanks for all the wealth of information.

Chris Kresser:  Thank you, Steve.  Pleasure, and see you all next time.

Steve Wright:  Yeah.  Thanks, everyone, for listening today.  If you would, please keep sending us your questions to ChrisKresser.com.  I swear I still have them, and we’re plowing through the list as we go.  When you get to ChrisKresser.com, use the podcast submission link to send them over to me.  And if you enjoyed listening to the show, please head over to iTunes and leave us a review.  Thanks.  We’ll talk to you next time.

A recent study by published in the New England Journal of Medicine (NEJM) has proposed a new link between eggs and coronary heart disease (CHD) that doesn’t involve cholesterol. A team of researchers, led by Dr. Stanley Hazen, showed that dietary choline—a nutrient found largely in eggs, beef liver and other animal foods—is metabolized by bacteria in our gut and then converted by the liver into TMAO.

They demonstrated this with a “choline challenge”: feeding volunteers two large hard-boiled eggs (with approximately 250 mg of choline each) along with 250 mg of supplemental choline that was tagged with a heavy isotope. The isotope acts like a chemical “label” that allowed the researchers to track what happened to the choline after it was ingested. Their data did indeed show an increase in both labeled TMAO and total TMAO (in urine and blood) in the volunteers after they consumed the eggs and supplemental choline.

In a second study, Dr. Hazen’s group showed that increased levels of TMAO in the blood are associated with cardiovascular disease (CVD). The researchers followed roughly 4,000 adults for three years. At the end of the study period, those with the highest levels of TMAO had a 2.5-fold increased risk of heart attack, stroke and death.

On the surface this sounds like very bad news for omnivores. But let’s take a closer look at the studies to see if it’s really time to swap your morning eggs for a tofu scramble.

Do choline-rich foods increase TMAO levels?

Dr. Hazen’s team did show a temporary increase in total TMAO after eating eggs. However, as Dr. Chris Masterjohn pointed out to me in an email dialog, the researchers’ own data show that there’s no way that the “choline challenge” could have contributed to this increase in total TMAO. If it had, we would expect to see an initial increase in labeled TMAO followed by an increase in labeled TMAO. This would indicate that the labeled choline supplement (that participants ate with the eggs) had been metabolized by the gut bacteria and then converted into TMAO in the liver.

But that’s not what happened. I re-created Figure 1C and 1D from the study. Figure 1C (below) shows an increase in total serum TMAO at one hour after the choline challenge. But by hour four, total TMAO is back to baseline and by hour 8 it’s even below baseline (i.e. the participants had lower TMAO at 8 hours than they did before they ate the eggs/choline).

However, Figure 1D (below) shows that labeled TMAO did not increase at all until hour four, and it didn’t increase significantly until hour six! This shows that the eggs and supplemental choline the participants ate had nothing to do with the increase in total TMAO that occurred one hour after the challenge.

What’s more, the researchers didn’t mention that other commonly eaten foods have a much more significant impact on TMAO than eggs. A 1999 study tested the effects of 46 different foods on the urinary excretion of TMAO in 6 human volunteers. (1) Eggs had no effect on TMAO excretion compared to a light control breakfast, yet 19 out of 21 types of seafood tested did. In fact, halibut generated over 53 times as much TMAO as eggs! This is not surprising, because although all species of seafood contain lower amounts of choline than eggs, they do contain trimethylamine and TMAO. Dr. Hazen’s team was aware of this study, because they referenced it briefly in the discussion section of the NEJM paper. They acknowledged that “TMAO has been identified in fish” and “the ingestion of fish raises urinary TMAO levels.” But remarkably, they did not explain how much greater fish’s impact on TMAO was when compared to eggs.

Finally, this paper did not prove that eating choline-rich foods (or any other foods) increases TMAO levels over time. In fact, the researchers themselves seem to suggest this is unlikely in the discussion section of the paper. They said: “the high correlation between urine and plasma levels of TMAO argues for effective urinary clearance of TMAO.” In other words, even if eating food does increase total TMAO levels, most people are able to quickly and efficiently clear that TMAO from their blood by excreting it in the urine. This makes it doubtful that dietary factors alone explain chronic elevations in TMAO.

Instead, there are several other factors that are more likely to explain such an increase, including:

• Impaired urinary clearance of TMAO due to impaired kidney function. This is at least partially supported by data in the NEJM paper. Those with the highest levels of TMAO had an average glomerular filtration rate (GFR) of 69 mL/min. According to National Kidney Foundation guidelines, a GFR between 60–89 ml/min is indicative of a reduced capacity to filter blood through the kidneys. (2)
• Differences in the gut microbiota that predispose toward increase TMAO production. Previous work by Dr. Hazen’s group has shown that people with higher levels of Prevotella bacteria in their gut produce higher levels of TMAO. (3) (Interestingly enough, other research has shown that consumption of whole grains—not animal products—is associated with higher levels of Prevotella bacteria.) (4)
• Enhanced conversion of trimethylamine to TMAO in the liver. An enzyme called Fmo3 carries out this conversion, and its activity is affected by genetic factors, iron or salt overload, and a number of common pharmaceutical drugs used to treat arthritis, GERD and infections. (5)
• Diabetes and metabolic syndrome. Fmo3 activity is upregulated in cases of insulin resistance and insulin deficiency. (6)

If food really did make a significant contribution to TMAO levels, and high TMAO levels cause heart disease, then we’d expect to see much higher rates of CHD among people who eat more fish—since fish has a much greater effect on TMAO than eggs. Yet this is the opposite of what studies indicate: Eating more fish (especially cold-water, fatty fish) has consistently been shown in both observational and randomized controlled trials to reduce the risk of death from heart disease. (7, 8)

Do choline-rich food cause heart disease?

At the end of their paper, Dr. Hazen’s group cautions against “excessive consumption of dietary phosphatidylcholine and choline” and recommends a high-fiber, vegetarian diet as a means of protecting against heart disease.

Yet as I’ve argued above, they failed to present convincing evidence that eating eggs significantly increases TMAO over time—especially when compared to other foods like fish. Moreover, if eating choline-rich foods did increase the risk of heart disease (via TMAO or any other mechanism), we’d expect to see higher rates of CHD in those that eat more eggs. Yet numerous studies have failed to find any such association. For example, a meta-analysis of prospective studies involving a total of 474,000 participants followed from 8 to 22 years published in the British Medical Journal found no association between higher egg consumption (up to one per day) and CHD or stroke. (9) An analysis of data from the National Health and Nutrition Examination Study found an inverse association between egg consumption and stroke, and a cohort study from Japan found that consumption of animal products including eggs was associated with reduced risk of death from stroke. (10, 11) The lack of association—or inverse association—between egg consumption and CVD is even more impressive when you consider that those who eat more eggs are also more likely to smoke and be physically inactive. (12)

Some studies suggest that eggs may even prevent heart disease. Egg consumption leads to the formation of larger, less dense LDL and HDL particles, which may be protective against atherosclerosis. (13) Eating eggs frequently may even lead to lower cholesterol; one study found that those eating four or more eggs per week had lower total serum cholesterol than those eating one or fewer per week.  (14) This same study found that egg consumers had diets higher in nutrients that have been shown to reduce the risk of cardiovascular disease compared to non consumers, including vitamins E, B12 and folate.

Finally, as I pointed out above, some research suggests that consuming large amounts of whole grain increase Prevotella bacteria in the gut, which were associated with the highest levels of TMAO in Dr. Hazen’s previous study on TMAO. If this is the case, consuming large amounts of fiber from whole grains may actually increase the risk of heart disease.

The hypothesis that increased serum TMAO is associated with heart disease is interesting and should be investigated further. But the data presented by Dr. Hazen’s group doesn’t support the conclusion that dietary choline is a major cause of increased TMAO, nor does it support their advice to avoid choline-rich foods like eggs, liver, beef and pork.

To read more about heart disease and cholesterol, check out the special report page.

In the last article in this series, I explained that LDL particle number (LDL-P) is a much more accurate predictor of cardiovascular disease risk than either LDL or total cholesterol. In this article, I’m going to briefly outline the five primary causes of elevated LDL-P.

Conventional medicine is primarily focused on suppressing symptoms. If your blood pressure is high, you take a medication to lower it. If your blood sugar is high, you take a medication to lower it. If your cholesterol is high, you take a medication to lower it. In most cases there is rarely any investigation into why these markers are high in the first place, with the possible exception of some basic (but often incorrect) counseling on diet and exercise.

On the other hand, functional medicine—which is what I practice—focuses on treating the underlying cause of health problems instead of just suppressing symptoms. If your blood sugar, blood pressure or cholesterol are high, the first question a functional medicine practitioner will ask is “why?” If we can identify the root cause of the problem, and address it at that level, medication is often unnecessary.

To use a simple analogy, if you have weeds in your garden, what happens if you just cut the weeds from the top? They grow right back—and sometimes faster than before! If you really want to get rid of them once and for all, you have to pull them up by their roots.

With this in mind, let’s look at some of the potential causes of elevated LDL particle number. If your LDL-P is high, it makes sense to test for and treat any of the conditions below (with the exception of the last, which is genetic and thus can’t be treated) before—or at least along with—taking pharmaceutical drugs.

5 common causes of elevated LDL particle number that can increase your risk of heart disease.

Insulin resistance and metabolic syndrome

LDL particles don’t just carry cholesterol; they also carry triglycerides, fat-soluble vitamins and antioxidants. You can think of LDL as a taxi service that delivers important nutrients to the cells and tissues of the body.

As you might expect, there’s a limit to how much “stuff” that each LDL particle can carry. Each LDL particle has a certain number of cholesterol molecules and a certain number of triglycerides. As the number of triglycerides increases, the amount of cholesterol it can carry decreases, and the liver will have to make more LDL particles to carry a given amount of cholesterol around the body. This person will end up with a higher number of LDL particles.

Consider two hypothetical people. Both have an LDL cholesterol level of 130 mg/dL, but one has high triglycerides and the other has low triglycerides. The one with the high triglyceride level will need more LDL particles to transport that same amount of cholesterol around the body than the one with a low triglyceride level.

Numerous studies have found an association between increased LDL particle number, and metabolic syndrome. One study measured ApoB, a marker for LDL particle number, in a group of 1,400 young Finns with no established disease. The participants with the highest LDL particle number were 2.8 times more likely to have metabolic syndrome than those with the lowest levels of LDL-P. (1) A much larger study of over 300,000 men also found a strong association between LDL-P and metabolic syndrome and its components (i.e. insulin resistance, abdominal obesity, high blood pressure, etc.). (2)

Poor thyroid function

Poor thyroid function is another potential cause of elevated particle number. Thyroid hormone has multiple effects on the regulation of lipid production, absorption, and metabolism. It stimulates the expression of HMG-CoA reductase, which is an enzyme in the liver involved in the production of cholesterol. (As a side note, one way that statins work is by inhibiting the HMG-CoA reductase enzyme.) Thyroid hormone also increases the expression of LDL receptors on the surface of cells in the liver and in other tissues. In hypothyroidism, the number of receptors for LDL on cells will be decreased. This leads to reduced clearance of LDL from the blood and thus higher LDL levels. Hypothyroidism may also lead to higher cholesterol by acting on Niemann-Pick C1-like 1 protein, which plays a critical role in the intestinal absorption of cholesterol. (3, 4)

Studies show that LDL particle number is higher even in subclinical hypothyroidism (high TSH with normal T4 and T3), and that LDL particle number will decrease after treatment with thyroid hormone. (5)

Infections

Another cause of high cholesterol profile is infection. Multiple studies have shown associations between bacterial infections like Chlamydia pneumoniae and H. pylori, which is the bacterium causes duodenal ulcers, and viral infections like herpes and cytomegalovirus and elevated lipids. (6) For example, H. pylori leads to elevated levels of total cholesterol, LDL cholesterol, lipoprotein (a), ApoB or LDL particle number, and triglyceride concentrations as well as decreased levels of HDL. (7)

Several mechanisms have been proposed to explain the association between infections and elevated blood lipids. Some evidence suggests that viral and bacterial infections directly alter the lipid metabolism of infected cells, and other evidence suggests that lipids increase as a result of the body’s attempt to fight off infection. Other evidence suggests that LDL has antimicrobial properties and is directly involved in inactivating microbial pathogens. This has been confirmed by studies showing that mice with defective LDL receptors—and thus very high levels of LDL—are protected against infection by gram-negative bacteria like H. pylori. (8)

Leaky gut

One of the primary functions of the intestinal barrier is to make sure that stuff that belongs in the gut stays in the gut. When this barrier fails, endotoxins such as lipopolysaccharide (LPS) produced by certain species of gut bacteria can enter the bloodstream and provoke an immune response. Part of that immune response involves LDL particles, which as I mentioned above, have an anti-microbial effect. A protein called LPS-binding protein, which circulates with LDL particles, has been shown to reduce the toxic properties of LPS by directly binding to it and removing it from the circulation. (9) Studies have also shown significant increases in LPS-binding protein (and thus LDL particles) in cases of endotoxemia—a condition caused by large amounts of circulating endotoxins. (10)

Though more research is needed in this area, the studies above suggest that a leaky gut could increase the level of LPS and other endotoxins in the blood, and thus increase LDL particle number as a result. I have seen this in my practice. I recently had a patient with high LDL-P and no other risk factors. I tested his gut and discovered H. pylori and small intestine bacterial overgrowth (SIBO). After treating his gut, his LDL-P came down to normal levels.

Genetics

The final cause of elevated LDL-P is genetics. Familial hypercholesterolemia, or FH, involves a mutation of a gene that codes for the LDL receptor or the gene that codes for apolipoprotein B (ApoB). The LDL receptor sits on the outside of cells; the LDL particle has to attach to the LDL receptor in order to deliver the nutrients it’s carrying and be removed from the circulation. ApoB is the part of the LDL particle that binds to the receptor. If we use a door lock as an analogy, apolipoprotein B would be the key, and the LDL receptor is the lock. They both need to be working properly for LDL to deliver its cargo and to be removed from the bloodstream.

Homozygous carriers of FH have two copies of the mutated gene. This condition is very rare. It affects approximately 1 in a million people. And people that are homozygous for this mutation have extremely high total cholesterol levels, often as high as 1000 mg/dL. And unfortunately they usually die from severe atherosclerosis and heart disease before the age of 25.

Heterozygous carriers, however, only have a single copy of the mutated gene, and the other copy is functioning normally. This is much more common. The prevalence is between 1 in 300 to 1 in 500 people, depending on which study you look at. These heterozygous carriers of FH have total cholesterol levels that often range between 350 and 550 mg/dL, along with very high LDL particle number. They have about three times higher risk of death from heart disease than people without FH if it goes untreated.

It’s important to note that people with FH have primarily large, buoyant LDL particles, and yet are still at much higher risk for cardiovascular disease. While it’s true that small, dense, oxidized LDL particles are more likely to cause atherosclerosis, large, buoyant particles can also be harmful when their concentration is high enough. This is one reason why LDL particle number is a superior marker to LDL particle size.

In the next article in this series, I will debunk the myth that statins extend lifespan in healthy people with no pre-existing heart disease.

Here is The Roundup, Edition 4, bringing you the best from around the web from the past two weeks! This week, I’m focusing on articles that address diabetes, obesity, and related metabolic disorders.

Blast from the Past

In 2011, I wrote an article explaining the many factors affecting the development of diabetes and obesity, and how many of the proposed mechanisms could conceivably contribute to the development of the disease. As obesity and diabetes research advances, however, the interconnection between these proposed mechanisms is becoming more clear, yet no primary treatment protocol has been established. And as I’ve mentioned before, I doubt one single treatment will ever be devised; after all, we’re not robots!

Recently, two studies were published suggesting alternative treatments that could help obese and diabetic patients lose weight and improve metabolic function. One study found that intermittent fasting (IF) may be a possible treatment protocol to help with weight loss and recover metabolic function, as IF has been found to limit inflammation, boost pancreatic function, and decrease levels of sugars and lipids in circulation. Another study demonstrated that intestinal parasites may be a potential diabetes and obesity treatment, as certain parasites may be able to mitigate inflammation, improve glucose tolerance, and prevent excess weight gain. Perhaps in the future, the recommendation to “eat less and exercise more” will be a distant memory, and these novel treatments will be considered the norm!

Research Report

• Fossil record shows early hominids hunted animals and ate their brains as early as 2 million years ago.
• A psychiatrist says that ADHD might actually be a misdiagnosed sleep disorder
• A study shows that increased efforts are needed to regulate the supplement industry.
• A small clinical trial suggests that fecal transplantation may help reduce or eliminate symptoms of ulcerative colitis in most children and young adults.
• Collaboration between veterinary and human medicine offers a cross-species perspective on a range of human health problems.
• Research by the NIH finds that women with sufficient amounts of vitamin D have a 32% lower risk of developing uterine fibroids.

Worth A Look

• Mercola.com: My interview with Dr. Mercola on one of the most important tests for heart disease you can get.
• Stumptuous.com: Krista Scott-Dixon explains hormones, homeostasis, and why you (probably) need carbs.
• Ancestralize Me: A young woman shares her experience with using ancestral nutrition to manage her autoimmune condition.
• Rodale: Carageenan hides out in a lot of your favorite foods, causing inflammation, gut irritation, and potentially even cancer.

For the Foodies

• Mark’s Daily Apple: Crock Pot Pork-Stuffed Peppers
• PaleOMG: Easy Delicious Breakfast Hash
• NomNomPaleo: Spicy Salmon Cucumber Bites
• Against All Grain: Baked Omelette with Ham and Gruyere
• Civilized Caveman: Dill Roasted Carrots
• The Food Lovers: Korean Inspired Beef and Vegetable Noodle Bowl

Gather, the Art of Paleo Entertaining by Bill Staley and Hayley Mason, is a brand new Paleo cookbook designed to inspire year-round celebrations with family and friends. No gathering of loved ones is complete without a table full of delicious food, yet it can be difficult to prepare multi-course meals that can be enjoyed by those who are following a Paleo diet. Bill and Hayley’s book is proof that it’s possible to eat and entertain like a gourmet without gluten, grains, or other “non-Paleo” ingredients.

Gather is not only visually stunning, it also contains impressive multi-course meals perfectly designed for a variety of holidays and celebrations throughout the year. The index is divided by the four seasons, and each season has its own set of menus to guide and inspire you for your own gathering of friends and family.

If you’re on a Paleo diet and you love food, Gather is the cookbook for you.

With Gather, you’ll be able to organize a casual Sunday brunch in the spring, a Tuscany-inspired dinner party in the summer, a Paleo Thanksgiving feast in the fall, and lovely winter holiday meal. The menus cover a variety of cuisines, such as Chinese, Cuban, and Caribbean, and there are kid-friendly menus, including a Halloween spooky supper, and even a birthday party, complete with chicken nuggets and birthday cake – all grain-free of course!

The best part of serving food from Gather is that you can feel confident you’re serving your loved ones nourishing food while pleasing their palates. A lot of early Paleo cookbooks were long on health and short of flavor and creativity. Gather is the best of both worlds: the dishes are worthy of a 5-star restaurant, with nutrient-dense ingredients such as pastured meats, wild seafood, green and root vegetables, and healthy fats like coconut oil and grass-fed butter.

Gather would also make a wonderful gift for a friend or family member who is tempted to try Paleo but is concerned that the idea of a “diet” is restrictive, or insist that they can’t live without their favorite foods. This book will be more than enough to convince them that they can eat healthily without sacrificing flavor and enjoyment. (But you might try cooking them a recipe from the book first!)

If you’re a Paleo foodie like I am, Gather is a must on your kitchen shelf. The book releases today (April 30th, 2013), and can be ordered on Amazon.com.

A beautiful side dish with a small ingredient list that packs great flavor.

Type of dish: Side Dish
Equipment: Pot with steamer basket and lid, sauté pan
Servings: Makes 4 servings.

Ingredients:

• 2 to 2 1/2 pounds asparagus, washed, tough bottom parts broken off, and sliced into one-inch pieces
• 1 TB traditional fat of choice
• 5 cloves garlic, minced or pressed
• 1/2 cup almonds, sliced or roughly chopped
• juice of one lemon
• salt to taste

Directions:

1. Steam asparagus in covered pot with steamer basket, with one to two” of boiling water, until bright green, about 5 minutes.
2. Remove asparagus from heat and drain any excess water.
3. In a sauté pan, heat the oil over medium heat. Add the garlic and cook for one minute, stirring.
4. Add the almonds and toast lightly, stirring for about another minute.
5. Remove pot from heat and add in the steamed asparagus. Stir well.
6. Finally squeeze in the juice of the lemon and salt to taste. Serve.

Enjoy!

To read more about heart disease and cholesterol, check out the special report page.

Cardiovascular disease is one of the most misdiagnosed and mistreated conditions in medicine. In the first article in this series, I explained the evidence suggesting that eating cholesterol and saturated fat does not increase cholesterol levels in the blood for the majority of the population.

In this article, I will debunk the myth that high cholesterol in the blood is the cause of heart disease.

Myth #2: High cholesterol is the cause of heart disease

Part of the confusion about cholesterol and its role in heart disease is caused by imprecise terminology. So, before I explain why high cholesterol is not the underlying cause of heart disease, we have to cover some basics.

Cholesterol is not technically a fat; rather, it’s classified as a sterol, which is a combination of a steroid and alcohol. It’s crucial to understand that you don’t have a cholesterol level in your blood. Cholesterol is fat-soluble, and blood is mostly water. In order for cholesterol to be transported around the body in the blood, it has to be carried by special proteins called lipoproteins. These lipoproteins are classified according to their density; two of the most important in cardiovascular disease are low-density lipoprotein (LDL) and high-density lipoprotein (HDL).

I know this can get confusing quickly, so let me use an analogy to make this more clear. Imagine your bloodstream is like a highway. The lipoproteins are like cars that carry the cholesterol and fats around your body, and the cholesterol and fats are like passengers in the cars. Scientists used to believe that the number of passengers in the car (i.e. concentration of cholesterol in the LDL particle) is the driving factor in the development of heart disease. More recent studies, however, suggest that it’s the number of cars on the road (i.e. LDL particles) that matters most.

The crucial test for heart disease risk you’ve probably never heard of.

Coronary arteries are essentially hollow tubes, and the endothelium (lining) of the artery is very thin—only one cell deep. The blood, which carries lipoproteins like LDL, is in constant contact with the endothelial lining. So why does the LDL particle leave the blood, penetrate the endothelium and enter the artery wall? The answer is that it’s a gradient-driven process. Going back to our analogy, the more cars there are on the road at one time, the more likely it is that some of them will “crash” into the fragile lining of the artery. It’s not the number of passengers (cholesterol) the cars are carrying that is the determining factor, but the number of cars on the highway.

The significance of this in terms of determining your risk of heart disease is profound. When you go to the doctor to get your cholesterol tested, chances are he or she will measure your total, LDL and HDL cholesterol. This tells you the concentration of cholesterol (passengers) inside of the lipoproteins (cars), which is not the driving factor behind plaque formation and heart disease. Instead, what should be measured is the number of LDL particles in your blood.

LDL cholesterol levels and LDL particle number are often concordant (i.e. when one is high, the other is high, and vice versa), and this is probably why there is an association between LDL cholesterol and heart disease in observational studies. The elevated LDL cholesterol was more of a proxy marker for elevated LDL particle number in these cases. But here’s the kicker: they can also be discordant. In layperson’s terms, it’s possible to have normal or even low cholesterol, but a high number of LDL particles. (1) If this person only has their cholesterol measured, and not their particle number, they will be falsely led to believe they’re at low risk for heart disease. Even worse, the patients that are the most likely to present with this pattern are among the highest risk patients: those with metabolic syndrome or full-fledged type 2 diabetes. The more components of the metabolic syndrome that are present—such as abdominal obesity, hypertension, insulin resistance, high triglycerides and low HDL—the more likely it is that LDL particle number will be elevated. (2)

On the other hand, patients with high LDL cholesterol (LDL-C) and low LDL particle number (LDL-P) are not at high risk of heart disease. In fact, studies suggest they’re at even lower risk than patients with low LDL-C and low LDL-P. (3) Yet they will often be treated with statin drugs or other cholesterol lowering medications, because the clinician only looked at LDL-C and failed to measure LDL particle number. This is a concern for two reasons. First, statin drugs aren’t harmless. (I’ll go into more detail on this in the third post of the series.) Second, studies suggest that low cholesterol can increase the risk of death, especially in women and the elderly.

In one study of over 52,000 Norwegians, researchers found that women with total cholesterol levels below 195 mg/dL had a higher risk of death than women with cholesterol levels above that cut-off. (4) And a study published in the American Journal of Medicine found that people over 70 years of age with total cholesterol levels below 160 mg/dL had twice the risk of death than those with cholesterol levels between 160-199 mg/dL. (5) Low cholesterol is also associated with increased risk of disease—especially mental health and brain disorders. For example:

• A study in the Journal of Psychiatric Research found that men with low total cholesterol levels were 7 times more likely to die prematurely from unnatural causes such as suicide and accidents than other men in the study. (6)
• A 1993 study published in The Lancet found that depression was 3 times more likely in men over 70 with low cholesterol than in those with normal or high cholesterol. (7)
• A Swedish study found that women with the lowest cholesterol suffered significantly more depressive symptoms than other women in the study. (8)
• A study in the journal Neurology showed that low cholesterol is associated with increased risk of dementia. (9)
• A paper published in the European Journal of Internal Medicine linked low cholesterol levels with Alzheimer’s disease. (10)

It’s important to note that all of these studies were observational, which means that they don’t prove that low cholesterol was the cause of the increased risk of death or disease that was observed. It’s possible, for example, that these patients had another disease that caused both the lower cholesterol and increase in disease or mortality. However, given what we know about the important roles of cholesterol in the body, it’s certainly plausible that low cholesterol is capable of contributing to these problems directly.

Wrapping up: The map is not the territory!

Before concluding, I’d like to point out that although LDL particle number is superior to LDL cholesterol as a marker for heart disease, it’s still just that—a marker. A marker is not a disease. It’s a risk factor for a disease. Having a risk factor for a disease does not guarantee that you will get that disease—it just increases the chance that you will. There are still several gaps in our knowledge about LDL-P and its usefulness in a clinical setting. For example:

• Imagine two people with an LDL-P above 2,000, which puts them in the highest risk group. Person A follows a Paleo diet and lifestyle, gets plenty of sleep, manages stress and has no other significant risk factors for heart disease. Person B eats a Standard American Diet, doesn’t exercise, doesn’t get enough sleep, is stressed out and has several other risk factors for heart disease. Logic would dictate that Person A would be at much lower risk for heart disease than Person B, but there isn’t any comparative data to quantify the difference in risk and it’s unlikely such a study will ever be done. (Who would pay for it?)
• Imagine two people following a healthy Paleo-type diet and lifestyle. Person C has no conventional risk factors for heart disease. Person D has no conventional risk factors either, but does have an LDL-P of 2,000. Logic here would dictate that Person D is at higher risk than Person C, but again, we don’t have actual data to quantify the difference in risk.

Heart disease is a complex, multifactorial process. The likelihood that we’ll have a heart attack depends on numerous factors, including genetics, diet, lifestyle and living environment. The purpose of this article is not to suggest that LDL-P is the only risk factor that matters, or that other risk factors shouldn’t be taken into consideration. It is simply to point out that existing evidence suggests that LDL-P is a much better predictor of heart disease risk than LDL or total cholesterol, and that it appears to be one of the better markers available to us now.

I was going to follow this article with one on statin drugs. But I’m almost certain that all of you are going to ask what increases LDL particle levels after reading this, so I think I’ll cover that next and then move on to statins after that.

Note: if you’re interested in a much more thorough discussion of how to determine your risk of heart disease and how to use diet, supplements and lifestyle changes to protect yourself and those you love, check out the High Cholesterol Action Plan.