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
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.
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!
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.
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.
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.
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.
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.
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.
Tagged as: anxiety, cholesterol, ldl, magnesium, pregnancy
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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.
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.
