The quality of our drinking water is a major determinant of our health and wellbeing. It is important to consider not only the presence of pathogens or contaminants, but also the routine addition of chemicals that may cause us harm. Chlorine is a chemical typically used as a disinfectant in public water supplies as an effective way to reduce the level of pathogenic bacteria in our drinking water. (1)

Unfortunately, this chemical, and other common chemical disinfectants, may have a damaging impact on our bodies’ beneficial bacteria as well.

When chlorine is used as a water treatment, it combines with organic matter to form compounds called trihalomethanes (THMs), also known as disinfectant byproducts. One of the most common THMs formed is chloroform, which is a known carcinogen. (2) Other THMs formed include the di- and trichloramines formed when chloramine is used as a disinfecting agent. (3) These compounds are toxic when consumed, inhaled, or applied to the skin.

Research conducted on the health effects of chlorinated drinking water have demonstrated a variety of toxicity issues. Several studies have found that communities using chlorinated or chloraminated drinking water have an increased risk of bladder, kidney, and rectal cancers. (4, 5, 6) THMs from chemically treated water have been associated with a variety of poor birth outcomes, such as spontaneous abortion, birth defects, and low birth weight. (7) Chlorine and chloramine vapors are associated with greater risk of asthma, and may damage the mucosal lining of the respiratory tract. (8) Free radicals in chlorinated water have been linked to liver malfunction, weakening of the immune system and pre-arteriosclerotic changes in arteries. (9)

While there hasn’t been substantial research on the topic, it’s reasonable to assume that chlorinated water adversely affects beneficial intestinal flora. Chlorine is a powerful antimicrobial agent, and is an effective pesticide against many different strains of bacteria. (10) The compounds in disinfected water may be able to reach the gut not only through our drinking water, but also through daily showers and baths.

A recent post at the Food Renegade blog (11) brought this disturbing theory to light, not only highlighting the harmful effects of chlorinated drinking water, but emphasizing the possibly greater effect that showers and baths could have on our intestinal flora. As we know, there’s a strong connection between asthma, acne, autoimmune conditions and the health of our gut flora. We might speculate that dysbiosis induced or made worse by excess chlorine exposure could contribute to these conditions.

Showering and bathing in chlorinated water may expose us to even more chlorine and its byproducts than drinking this disinfected water.

While our bodies can filter out much of the chlorine from our drinking water, the THMs and other disinfectant byproducts we inhale during showers and baths may be much more harmful, since the chlorine gas we inhale enters directly into our blood stream. (12) Therefore, even if you filter your drinking water, the amount of toxins you are exposed to from your daily shower or bath, through inhalation or skin absorption, may be cause for greater concern.

Research has demonstrated that the cancer risk associated with chlorinated water may actually be due to showering and bathing, rather than drinking the disinfected water. (13, 14) This suggests that many health risks of chlorine may be specifically related to dermal and inhalation exposure. In fact, the chloroform dose from a single, ten minute shower is equal to, and possibly greater than, that from the average two liters of water ingestion on a daily basis. (15, 16)

Therefore, the filtration of your shower and bath water may be even more important than the water you drink.

Chlorine filtration is fairly simple, provided you use some level of technology to remove it from your shower or bath water. There are resources on the Food Renegade blog about where to find chlorine-filtering shower heads and bath filters. (17) This includes the Rainshow’r Shower Filter and the Crystal Ball Bath Dechlorinator, both sold by the Radiant Life Company.

I’d like to point out that chlorine isn’t in everyone’s water supply, but there is another disinfectant that is also of concern. I checked my local water company’s website, and discovered they use chloramine (chlorine + ammonia) to disinfect the water supply. (17) Chloramine exposure may be even more damaging to the lung epithelium than chlorine, and may release ammonia as another toxic byproduct as well.

The filters that remove chlorine don’t necessarily remove chloramine.

Chloramine can be removed for drinking water purposes by a carbon block or activated carbon filter that can be installed on a kitchen faucet. Also, both chlorine and chloramine can be removed for bathing purposes by dissolving Vitamin C in the bath water. One 1000 mg Vitamin C tablet will neutralize chloramine in an average bathtub. (18)

There are no shower filters on the market that completely remove chloramine. (19) There are, however, whole house water filters that remove chlorine, chloramine, and other contaminants.   Unfortunately, they’re quite expensive and thus may not be an option for many people.

Vitamin C shower filters may be a good choice for those looking for an inexpensive way to reduce the chloramine (and chlorine) content of their showers. Vitamin C is an effective dechlorination agent, removing up to 99% of chlorine and chloramine, and vitamin C filters are much less expensive than the whole house filter featured above. The disadvantage to using them is they’re not as durable or effective as a whole house filtration system, and you would need a separate filter for each shower outlet in the house.

Other simple methods to reduce exposure to chlorine and chloramine include: taking shorter or less frequent showers, avoiding excessively hot showers (since high heat increases the amount of steam), and shutting the water off while soaping up. These techniques will help decrease your exposure if filtration or dechlorination is not an option.

I recommend you check with your local water supply company to determine what disinfecting agents they use to sanitize your tap water. You can then use that information to make a decision about which shower filter is most appropriate for you and your family. Until we know more about how chlorinated water affects our health, and especially our beneficial gut flora, it seems prudent to keep chlorine and chloramine exposure to a minimum.

Well, folks, I blew it with the audio this time.  My recording settings weren’t set properly, so we had to use the Skype back-up.  Sorry!

Pork has been getting a bad rap in the blogosphere lately.  In this episode we explore whether pork deserves the harsh treatment, or whether it’s merely a victim of misunderstanding.  We also discuss a novel treatment for chronic sinusitis, which by some measurements is the most common chronic disease in the U.S., as well as a few other great questions.  Enjoy!

In this episode, we cover:

4:38  Is pork a “dirty meat” that causes liver disease?
17:20  What do you recommend for chronic sinus infections?
27:58  Does high intra-abdominal pressure always cause GERD?
35:11  Are “properly prepared” grains OK to eat?
45:45  Is postnasal drip a sign of a bigger problem?
47:35  Should pregnant moms supplement with folic acid?

Links We Discuss:

• Ned Kock – Health Correlator Pork and Liver Disease Article
• Chronic Rhinosinusitis (CRS) and Biofilm Studies:

http://www.ncbi.nlm.nih.gov/pubmed/21739098
http://www.ncbi.nlm.nih.gov/pubmed/21814734
http://www.ncbi.nlm.nih.gov/pubmed/22144052
http://www.ncbi.nlm.nih.gov/pubmed/21865700
http://www.ncbi.nlm.nih.gov/pubmed/22088282
http://www.ncbi.nlm.nih.gov/pubmed/22182736
http://www.ncbi.nlm.nih.gov/pubmed/22241786
http://www.ncbi.nlm.nih.gov/pubmed/22287462

• Xlear Nasal Spray
• Histamine and Tyramine Diet Changes – Gut-Skin Axis Episode
• Pure Encapsulations Nutrient 950 Vitamins

Full Text Transcript:

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

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

Steve Wright:  I’m doing great, man.  I got my sling off yesterday, so I’m finally back to two arms.

Chris Kresser:  Glad to hear it.  I bet that’s liberating.

Steve Wright:  It is, it is; however, I have a bunch of new pains now, and I’m gonna have to learn how to sleep again.  So.

Chris Kresser:  Right.  Ah, well, it’s all part of the fun, huh?

Steve Wright:  Yeah.  Only like four more months, right?  So.

Chris Kresser:  Ha-ha.  You’ll hardly remember it in a few years.

Steve Wright:  Exactly!

Chris Kresser:  Cool.  So, we have some good questions.  We’re gonna do a 100% Q&A episode today, which is a little unusual, but lots going on for me right now, and didn’t have time to prepare anything for the show, and I actually like doing these Q&A episodes every now and then.  Before we do that, though, I want to tell everyone — I’m sure most of you have already heard of this, but in case you haven’t, I want to tell you about a really cool event that’s coming up starting on February 26 and running through March 4.  It’s put on by my good buddy, Sean Croxton, over at Underground Wellness, and it’s called The Paleo Summit.  So, this is an online conference with tons of great speakers in the Paleo/Primal niche, a lot of familiar names:  Mark Sisson, Jack Kruse, Erwin Le Corre from MovNat, Paul Jaminet, Diane Sanfillipo, myself, Sarah Fragoso, Mat Lalonde, Amy Kubal, Denise Minger.  So, it’s a great group of speakers.  And then even Matt Stone is gonna be there for the anti-Paleo perspective, so Sean is really interested in hearing from a number of different voices.  I think that’s great.  I enjoy that.  And it’s really cool because it’s free.  Free is good.  It’s gonna be accessible to everybody, and all you have to do is go there and register and you get a couple of bonus videos:  an interview with Mark Sisson and Sean and another with Sean interviewing Gary Taubes.  So, definitely check it out.  It kicks off on Sunday, February 26, and go to CKPaleoSummit.com to register.  So that’s CKPaleoSummit.com.  And I hope you enjoy it.  It’s a great opportunity to get exposed to some cool stuff, and unlike the Ancestral Health Symposium and PaleoFX, which are awesome events too that I’m speaking at this year, this one’s totally free, and you can participate from the comfort of your own home.

Steve Wright:  Yeah, I’m pretty jacked about this.  I’m all signed up, and I think it’s gonna be great.  I think the speaker lineup is just amazing.  There are 24 people, right? 

Chris Kresser:  Yeah, 24 people.  I think eight days and three people on each day, and then there’s gonna be full transcripts and PDFs and videos and a whole package.  That part is not free, but if you want to have the whole thing so you can refer back to it afterwards, you’ll be able to do that.  So, it’s a cool format.  I think Sean is doing a great thing, and I’m looking forward to being a part of it.  My talk actually is gonna be — it’s called An Update on Cholesterol, so I take a lot of the information that we discussed in the three-part series with Chris Masterjohn, and I distill it down into a really practical framework of what to do — if anything — if you have high cholesterol, when is it a problem, when is it not a problem, and what do you do about it from a natural perspective.  So, yeah, check it out.  It’s pretty exciting.

Steve Wright:  All right, so should we roll on to the first question?

Chris Kresser:  Yeah, let’s do it.

Is pork a “dirty meat” that causes liver disease?

Steve Wright:  OK, so here’s question number one from Marianne:  “I would love to hear what you think about pork consumption and liver disease, as referenced from an article this week from the Perfect Health Diet website.”

Chris Kresser:  Yeah, this has caused a little bit of a stir.  So, for those of you that didn’t see it, Paul wrote an article quoting a 2009 study by Bridges showing a stronger correlation between liver cirrhosis and pork than liver cirrhosis and alcohol.  And Paul’s argument was, therefore, that eating pork may cause liver cirrhosis.  But, of course, correlation is not causation.  We talk about this a lot.  That’s research 101.  Two things occurring together does not necessarily mean that one thing causes the other.  So, it’s really crucial and important to understand that basic principle.  And Ned Kock, who has a blog called Health Correlator, which is pretty technical — he’s a statistician and sometimes it’s over my head.  I’m not a statistician.  I get basic statistics, but when it gets really advanced, my eyes start to glaze over.  But this article is pretty easy to follow, and you should check it out if you are concerned about pork consumption after reading Paul’s article.  Ned did a more sophisticated multivariate analysis on the same study, and he found that the total effect of alcohol consumption on cirrhosis was actually 94% stronger than the total effect of pork consumption on cirrhosis.  He also pointed out that another factor that’s associated with liver cirrhosis is obesity, so in countries where pork is a staple, you might think it’s reasonable to assume that pork consumption may be correlated with obesity, but people who consume a lot of junk food also consume a lot of saturated fat, and they show up in the disease stats, but this is exactly the kind of confusion that led to the mistaken idea that saturated fat causes heart disease, right?  So, that idea rose out of epidemiological studies that saw:  Oh, these people are eating a lot of saturated fat and they have heart disease.  But what they didn’t control for was the fact that those people were also eating tons of other processed junk food that could very well have been contributing to heart disease, and it had nothing to do with the saturated fat, because later when they looked at studies that isolated those variables and they just compared saturated fat with other types of fat, they found that saturated fat did not increase the risk of heart disease.  So, we don’t want to make that same mistake here with pork and liver cirrhosis, and that’s why we can’t look at epidemiological data like this and draw causal relationships from it.  So, Ned went on to — just for the other side of the coin — to look at evidence that pork might be good for you.  And he took some data from NationMaster.com on pork and alcohol consumption and life expectancy, and it was a much larger list of countries than was used in the Bridges study, so it included Australia, Brazil, Canada, China, Denmark, France, Germany, Hong Kong, Hungary, Japan, Mexico, Poland, Russia, Singapore, Spain, Sweden, the UK, and the US — so a broad representative sample from all different parts of the world.  And in that study, the link between pork consumption and life expectancy is actually positive, with a 0.36 correlation.  So, according to this data set, the more pork is consumed in a country, the longer people live.  And in fact, the data suggested that each additional gram of pork consumed per person per day adds an extra 13 days to their life expectancy.  Now before everyone runs off and goes on a 100% pork diet, you have to realize that this is merely a correlation too, so we can’t draw conclusions about causal relationships from this data either, but we can say that the data don’t prove that pork consumption causes liver cirrhosis unless, perhaps, you become obese from eating it.  Now there was a second part to that question, which was:  What about the idea that pork is a “dirty meat”, which is somewhat prevalent in the mainstream?  Conventionally raised pigs or pigs raised in confinement feeding operations are given a lot of antibiotics because of the conditions of their confinement, and the problem with this is that just like in humans, if you give animals a lot of antibiotics, they’ll develop antibiotic-resistant super strains of bacteria.  So, Canadian researchers have found antibiotic-resistant staph bacteria in conventionally raised pork products, and that could, indeed, be a problem.  Also improperly cooked and prepared pork may harbor parasites that can cause disease in humans, and there are two helminths or worms that we have in common.  Both humans and pigs can be affected by them, and they cause the same diseases in pigs and in us.  One is the nematode Trichinella spiralis, which causes trichinosis.  That’s the disease most people have heard of associated with pork.  And then a tapeworm, Taenia solium.  And both of these diseases were known to ancient cultures, including the Egyptian and Greek cultures, and then later on Jews and Muslims, which is probably why both Judaism and Islam proscribe the eating of pork.  But today, I mean, if you completely cook pork, if you cook it thoroughly, that should effectively kill the parasites if they’re present, and that’s probably why trichinosis has become pretty rare in the US, because cooking pork thoroughly has become a widespread practice.  And traditionally pork was marinated or cured, i.e. bacon, before cooking because the marinating and curing helped kill the pathogens, as well.  So, if you’re concerned about the potential of pathogens in pork, (1) don’t eat conventionally raised pork.  Get grass-fed, pasture-raised pork from a local farmer or a farmers’ market or a store that sells that.  And that will reduce the risk of super strains of antibiotic-resistant staph that you would find in conventionally raised pork.  (2)  You can marinate or cure pork before eating it.  One way to do that without using nitrates or nitrite salts is just to use a little bit of salt and a natural sweetener, like maple sugar, to treat the meat, to marinate it for a period of time, maybe 18 hours, 24 hours, and some spices with flavor, and then just make sure to cook it all the way through, and it shouldn’t be an issue.  So, you know, based on the evidence that I’ve seen, I don’t think that you can make an argument that pork is unhealthy or is associated with disease.  I think you can make an argument that undercooked pork or improperly prepared pork that’s raised in confinement feeding operations can contribute to that, but I think we need to be a little more specific, you know, when we make these kinds of statements. 

Steve Wright:  I’m glad you cleared that up, because I was really sweating about my bacon.

Chris Kresser:  Ha-ha, I know!  A lot of people out there were freaking out.  Don’t mess with their bacon.

Steve Wright:  Do you eat pork on a regular basis at all?

Chris Kresser:  I do eat pork.  I like pork, and we get it from a local farm, and we do marinate it and prepare it that way, and we often, you know, we cook it for — we’ll usually slow cook pork, like, if we get a pork shoulder roast or something like that, and we’ll turn it into carnitas, and we’ll roast it for a long period of time at a low temperature, and that will kill any potential pathogens in there.  I do eat bacon.  I’m not, you know, I don’t eat it every day, but I have it probably two or three times a week.  And I love pork chops, actually.  That’s one of my favorite kinds of meat.  So, I think, like I said, as long as you prepare it well and as long as you cook it thoroughly, it shouldn’t be a problem.  Now the other issue with pork is the omega-6 content, and this has less to do with how the pork is raised, although certainly pork that’s raised in confinement feeding operations is likely to have more omega-6 because of the food that they’re given, but even pasture-raised pork will have more omega-6 than beef or lamb or any other kind of wild game meat, of course.  But it has less omega-6 than chicken, than dark-meat chicken, so I don’t think the omega 6 issue is a reason to completely avoid pork.  I just think it’s probably a reason not to make it your staple meat that you eat every day, twice a day, but I don’t think it’s a reason to avoid it completely.

Steve Wright:  I’m glad you brought that up, because I think most people hold chicken to be like the super-safe meat, but little do they know that it might not be so safe. 

Chris Kresser:  Yeah, I mean, it’s all in moderation.  Like, we have the ability to deal with some amount of omega-6, and eating dark-meat chicken, you know, once or twice a week, I don’t think it’s gonna cause any serious health problems for anybody.  I think that the risk in doing what I do and making people aware of these things is it’s sometimes difficult to convey the — What am I trying to say?  It’s easy, I think, sometimes for it to come across too literally, and I’d like to find a way of communicating it where that’s less likely to happen.  But, you know, if I write an article that says omega-6 is proinflammatory in excess and contributes to various disease states, then sometimes that gets interpreted like I shouldn’t eat any omega-6; you know, like even half of an avocado is gonna make me keel over and die of a heart attack.  And I just don’t think that’s the case.  I don’t see evidence really to support that, and I don’t see it clinically in my practice.  I think it’s wise to reduce our omega-6 consumption significantly, as I’ve pointed out several times, but that doesn’t mean we can’t have dark-meat chicken or avocados or walnuts or things like that occasionally as part of an overall healthy diet.  And so, I think the same is true with pork, provided you follow the guidelines that I just mentioned.

Steve Wright:  Yeah, I’m glad you brought that up.  I didn’t mean to demonize chicken in favor of pork or anything, because I think you’re right.  It’s hard for us as we read what you write and as we all do our own research, we’re always looking for a black-and-white answer.  And I think I’ve learned as you get deeper and deeper, you start to become more appreciative of the body we have and its systems, and you start to realize that everything is kind of on a continuum.

Chris Kresser:  Um-hum.

Steve Wright:  And there’s usually never a supremely right or supremely wrong way to eat some things. 

Chris Kresser:  Um-hum.  Very well said.

Steve Wright:  Or natural foods, that is.

Chris Kresser:  Um-hum.  Yeah, and it depends on a lot of factors too, like how healthy you are now, what your goals are, you know, where you’re coming from, and I think there’s a question later where we’ll get into more detail about this, but it’s just good to point out in the context of the whole pork thing.

What do you recommend for chronic sinus infections?

Steve Wright:  Cool.  Well, let’s roll on for the next question from David.  He asks, “What do you recommend for chronic sinus infections?  This is, according to some reports, the most common chronic disease in the United States.  Research by Mayo Clinic in 1999 found that virtually all (96%) cases of chronic sinusitis are caused not by bacteria but by fungus.  So, what is your approach to this?”

Chris Kresser:  Yeah, this is a big topic, and maybe we’ll do an entire show on it, and we’ll have Kurt Harris come and help us out.  He is somewhat of an expert on this topic, and I’ve consulted him about it a few times.  And, yeah, I’ve read that Mayo Clinic thing, and it turns out to be a little bit of a red herring.  The consensus that I respect on fungus is that except for true fungal rhinosinusitis — which is what the technical term is for chronic sinus infections, chronic rhinosinusitis or CRS — true fungal CRS is easily diagnosable by the presence of eosinophilic mucin, but that’s actually pretty rare, and fungus in the nose is commensal, meaning it’s just part of the body’s natural terrain, and most cases of CRS have nothing to do with fungus being present, and furthermore, there is no good evidence that antifungal agents help in the treatment for fungal rhinosinusitis, which is relatively rare.  So, I don’t actually buy the fungus hypothesis for that reason, and my view on it is that it’s probably more like chronic, recalcitrant, difficult-to-treat sinus infections are more related to biofilm than fungus, and particularly in those who have had surgery and those who have poor immune function.  And there’s a bunch of studies that I’ve looked at connecting CRS to biofilm — and we can put those studies in the show notes for anybody that’s interested — but there are some pretty interesting emerging treatments for chronic sinusitis that relate to this biofilm hypothesis, and one of them is nasal irrigation with Johnson’s baby shampoo solution.

Steve Wright:  What?!

Chris Kresser:  Ha-ha, yeah, no joke.  This is in the scientific literature.  You’ll find studies in PubMed about this.  So, it’s a 1% Johnson’s baby shampoo solution, so you do kind of like a Neti or a nasal irrigation with the 1% baby shampoo.  And in the study, 60% of patients noted a significant improvement in symptoms, you know, reduction of thickened mucus and postnasal drainage.

Steve Wright:  Is this biofilm, is this in the gut or is this in the nose or the cavities?

Chris Kresser:  Biofilm is everywhere.  Biofilm is an extracellular matrix that bacteria reside in, and most pathogens actually we think now.  One really good example of biofilm is plaque, you know, the thin film that covers our teeth.  And this extracellular matrix allows the bacteria to share nutrients and also even DNA, and it protects them from our own innate immune defenses and also from any external antimicrobials that we might take.  So, it’s kind of like a protective community, strength in numbers, and as long as the bacteria are in the biofilm, a lot of the antibacterial agents that we use don’t really work.  So, that explains why some people take antibiotic after antibiotic after antibiotic with sinus infections and they just don’t recover.  So, one therapeutic approach is to disrupt the biofilm, and there are ways to do that topically, and there are ways to do that systemically.  So topically, one way is this Johnson’s baby shampoo irrigation, and the way it works is that Johnson’s baby shampoo has chemical surfactants in there, and you can think of them as like a therapeutic detergent to break up and assist in the eradication of biofilms, and that’s been known for a while.  That’s been used in the orthopedic literature, this use of chemical surfactants to break up biofilm.  But in chronic sinusitis, it probably has two benefits:  One is as a mucoactive agent, and mucoactive agents work either to increase the ability to expectorate sputum or to decrease mucus hypersecretion.  Or, number two, it has potential bactericidal activity; in other words, antibiotic activity.  So, that’s one.  Another solution that’s maybe a little bit more accessible to people and a little bit easier to get your head around are xylitol nasal drops.  Now xylitol is a sugar alcohol, but it has activity against biofilm, and this is one of the reasons why xylitol chewing gum has become popular amongst dentists.  As I just mentioned, plaque is a biofilm, so if you chew xylitol gum, that can actually help break up plaque.  So, these xylitol nasal drops, or there’s actually a nasal spray that’s called — I’m not sure how to pronounce it.  It’s a very bad name.  Anyways, Xlear nasal spray.  And I’ve read a couple studies that use a similar solution and some accounts from doctors who are working with this stuff, and the consensus seems to be that it needs to be used pretty frequently, like up to three to four times a day, for it to work.  But unlike steroid sprays, which are often used in nasal sprays, xylitol doesn’t dry out the nasal passages, and it doesn’t inhibit the immune defense of the body.  Instead, it acts more as a lubricant, which makes it easier for natural mucus secretions to occur that kind of eliminate the pathogens.  I mean, the way it should work is that the mucus forms, and then you blow your nose and it carries the pathogens out of the nasal passage, and xylitol helps that to happen by lubricating them and acting as a surfactant that allows the nasal passages to clear.  So, another potential avenue, although I haven’t seen any research on this, is using a systemic biofilm disruptor, which would be something like InterFase Plus, and that’s a product that has EDTA and some enzymes that chelate — Well, EDTA chelates some of the minerals that are needed to produce biofilm, that biofilm formation depends on.  And then there are some systemic enzymes that have been shown to break up biofilm.  So, that needs to be taken on an empty stomach, because if you take it with food, the enzymes in there will help digest the food, which is nice but it’s not really, you know, what you’re taking it for.  So, InterFase Plus needs to be taken on an empty stomach a couple hours after a meal or a half hour before a meal.  And, like I said, I haven’t seen any studies on systemic biofilm agents like this in chronic rhinosinusitis, but I do use InterFase for other kinds of infections, and I’ve found it to be extremely effective in most cases.  In fact, it seems to cause more of a Herxheimer or die-off reaction in treating infections than a lot of the botanical antimicrobials, which is indicative that it’s working. 

Steve Wright:  Interesting.  So, let’s back up to the very beginning of the question just to clarify this for everyone.  Chronic rhinosinusitis, you said, was kind of rare, so what’s –

Chris Kresser:  No, chronic rhinosinusitis is actually pretty common.  It might be one of the most common diseases there is, but the fungal chronic rhinosinusitis or fungal RS, as it is called, which is caused by a fungus, that’s rare. 

Steve Wright:  OK.

Chris Kresser:  And that is easily diagnosed by looking for eosinophilic mucin, and there’s been an idea that — I don’t know if it started with that Mayo Clinic article, but it’s been bounced around a lot in the blogosphere that all sinus infections are fungal in origin, and what I’m saying is I don’t think the evidence really supports that.

Steve Wright:  All right, I gotcha.

Chris Kresser:  Yeah, it’s more about biofilm than it is about fungus.

Steve Wright:  OK.  That makes much more sense now.

Chris Kresser:  Yeah, so I mean, of course, all of the other things apply, like all of the other things that you would do to regulate your immune system and not eating food toxins and making sure you have the micronutrients that support immunity, like vitamin C and iodine and selenium and, you know, exercise, all the basics apply here.  But I am assuming a lot of people are already doing that who are listening to this show, and they’re already eating a Paleo/Primal type of diet, and if they’re still having sinusitis, then you might want to investigate this biofilm angle.  I think the easiest way to do that is the Xlear — or however you say that — nasal spray and then possibly a systemic biofilm agent like InterFase Plus.

Steve Wright:  OK, and don’t forget to check your vitamin D if this is a problem for you, as well. 

Chris Kresser:  Absolutely.

Does high intra-abdominal pressure always cause GERD?

Steve Wright:  All right.  So, let’s move on to the next one.  This comes from Brendan:  “I’ve got one regarding your position on GERD.  In my medical nutrition therapy class at school my professor taught us that increased pressure from the other side of the lower esophageal sphincter actually helps to keep the sphincter closed and that a lack of pressure allows it to relax and allows the reflux to occur.  This seems to conflict with your idea that bacterial overgrowth leads to increased intra-abdominal pressure and causes reflux.  I tend to trust your information more, but I wanted to get your opinion on this.”

Chris Kresser:  A real tongue-twister, huh?

Steve Wright:  Man!  Got me all messed up.

Chris Kresser:  Ha-ha.  So, I think the first thing I want to say is I don’t believe that all GERD is caused by one thing.  GERD is a pretty vast landscape of varying conditions, and a lot of what is referred to as GERD, gastroesophageal reflux disease, is actually NERD, which is non-erosive reflux disease.  There are lots of different presentations, lots of ways that it shows up and manifests, and I don’t think they’re all caused by the same thing.  In fact, some people do produce excess stomach acid, and that is the cause of their problem.  That’s a minority.  According to the scientific literature, it’s a small number of people, but it doesn’t mean that, you know, the fact that I wrote that series suggesting that GERD is caused by low stomach acid primarily and bacterial overgrowth doesn’t mean that that’s true in 100% of cases.  So, just wanted to clarify that.  The main pathology involved in GERD or NERD is transient lower esophageal sphincter relaxations or TLESRs, as they are referred to in the literature.  And so, just a little anatomy/physiology here:  The esophagus is separated from the stomach by the lower esophageal sphincter, and that sphincter should most of the time be closed, and it opens, of course, when we eat and when we burp and things like that.  One of things, I mean, the main thing that happens with GERD or NERD is that you get these transient relaxations of that sphincter at inappropriate times, so the sphincter will open or relax when it should be closed, and then you get a reflux of acid or bile into the esophagus, and that causes the symptoms associated with reflux.  So, studies have shown that gastric distension increases the number of TLESRs, the number of these transient relaxation events.  And, of course, gas can increase gastric distension and thus can increase the number of transient relaxations and reflux.  So, I think you can make an argument — I understand where the question is coming from, and it’s true that pressure could, in theory, keep the sphincter closed, but it turns out that, according to the studies, that this gas and gastric distension actually increases the number of relaxations that happen.  And if you do a search on PubMed for gastric distension and TLESRs, you’ll see the study come up, and you can take it in and show it to your professor.  Also, I think it’s important to look at actual clinical results.  I’ve talked about this three-legged framework I use for determining whether something is valid or for testing a hypothesis.  And one of those legs is modern scientific research; that’s important.  Another leg is traditional wisdom, evolutionary medicine, which is also important.  You know, does it check out according to what we know about ancestral health?  And then the third leg, which I think is also very important, is clinical experience.  And, so, for something to really check out for me, it has to pass all three of those tests.  And if you look at the comments on some of those GERD articles, particularly the three steps to curing GERD article, you’ll see literally hundreds of people that have tried this protocol and that were suffering tremendously and had been on PPIs in some cases for as much as 20 years or acid-suppressing drugs for 20 years and were able, using this protocol, which is geared, you know, towards reducing the bacterial overgrowth in the small intestine and improving, increasing stomach acid production via HCl, have been able to stop for the first time in their lives their acid-suppressing drugs and have been able to eat food without reflux for the first time in their lives.  So, I think that’s highly significant and shouldn’t be ignored as part of this whole picture of figuring out reflux and GERD.  I will say that there are some people that that protocol doesn’t work for, and they very well may be the people that do produce excess stomach acid for other reasons, and in those cases something like melatonin and methylation precursors, serotonin precursors might be a better option because melatonin has been shown to regulate the contractility of the lower esophageal sphincter, and that’s probably why it works in a couple studies as well as PPIs, a combination of melatonin and serotonergic nutrients like 5-HTP and methyl donors like B6 and B12 and folate.  So, I think that’s it.  That’s how I’m tying together the gastric distension and gas and the transient lower esophageal relaxations.

Steve Wright:  You know, the one thing I’ve never really understood, Chris, is with the lower esophageal sphincter, is that like a flap, like a trapdoor flap, or is it more like an opening and closing of, like, a hole?  How does it actually work?

Chris Kresser:  It’s more like a flap, I think.

Steve Wright:  OK.

Chris Kresser:  I’m not totally sure, actually.  It would be interesting to see a picture.

Steve Wright:  Yeah, I’ve never seen one, and I was just curious because with some of these, you know, low pressure / high pressure kind of is determinant upon how it actually mechanically works.

Chris Kresser:  Yeah, I’m pretty sure it’s a flap.

Are “properly prepared” grains OK to eat?

Steve Wright:  Interesting.  OK.  Let’s more on to the next one.  This comes from Monica, and she would like to know your thoughts regarding several real food bloggers who are recently posting about wheat, grains, and even gluten and the fact that they are not inherently bad and if properly prepared after having undergone a gut-healing protocol, can be consumed without ill effects.

Chris Kresser:  I bet she’s talking about Matt Stone.

Steve Wright:  Yeah, I’ve seen some from, I think, Cheeseslave, as well.

Chris Kresser:  Yeah.  Just getting a little sip of water here.  Let’s get back to what you and I were talking about at the end of the first question on pork.  Health is a continuum, so if you have on the one hand death, which is the end of health, and on the other hand you have perfect health, then there’s a huge, huge spectrum of what you can experience in between those two extremes.  And I just assume that most people who are listening to the show and who are reading my website are interested in optimizing their health, and so that’s the audience that I’m speaking to.  I’m also, because I’m a health care practitioner, I’m speaking in particular to an audience that’s dealing with chronic health issues and disease, so you know, above and beyond just people who want to optimize their health, I’m really more focused on people who have health problems, and I’m trying to help them recover.  So, a lot of what I speak and write about is geared towards that audience, and that’s important to understand because that audience is more likely to experience difficulties with foods that may not be problematic for people that are otherwise healthy, and I think grains and wheat and even gluten fall into this category, where — Well, let’s break them down separately.  So, gluten, I think, is an inflammatory protein on its own, and so I don’t actually recommend that even healthy people eat it for that reason, but does that mean if someone who is very healthy, has a really healthy gut and no real health issues to speak of is gonna keel over and die if they eat a piece of bread a few times a week?  I don’t think so.  Probably not.  And, you know, we can handle some amount of inflammation.  We can handle some amount of toxicity, of toxins.  You know, there’s a concept called hormesis where a small amount of toxin actually sensitizes our immune system and our ability to cope with larger amounts of toxins.  So, I think that you really have to consider who is asking the question, where are they coming from, again, what are their goals, are they trying to optimize their health to the greatest possible degree and feel as good as they possibly can?  Most people in that situation do better without wheat and gluten, in my experience.  That doesn’t mean there aren’t people that are exceptions.  It doesn’t mean that you can’t eat some wheat and gluten if you’re healthy and still feel fine.  But if you’re interested in absolutely optimizing your health, I think you’re better off without it.  Now, with grains — and there is a distinction here between grains that are not properly prepared and grains that are properly prepared.  Grains that are not properly prepared have a number of food toxins in them that are part of the plant’s natural defense system, and of course, people who are following a Paleo and Primal type of diet are well aware of all of this.  But again, you know, for someone who is basically healthy, some small amount of grain may not be that big of a deal.  And even for people who are not that healthy, if you properly prepare the grains and break them down, break down the phytic acid, break down some of the food toxins by soaking or fermenting or sprouting, then grains may not present any problem at all, even for someone who is not at the top of their health.  But I’ll say in my experience as a clinician that most people who are sick or who are dealing with gut issues or immune dysregulation or any number of other conditions generally feel better without grains, as a general rule.  But these are all general guidelines, and they’re all subject to all of the variables that I’ve mentioned.  You know, what’s the current health status, what’s the constitutional health, what are the goals?  So, I think that’s why I get a little bit irritated about all of the debating because it’s kind of nonsensical unless you know what the context is. 

Steve Wright:  That makes sense, and I think you brought up something really important there, which is the toxic load.  You know, if you’re pretty healthy and you recovered your health, if you keep the toxic load pretty low and you eat a non-prepared grain every once in a while, it’s likely that you probably wouldn’t see a problem because your body is designed to handle that load.

Chris Kresser:  That’s right.  Exactly.  And then let’s take it a step further:  I’ve said this in the Beyond Paleo, previously the 9 Steps series, but there’s more to health than food.  You know, there is!  There’s a lot more to health than food.  There’s movement and exercise.  There’s sleep.  There’s stress management.  There’s cultivating pleasure.  There’s having a purpose and feeling like your life is meaningful and you’re serving others or some higher purpose that goes above and beyond just, you know, getting what you want.  I think that’s actually a really crucial element that contributes to health.  There’s relationships, how you relate to your partner, your kids, your colleagues at work.  There’s connection with nature, and you know, this whole earthing movement that’s kind of taken on steam lately in the Paleosphere; there’s concern with that.  So, there are so many things that contribute to whether we feel healthy on a daily basis and whether we prevent disease or recover from disease, and food is a huge part of that equation, of course.  I think it’s pretty clear that I believe that from what I write.  But it’s not the only variable, and when obsession with food happens at the expense of all of those other things that contribute to health, then actually even eating really healthy food can become problematic.  I think we talked about this on a previous episode, my beer and pizza story. 

Steve Wright:  Yeah, I’m not sure I remember that, but sounds like a fun diet, maybe?  I don’t know.  Ha-ha!

Chris Kresser:  Ha-ha!  OK, I’ll tell it again.  It’s not my beer and pizza story, but I’ll tell it briefly again for people who are new to the show.  So, I was in San Diego way back when I was in school, and I was interning with a holistic doctor, and he specialized in, you know, treating people who were dealing with chronic mysterious kind of diseases.  And we had a young guy, I think he was like in his early 20s, and he came to us and he was really emaciated, really sick, and just couldn’t eat anything.  And, so, the doctor further restricted his diet, and I mean, he got down to the point where he was eating like boneless, skinless chicken breasts, broccoli, and quinoa, I think were the only three foods he was eating.  And each time he came back to the office, he was just literally wasting away in front of our eyes.  He looked like death.  You know, he looked so sick.  And he was this young guy, you know, like totally in the prime of his life.  So, he disappeared, stopped coming.  We didn’t see him for, like, six to seven months, and then he came back to the office and he was literally — We didn’t even recognize him.  He looked like a different person.  He had gained like 40 pounds, no dark circles under his eyes, really good complexion, you know, looking extremely healthy.  And the doctor and I were both like, “Whoa!  What happened here?  What was it?  Was it diet?”  And he’s like, “Yeah, it was diet.”  And we said, “Well, what was it?  The anti-candida diet or the macrobiotic diet?  Which one was it?”  And he said, “It was the beer and pizza diet!”  Ha-ha, and we were like, “What?”  And he said, “Yeah.  I just got to the point where I thought if I’m gonna die,” which he though he might, “I’m gonna just forget about all these dietary restrictions and have some fun before I check out.”  And so, he decided that at three days a week he would go out with his friends and have beer and pizza and the rest of the time he would eat whatever he wanted.  And after, you know, several months of doing that, he was completely transformed and completely well.  And, you know, there are a lot of caveats to the story, but in his case, I think, a lot of what was happening was social isolation and he had broken up with his girlfriend because she just, you know, couldn’t handle being with him, and there was a lot going on behind the scenes there, and I’m not suggesting that it’s as simple as just, you know, having fun and eating whatever you want.  That’s ridiculous.  It doesn’t work that way for everybody.  But I am suggesting that that’s how powerful the mind and the heart can be in the healing process and that sometimes eating the wrong food with the right attitude is a better choice than eating the right food with the wrong attitude. 

Steve Wright:  Hmm.  Good advice.  OK, well I know we don’t have that much more time here, so let’s ask at least one more question.

Chris Kresser:  All right.

Is postnasal drip a sign of a bigger problem?

Steve Wright:  This one comes from Warren, and he’s wondering — and it kind of might relate to a previous question — he’s wondering about postnasal drip.  Is it a sign of a larger problem, and could it be helped by just eliminating dairy?

Chris Kresser:  Uh, yes, it is a sign of a larger problem.  That’s not a normal physiological process.  And eliminating dairy is certainly a good step.  I think if you’re not already eliminating wheat and grains, that’s important too.  Wheat tends to have a really strong connection with sinus problems, in my experience.  And, so, a Paleo type of diet as a starting place, maybe a 30-day challenge where you eliminate dairy and — I don’t really know necessarily that an autoimmune version is necessary, but if you wanted to be really thorough, you could do that and eliminate eggs and nightshades and all dairy for 30 days and then start adding those things back in sequentially.  And if you’re still having the postnasal drip at that point, it’s possible that there’s a histamine issue there.  You could try a low histamine and tyramine diet, which we’ve talked about before on the show when we talked about skin problems, the gut-skin issues.  And then if you’re still, after that, having issues, it’s probably time to seek out some help and see what’s happening with the immune system.

Steve Wright:  So, if you’re already on a Paleo diet and you don’t think you have a histamine problem, it’s indicative of an immune system dysregulation?

Chris Kresser:  Yeah, immune dysregulation, some inflammation there in the sinuses.  Yeah, definitely.

Steve Wright:  OK.

Chris Kresser:  We can do one more.  I see that the next one is pretty short, too.

Should pregnant moms supplement with folic acid?

Steve Wright:  All right.  This one comes from Sally, and she would like some advice on the whole folic acid issue.  Is there any prenatal vitamin you do recommend?  And if so, which?

Chris Kresser:  Yeah, so, folic acid is a synthetic form of the active methyltetrahydrofolate, or there are different versions of active folates other than that.  But folic acid — the important thing to realize is it’s a synthetic chemical that’s not found in nature in the body, and it has to be converted via several steps into the active forms of folates, which are what the body needs and can utilize.  So, the problem is that most multivitamins, including prenatal vitamins, use folic acid, and what happens in a lot of people is that that conversion is poor from folic acid to active folates, and you get a buildup of unmetabolized folic acid.  And unmetabolized folic acid has been linked with cancer and other health problems, and this can happen at doses as low as 400 mcg a day.  It certainly is more likely to happen at higher doses of 800 mcg per day, which is often what’s in pregnancy multis.  So, you want to make sure if you’re taking supplemental folate that it’s an active form of folate.  So, sometimes it’s abbreviated as L-5-MTHF, which is 5-methyltetrahydrofolate.  There’s a brand name called Metafolin.  It is used in Thorne products and Pure Encapsulations and some other products.  You just want to make sure on the bottle that it says “folates” on there and not “folic acid.”  But in terms of a prenatal that I do recommend, there aren’t that many because most multivitamins, in my opinion, have too much of the wrong thing and not enough of the right thing.  But the one I would recommend is Nutrient 950 with Vitamin K, and that’s by Pure Encapsulations, and you can find it online.  It’s more expensive than other choices, but it’s definitely worth it.  There’s not much that’s more important than nourishing your body with the right nutrients if you’re trying to conceive.  That said, I think prenatals are not strictly necessary if you’re getting all of the nutrients that you need from food.  Additional folate is one of the few things that I think is crucial even if you’re eating a Primal/Paleo type of diet because it’s so important for the development of the fetus and the prevention of neural tube defects that I think it just makes sense to take some extra folate during prenatal period and during pregnancy. 

Steve Wright:  And you couldn’t really get that from food or you’d have to eat too much greens or anything probably?

Chris Kresser:  Yeah, I mean, you can get some folate from foods, but folate is highest in chicken liver, lentils, and leafy greens.  You’d have to eat a lot of, you know, like, six to eight cups of dark leafy greens a day to get the recommended folate amount.  You’d only have to eat 3 ounces or so of chicken liver, but I don’t know that many people that are eating 3 ounces of chicken liver.  And then grains and legumes are other sources of folate, and those are not happening on the Paleo and Primal type of diet, so I think supplemental folate is a good idea.

Steve Wright:  OK, awesome.  Good to know.  I think that will help a lot of people.

Chris Kresser:  Yeah, and if, you know, folks need more guidance on this specifically, you can check out The Healthy Baby Code, HealthyBabyCode.com.  That’s my whole program with a lot of detailed information about fertility and pregnancy nutrition. 

Steve Wright:  If someone is thinking about getting pregnant, how soon should they begin supplementing?  Is it a couple months or a year?

Chris Kresser:  Well, yeah, probably.  I mean, honestly, in some ways the sooner the better.  I mean, to an extent.  There’s no need to start 10 years in advance, but if you started a year in advance, you would just improve your chances of conceiving easily probably.  And, you know, there’s no reason not to do that maybe other than expense because folate at the kind of dose I’m recommending is well tolerated and is not gonna cause any problems.  So, you know, six months to a year before, I think, starting the special fertility stuff is a good idea. 

Steve Wright:  You definitely want to pick up The Healthy Baby Code so you get all the info about what you should be doing. 

Chris Kresser:  All right.  I think that’s it.

Steve Wright:  Yeah, I think that’s what we got for questions this time.

Chris Kresser:  Let’s call it a wrap.

Steve Wright:  All right.  It’s been a good show.  If you’re new to the Paleo Diet or you’re just interested in optimizing your health, check out Beyond Paleo.  It’s a free 13-part email series on burning fat, boosting energy, and preventing and reversing disease without drugs.  To sign up, go to ChrisKresser.com and look for the big red box.  Chris and I want to thank you for listening today, and please keep sending us your questions at ChrisKresser.com using the podcast submission link.  If you enjoyed listening to the show today, head over to iTunes and leave us a review.

For decades, fiber has been touted as an essential component of a healthy diet. The supposed benefits of a high-fiber diet have been drilled into us through recommendations by our doctors, government, and the food industry alike, yet many of these health claims have not been proven by research.

In fact, many studies have demonstrated that excess intake of fiber may actually be harmful, particularly for gut health.

The majority of the research supporting the benefits of dietary fiber come from epidemiological studies that link the consumption of fiber-rich fruits and vegetables with a lowered risk of certain diseases such as obesity, heart disease and cancer, particularly colon cancer. (1) Yet when tested in the lab, controlled intervention trials that simply add fiber supplements to an otherwise consistent diet have not shown these protective effects. (2) (3) (4)

The Institute of Medicine recommends a daily fiber intake of 38 grams for men and 25 grams for women (5), which may come from dietary fibers, both soluble or insoluble, or the addition of “functional fibers” to the diet. The IOM defines functional fibers as non-digestible carbohydrates that have been isolated or extracted from a natural plant or animal source, or they may be manufactured or synthesized. Examples of functional fibers are psyllium husks, chitin from crustacean shells, fructooligosaccharides, polydextrose, and resistant dextrins. (6)

These functional fibers are often added to processed foods as a way to bulk up the fiber content for consumers looking to meet the IOM intake guidelines. A recent report by NPR commented that despite the lack of significant evidence linking fiber intake to health outcomes such as reduced heart disease or cancer, many consumers are buying foods that are fortified with synthetic fiber additives under the guise of health promotion. (7) Three grams of added fiber is enough to allow these food products to claim to be a good source of fiber, and the food industry has used these fiber guidelines as a way to increase their sales of grain-based products in particular. (8)

Tan and Seow-Choen, in their 2007 editorial on fiber and colorectal disease, call insoluble fiber “the ultimate junk food”, as “it is neither digestible nor absorbable and therefore devoid of nutrition.” (9) Excess insoluble fiber can bind to minerals such as zinc, magnesium, calcium, and iron, preventing the absorption of these vital nutrients. (10) Large excesses of certain soluble fibers like pectin and guar may also inhibit pancreatic enzyme activity and protein digestion in the gut, leading to an anti-nutritive effect. (11)

The addition of insoluble and soluble fibers to processed foods may actually cause these foods to be even less nutritious than if they were not enriched with any fiber at all.

A high-fiber diet has also been described as a preventative strategy for the development of diverticulosis, a disease that is markedly more common in Western countries. However, when researchers tested the theory that a high-fiber diet prevented diverticulosis, they not only found that a high intake of fiber did not reduce the prevalence of diverticulosis, but that a high-fiber diet and greater number of bowel movements were independently associated with a higher prevalence of diverticula. (12) Interestingly, this study found no association between the presence of diverticulosis and red meat intake, fat intake, or physical activity, which are other factors commonly attributed to diverticulosis.

The researchers hypothesized that one possible effect of a high-fiber diet in the development of diverticulosis could be the quantitative and qualitative changes in gut bacteria due to the excessive fiber intake. Both insoluble and soluble fibers are shown to alter gut bacteria in as little as two weeks. (13) It is possible that the high levels of excess fiber and overgrowth of intestinal bacteria may have contributed to the development of diverticular pouches in the colon.

This hypothesis brings up another side to the fiber debate: the effect of dietary fiber on beneficial gut bacteria, as well as the bacterial fermentation of undigested soluble fiber into short-chain fatty acids such as butyrate. When we eat the soluble fibers found in whole plant foods, the bacteria in our gut ferment these fibers into short-chain fatty acids like butyrate, proprionate, and acetate, and greater amounts of fiber consumed will lead to greater short-chain fatty acid production. (14) In this case, naturally occurring soluble fibers are very important for feeding the friendly bacteria that live in our guts.

One of the risks of long term very low-carbohydrate (VLC) diets, in my view, is the potentially harmful effect they can have on beneficial gut flora.  VLC diets starve both bad and good gut bacteria, which means these diets can have therapeutic effects on gut infections in the short term, but may actually contribute to insufficiency of beneficial strains of gut bacteria over the long term. Providing adequate levels of carbohydrate and soluble fiber to feed friendly bacteria is important for optimizing digestive health and maintaining the integrity of the gut lining through the production of short-chain fatty acids.

Stephan Guyenet has written an excellent blog post describing the benefits of butyrate and other short-chain fatty acids on the maintenance of healthy gut integrity. (15) Butyrate has anti-inflammatory effects, increases insulin sensitivity, and may delay the development of neurodegenerative diseases. It may also be helpful in the treatment of diseases of the colon such as Crohn’s, IBS or ulcerative colitis. (16)

Stephan believes that butyrate may play a significant role in healthy metabolic function, stress resistance, and the immune response. He also asserts that the epidemiologically observed benefits of a diet high in naturally occurring fiber are likely due to the higher butyrate production from these diets. In this case, a higher fiber diet could be protective and beneficial for health, particularly if the fiber is soluble.

So what does this mean for our own consumption of fiber?

Ideally, dietary fiber should be coming from whole food plant sources. Many foods in the Paleo diet are great sources of both soluble and insoluble fiber, such as yams and sweet potatoes, green leafy vegetables, carrots and other root vegetables, fruits with an edible peel (like apples and pears), berries, seeds, and nuts. Interestingly, butyrate itself is also found in high-fat dairy products such as butter and cheese, and can also be provided by the bacteria found in fermented foods. (17)

Although I recommend that most people get fiber from whole foods, there are some people that may benefit from soluble fiber supplementation – including those that aren’t able to eat fruit or starch due to blood sugar issues or weight regulation, and those with severely compromised gut flora or gut dysbiosis.  In these cases I’ve found soluble fiber and/or prebiotic supplements to be helpful.

For healthy people, including a variety of fibrous whole plant foods, fermented foods, and high-fat dairy as tolerated should eliminate the need to supplement with extra fiber, especially those insoluble fibers that are from sources high in anti-nutrients. A Paleo diet with some level of attention paid to the quality and quantity of vegetables, fruits, and starchy tubers can provide adequate levels of soluble fiber to feed the friendly bacteria in the gut that convert these fibers into beneficial short-chain fats like butyrate.

Recommended supplements if needed:

Prebiotic: Klaire Labs Biotagen

Soluble fiber: Organic Acacia Fiber

Caution: it’s crucial to start with a very low dose of prebiotic or soluble fiber and build up slowly over time.  This will minimize any potential adverse reaction that can occur with significant changes (even positive changes) to the gut microbiome.  For Biotagen, start with 1/4 of 1/8 of a tsp (1/32 tsp.) and increase by 1/32 of a tsp every 4-5 days.  For Organic Acacia Fiber, start with 1/4 of a tsp. once per day and build slowly from there.

Sean Croxton over at Underground Wellness is hosting an online Paleo extravaganza called the Paleo Summit.

Whether you’re hardcore into paleo, just getting started, don’t really know anything about it, or hate it and think it’s all hype — this event has something for you.

Mark your calendars, because this event (8 days of in all) starts Sunday, February 26th.

Speakers include Mark Sisson, Mat LaLonde, Jack Kruse, Paul Jaminet, yours truly – and many more. On Day 5 I’ll be giving a talk called “An Update on Cholesterol” summarizing and boiling down the latest research on cholesterol and heart disease.

The best part? It’s completely FREE.

As an added bonus, when you register today, you’ll also get an awesome video interview with Mark Sisson regarding why we should eat like our ancestors, as well as a 40-minute interview with Gary Taubes on why we get fat – I know you’re going to love them.

Pre-registration is now available – so make sure you head over to right now to sign up.

I’ve got four speaking engagements in 2012 I’d like to let you know about, beginning with one right here in Berkeley on Sunday, February 26th. I’m hoping I get to meet some of you in person at these events.

Three Stone Hearth in Berkeley, CA – Sunday, February 26th from 3-5pm

Topic: What to do – or not do – about high cholesterol

Three Stone Hearth is a community-supported kitchen (CSK) in Berkeley, CA. What the heck is a CSK, you ask? From their website:

Three Stone Hearth is pioneering a new business model: a community-supported, worker-owned cooperative, and a teaching kitchen all in one.

Our work is grounded in shared values of sustainability, community, and health.

Inspired by diverse cuisines, our weekly menus are prepared using the nourishing traditions approach to ensure maximum digestibility and nutrient absorption.

Ordering from us helps reduce your carbon footprint. We pack our foods in re-usable glass containers, compost waste, and purchase from local farms.

Elanne and I order food from them each week, and it’s delicious, nourishing and very convenient for us. We cook a lot, of course, but as anyone running their own business with young kids knows, sometimes it’s just hard to pull off cooking a nice meal at the end of a long day.

It’s like having your own Primal/Paleo chef, except a lot cheaper. If you live in the Bay Area and haven’t checked them out, click here to sign up and place your first order!

I’ll be speaking about cholesterol and heart disease. This is an updated talk focusing on a practical framework for determining whether high cholesterol is a problem for you or not, and if it is, what to do about it.

Click here to register. (Scroll down to the green-mutant picture of me.)

PaleoFx in Austin, TX – March 14th – 16th

Topic: What to do – or not do – about cholesterol

The PaleoFX Ancestral Momentum – Theory to Practice Symposium fosters collaboration among fitness professionals, healthcare professionals, nutritionists, research scientists and laypersons who approach their respective practices from an evolutionary perspective in order to successfully address modern health challenges through the application of ancestral based theory in practice.

I’m giving a 40-minute talk on my practical framework for determining whether high cholesterol is a problem, and what to do about it. I will also be on a panel discussion exploring the pros and cons of whole foods vs. supplements.

Click here to learn more and buy tickets. Should be a blast because this is happening during the same week as SXSW.

Ancestral Health Symposium in Cambridge, MA – August 9th – 11th

Topic: Iron Behaving Badly: A Protective Mutation Gone Wrong

The Ancestral Health Symposium is the premier conference for scientists, healthcare professionals and laypersons interested in evolutionary health and medicine. If you’ve been around the Paleo/Primal scene for any length of time, I’m certain you’ve heard of it.

I’ll be giving a 40-minute presentation on the under-diagnosed phenomenon of iron overload, and its impact on blood sugar regulation and male reproductive health in particular.

Click here to learn more and buy tickets.

Wise Traditions Conference in Santa Clara, CA – November 9th – 12th

Topic: The gut-brain-skin axis

The Weston A. Price approach to nutrition was my entry point into the world of nutrient-dense food, and I’m a big supporter of their mission and activities. They have invited me to present on a favorite topic of mine, the gut-brain-skin axis. And they were nice enough to host the conference in the Bay Area this year. Hooray!

It looks like registration isn’t active yet, but check back at this page in a few weeks to get signed up.

Okay, that’s it. I hope to see you at one of these events in 2012.

Maintaining proper balance of healthy gut flora is a crucial yet widely misunderstood component of human health. While the development of antibiotics has lengthened our lifespans, our excessive and inappropriate use of these drugs may be causing serious long-term consequences we are only now becoming fully aware of.

These consequences not only affect our individual health, but may even be causing permanent changes to the microflora of all people from generation to generation.

Martin Blaser’s recent (2011) article published in Nature highlights the potentially dangerous long-term consequences that arise from the rampant overuse of antibiotics. (1) He argues that changes in our microbiota may even be promoting the transmission of deadly organisms, as one of the important roles of an intact microflora is to resist colonization by pathogenic organisms.

Blaser also points out that not only does the individual use of antibiotics cause permanent changes in the gut flora, but that infants born to women given antibiotics during pregnancy, or the 30% of children delivered via cesarean section, may be starting life with a significantly altered and insufficient level of friendly gut flora. (2) This is a serious concern because lack of diversity in friendly gut bacteria has been shown to contribute to a large number of diseases and complications.

Unfortunately, even a single course of antibiotics can permanently alter the gut flora.

One study found that after a single treatment of intravenous antibiotics, fecal bacteria tests demonstrated a significant change in the variety of bacterial strains, and the development of the pathogen Clostridium difficile. (3) C. difficile colonization in the gut can lead to serious complications such as severe diarrhea and colitis. (4)

Another study demonstrated that a short course of the antibiotic ciprofloxacin reduced the diversity of the intestinal microbiota, with significant effects on roughly one-third of the bacterial species. (5) This study also found that while much of the diversity eventually recovered, there were still several species that failed to recover after six months, suggesting that even a short course of antibiotics may cause permanent changes to the community of friendly flora in the gut.

Antibiotics are known to cause diarrhea, which may be due to infection by antibiotic resistant pathogens such as salmonella, C. perfringens type A, Staphylococcus aureus, and possibly Candida albicans, as well the various metabolic consequences of reduced concentrations of fecal flora. (6) These results suggests that disturbance of the normal intestinal flora following antibiotic use may be responsible for the overgrowth of dangerous pathogens.

Research also indicates that infants’ gut flora is significantly affected by cesarean delivery, which requires the administration of antibiotics to the mother. One study demonstrated significant changes in the primary intestinal flora of infants born through cesarean delivery, lasting at least six months. (7) Primary colonization of the newborn’s sterile intestinal tract normally happens during vaginal birth, and it is unknown whether an infant born with inadequate or unbalanced colonization will ever develop normal intestinal flora without intervention. 

While breastfeeding can help restore some of the natural balance to the microflora, only about 44.3% of American women breastfeed (with only 14.8% breastfeeding exclusively) for the full six months that is recommended. (8, 9) Furthermore, breastfeeding alone may not compensate for the changes in flora associated with cesarean sections, suggesting that many infants may be at an even greater disadvantage when it comes to the proper development of a healthy, functional digestive tract. (10)

Research from diverse fields demonstrates the negative effects of gut dysbiosis and inadequate friendly flora on a variety of health outcomes.

For example, resident bacteria of the normal flora are involved in intestinal mucosal inflammation and patients with inflammatory bowel disease (IBD) have higher amounts of bacteria attached to their intestinal mucosa than do healthy people. (11) Patients with Crohn’s disease and ulcerative colitis are found to have reduced concentrations of fecal Lactobacillus and Bifdobacteria, which protect against pathogenic bacteria, increase mineral absorption and induce the production of growth factor in the gut. (12)

An unbalanced microbiota in the gut is also a contributing factor in autoimmunity. (13) Infection with certain microbial pathogens can trigger autoimmune reactions in joints and other organs. (14) The destruction of healthy gut flora can make the mucosal lining more susceptible to leakage, which some researchers believe is a precondition for developing autoimmunity. (15, 16) It is well-established that the balance of gut bacteria plays a key role in the formation of a proper immune response. (17, 18) A lack of healthy gut bacteria is associated with allergies, IBD, and general autoimmune reactions when this immune modulation goes awry.

New research has linked changes in gut bacteria with obesity. One study found that the gut bacteria of obese subjects different significantly in species type than lean subjects, and that low calorie diets, restricting either fat or carbohydrates, changed the gut flora and increased the abundance of the bacterial strains found more predominantly in the lean subjects. (19) Another study found that transplanting fecal bacteria from lean or obese mice into mice with sterile guts could affect whether these mice gained body fat, even when food intake was controlled. (20) Those mice implanted with fecal bacteria from obese mice gained a significantly larger percentage of body fat than those transplanted with bacteria from lean mice. The authors hypothesized that certain types of gut flora are associated with obesity due to the increased extraction of energy from the diet. I’ve written about this in more detail here.

These studies demonstrate the wide range of potential consequences caused by the improper development or destruction of the intestinal flora.

Though antibiotics may be necessary in certain situations, it’s important to weigh the benefits of using them with the potential risks that may come from the permanent alteration of the gut flora. If antibiotics must be used (and there are certainly situations where this is the case), special care should be taken to not only restore their gut flora using probiotic foods and supplements, but to eat a diet that supports healthy gut microbiota with plenty of fermentable fibers from starch and the removal of food toxins.

To protect infants’ gut health, especially those infants born through cesarean section, it is crucial to exclusively breastfeed for at least six months, with breastfeeding continuing on-demand throughout the complementary feeding period (up to 2 years of age). I also recommend using a high-quality infant probiotic to help populate your baby’s gut with beneficial flora, as I explain in this article from my natural childbirth series.

Infancy is a critical time where the development of a healthy gut microbiota is essential for the long term health of your child. You can read more about protecting the gut health of your child in The Healthy Baby Code.

In medicine and health, as in all other areas of life, each choice we make comes with consequences. The purpose of this post is not to suggest that antibiotics are “bad” and we should never take them. As I said in the beginning of the article, antibiotics save lives and have significantly lengthened our lifespans. But that benefit has come with a price, and it’s one that we’re only just beginning to understand the full implications of. My goal here is simply to raise awareness of this price – the harmful and potentially lasting effects of antibiotics – so that you can make a more informed choice.

What are some alternatives to antibiotics?

Mark Sisson wrote a good post listing some alternatives to antibiotics a few months back. In my practice I use a combination of botanical anti-microbials, biofilm distruptors (bacteria often live in extracellular matrices called biofilm, which protect them from our innate immune defenses and any external anti-microbials we might take), and probiotics – as well as micronutrients to support immune function, like vitamin C, iodine and selenium.

While these botanicals do have an impact on the gut flora, it is less pronounced than the effect of broad-spectrum antibiotics. Still, I recommend taking any strong anti-microbials under the supervision of a qualified health care provider.

In this episode we conclude the excellent 3-part series on cholesterol and heart disease with Chris Masterjohn.  It’s been a pleasure to have Chris with us throughout the series, as he’s the most knowledgeable person I know about these topics.  We’ll certainly have him back in the future!

In case you missed them, here are links to Part 1 and Part 2.

In this episode, we cover:

2:30 The role of cholesterol in heart disease
11:26 What to do – or not do – about high cholesterol
24:11 The thyroid-LDL connection and why iodine matters
29:36 Are goitrogenic foods inhibiting your thyroid function and raising your cholesterol?
46:01 The telltale sign you need more carbs

Links We Discuss:

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

Full Text Transcript:

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

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

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

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

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

Chris Kresser:  Woo-hoo!

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

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

Chris Masterjohn:  Ha-ha, yeah.

Steve Wright:  Yeah, that’s a mouthful! 

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

The role cholesterol plays in heart disease

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

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

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

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

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

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

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

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

What to do – and not do – about high cholesterol

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

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

Chris Masterjohn:  Absolutely.

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

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

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

Chris Masterjohn:  For the test?

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

Chris Masterjohn:  Right.

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

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

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

Chris Kresser:  Wow.

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

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

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

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

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

Chris Kresser:  OK.

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

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

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

Chris Kresser:  Right.  Great point.

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

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

The Thyroid-LDL connection and why iodine matters

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

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

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

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

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

Are goitrogenic foods inhibiting your thyroid function?

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

Chris Kresser:  Yeah.

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

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

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

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

Chris Masterjohn:  Yeah.

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

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

Chris Kresser:  Right.

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

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

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

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

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

Chris Kresser:  Ha-ha!

Steve Wright:  Oh, yeah.

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

Chris Kresser:  Sure.

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

Chris Kresser:  Right.

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

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

Chris Kresser:  Ha-ha!

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

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

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

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

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

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

Chris Masterjohn:  Right.

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

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

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

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

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

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

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

Steve Wright:  Do either of you take iodine?

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

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

Chris Kresser:  Yeah, keep us posted.

Steve Wright:  Yeah, I’m looking forward!

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

Chris Kresser:  Yeah, sounds good.

The telltale Thyroid-Cholesterol signs you need more carbs

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

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

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

Chris Kresser:  Yeah, let’s hear it.

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

Chris Kresser:  Wow.

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

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

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

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

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

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

Chris Masterjohn:  Yeah, I look forward to it!

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

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

If you’re confused about what to eat, check out the Personal Paleo Code.  It’s a 3-step process designed to help you discover your own ideal diet and create highly customized meal plans with a few clicks of a button.  Visit PersonalPaleoCode.com to learn more.  And if you’re trying to get pregnant or are already pregnant or nursing, don’t miss The Healthy Baby Code.  It guides you through the essential steps to naturally boost fertility and promote lifelong health for you and your baby.  Find out more at HealthyBabyCode.com.

Please keep sending us your questions at ChrisKresser.com using the podcast submission link.  And if you enjoyed listening to the show, head over to iTunes and leave us a review.  Thanks.

A healthy thyroid is a critical component of one’s overall health, and many people are struggling with thyroid disorders such as hypothyroidism, specifically Hashimoto’s autoimmune thyroiditis. In this autoimmune condition, the immune system attacks the thyroid gland, with the resulting inflammation leading to an underactive thyroid gland or hypothyroidism. Hashimoto’s disease is the most common form of hypothyroidism and was the first condition ever to be classified as an autoimmune disease.

I’ve written extensively about thyroid health, focusing on a multitude of environmental factors that may affect thyroid function, including gluten, gut health, stress, excess iodine, and vitamin D deficiency. I’ve also discussed why dietary changes are always the first step in treating Hashimoto’s, and why replacement thyroid hormone is often necessary for a successful outcome.

There is yet another nutritional factor that may play a role in thyroid health: selenium.

Selenium deficiency is not thought to be common in healthy adults, but is more likely to be found in those with digestive health issues causing poor absorption of nutrients, such as Crohn’s or celiac disease, or those with serious inflammation due to chronic infection. (1, 2) It is thought that selenium deficiency does not specifically cause illness by itself, but that it makes the body more susceptible to illnesses caused by other nutritional, biochemical or infectious stresses, due to its role in immune function. (3) Adequate selenium nutrition supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage from excessive iodine exposure. (4)

Several research studies have demonstrated the benefits of selenium supplementation in treating autoimmune thyroid conditions. One study found that selenium supplementation had a significant impact on inflammatory activity in thyroid-specific autoimmune disease, and reducing inflammation may limit damage to thyroid tissue. (6) This may be due to the increase in glutathione peroxidase and thioredoxin reductase activity, as well as the decrease in toxic concentrations of hydrogen peroxide and lipid hydroperoxides which result from thyroid hormone synthesis. (7)

Another study followed patients for 9 months, and found that selenium supplementation reduced thyroid peroxidase antibody levels in the blood, even in selenium sufficient patients. (8) While these studies show promise for the use of selenium supplementation in preventing thyroid tissue damage, further research is needed to determine the long-term clinical effects of selenium treatment on inflammatory autoimmune thyroiditis.

Additionally, selenium is also essential for the conversion of T4 to T3, as deiodinase enzymes (those enzymes that remove iodine atoms from T4 during conversion) are selenium-dependent. As I’ve explained before, T3 is the active form of thyroid hormone, and low T3 can cause hypothyroid symptoms. A double-blind intervention study found that selenium supplementation in selenium deficient subjects modulated T4 levels, theoretically by improving peripheral conversion to T3. (9) In cases of severe selenium deficiency, conversion of T4 to T3 may be impaired, leading to hypothyroid symptoms. As T3 conversion is not performed by the thyroid, the dependence on selenoproteins for this conversion demonstrates how significant selenium deficiency could lead to hypothyroid symptoms.

So the question is, should you start supplementing with selenium if you have hypothyroidism, Hashimoto’s thyroiditis, or low T3 levels?

As the answer often is, it depends. These preliminary studies show the positive effects of selenium supplementation on inflammatory activity in autoimmune thyroid conditions, but the long term effects of supplementation on thyroid health are still unknown. And we know that selenium is an essential component of the enzymes that convert T4 to T3, but whether supplementation will increase serum T3 levels is unclear.

While it seems that selenium supplementation would be an obvious solution to poor thyroid function, long term consumption of high doses of selenium can lead to complications such as gastrointestinal upsets, hair loss, white blotchy nails, garlic breath odor, fatigue, irritability, and mild nerve damage. (10) Additionally, supplementing selenium in the context of low iodine status may actually aggravate hypothyroidism. Mario Renato Iwakura discusses this particular topic extensively on Paul Jaminet’s Perfect Health Diet blog.

For now, the best option for most people may be to include selenium-rich foods in the context of a healthy Paleo diet. Great sources of selenium include: brazil nuts, crimini mushrooms, cod, shrimp, tuna, halibut, salmon, scallops, chicken, eggs, shiitake mushrooms, lamb, and turkey. For those concerned with the high level of omega-6 fats in brazil nuts, it may be worth considering the fact that it only takes one or two brazil nuts per day to improve your selenium status and boost immune function. (11)

For those who choose to supplement, I consider 200 micrograms of selenium to be a safe supplemental dose for people with thyroid issues. The brand of selenium I recommend is Life Extension Super Selenium Complex, which has four different forms of selenium, totaling 200 micrograms. It also provides vitamin E, which works synergistically with selenium as an antioxidant. This dosage is enough to be therapeutic for treating selenium deficiency, but has a lower risk of causing overdose symptoms.

Making sure your selenium intake is optimal may give your immune system and thyroid the boost it needs to help it function better. Whether through selenium-rich foods or supplements, it is especially important for those managing thyroid conditions to ensure their selenium status is adequate.

Has anyone had any experience with selenium supplementation? Was it a positive or negative experience? Let me know in the comments below.

Vita-mix Giveaway

I have a couple of announcements to make. First, I’m switching over to a new Facebook page. My current page is still called “The Healthy Skeptic”, and as it’s not possible to change the name of a Facebook page, I had to create a new one.

In order to entice you to come join us on my new page, I’m giving away a Vitamix blender and free lifetime access to both the Personal Paleo Code and the Meal Plan Generator.

To enter the drawing, just like my new page and fill out the entry form. The contest ends on February 29th at 11:59pm, so make sure to enter before then!

Personal Paleo Code Affiliate Program

I’ve received a lot of inquires about an affiliate program for the Personal Paleo Code, and I’m happy to say that it’s now available. You can sign up by clicking here and filling out the form. We will then contact you with details.

The affiliate program is a great way to help others experience the life-changing benefits of a Paleo diet and lifestyle, while earning a little extra cash for your efforts. Here’s how it works:

• You place banners or links to the Personal Paleo Code on your website.
• If someone purchases the PPC through through your site, you earn a 33% commission.
• If they continue with the Meal Plan Generator after the 30 day trial, you’ll earn a 25% commission on their monthly subscription fee.

If you plan to promote the PPC offline – at your gym or health clinic, for example – you can still be an affiliate and earn commissions. Just make sure you indicate that you will be promoting PPC offline in the “Website/location where you will promote PPC” field on the sign up form, and we will send you special instructions.

Healthy Baby Code Affiliate Program

We also have an affiliate program for the Healthy Baby Code. It works in a similar fashion. You will earn a 33% commission for anyone who purchases through your website or gym/clinic. Click here to sign up.

Exercise is a major component of a healthy lifestyle, and the benefits of regular physical activity are well established. When adopting a Paleo lifestyle, modifying your fitness routine to include more high intensity exercise can bring great benefits to energy, body composition, and overall fitness.

However, there are many people who take their physique and physical fitness to an extreme level, particularly in the Paleo community. Certain styles of exercise take the participant to a state of physical exhaustion on a regular basis, which may do more harm than good.

While a consistent, high intensity workout routine may provide some benefits for those people looking to lose body fat and increase their strength and fitness, there is a fine line between training hard and overtraining. While running fast and lifting heavy may be major components of an active Paleo lifestyle, engaging in these physically demanding activities too regularly or too intensely can contribute to many different symptoms of overtraining.

Overtraining goes beyond just excessive “chronic cardio” or too many hours spent at the gym. Certain high-intensity exercise routines may push the body’s stress response too far, leading to a cascade of biochemical responses that can cause serious damage to one’s health in both the short and long term.

While short, intense workouts can be great for inducing fat loss, increasing aerobic capacity, and reducing risk for cardiovascular disease, excessively intense exercise can cause a variety of health problems, especially for those dealing with other concurrent stressors such as autoimmune disease, gut dysbiosis, or adrenal fatigue.

Overtraining has been shown to affect blood levels of important neurotransmitters such as glutamine, dopamine and 5-HTP, which can lead to feelings of depression and chronic fatigue. The stress caused by intense, excessive exercise can negatively affect the hypothalamic-pituitary axis, possibly causing conditions such as hypothyroidism. Hypothyroidism is known to cause depression, weight gain, and digestive disfunction along with a variety of other symptoms. As we know, high stress in general can cause symptoms of hypothyroidism, and the stress caused by excessive, intense exercise is no exception.

Another major effect that extreme exercise has on our bodies is an immediate increase in cortisol, the hormone that is released when the body is under stress. Heavy-resistance exercises are found to stimulate markedly acute cortisol responses, similar to those responses found in marathon running. Chronically high levels of cortisol can increase your risk for a variety of health issues, such as sleep disturbances, digestive issues, depression, weight gain, and memory impairment. Excess cortisol also encourages fat gain, particularly around the abdomen.

When a goal of exercise is to lose weight or improve energy, overtraining can clearly be a major barrier to achieving those goals.

Overtraining can also have harmful effects on the immune system. Research has shown that the cellular damage that occurs during overtraining can lead to nonspecific, general activation of the immune system, including changes in natural killer cell activity and the increased activation of peripheral blood lymphocytes. This hyperactivity of the immune system following intense overtraining can possibly even contribute to the development of autoimmune conditions.

This type of nonspecific immune response is associated with symptoms such as chronic fatigue, weight loss, decreased appetite, and sleep changes. Altered immune status is also known to affect the hypothalamic-pituitary axis, and may be responsible for the hypothalamic-pituitary dysfunction and hypothyroidism known to occur in overtrained athletes.

Mark Sisson talks about the different signs of overtraining, which may be more common in endurance training but is nonetheless possible in high intensity training as well. Feeling ill or rundown, losing muscle mass, gaining fat, and constant exhaustion can all be signs of excessive exercise of any type. Not only is this counterproductive to most people’s fitness and health goals, but it is also a sign of sickness. In the path to better health, any activity that makes you more fatigued and more prone to infection is definitely something to be avoided.

So does this mean you should quit CrossFit, or stop pushing towards your weightlifting goals? Not necessarily.

Here are a few techniques to avoid overtraining while still enjoying high intensity exercise:

1. Reduce the frequency. While pushing yourself hard at the gym is not inherently problematic, doing it too often during the week is overtraining. High intensity, high stress exercise should be limited to two or three times a week, especially for those who are dealing with other health issues such as autoimmune conditions or digestive troubles. Compounding those stressors with extra stress from your exercise routine will not leave you healthier, and can easily cause you to become more sick.
2. Get adequate rest. I’ve written before about how important sleep quality is for health. Not only is taking breaks from exercise important, but getting adequate sleep to allow recovery from intense exercise is vital to avoiding the overtraining syndrome. Make sure you are getting adequate sleep, particularly on the days you train. Interestingly, one symptom of overtraining is disturbance of sleep, so if you’re feeling restless and having trouble sleeping through the night, you may want to reconsider the intensity of your training schedule.
3. Mix it up. While high intensity exercise may be ideal for losing body fat and improving lean muscle mass, we know that high levels of cortisol can cause the body to hold onto fat. For this reason, you may consider trying a type of exercise that can help modulate your cortisol levels. Some may knock yoga as being too easy to affect weight loss, but regular yoga practice is shown to reduce cortisol levels, which may help in reaching your weight and fitness goals. Instead of doing a fourth day of CrossFit, try doing a yoga class instead. You may find that this stress reducing exercise helps you recover more quickly from your more intense exercise schedule.
4. Eat more carbohydrates. While cutting down carbohydrate consumption is often seen as the best way to decrease body fat, a combination of overtraining and low-carb eating can actually raise cortisol significantly and negatively impact immune function. There is also a possibility that very low carbohydrate (VLC) diets suppress thyroid function, a debate thoroughly discussed by Paul Jaminet on his blog. So if you’re regularly doing high intensity training and want to avoid symptoms of overtraining stress, don’t skimp on the carbs!

High intensity exercise can be a great way to improve body composition and enhance your general health, if done the right way. As with all components of our lifestyle changes, the key is moderation and listening to your body. If you choose to participate in these high intensity training programs, always use your best judgment and don’t let coaches or fellow athletes push you past your comfort zone.

Now, I’d like to hear your experiences with different exercise programs – did your health improve or suffer after increasing the intensity of your training? Have you been able to find a balance between intensity and adequate recovery?

**Special announcement: you’ll notice we’re now providing a full transcript for each new episode of the show.  Special thanks to Lindsey Gosling from our community for volunteering to do this.  She’s my hero.

One of the most hotly debated subjects in the Paleo-sphere over the last several months has been the causes and treatment of obesity and overweight.  Some claim that it’s simply a matter of “calories in, calories out”, and weight loss is just a question of “eating less, and exercising more”.  Others claim that it’s all about macronutrients (fat, carbs & protein), and calories don’t make a difference at all.

Over the last two decades a more sophisticated theory of weight regulation has emerged that encompasses the seeming contradictions in the prevailing paradigms.  This theory holds that the brain is the primary driver of weight gain and loss, and that environmental and genetic factors that influence this neurobiological system are what account for the alarming rise in obesity we’ve seen in the Western world since the early 80s.

2:57 Why it’s so hard to lose weight and keep it off
8:00 The truth about food reward, calories in vs. calories out, and “the metabolic advantage”
13:32 The Body Fat Setpoint making you “gain the all weight back”
21:06 Why leptin is the master fat hormone and what happens when you’re leptin resistant
26:05 The link between inflammation and obesity
31:00 Are modern foods engineered to make us fat?
49:48 The one thing any successful weight loss intervention must have

Links We Discuss:

• Stephan Guyenet: Author of The Whole Health Source Blog
• Stephan Guyenet: Body Fat Setpoint Series
• “The End of Overeating”

Full Text Transcript:

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

Chris Kresser:  I’m pretty good.  I have to confess to being quite sleep deprived.  Sylvie is usually a pretty good sleeper actually, but the last several nights she has been — I don’t know what’s happening, maybe a growth spurt or something, but she has just been squirrelling around the bed like a little monkey all night.  Yeah, so if I start slurring my speech or just have large pauses or gaps, you’ll know what’s going on.  How are you doing, Steve?

Steve Wright:  We’ll be a pretty good tag team today then, because I’m working one-handed here, so I can basically only talk.  I had shoulder surgery nine days ago, and everything went well.  It appears to be good.  I had a labrum tear, but I do have an arm in a sling for four weeks, so that kinda slows down life.

Chris Kresser:  Oh, wow.  Well, all right, so we’re injured and impaired, but we’re still here.

Steve Wright:  That’s right.  We can still talk!

Chris Kresser:  Yeah, thank God for the radio show!  So, let’s see, we have one announcement to make before we get started.  Some people are already aware of this, I’m sure, but we now have full transcripts for all of the Revolution Health Radio and previous Healthy Skeptic podcasts in the works, which is really exciting.  We loved you so much that we just decided that we were finally gonna do it, and we have a volunteer from the community, Lindsey, who is helping us with this on an ongoing basis, and we’re really grateful to her.  She’s doing an awesome job, and so we’ve already put some of the transcripts up on the website, on the actual episode posts, and some of the older ones are in progress right now, and we’ll be adding them as we get them done.  But in the future, I think we’re gonna be able to have the transcript up there right as the podcast or the radio show goes live, so that’s really exciting, and I hope you enjoy the transcripts, all of those who have been asking for them.  I hope you enjoy it!

Steve Wright:  Yeah, it will make things much easier to find with the Ctrl+F function.

Chris Kresser:  Yeah, definitely.

Why is it so hard to lose weight and keep it off?

Chris Kresser:  So, today I decided to review a study that was recently published by a friend of mine who I’m sure many of you know and a colleague, Stephan Guyenet, from Whole Health Source, one of my favorite blogs, and if you don’t know his work, I would highly recommend checking it out.  I think it’s WholeHealthSource.blogspot.com.  And Stephan published this paper with his mentor, Michael Schwartz.  Both of them are at the University of Washington School of Medicine.  And Stephan is an obesity researcher.  He has spent his career studying the mechanisms involved in particularly the neurobiology of weight regulation, and he just published a paper called Regulation of Food Intake, Energy Balance, and Body Fat Mass:  Implications for the Pathogenesis and Treatment of Obesity.  And we’ll put a link to the paper in the show notes.  Unfortunately the full text is not available for free, but the abstract is, and if you’re really interested you can cough up the, I think, 30 bucks or 35 bucks for the full text.  I want to talk about it because Stephan’s been on the show twice already to discuss obesity and all the various factors involved in obesity, but I wanted to take another opportunity to revisit this because I think it’s much misunderstood.  I think our understanding of it is continually evolving, and this paper, I thought, was the most concise and thorough synopsis of all of the various mechanisms that are supported in the scientific literature in terms of what causes weight gain and what might cause weight loss and keeping the weight off, because as everybody knows, losing weight is hard and keeping it off is even harder, and I want to explain in some detail why that is because, again, I think there is a lot of misunderstanding about that.  So, we’re gonna spend quite a bit of time talking about this.  It might even take the whole show.  If we have a chance, we’ll answer some questions at the end, and I’m sure we’ll come back to this again.  I’m not gonna get too far into what this means in terms of practical mechanisms because we’ll probably devote another show to that later, so this is just gonna be more of the background theory.

Steve Wright:  Sounds good.

Chris Kresser:  OK, shall we do it?

Steve Wright:  Yeah, are you gonna start with a high-level overview or just dive right in?

Chris Kresser:  Yeah, I’m gonna do a high-level overview, and so I’ll just give you kind of the basics of what we’re gonna be talking about, and then we’ll get into more detail about each point.  The high-level overview, I’ve written about this on my blog as well, and as most of you know, I think, obesity is a multifactorial disease, and I think pretty much anybody who researches it seriously agrees with that.  Anybody who says obesity is as simple as, you know, too much fat or too much carbohydrate or something like that is either misinformed or is intentionally misleading you.  It’s far more complex than that, but I can boil it down into one simple phrase, which is modern lifestyle + genetic predisposition = obesity.  And this is supported by the fact that obesity is virtually unheard of in populations that still follow their traditional diet and lifestyle.  In modern hunter-gatherer societies, it is basically nonexistent.  And then on the other hand, we know that there must be some genetic predisposition because not everyone who adopts a modern lifestyle becomes obese.  I mean, surely we all have friends or family members that eat like crap and they’re still really lean, so there are obviously some genetic and epigenetic factors, as well.

Steve Wright:  And lifestyle is food, stress, environment, everything?

Chris Kresser:  Yeah, exactly, so everything from the food we eat to our — I mean, actually it starts even before that.  It starts with our mother’s diet while she was pregnant with us, and it’s our gut flora particularly at the time of birth, whether we were breastfed.  So, that’s maybe kind of depressing news for some people because we obviously didn’t have any control over that, but it turns out that those things can have a very significant impact on our risk for obesity as we get older.

The truth about food reward, calories in vs. calories out, and “the metabolic advantage”

Chris Kresser:  One thing I want to talk about right up front is this whole — many of you who follow the Paleo blogs and are involved in this kind of thing have been aware of this debate that has been going on about food reward and calories in / calories out vs. the metabolic advantage or the idea that carbohydrates in particular predispose people to weight gain.  You know, on one end of the spectrum you have people say that calories don’t matter at all; it’s more a matter of carbohydrate density and the type of carbohydrates that you eat, and if you eat a low-carb diet, for example, you can eat as many calories as you want and you won’t gain weight.  And then you have on the other end of the spectrum people that say it’s all about calories, and as long as you’re in a negative energy balance, meaning as long as you expend more calories than you eat, then you will lose weight, and if you have an energy balance where you eat and expend about the same amount of calories, then you’ll maintain your weight.  That’s a little bit of a false dichotomy, and I’ll explain why in a second, but I just want to say for the record that I think that calories do matter, and I think the research definitely supports the idea that calories matter.  If you look at per capital energy intake — there’s actually a great graph in this study — in the U.S. it has increased about 20% since 1980, and that increase in energy intake or food intake over that period has closely paralleled the rapid rise we’ve seen over this past 30 years in obesity.  I think where people get confused about this is that they mistake the idea that calories matter with the idea that eating less and exercising more is effective weight loss advice; and it’s not.  And, you know, I absolutely agree with that.  That’s been a monumental failure.  The idea that you can just tell somebody to eat less and exercise more to lose weight is ridiculous and doesn’t work in the vast majority of cases, and we’re gonna talk a lot about why that is in the show today.  But that doesn’t mean that calories aren’t a factor and that some interventions that reduce caloric intake wouldn’t contribute to long-term weight loss.  This will be more clear as we get into it.  I’m already kind of ignoring my own top-line review thing here.

Steve Wright:  Hey, Chris, what was the 20%?  Was that 300 extra calories a day or 400?

Chris Kresser:  I don’t know the exact number, actually.  Let me look here.  I don’t know the exact number.  I’d have to look it up.  I just the percentage.

Steve Wright:  OK.

Chris Kresser:  So, another thing that we’re gonna focus on here is that over the last 20 years or so, research has shown that food intake and body fat regulation are primarily orchestrated by the brain.  And of course, the brain gets input from another of other body systems, but it turns out that the hypothalamus in particular, and other regions of the brain play a really essential role in regulating weight and body fat mass and that obesity involves the biological defense of an elevated body fat mass, or another way of putting that is an increased setpoint, and we’ll talk more about this.  And the increase in the setpoint, in turn, is mediated by interactions between the hedonic or pleasure/reward-seeking system and the homeostatic or energy-regulating system.  And these, in turn, are influenced by inflammation, both peripherally, like in the gut and other parts of the body, and then in the brain, by leptin resistance and by other mechanisms that impair the function of the hypothalamus or those other parts of the brain that are involved in regulating weight.  So, that’s the birds-eye view of what we’re gonna talk about, and it unfortunately gets a little bit complex in certain areas, so bear with me, and I hope it’s not overwhelming in those parts, but since we do have a transcript, you can go back and read it if it gets to be too much.  So, all clear, Steve?  Shall we go on?

Steve Wright:  Yeah, I think one more time really fast do that crescendo of the various parts.

Chris Kresser:  Well, basically obesity = modern lifestyle + genetic predisposition, and one of the ways that that is mediated, and the primary focus that we’re gonna talk about today, is the interaction between the hedonic and the homeostatic weight regulation mechanisms, and those are governed primarily by the brain.  So, that’s kind of the gist of what we’re gonna get to today.

Steve Wright:  OK, and then a bunch of things, like inflammation, affect the brain.

Chris Kresser:  Yeah.

Steve Wright:  Gotcha.  Cool.

The Body Fat Setpoint making you “gain all the weight back”

Chris Kresser:  OK, so let’s talk about the body fat setpoint.  I mean, I don’t know if anyone has thought about this, but if you’ve wondered how most lean people stay the exact same weight or within a couple of pounds for years or maybe their whole life without counting calories or weighing what they eat, it’s actually a pretty remarkable system if you think about it.  I mean, if it is true that the amount of calories you take in and the amount of calories you expend is what determines your weight, then it’s a pretty exquisitely regulated system to be able to maintain a range of weight within this 1 or 2 pounds without the person even thinking about it at all.  So, this happens because survival in a natural environment is threatened by either too little or too much fat.  If we have too little fat, we can’t survive periods of food scarcity and we starve; and if we have too much fat and we become obese, then we aren’t as fit to hunt and gather food and evade predators and survive.  So, the body has a system for maintaining a level of fat that’s appropriate for the human ecological niche, and this is called the energy homeostasis system or the homeostatic regulation of weight, and it’s this system that’s one of the main reasons it’s so hard to keep weight off once you lose it, because the homeostatic system responds to any reduction in fat.  Like if you lose 20 pounds, let’s say, this homeostatic system will increase hunger, it will decrease your resting energy expenditure, so even when you’re just sitting down the number of calories that you’ll burn will be lower, and it extract more calories from the food that you eat, so your metabolic efficiency goes up.  So, it has all of these mechanisms that are basically working against you when you lose weight to get you back to that body fat setpoint or what it thinks is the ideal weight for you.  On the other hand, if you were to gain 10 or 15 pounds, the body responds in the opposite way.  It would decrease hunger, it would increase your resting energy expenditure, so you burn more calories just sitting there, and it would extract fewer calories from the food that you eat, and by doing that your weight would also fall back down to the setpoint.  And so, a good analogy for this setpoint is a thermostat, and everyone knows how a thermostat works.  Let’s say the thermostat is set at 70 degrees, and that’s the setpoint for the temperature in the house.  And, you know, overnight the temperature drops down to 60 degrees, the heating system kicks in, and it brings it back up to 70 degrees.  And then during the day the sun comes out, maybe the temperature goes up to 80 degrees, and then the air conditioner kicks in and brings it back down to 70 degrees.  So, likewise, that’s how the body fat setpoint regulates our weight.  That’s what happens in a normal-weight person, but what happens in obesity is that the thermostat, or the body fat setpoint, gets thrown off and the body defends a higher setpoint, which corresponds to a higher fat mass.  And then when that person tries to lose weight, all of their efforts to reduce the fat mass are fought pretty strenuously by the body in the same way that a lean person maintains their normal weight.  So, it’s an extremely effective system, and anyone who has tried to lose weight and keep it off knows exactly what I’m talking about.  It’s really an up-hill battle, and that’s the depressing part about weight loss, and it’s probably why after all these years nobody has come up with the magic bullet.  You know, weight loss is a billion dollar industry, it’s still a huge hot topic in the research literature, and really it still hasn’t been cracked, and that’s because we’re talking about some very old, very powerful, innate evolutionary mechanisms that are working against us, and any time we’re up against mechanisms like that, you know, that are mediated by our brain and not in our conscious control, it’s a challenge.

Steve Wright:  So, when it comes to the setpoint, do we know anything about, like, how long it takes to slowly reset?  Because there are a lot a people who do lose the weight.  I’m not sure how many.  There are people who lose the weight and keep it off, and then there are definitely plenty of people who lose the same amount of weight but then gain half of it back, so is it more of a time-based thing, do you think?

Chris Kresser:  There are a number of factors that control what dysregulates the setpoint, which we’re gonna talk about, and as you say, there are some people who seem to be able to lose weight and keep it off, but statistically speaking, there is only really one treatment that we know of that reliably and substantially and durably lowers the setpoint in pretty much everybody that tries the treatment, or a vast majority of the people, and we’ll talk about that towards the end of the show.  But in answer to your question, I don’t think that it’s an easy formula and certainly not black or white, and it depends on so many factors, beginning with genetics, you know, gene mutations, single gene mutations, which are relatively minor, and then epigenetic and developmental factors like I just was talking about, maternal status, maternal weight, birth weight, exposure to initial bacteria, gut flora, breast feeding, food, environmental toxins.  I mean it’s so vastly complex that I don’t think there will ever be an easy, straightforward answer to that question.

Steve Wright:  OK, and then did you say that the homeostatic system basically will also stimulate more hunger, as well?

Chris Kresser:  Yeah, if you lose weight and you’re below what your setpoint is, then you’ll get hungrier.  And that’s one of the ways that the homeostatic system regulates energy balance.  You know, it’s one of the ways it tries to get you back to what it considers to be your normal weight.  And that’s fine, that’s exactly how it should work in a lean person, but the problem in obesity is that the setpoint has become too high, and so the weight that the body is defending is inappropriate, and that’s again, of course, why weight loss and keeping it off is so difficult.

Why leptin is the master fat hormone and what happens when you have too much

Chris Kresser:  So let’s talk about leptin because, as I’m sure most people have heard by now, leptin is really the master control hormone in this process.  It is made by fat cells in proportion to body fat mass, so more body fat means you’ll be producing more leptin.  And leptin basically informs the brain of changes in energy balance and the amount of energy stored as fat, so it’s a communication system where leptin signals to the brain how much energy is stored as fat, how much fat mass you have.  And that leptin signal acts primarily on the hypothalamus in the brain.  The hypothalamus is a little, pea-shaped gland kind of right between your eyes; if you were to extend back beyond that, that’s about where it would be.  But there are also other more specific areas like the arcuate nucleus; the paraventricular nucleus; the ventromedial hypothalamic nucleus; and the lateral hypothalamic area, which is often referred to as the LHA; and then other parts of the brain that are leptin sensitive.  So, clearly we know now from the last 20 years that leptin acts on several different areas of the brain, and that’s probably the main nexus of where leptin acts.  So, in a normal-weight person, here’s what happens:  When fat mass increases — if you go through a period of overfeeding or overeating, for example — leptin goes up, and then the brain gets the message to constrain the fat mass by reducing food intake and increasing energy expenditure, all of those mechanisms that we already talked about.  And then, on the other hand, when fat mass decreases, leptin will go down, and then the brain will stimulate mechanisms that increase food intake and reduce energy expenditure and cause body fat accumulation.  And so that’s how leptin regulates that homeostatic system.  But in obesity, what we see is an increase of fat mass and a corresponding increase then in circulating leptin, but the appropriate response of reducing food intake and increasing energy expenditure doesn’t happen, and this suggests a state of leptin resistance, where increasing amounts of leptin are required to overcome the insensitivity to leptin in the brain.  For people have heard of insulin resistance, and that’s a condition where the liver or the fat cells or the muscles cells become resistant to insulin, and the pancreas has to just continue to make more insulin in order to have the same response, in order to perform the functions that insulin should perform, because it’s basically like somebody is knocking on the door and nobody is answering, and so then they have to knock louder and louder or you have to get a couple more people to knock on the door before the person inside can actually hear it and open the door.  So, that’s possible with the pancreas and insulin resistance because the pancreas can just make more insulin, right?  But what happens with leptin resistance and in obesity, because leptin is produced by body fat, when there’s leptin resistance in the brain, the only way for the message to get through is for the body to increase fat stores, and that’s what will lead to a higher amount of leptin so that the message can finally get through.  So, this is how leptin resistance promotes the defense of a higher setpoint for body fat mass, and we see this borne out in studies that show the genetic interventions that prevent leptin resistance in the hypothalamus will also prevent obesity, diet-induced obesity.  We see this in rat studies, and we also have seen that leptin resistance precedes weight gain, so for example it can be detected in the brain even after relatively short periods of overfeeding, which suggests that it’s the leptin resistance that comes first, not the obesity.

Steve Wright:  So, once you’re obese then, you don’t want to focus on more leptin, you want to focus on the leptin resistance and making new receptors.

Chris Kresser:  Yeah, decreasing the factors that cause leptin resistance — and inflammation is a big one, improving leptin sensitivity, and decreasing fat mass because that’s part of what caused the problem in the first place.

The link between inflammation and obesity

Chris Kresser:  Let’s talk about what causes leptin resistance then, because we just touched on it.  So, one of the main causes is inflammation, and Stephan has written some good articles about this on his blog.  Maybe we can link to them, as well, in the show notes.  But we know that proinflammatory cytokines inhibit leptin signalling in a whole bunch of different cell types, so leptin is getting to the brain, again, but the hypothalamus can’t hear it, and then the fat mass has to increase to produce more leptin.  This inflammation can be caused by a lot of different factors.  There are, of course, a lot of foods that promote inflammation:  processed and refined foods in particular and sugar and some unprocessed, improperly prepared grains.  Gut infections that produce an increase in endotoxins like lipopolysaccharide and then intestinal permeability, which allows those endotoxins to get out of the gut and into the blood stream, that promotes inflammation and has been implicated in hypothalamic leptin resistance.  Then certain micronutrient deficiencies and fatty acid imbalances can also promote inflammation and leptin resistance in the brain.  And finally, another cause of leptin resistance is injury to the neurons that is, in turn, caused by accumulation of free fatty acids in the brain, and this has been shown in experiments with rodents, where researchers overfeed them, you know, they feed them a purified, which means processed, high-fat diet, and then they observe the damage to the neurons prior to the onset of obesity.  So, just like leptin resistance seems to precede obesity, then the damage to the neurons also precedes obesity.  So, let’s talk about now what else increases the body fat setpoint.  We just discussed inflammation, and inflammation is a pretty broad term that can include causes like gut infections and intestinal permeability and environmental toxins and food toxins and micronutrient deficiencies, etc.; but there’s another main cause, I think, and this is one that Stephan has really spent a lot of time and energy highlighting on his blog, and he has taken a lot of flack for it, which I don’t really understand why.  I mean, I understand people’s reaction, but I think he has presented really solid evidence supporting this.  I mentioned before that the modern lifestyle is one of the primary causes of obesity, and one aspect of that lifestyle that affects weight regulation is the availability of highly energy-dense and palatable and rewarding foods.  So, again, we have two systems that interact to regulate fat mass, and one is the hedonic or pleasure-seeking system and the other is the homeostatic system.  And we’ve talked a bit about the homeostatic system, but the hedonic system evolved to help our hunter-gatherer ancestors seek out and take advantage of any highly palatable, energy-dense foods they happened to come upon, and its job is to make it hard to resist those foods because they’ve been so rare for most of evolutionary history.  You know, having a 7-Eleven on the corner and being able to access extremely calorie-dense, rewarding, palatable foods is a very recent development on the overall scale of human history, so the hedonic system evolved at a time where that wasn’t the case, and it was to our survival advantage to be naturally drawn to those energy-dense foods and eat pretty much as much as we could of them and then store them because inevitably there were would be times where those foods were scarce and possibly even most of the time.

Are modern foods engineered to make us fat?

Chris Kresser:  But, like I said, over the last 50 years in particular, there has been a huge increase in the availability of these foods and actually a systematic effort by food manufacturers to increase the reward value of food, and there’s a book that’s all about this that Stephan referenced in one of his blog posts.  I can’t remember the title off the top of my head, but the book covers the intentional effort on the part of food manufacturers who hire scientists, people who really understand all of these mechanisms in depth, and they purposely engineer the food to be highly rewarding.  And reward in this context is actually a term borrowed from psychology literature, which means that it reinforces a particular behavior in response to a stimuli; in this case, eating.  So, eating a rewarding food makes you want to eat more of it, and there are a number of factors that influence the reward value of food — and believe me, the processed food industry has, like I said, teams of scientists that study these factors — and they include caloric density, the texture of food, the content of fat and starch and simple sugar and salt and free glutamate.  They talk about it with terms like ‘mouth feel,’ like when you put a food into your mouth, how it feels in the mouth; and they study the neurobiology of it, like what centers in the brain are stimulated when you eat that particular food.  It’s really quite insidious, and if you study it and become aware of how much effort has gone into this, it starts to become obvious, at least from this perspective, why there is such a dramatic increase in obesity.

Steve Wright:  Is that book The End of Overeating?

Chris Kresser:  It might be.  Is it?  Have you read it?

Steve Wright:  I think it is.  I’ve read that one.  There’s also Mindful Eating, I believe.

Chris Kresser:  I don’t think it’s Mindful Eating.  It could be The End of Overeating.  We’ll look it up and put it in the show notes.

Steve Wright:  Yeah, if it’s that book, that book just literally blew my mind.  It talks all about that, about the chemistry and the various — I think they have five variables that they rate food on.

Chris Kresser:  Right, so this is a highly developed science, right?  I mean, they talk about that in the book.

Steve Wright:  Yeah.  I think they talk about — I think it’s over a billion dollars that is kind of spent in R&D, or it’s some astronomical number that’s spent in R&D just to make us like the food, and they call it a craveability.  So, they want to create foods that just — like, for some people maybe it’s a Dorito, like the Cool Ranch Doritos, or something — and they’re only looking to promote foods that are craveable.  In a capitalistic, you know, consumer marketplace, that’s the only thing that’s gonna survive is that one food where you’re like, “Man, I just want some of that Cool Ranch,” or something like that.

Chris Kresser:  Yeah, exactly.  So, like I said, it’s an insidious and very highly developed industry.  Well, we know from many animal and human studies that the reward value of a food has repeatedly been shown to influence food intake and body fatness in both animals and humans; whereas, palatability, on the other hand, is defined as the pleasure or the hedonic value associated with a food.  So, when Stephan was writing this series, people got reward and palatability really confused, so let’s say again reward value reinforces a particular behavior; in this case, eating more of it; so eating a rewarding food makes you want to eat more.  Whereas, a palatable food is just one that tastes good, and you know, of course, they often are related.  Like, a highly palatable food might be one that is highly rewarding, in that since it tastes so good, you want to eat more of it.  But it’s not necessarily to the same degree.  A good example of this is steak.  Steak, in my opinion, is a pretty palatable food.  It tastes great.  I love it.  But how often do you hear somebody say, “I’m really addicted to steak.  I can’t get enough steak”?  People like it, they eat it, but it doesn’t tend to stimulate addictive eating behavior, right?  But you do often hear people say that about chocolate or ice cream or chips and crackers.  I mean, the whole Pringles thing, right?  What was their slogan?  “I bet you can’t eat just one.”

Steve Wright:  Perfect.

Chris Kresser:  Yeah!  There’s a reason for that, because the scientists have designed it that way, and their marketing department is even making a baldfaced bet against you in their advertising slogan.  They’re betting that your hedonic system’s evolutionary effectiveness is gonna override any willpower that you might have and that you won’t be able to eat just one, and so they’re doing everything they can to make sure that’s possible, and they’re capitalizing on our innate, you know, our evolutionary mechanism here that was designed from the beginning to be a survival advantage, but in an obesogenic environment where you have access to all these super-energy-dense, palatable, rewarding foods, that system kind of backfires.

Steve Wright:  So, let me repeat that back really quick.  So, palatability is just all about the food in itself and our judgement of whether it tastes good.

Chris Kresser:  Right.  It’s the pleasure and taste.  If you find a food to be palatable, that means you like it and it tastes good.

Steve Wright:  And then the reward that we’re talking about is multilevel — it’s a chemical in the brain, it’s psychological in our actions, and it potentially is also driven from, like, our ancestors in a deeper lizard brain as far as seeking certain nutrients, as well?

Chris Kresser:  Well, I think they’re both driven by neurobiological mechanisms, which we’re gonna talk about a little bit more.  I think that the easiest way to simplify it is that palatability doesn’t necessarily imply a change in behavior.  It just means that it tastes good and you like it and you get pleasure from eating it.  Whereas, food that’s rewarding will make you want to eat more, so it will actually influence your behavior.  And I think, again, the really good way to piece that out in your mind is just to think of certain foods that you like the taste of but you don’t have any kind of addictive relationship with them, like steak or something.  And those would tend to be foods that taste good and they’re probably part of our evolutionary history in terms of eating them, you know, like a plain sweet potato.  I think most people would think a plain sweet potato tastes pretty good.  It’s sweet and it’s pleasurable to eat, but how many people, again, do you know that just would go crazy eating plain sweet potatoes?  It just doesn’t really happen.  On the other hand, chips that have fat and salt and a particular mouth feel all engineered to stimulate the centers in your brain that motivate a particular behavior, that’s gonna have a really high reward value.  Does that make sense?

Steve Wright:  Yeah, it totally makes sense, and I think a lot of people listening probably in the Paleo crowd or the Specific Carbohydrate Diet crowd will relate, because I know that previously if I ate mashed potatoes or sweet potatoes I never thought of them as particularly intensely flavorful, and I think that’s just because I was eating that other stuff.  Then once you drop off and you eat something that has some more carbs in it like that, you can definitely taste the sweetness and it’s much more subtle.

Chris Kresser:  You got it, and I’m glad you brought that up, because one of the reasons I love this overarching theory is that it can explain why both low-carb and low-fat diets can be effective for weight loss and why when people tend to start adding carbs back if they have been on a low-carb diet or they start adding fat back when they’ve been on a low-fat diet that they tend to gain the weight back, and that’s because carbohydrates and fat have reward value on their own.  And so, when you remove or really limit a whole entire class of macronutrients, that reduces the reward value of that diet.  And then when you bring them back in, that increases the reward value and it tends to make you want to eat more of that.  So, in your example that you just used, if you’re on a low-carb diet, which the SCD and GAPS typically are, and then you start eating carbohydrates, you’re adding reward value back to your diet, and if you had a weight problem before and the setpoint hadn’t been actually adjusted, then the chances are that you’ll gain weight back.  We’re gonna talk a litte bit more about that in a moment here.  So, one of the best examples of how reward and palatability affect weight regulation is something called the cafeteria diet model of rodent obesity, and this is where they give rats a bunch of human junk food, so you know, just chips, crackers, candy — it’s all human, processed food — and then they also give them an unlimited amount of the standard rat chow, which compared to the human junk food is pretty boring.  And what do you suppose happens?  I mean, you can probably guess.  They over consume the junk food, and they don’t even touch the rat chow.  And the rats that are genetically susceptible become obese, and how addicted do they get to the junk food?  Well, the rats that are put on this cafeteria diet will voluntarily endure foot shocks and extreme cold just to obtain the cafeteria diet, even when the standard rat chow is freely available.

Steve Wright:  That’s how good those researchers are.

Chris Kresser:  Exactly!  So, I mean, it’s pretty amazing, and it works the other way around, and again, we’re gonna talk about that in a second, but before we do that, I want to back up a little bit and talk at least a little about how food reward and the central nervous system interact and the regions of the brain that are involved in this, because I thinks it’s important to have a basic understanding of it.  So, there are a lot of regions of the brain involved in evaluating and reinforcing the reward value of food, including the corticolimbic system, the hypothalamic system, and parts of the midbrain, and we know that signalling of dopamine and opioid peptides is especially important in the reward and hedonic value.  And this kind of gets at what you were asking before, Steve.  Dopamine signalling is thought to contribute particularly to reward, to the wanting of food and to the motivation to obtain food, and this is supported by the observation that changes in dopamine signalling are associated with other kinds of addictive behavior like drugs and alcohol and other substance abuse.  There are lots of studies showing in drug addicts or alcoholics that there is a problem in the dopamine signalling system.  We also know that interventions that alter dopamine signalling in the central nervous system have been shown to powerfully influence food intake and body fat mass, and we know that inherited or acquired reduction of dopamine signalling favors the accumulation of body fat.  And one theory on this is that overexposure to these highly palatable, rewarding, and energy-dense foods desensitizes the dopamine circuits, although there is some controversy about that.  Now on the other hand, opioids are connected to the liking or the hedonic value or palatability of food, and studies have shown that opioid receptor agonists — an agonist is a substance that mimics the action of a natural substance, so an opioid receptor agonist would be something that increases the effect of opioids.  They strongly increase intake of palatable food in rats, so if you stimulate the opioid receptors, rats will really go crazy for palatable food.  Whereas, on the other hand, opioid antagonists have the opposite effect.  So, we’ve talked a lot about low-dose naltrexone on the show, but full-dose naltrexone at 50 mg is an opioid antagonist, so it completely blocks the opioid receptors, and that’s why it was used for opiate and heroin and alcohol withdrawal, because if a heroin addict, for example, is on 50 mg of naltrexone and they shoot heroin they’ll feel absolutely nothing.  So, the naltrexone has been shown in clinical trials to reduce body weight because when people are taking it, they’re not inclined to eat as much palatable food, so that’s more evidence that these parts of the brain are involved.

Steve Wright:  I was just going to repeat that back:  So, dopamine is the craving, it’s the wanting, and then opioids are the high?

Chris Kresser:  Opioids are the liking.  Yeah, the hedonic — it goes to palatability.  So, dopamine is connected to reward and the motivation and the behavior, and opioids are connected to the liking or the experience of pleasure or the high, yeah, if you want to put it that way.  Definitely.

Steve Wright:  So, that’s how LDN works, is by taking away the high, then all you’re left with is craving, and you could eat a case of chocolate and –

Chris Kresser:  Well, that’s how full-dose naltrexone would work, but the problem with that is that it also, I mean, opioids are what regulate our sense of pleasure overall, so if you’re taking 50 mg of naltrexone, yeah, you won’t experience pleasure when you shoot heroin, and you won’t experience pleasure when you eat that bowl of ice cream, but you’re not going to experience much pleasure any other time.  So, there are pretty obvious problems with that.

Steve Wright:  Yeah.

Chris Kresser:  And then a third neurochemical that’s involved in this whole process are the endocannabinoids.  These are involved in the brain reward area, and of course, they earn their name after it was discovered that marijuana acts primarily through the CB1 endocannabinoid receptor.  Stimulating that receptor selectively increases the consumption of highly palatable foods, and this explains, of course, why people get the munchies when they smoke pot.  So, if they smoke pot and then those endocannabinoid receptors are activated, then they’re gonna want to increase palatable foods, and when people get the munchies they’re seeking out particularly palatable foods, right?  They’re usually not getting the munchies for, I don’t know, brussels sprouts.  I mean some people find them to be palatable.  I actually like them, but it’s not the food that people tend to eat when they get the munchies, right?  They’re going for the more palatable and probably more rewarding foods, as well.  On the other hand, just like naltrexone, drugs that block the endocannabinoid receptors have been shown to cause weight loss and selectively suppress the consumption of highly palatable foods in rodents.  So, that means it didn’t suppress consumption of all food across the board; it just selectively suppressed the consumption of the highly palatable foods.  But, again, there are some problems with using this as a treatment for human obesity because these drugs are known to have psychiatric side effects including an increased risk of suicide because the endocannabinoid system probably, again, plays a role in our overall experience of pleasure and enjoyment or life.  So, you have a drug that blocks those receptors, it does serve the goal of reducing consumption of palatable food, but it also, you know, really screws up people’s mood.  And, of course, that’s often the problem with drugs is they suppress function.  So, they suppress symptoms, but they also suppress functions, and that means that in solving one problem, they end up causing several others, because the receptors and proteins and things that drugs affect in the body don’t tend to have just one effect; they tend to have several different effects.  And so, when you suppress something, you’re not just suppressing the one effect that you want to get rid of.  You’re suppressing multiple effects, many of which are beneficial.  So, when you put all of this together, it suggests that in an environment where humans are exposed to food that’s way more palatable and way more rewarding than what we’re adapted to, that’s when you get obesity.  And I just want to reiterate that I don’t think that food reward and palatability is the only environmental factor involved in the obesity epidemic by a long shot.  We’ve already talked about other factors like food environmental toxins and genetics and micronutrient deficiencies and gut flora and birth weight, etc.  But I do think that reward and palatability is definitely a factor, and I think the research pretty clearly supports that it is.

The one thing any successful weight loss intervention must have

Chris Kresser:  So, let’s wrap all of this up and talk a little bit about what it means for people who are trying to lose weight, and as I said in the beginning, we’re not gonna — you know, we’re already getting to the end of the show here, so we’re not gonna have time to cover this in detail, but we will revisit it later.  At the simplest level, what it means is that any successful weight loss intervention has to involve lowering the setpoint.  And if it doesn’t lower the setpoint, the effect is just flat-out not gonna work at all or it’s gonna work for a short period of time and then the weight will come back, and of course, that explains why something like over 90% of people who go on calorie-restricted diets end up gaining the weight back at some point, and oftentimes they gain more weight back than they lost in the first place.  There is some evidence that low-carb diets and Mediterranean diets have been shown to induce moderate fat loss over the long term, and I think Paleo Diets can do that, too.  There are a few studies that suggest that, but we don’t have any long-term Paleo Diet studies yet on weight loss.  I certainly, you know, anecdotally in my practice have seen that, and I’m sure a lot of other people have had that experience, as well.  But on the other hand, I have a lot of patients in my practice who come to me for weight loss, and they’ve been on a Paleo Diet, they lost weight to begin with, sometimes quite a bit of weight, and then they either plateau and can’t lose the last 10 or 15 pounds or they start gaining the weight back and eventually gain it all back.  So, even though the Paleo Diet, I think, helps a lot of people and in some cases is the only thing that people need to lose weight and keep it off, there are clearly a lot of people whom that’s not enough for, and that’s one of the reasons I wanted to do this show, is I wanted to explain some of the mechanisms involved and help people appreciate how deeply rooted those mechanisms are, that they’re evolutionary in nature and that it’s not a failure of willpower, it’s not your fault that these systems are in place and that they work so strenuously against our efforts to lose weight.  So, getting back to the setpoint, right now, as I mentioned earlier in the show, the only intervention that we know that substantially and consistently and durably, meaning in a lasting way, reduces the defended level of body fat or the setpoint is bariatric surgery or gastric bypass.  So, this is a surgery where they divide the stomach into a small upper pouch and a much larger lower remnant pouch, and then they rearrange the small intestine to connect to both of these chambers.  In the most popular variation of this, the small intestine is divided about 18 inches below the lower stomach outlet, and then it is rearranged into a Y-configuration, and that enables outflow of food from the small upper stomach, and what it does is it causes a rapid onset of satiation, which is feeling full.  So, people who have had this surgery will feel full very quickly after they start eating, and then that is followed by growing satiety, which is an indifference to food or a lack of appetite after you’ve started eating.  So, people who have had gastric bypass, on average, they lose about 60% of the excess body weight that they were carrying — at least, morbidly obese people do, and those are the ones who generally have this surgery.  And in contrast to calorie restriction and other weight loss programs, the bariatric surgery causes a reduction in hunger and reduced cravings for energy-dense foods, and it doesn’t cause any change in circulating thyroid hormones that would suggest a compensatory homeostatic response to fat loss.  In other words, the body doesn’t respond to this surgery in the same way that it responds to caloric restriction that I described earlier by increasing hunger and decreasing resting energy expenditure and decreasing the conversion of T4 to T3 and all of those things.  And then we have studies that suggest that gastric bypass alters food reward processing in the brain, and so it’s changing the food reward system in some way, but those mechanisms aren’t entirely clear at this point.  So, at this point, it may seem like I’m recommending gastric bypass, and –

Steve Wright:  Are you?

Chris Kresser:  I’m not really.  I think it has some use in people who are extremely obese and who have tried every other way of losing weight and haven’t been able to because morbid obesity along with extreme, you know, metabolic syndrome is a real significant risk factor for a number of different diseases that can kill you.  So, in those situations, gastric bypass might actually be a valid alternative, but I’m not bringing it up to suggest it for people who are just trying to lose a little bit of weight or are even 10, 20, 30, 40, 50 pounds overweight.  I don’t think it’s a viable alternative in that situation.  There are risks, of course, associated with any invasive procedure like that, and you know, I’m more talking about this as a way of, first of all, just sharing what this surgery and what happens after it can tell us about the setpoint and other interventions that might help to lower the setpoint, because at this point that’s not altogether clear.  And that’s the million dollar question, really.  I talked earlier about how we just haven’t cracked the nut yet in this whole weight loss thing, and whoever figures out what nonsurgical method can reliably lower the setpoint is gonna get the Nobel Prize and be a multi-billionaire — if there even is such a, I mean, I frankly don’t think that there is gonna be just one thing and that it’s that simple because this is so complex.

Steve Wright:  Yeah, I think you made it pretty clear that this is pretty complex, and any thought that a surgery could just magically turn things around — because I think there is a lot of new stuff coming out now about long-term studies with the bypass surgeries, and they’re having onset of other diseases because of lack of nutrients now and that kind of thing.

Chris Kresser:  Absolutely.  Those are the complications that I was referring to, so there’s no magic bullet.  It does work for weight loss, that’s for sure, but as you pointed out, there are a lot of other problems that the surgery causes, and there is a lot more to health than weight.  There are some other interventions, though, that might lower the setpoint that research supports, and Stephan, again, of course, has written about this.  Just as increased food reward and palatability can increase the setpoint, there are studies that suggest that decreased reward and palatability lowers it in both rodents and humans.  And Stephan blogged about a really great 1965 paper that was published in the Annals of the New York Academy of Sciences, and in this study researchers developed a machine that basically dispenses bland liquid food through a tube at the push of a button, and it was kind of like sci-fi, if you look at the picture; it’s pretty funny.  And the formula was 50% carbohydrate, 20% protein, and 30% fat.  So, at first they fed two lean people with no weight problems for 16 and 9 days, respectively, and both people maintained their typical caloric intake and weight eating this really bland liquid food.  And then they fed morbidly obese volunteers, and over the first 18 days, one obese volunteer ate only 275 calories a day, and the second volunteer ate even less, 144 calories a day over 12 days, and that person lost 23 pounds in 12 days.  The first volunteer continued eating from the machine for 70 more days in the ward and lost 70 pounds total in that 70 days, and then he was sent home with the formula and instructed to eat about 400 calories a day with it for another 185 days, and he ended up losing 200 pounds in that 185-day period and, remarkably, never complained of hunger or GI discomfort.  So, some people might say, yeah, big deal; of course you’re gonna eat less food when it’s not palatable or rewarding.  But that doesn’t explain why the lean people maintained their weight and their caloric intake on that diet, because if both lean and obese people ate less of it, then you would expect the lean people to lose weight, but they ate the same amount of it, and they maintained their weight over that period of time.  And then there was another study in 1976 that confirmed that reducing food reward by feeding bland food lowers the body fat setpoint in humans.  So, all of this implies that, of course, highly rewarding food can increase the body fat setpoint in certain susceptible people, not in everybody, and that food with few rewarding properties can allow them to return to a lean state, and that doesn’t happen necessarily with everybody either.  And there’s also some evidence that suggests another technique called the protein sparing modified fast may reset the setpoint, but we’re out of time here, so we can’t talk about that in any detail.  Before we close, I just want to say a brief word about genetics.  There’s absolutely no doubt, as I’ve said a few times already, that genetics play a role in fat gain and fat loss, but how much is the question.  We know that heritable factors, when you combine genetics and epigenetics, are estimated to account for somewhere between 45% and 75% of body mass index variability.  But we also know that monogenic disorders, which mean mutations of one single gene, account for less than 5% of obesity, and some estimates say it’s even less than 2%.  So, this means, of course, that obesity is a polygenic trait, which means that it involves both developmental and epigenetic factors, as well as genetics, and we’ve talked about some of those before.  Things like low birth weight and maternal obesity and maternal overnutrition can increase subsequent obesity risk.  And likewise, prepregnancy fat loss, like women who have had the bariatric surgery before they get pregnant, tends to reduce the future risk of obesity.  So, this suggests that genetics do play a role, but that role is pretty small on its own but pretty large when you combine genes with environmental and developmental factors.  So, again, it’s the interaction of the genes and the environment that really makes a difference.  OK, I think that’s it!

Steve Wright:  Yeah, that’s pretty powerful!  So, the moral of the story is that you could have been set up from the beginning, unbeknownst to you, from genetics.  And there are a bunch of scientists and a large, billion dollar industry that are trying to set you up on the corner, and so you definitely need to get some help, right?

Chris Kresser:  That’s it!  I hope that the effect of this — one interpretation of this is to get really depressed and say, “Wow!  It’s just pointless to even try to lose weight.”  But I hope that’s not the result of this.  My intention was that people who have been having a hard time might be able to find some more compassion for themselves, because if you think about the forces you’re up against — as you pointed out, so you’ve got genetics, genetic predisposition.  Then you’ve got epigenetic factors that start from before you were even born.  I mean they basically start at conception or even before conception with your mom’s nutritional status during her pregnancy and then your birth and the manner of your birth and whether you were breastfed and your early exposure to all of these environmental factors.  And then you encounter the food industry, which, like you said, is on every corner, trying to get you to eat these highly energy-dense, palatable foods, and that is interacting with all kinds of neurobiological mechanisms, opioids, endocannabinoids, dopamine, and the whole hedonic, pleasure-seeking system that we’ve had as part of our wiring for millions of years.  So, when you put all that together, I hope it leads to just an appreciation of the difficulty of the task and maybe some compassion for yourself if you’re struggling with this for why it is so difficult, and hopefully in the future we’ll get a chance to dive more into what can be done about it, and I will frankly say that weight loss is difficult.  It’s one of the hardest things for me to treat in my practice.  I’m experimenting with some different programs designed to reduce the body fat setpoint, and sometimes they’re successful and sometimes they’re not.  And I’d be really suspicious of anybody who claims to have a program that works for everybody.

Steve Wright:  Yeah, I hope this isn’t depressing either.  I hope this is eye-opening, as you said, and I think it should be eye-opening in the fact that there is no magic pill.  There’s not a magic pill that’s even in testing that could come, and the appreciation that it’s a multifaceted problem, which means that the answer is likely multifaceted.  So, it’s a food problem; therefore, there’s gonna be a food answer.  It’s potentially a psychological problem; there might be a psychological component. It’s a chemical problem; there’s probably a chemical answer.  And altogether, I think it should be encouraging to take multiple steps in every area.

Chris Kresser:  Yeah, that’s very well said, and the takeaway is that it’s extremely individual, and it’s really important to first identify what all the mechanisms are in each individual case and then address those one by one, and that’s, of course, why there is, again, no magic bullet that works for everybody in the same way.  OK, so thanks everybody for listening, and we’ll see you next time!

Steve Wright:  Yeah, it’s been a great show!  OK, so if you’re confused about what to eat, which, after the show, you might be, check out the PersonalPaleoCode.  It’s a 3-step program designed to help you discover your own ideal diet and create highly customized meal plans with a few clicks of a button.  You can visit PersonalPaleoCode.com to learn more.  And if you’re trying to get pregnant or are already pregnant or nursing, don’t miss out on The Healthy Baby Code.  It guides you through the essential steps to naturally boost fertility and promote lifelong health for you and your baby.  Find out more at HealthyBabyCode.com.

Thanks for listening, and keep sending us your questions at ChrisKresser.com using the podcast submission link.  If you enjoyed listening to the show, please head over to iTunes and leave us a review.

I’m going to be speaking as well as participating in a couple of mastermind panels at the PaleoFx conference in Austin, TX from March 14th – 16th.

The symposium theme is “Theory to Practice”. PaleoFx is the practical, hands-on, how-to version of the Ancestral Health Symposium. Speakers include myself, Robb Wolf, Mark Sisson, Jack Kruse, Keith Norris, and many others. All of your favorite Paleo & Primal diet and lifestyle folks will be there.

In addition to fitness and healthcare professionals, nutritionists, and research scientists, there will be top strength and conditioning and natural movement coaches giving hands-on demonstrations. The symposium is intended for laypersons, practitioners, researchers, and everyone in between.

Tickets are now on sale. Stay tuned for announcements on ticket giveaways. For full details, visit www.paleofx.com and www.facebook.com/paleofx.

Looking forward to seeing you there! Are any of you planning to go?

GERD is an extremely common problem in the U.S.. 44% of Americans suffer from it at least once a month, and 20% suffer from it weekly. (1) Drug companies make $7 billion a year selling acid suppressing drugs – primarily proton pump inhibitors (PPIs) like Prilosec and Aciphex.

The popularity of these drugs is predicated on the idea that GERD is caused by stomach acid burning the esophagus. This is known as the “chemical burn” theory. It holds that GERD develops from caustic, chemical injury that starts at the surface layers of the esophagus and progresses through the tissue to the deeper layers (the lamina propia and submucosa). (2)

Early animal research seemed to support this. Studies showed large quantities of stomach acid with a pH of less than 2 does damage the esophagus. (3) However, the concentrations of acid used in these studies are much higher than those normally found in human episodes of reflux. In fact, the vast majority of human reflux episodes have a pH of more than 2 and are incapable of causing esophageal damage. (4)

What if GERD is not caused by acid burning the esophagus?

In a 2009 study Souza and colleagues connected the esophagus directly to the duodenum (the upper part of the small intestine) in a group of rats, thus permitting acid to reflux freely into the esophagus. (5) To their surprise, it took 3 weeks for damage to the esophagus to occur. Commenting on the results, senior author Stuart Spechler said:

That doesn’t make sense if GERD is really the result of an acid burn, as we were all taught in medical school. Chemical injuries develop immediately. If you spill battery acid on your hand, you don’t have to wait a month to see the damage.

If acid itself caused the damage, we’d expect to see the damage start at the superficial layers of the esophageal tissue, and then progressively deepen. Instead, this study found the opposite. 3 days after the initial acid exposure, there was no surface damage – but inflammation had already begun to develop at the deepest layer of the tissue. This inflammation didn’t rise to the surface layers until about 3 weeks after the initial acid exposure.

This suggests that GERD is an autoimmune disease.

Acid refluxing into the esophagus doesn’t damage the mucosal lining. Instead, it causes the esophagus to release inflammatory cytokines that attract inflammatory cells like interleukin-8, interleukin-6, and others. It is this inflammatory process – and not the initial exposure to stomach acid – that causes the tissue damage characteristic of GERD.

Do you have GERD – or NERD?

The theory that GERD is not caused by chemical injury is supported by the fact that 70% of westerners diagnosed with GERD have no visible tissue damage.

In fact, these people don’t have GERD at all. They have NERD, or Non-Erosive Reflux Disease. Tissue biopsy of their esophagus shows inflammation developing at the base layers of the esophagus like GERD sufferers, but no damage to the surface layers as the conventional theory would predict. It’s unclear at this point why the tissue injury progresses to the superficial layers in GERD – but not NERD – sufferers, but this study suggests that the answer may be an autoimmune mechanism.

So what does this mean for you? How do you avoid GERD and NERD in the first place?

Even if GERD is caused by an autoimmune process as this study suggests, the initial trigger seems to be acid inappropriately moving from the stomach to the esophagus. But that does not mean GERD & NERD are caused by too much stomach acid, as the common dogma holds.

In an earlier series of articles I presented evidence that acid reflux is caused not by too much stomach acid, but by not enough. I argued that low stomach acid causes bacterial overgrowth in the gut, which in turn produces gas that puts pressure on the lower esophageal sphincter, causing it to open and inappropriately allow acid into the esophagus.

I also offered a simple, 3-step protocol for treating reflux and GERD without drugs that thousands of people have now successfully used (check out the 190 comments) – including people that had been on acid suppressing drugs for 20 years or more. This is important because acid-suppressing drugs have numerous side effects and complications.

Why you should think twice about taking acid-suppressing drugs.

Acid stopping drugs promote bacterial overgrowth, weaken our resistance to infection, reduce absorption of essential nutrients, and increase the likelihood of developing IBS, other digestive disorders, and cancer. The pharmaceutical companies have always been aware of these risks. When acid-stopping drugs were first introduced, it was recommended that they not be taken for more than six weeks. Clearly this prudent advice has been discarded, as it is not uncommon today to encounter people who have been on these drugs for decades – not weeks.

What’s more, a recent study showed that proton-pump inhibitors (PPIs) – the most popular class of acid-suppressing drugs – induce “rebound acid reflux” in healthy people. The researchers took a group of people without any history of reflux and put them on PPIs for 8 weeks (where did they find these volunteers???) More than 40% of the healthy volunteers developed rebound acid-related symptoms like heartburn, acid regurgitation and dyspepsia once they stopped taking the drugs. (6) The authors of the study stated:

If rebound acid hypersecretion (RAHS) induces acid-related symptoms, this might lead to PPI dependency and thus have important implications.

I’d say!

If you suffer from acid reflux, make sure to read the entire series, and then follow the 3-step protocol I laid out. In a future article I’ll be covering some additional natural treatments that studies have shown to be just as effective as PPIs, with virtually no side effects or risks.

When addressing our health, many of us tend to focus on the quality of our diet and exercise as the primary methods of improving our overall wellness. We often believe that if we perfectly “dial in” our diet and exercise routine, then optimal health will surely follow. This concentration on perfecting both food and fitness in the quest for well-being can often lead to the neglecting of certain important relationships in our lives, particularly relationships with others.

But what about your relationship with nature?

You may not have considered the possibility of fostering a “relationship” with nature – after all, how can you have a relationship with a non-human entity?

From an anecdotal perspective, how many of us have taken a long walk in the woods, and felt soothed by the sound of the wind in the trees and the crisp smell of leaves? Or have been moved by the beauty of a snow-capped mountain range? Who wouldn’t enjoy an evening watching the sunset at the beach, sand between the toes, with the rhythmic ocean waves lapping at the shore?

Experiencing these profound moments of peace, happiness, or wellness in the context of nature is a universal event, and demonstrates that contact with nature is an integral part of our well-being as humans. In a public health context, exposure to nature has been used as therapy for short-term recovery from stress or mental fatigue, faster physical recovery from illness, and long-term overall improvement on people’s health and well being (1).

Research supports the theory that our relationship with nature is a fundamental component of maintaining good health. This “biophilia hypothesis” suggests that there is an innate affiliation of human beings to other living organisms, both flora and fauna, and perhaps even an innate bond with nature more generally.

The biophilia theory is supported by both common sense and clinical evidence. Many controlled trials and observational studies have demonstrated the positive therapeutic value of both the physical and visual exposure to nature, with benefits shown for a diverse range of diagnoses spanning from schizophrenia to obesity.

This biophilia theory makes sense in an evolutionary context as well.

Many species of animals use habitat selection as a criteria for successful survival, focusing mainly on patterns of tree density and openness of view. Early humans were no different; a preference for living near water and an abundance of green plants would have indicated greater food availability, with both edible vegetation and herbivorous animals in plentitude (2).

The ability to identify relaxing, restorative natural settings would have also allowed paleolithic humans the opportunity to recover from stress or fatigue, and would have been adaptive to survival. Those individuals who were able to settle in these types of environments would have gained a survival advantage, which may explain human beings’ preference for certain landscapes.

While we evolved outdoors and amongst nature for most of the last two million years of our species’ existence, the movement to a largely indoor environment has been a recent development for humans. Much like our diet, our physical environment has changed drastically in a comparatively short amount of time.

We have broken our strong connection with the natural environment very recently, and have not had the chance to adapt to our new life of shelter and confinement. The advent of electricity has been even more recent, allowing our world to be inundated with artificial light at any time of day (or night).

A lack of sunlight and/or excessive amounts of artificial light can have a variety of negative health consequences. (Diane Sanfilippo of Balanced Bites has written an excellent post regarding the problems with artificial light and the different ways you can reduce your exposure.)

Our relationship with nature has been overcome by our relationship with technology.

Recent news stories have focused on the idea of “nature deficit disorder”, suggesting that children who spend too much time staring at screens may develop attention deficits, hyperactivity, or depression (3). While our children may be bearing the brunt of this nature deficit, it stands to reason that those of us that spend forty hours a week or more with our eyes glued to a computer screen may have similar negative health consequences.

While we may not be able to quit our jobs, sell our houses, and move out into the wilderness (or can we?), there are many ways to alleviate our growing nature deficit:

1. Take your exercise outside – Research shows that exercising outside confers even greater physical and mental benefits compared to the same exercise indoors. Take a long walk at your local park (bundle up if it’s cold) rather than plugging away on the treadmill in your fluorescent-lit gym. Take advantage of warmer, sunny days and move your workout into the wilderness. It may take some creativity or extra planning, but the mental and physical benefits will be worth the effort. You may even find yourself enjoying your workout more than usual!
2. Invest in a pet – Companion animal relationships have been essential to the survival of primitive humans, and pet-keeping was common in hunter-gatherer societies. Pet ownership not only gives people a sense of companionship and nurturance, but also provides a connection to nature in a more tangible sense. Contact with animals has been shown to decrease risk of heart disease, lessen anxiety, and reduce depression. Not to mention, there’s nothing more motivating to get outside than a hyperactive dog!
3. Grow an indoor garden – If getting outside on a regular basis is too challenging, consider the addition of indoor foliage to your home’s interior design. Studies show that indoor plants can boost mood, improve air quality, and reduce anxiety and fatigue. Even if you live in an urban environment, bringing green foliage into your living space can greatly benefit your connection with the natural world.

Our relationship with nature is a vital component of our wellbeing, and one often neglected due to the concerns of modern life. In order to more fully address our health and wellness as humans, we must consider the biological appropriateness of our environment to be just as important as that of our diet and exercise choices.

Now I’d like to hear from you. How do you nurture your relationship with nature? What are your favorite ways to interact with the natural world?