The Gut as the Second Brain, Group B Strep During Pregnancy and Unwanted Synthroid Side Effects

In this episode, we cover:

4:40 The role of neurotransmitters in gut health and why it’s called the “second brain”
12:39  How abnormalities in gut-brain signaling and serotonin metabolism play a role in IBS
27:00  Everything you need to know about testing positive for Group B Strep during pregnancy
44:20  What to do about unwanted Synthroid side effects

Links We Discuss:

• Paper – A Gut Feeling about GABA: Focus on GABA(B) Receptors
• Paper – Late-onset infections in infants exposed to antibiotics during birth
• Life Extension Super Selenium Complex
• Nature’s Way – Alive Organic Vitamin C
• Life Extension Vitamin D3, 2000 Iu Emulsion
• Herb Pharm – Echinacea

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Full Text Transcript:

Steve Wright:  Hey everyone, and welcome to another episode of 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.  Chris, how are you doing today?

Chris Kresser:  I’m pretty good, Steve.  Other than nearly cutting my thumb off making taro chips the other day, I’m great.

Steve Wright:  Yeah, so what kind of kitchen appliance harmed you?

Chris Kresser:  The evil mandoline, which is probably…I don’t know if there’s a more dangerous appliance in the kitchen.  If there is, I haven’t found it.  You know, a mandoline is a very sharp tool used to slice vegetables, particularly root vegetables, and other things thinly.  It’s got a very sharp blade on it, and it comes with a little hand protector, a plastic thing with spikes on it that you’re supposed to attach to the vegetable as you slide it back and forth, but I’ve always found that thing to be really kind of awkward and tricky to use.  I do use it when the vegetable gets small, but I was using a big hunk of taro, and it was going back and forth, and I was paying attention, but I just thought that I could get it a little bit closer before I had to switch over to that irritating hand guard tool thingy, and I misjudged it, obviously.  Took a little chunk off the corner of my thumb and managed to get blood all over the taro chips.

Steve Wright:  It’s those dang safety devices, I tell you.  They’re messing up our lives.

Chris Kresser:  Yeah, I mean, it’s fine.  I just used a couple butterfly bandages to try to keep that little chunk on there and see if the wonders of regeneration can leave it intact there or mostly intact.  And I posted it on Facebook, and it was surprising to see…well, maybe not surprising to see how many other people have suffered the same fate.  And there apparently actually are some metal-lined kitchen gloves that you can use that help protect your hand from similar kind of events, so I think I’m gonna get one of those even though, you know, I’m sure I’ll be more careful.

Steve Wright:  So is it like chainmail?

Chris Kresser:  It looks like it, you know, like a kind of Knight of the Templar thing when you’re wearing those gloves!

Steve Wright:  That’s taking cooking up to a whole other level!

Chris Kresser:  Yeah, exactly.  So, yeah, I think I’ll give those a shot just to be safe now.  But the mandoline, I mean, you can make taro chips with just a sharp knife.  We have, like, a really nice MAC knife, but it takes longer that way, and the consistency of the thickness is not as good as it is with the mandoline.  Kitchen injuries.

Steve Wright:  Well, I’ve cut myself many times as well, so I can sympathize.

Chris Kresser:  Yeah.  How are you doing?

Steve Wright:  I’m doing well.  I’m doing very well.  I’m looking forward to Memorial Weekend here and having some cookouts.

Chris Kresser:  Sounds good.

Steve Wright:  OK, so on this episode of the Revolution Health Radio Show, we’re gonna give you an update on the gut-brain axis and some of the various neurotransmitters that are gonna be affected in this axis.  We’re also gonna do some Q&A, and one of the main topics we’re gonna cover in the Q&A is group B strep and its effects on pregnant moms.

OK, so, before we get started here, Chris, go ahead and take a break, get a drink of water, and in the meantime, I’m gonna tell our listeners about our sponsor today.  Now if you’re new to the paleo diet, to this radio show, or you’re just interested in optimizing your health, you’re gonna want to check out Beyond Paleo.  Now, what’s Beyond Paleo, you ask.  Well, it’s a free 13-part email series that covers the topics of burning fat, boosting energy, and preventing and reversing disease without drugs.  Now, we’ve had over 10,000 people download this so far, so you’re probably gonna want to check it out.  If so, go over to ChrisKresser.com and look for the big red box.

OK, Chris, are you ready?

Chris Kresser:  I’m ready.  Let’s do it!

Steve Wright:  Perfect!  So, we’re starting with gut-brain axis, right?

The role of neurotransmitters in gut health and why it’s called the “second brain”

Chris Kresser:  Yeah.  This is one of my favorite topics.  You know, we’ve had a whole show on it in the past.  I write about it a lot, and the more I treat people with gut issues, which is probably 80% of my patient population, I mean, even people who don’t come to see me ostensibly for gut issues very often have gut issues.  So, I think it’s probably one of the major health issues that impact us these days, and if anything, it just seems to be getting more and more common because there are so many aspects of the modern lifestyle that are antagonistic to gut health, and I really believe that healing the gut is probably the single most important thing we can do to improve our health.  And I’m not just talking about our gut health.  We know, as we’ve discussed many times on this show, that gut health contributes to proper immune function because 70% to 80% of the immune system is in the gut.  Poor gut health can predispose us to everything from autoimmune disease to allergies and asthma to skin problems like eczema and psoriasis to cognitive difficulties, depression, anxiety, to metabolic problems like obesity and fatty liver.  I mean, the list really goes on and on, and it’s quite astounding when you dive into the literature and see all of the various connections between the gut and other systems of the body and all aspects of health.

So there’s a lot of discussion about the gut flora and gut barrier integrity and leaky gut and gut infections and things like that that affect gut health, but recently there has been more and more focus in the research literature on this gut-brain axis that we discussed in the previous show, and briefly, to review, there’s a very tight connection, and it’s maybe even inaccurate to say “connection” because that implies we’re talking about two separate systems.  Really the gut and the brain are part of one unified central nervous system, and you can think of the gut as just a big nervous system tissue, and some people even consider it to be the second brain, and the scientific term for that is the enteric nervous system.  A large percentage of the output, I think it’s over 80% of the output, of the brain goes into the pontomedullary area, which in turn goes into the vagus nerve, and the vagus nerve innervates the entire digestive tract and influences things like hydrochloric acid secretion, pancreatic enzyme production, and intestinal motility.  And then inflammation in the gut, for example, when inflammatory cytokines are produced, they can travel into the bloodstream, go across the blood-brain barrier, and then suppress the activity of the frontal cortex, which in turn decreases the output into the gut and creates a vicious cycle of gut-brain axis dysfunction.

So that’s kind of what we focused on when we originally covered the gut-brain axis, but recently I’ve been reading some interesting papers on the role of neurotransmitters in the gut.  And people, I’m sure, are familiar with neurotransmitters like serotonin and melatonin and GABA for the role that they play in brain health and central nervous system function.  Serotonin imbalances have been linked, of course, with depression and other mood disorders, and GABA imbalance has been linked with anxiety because GABA is the major inhibitory neurotransmitter, which we’re gonna talk a little bit more about in a second.  But what a lot of people don’t know is that there are actually much higher levels of these neurotransmitters in the gut than anywhere else in the body, including the brain.  So, I came across a paper the other day about this GABA in the gut, and I thought it was a good opportunity to discuss some other recent research on neurotransmitters and gut health that I’ve been looking at.

So, again, GABA is the main inhibitory neurotransmitter, and it regulates a lot of physiological functions, especially in the gastrointestinal tract, and it’s found throughout the GI tract.  It’s localized primarily in enteric nerves and then in endocrine-like cells, and so you can think of GABA not only as a neurotransmitter but also an endocrine mediator in the gut.  And in fact, the myenteric neurons in the gut nervous system have been shown to regulate intestinal motility, and about 8% of those neurons contain GABA.  Baclofen, which is a GABA receptor agonist, something that activates the GABA receptors, has been used in the treatment of GERD.  In one study, it reduced the transient lower esophageal sphincter relaxations, or TLESRs, which are a characteristic of GERD and reflux, and it also reduced the number of reflux episodes in healthy subjects.  So, this drug that increases GABA has actually been shown to benefit patients with GERD.  Unfortunately in that study, about 80% of patients in the trial developed central nervous system-mediated side effects like dizziness.  So, the mechanism is interesting, and we know that increasing GABA can improve gut health, but using this particular drug is not a good idea because of the side effects that it led to.  But what I’ve been researching and experimenting with in my patient population has been other non-pharmaceutical approaches to increasing GABA that can have similar effects on gut health without the negative side effects that some of the more powerful drugs have.  So, that’s GABA, and there’s a lot more work to be done there, but I think it’s probably no surprise that if a major inhibitory neurotransmitter that can have pretty profound effects on anxiety might contribute to gut health because, as most of us know, anxiety and stress are antithetical to gut health.  So, something that could help mitigate the impacts of anxiety and stress or reduce anxiety and stress, it’s probably fairly obvious that that could contribute to gut health, but it’s not an avenue that’s been explored in a lot of detail.

Steve Wright:  So, GABA is the main inhibitory neurotransmitter, and now there’s also main excitatory transmitters.  What exactly is “inhibitory” meaning in this standpoint?

Chris Kresser:  Well, you have excitatory neurotransmitters and inhibitory neurotransmitters, like you just said, and we’d have to get an expert in brain chemistry to come in here and talk about the exact differences.

Steve Wright:  On a high level, I mean, GABA is gonna be downregulating some things?

Chris Kresser:  Excitatory turns on and inhibitory turns off.

How abnormalities in gut-brain signaling and serotonin metabolism play a role in IBS

Chris Kresser:  That’s probably the easiest way to explain it.  So, serotonin, there’s a lot of research that suggests that abnormalities in gut-brain signaling and serotonin metabolism play a role in IBS and similar conditions, and some people might have heard of a drug called Zelnorm, which I’ll come back to in a second.  That’s actually based on this idea that serotonin plays an important role in gut health, particularly gut motility.  There’s some more recent evidence that suggests that serotonin is involved in modulation of immune and inflammatory responses within the gut, and again, there’s about 400 times more serotonin in the gut than there is in the brain.  In fact, 95% of the body’s serotonin is found in the gut.  Most people when they think of serotonin, they think primarily of the brain, but really the main reservoir of serotonin is the gut and particularly the enterochromaffin cells in the gut.  So, we’ve known for almost 50 years, actually, that serotonin can influence gut motility, and studies have shown that IBS patients with diarrhea predominance have increased numbers of enterochromaffin cells, which means they have more serotonin, and these are activated by inflammation to release serotonin.  And on the other hand, constipation-predominant IBS patients have less serotonin in the gut.  Then there’s another interesting finding that patients with irritable bowel syndrome have genetic polymorphisms that can lead to lower expression of transport proteins and less serotonin reuptake, so there are changes in serotonin metabolism in the gut.

And then serotonin agonists, like Zelnorm (tegaserod), which we just mentioned, have been used for some time to increase the amount of serotonin in the gut, and it’s particularly used for IBS patients with constipation because it increases motility.  However, much like the GABA drug that we talked about earlier, baclofen, Zelnorm has had some serious problems, and it had a lot of side effects and was actually withdrawn in 2007 by the FDA due to concerns about possible serious cardiovascular adverse effects.  So, it’s no longer available.  It’s another example of where it was a promising mechanism for the therapeutic target, but the drug turned out to have a lot of issues that made it not a good choice.  So in the same way as I’ve been experimenting with GABA and gut health, I’ve been experimenting with serotonin and gut health.  There are, of course, natural ways of raising serotonin, like taking 5-HTP and doing some things to improve methylation, and those actually I’ve found to be pretty successful and without any of the negative side effects that Zelnorm has, because you’re mostly just dealing with…I mean, when you take tryptophan or 5-HTP, you’re just dealing with amino acids and serotonin precursors that are not gonna have the same kinda negative impacts that a drug like Zelnorm, a serotonin agonist, does.

Steve Wright:  Have you been using those for both diarrhea and constipation or just constipation-dominant?

Chris Kresser:  Yeah, actually for both, and it’s a little unclear how it works, but I think what it comes down to, and this is generally my philosophy with intervention, is it’s best to intervene in such a way that you still allow the body to regulate itself.  We’ve talked about this in the context of hormones.  It’s a better idea, if possible, to support the basic systems that lead to good hormone production and metabolism like blood sugar regulation, oxygen deliverability, gut function, liver/gallbladder function, etc.  When you give a hormone, you’re often bypassing the body’s natural regulatory mechanisms, and it makes it more difficult for the body to kind of determine what an appropriate amount is or response is, and then you run the risk of interrupting the natural feedback and causing hormone resistance.  So, working with precursors, then the body would still have some ability to determine what gets converted into whatever the end product is.  Whereas, if you just take the end product or you do something that alters the other end of that scale closer to the end product, then the body has less control over how it responds to that.  So yeah, it seems to work in both cases, though I’ve had more success with it in the case of IBS with constipation.  And for whatever reason, I seem to have more patients with that presentation even though I think diarrhea-predominant IBS is more common statistically.

Steve Wright:  Is it really?

Chris Kresser:  I think so.  I could be wrong about that, but I think it is.  So, melatonin…I can’t remember whether we’ve talked about this or I wrote about this somewhere.  It’s all kind of a blur these days, but melatonin is, like serotonin, 400 to 500 times more prevalent in the gut than it is in the brain.  Melatonin is produced in the pineal gland.  That’s where most people think about melatonin production.  And it plays a role, obviously, in regulating our sleep-wake cycles.  But it’s produced by the same cells, the enterochromaffin cells, that make serotonin in the gut, and it’s actually an important gut motility signal, so it regulates gastric emptying and peristalsis, and then it’s an important signalling molecule for communication between the gut and the liver.  Also interesting to note that there are significant amounts of melatonin and melatonin binding sites present in the esophagus, which is probably one of the reasons it can play a role in GERD treatment, which I’ll talk about in a second here.  And then melatonin also stimulates the production of nitric oxide and prostaglandin E2, both of which protect the esophageal mucosa from damage that can be induced by stress or oxidative damage, you know, excessive free radical production.  And finally, melatonin also inhibits gastric acid secretion while increasing gastrin release, and then gastrin stimulates the contractile activity of the lower esophageal sphincter.  And since GERD is characterized by these transient lower esophageal sphincter relaxations and problems with the tone of the LES, then something that stimulates the contractile activity can be helpful because it protects the esophagus by minimizing contact with reflux, with stomach acid and bile that would otherwise go back into the esophagus.

So, there was a pretty interesting trial a while back, where they compared two groups.  One was taking Prilosec, and then the other group they gave a pretty high dose of melatonin, like 6 mg of melatonin, and then some methylation cofactors like B6 and B12 and trimethylglycine and methionine and folate, and 90% of patients that took the nutrient/melatonin combination experienced relief after seven days, while 66% of those on Prilosec, which is a proton pump inhibitor, had similar relief after about nine days.  But after 40 days, 100% of the patients in the melatonin/nutrient group reported relief compared to only 66% of the Prilosec group.  And then at the end of that 40-day trial, the 60 patients in the Prilosec group who still had symptoms were switched over to the melatonin/nutrient combination for another 40 days, and at the end of that treatment period, 100% of the PPI nonresponders reported that all of their symptoms had resolved.  So, those are pretty amazing results, and I’ve used this protocol with some of my patients who have tried the starting place, which is increasing stomach acid with HCl and then possibly lowering carbohydrate intake, and if they’ve been tested for H. pylori and we’ve treated that and they don’t have H. pylori, or we’ve treated it and then they still have reflux, usually my next step will be a protocol with melatonin and these nutrients.  And it’s been remarkably effective.  I haven’t had 100% effectiveness, but it’s been really, really effective, and keep in mind that these are people who have had issues for a long time and they’ve tried numerous things, most of which haven’t helped, or if they have helped, the effect has been temporary.

Steve Wright:  Those are amazing results.  Do you think it’s mostly due to the contracting of the LES, or is there is stomach acid part here that isn’t being talked about, some extra secretion?

Chris Kresser:  It might depend on the patient.  You know, as we’ve discussed before, I think many people with GERD actually have low stomach acid, but there is a small subsection of people with GERD who do produce excess stomach acid, and there are ways of testing for that.  The tests aren’t very commonly done, but I have a few patients who have had that test and they have been shown to be producing excess stomach acid.  So, as I mentioned, melatonin inhibits gastric acid secretion, so that could have some effect there, but interestingly, it doesn’t do it in the way that a PPI does, so it doesn’t seem to negatively affect somebody who has low stomach acid in the same way that a PPI would.  That said, oftentimes when people are doing this protocol, if they have low stomach acid, they’ll be taking HCl, so it’s hard to say exactly what’s going on there if they’re taking HCl at the same time.  But I think it’s mostly about the tone and the contractility of the lower esophageal sphincter and the effects that melatonin has on gut motility.

Steve Wright:  Interesting.

Chris Kresser:  Yeah, I’ll report back on this later when it’s a little more solidified, and actually this might be a good time to very briefly mention that my next program that I’m really excited about, it’s not gonna be ready probably until early next year, but it’s gonna be called something like Restore Your Gut, and as I said when we first started talking about this, just the more I work with patients, the more convinced I am that healing the gut is the key step in recovering our health, almost regardless of what we’re…not regardless of what we’re suffering from, but in many, many cases and also in maintaining good health and preventing disease.  So I’m gonna do a program where I cover everything from how to identify and treat gut infections to particular dietary approaches for people with IBS and IBD and various food intolerances to how to work with gut-brain axis issues like this, and so what I continue to learn over the next year about treating the gut-brain axis will definitely be included in that program.

Steve Wright:  Well, I’m excited for it.

Chris Kresser:  Yeah, me too!

Steve Wright:  You know me, I love digestion!

Chris Kresser:  It’s gonna be a lot of work, but it’s a subject that I’m fascinated by, obviously, so I’m looking forward to it.

Steve Wright:  Yeah, well, there’s new research coming out, like you said, every month that’s linking all of the “lifestyle” chronic diseases back to the gut now, so it’s gonna be a product basically for everyone.

Chris Kresser:  You got it.  So, yeah, let’s go on to the first question we’re gonna talk about, and it’s an important question and a big topic, so it very well may take up the rest of the show, but we’ll see where we get to at the end, and then we’ll go on to a few other questions if we have time.

Everything you need to know about testing positive for Group B Strep during pregnancy

Steve Wright:  OK, so this question comes from Jessica.  She says:  “I’m going on 38 weeks pregnant, and I’ve tested positive for group B strep.  I reviewed your natural childbirth series to see if you had covered this topic there, but couldn’t find anything.  This is my second child, and I’m planning a homebirth in water.  At some point during labor, we’ll need to make a final decision regarding the administration of IV antibiotics.  I’ve been trying to find good information online about this topic, but it’s difficult to know whose opinion to trust.  One of the factors I’ve been considering is that my husband has a number of general autoimmune-related issues,” and she lists off a few of them including asthma, allergies, eczema, skin issues, gut issues.  “If our child is going to inherit these tendencies, having good gut colonization during birth will be especially important, so I’m really conflicted about using antibiotics that will disrupt this.  Have you researched this when preparing for your child’s birth?  And if so, could you shed some light on this for me?”

Chris Kresser:  Yes and yes, definitely.  Just a little background for people who aren’t familiar with this issue:  Group B strep is a type of bacteria that lives in the bowel and/or the vagina as part of normal flora, and the statistics I’ve seen suggest that somewhere between 1 in 3 and 1 in 10, depending on which study you look at, of pregnant women are carriers of GBS.  And during labor and birth, the baby can be exposed to GBS in the womb, which usually happens after the membranes have ruptured or through contact with the mother’s vaginal and bowel flora during birth.  Now, for some exposed babies, GBS will just colonize the skin and the crevices between the skin folds, and far less commonly GBS can actually enter inside of the baby’s body and cause serious infection, including pneumonia, septicemia, and meningitis.  And in fact, GBS is one of the leading causes of infection in newborns, but the absolute risk or the absolute number of infections is pretty small.  The statistics I’ve seen suggest that fewer than one baby per 2000 contracts early-onset GBS, which is GBS that occurs up to a week after birth, and then an equal number, 1 in 2000, contract late-onset GBS, which occurs between one week and three months after birth.  Now, of that number, 1 in 25 affected babies dies from GBS, totalling about 80 newborn deaths per year.  So, there are about 4 million births per year, and that means there’s about a 1 in 50,000 chance of an infant dying from GBS.

So in recent years, it’s become common, and in some settings almost mandatory, to screen for GBS during pregnancy, and they do that with a swab, and if GBS is positive it’s recommended that women are administered an IV antibiotic during labor to eliminate GBS both from herself and her baby.  And this is usually done by giving penicillin every 4 hours until birth unless the woman is allergic to penicillin, in which case other broader-spectrum antibiotics are sometimes used.  Now, that’s not ideal because the broader-spectrum antibiotics eradicate a wider range of bacteria than penicillin, including the friendly bacteria in the gut and the vagina, and that’s, in fact, one of the main problems with GBS treatment, which we’ll talk about more in a second.  There’s still a debate about whether all women should be tested in various western countries or women who just have risk factors should be tested.  Some of the risk factors are gestation of less than 37 weeks, membrane rupture lasting more than 18 hours, temperature of over 100 degrees in labor, having a previous baby that had GBS, or having GBS that’s diagnosed by urine culture in pregnancy.  But here in the US the CDC, Centers for Disease Control, currently recommends universal screening, and they estimate that universal screening will prevent two times as many infections as risk-based screening approaches.  So, according to current numbers, using universal screening, about 30% of pregnant women would receive IV antibiotics in labor.  That’s a pretty significant number, 3 in 10, and there’s no doubt that GBS screening has benefits.  Universal screening has been estimated to prevent early-onset GBS for between 60% and 90% of susceptible newborns, depending on what study you look at, which in turn would prevent about 800 infections and potentially save the lives of 40 newborns per year.

So, you know, we’re talking about saving babies’ lives.  It’s pretty hard to argue with those numbers.  But we need to note a few things here.  Number one is that screening and treatment does not prevent late-onset GBS, and rates of late-onset GBS in the US have been pretty stable despite widespread screening and antibiotic use over the last several years.  And the other thing to note is that treatment of laboring women with antibiotics does not come without risks and unintended effects both for mothers and babies.  And these can include everything from nocebo effects of having a positive test result.  We’ve talked about the nocebo response, where being told that you have a problem or a condition can actually create real physiological changes that are negative or adverse.  Risks to pregnant women with antibiotic allergies.  Penicillin allergy is not common, but it happens, and so if a woman is not screened for that and she’s given penicillin, that could be very problematic.  Possible increased risk of late-onset infections, increased rates of antibiotic resistance, and then impact on newborn gut flora.

So I’m gonna focus on the possible increased risks of other types of infection as well as the impact on gut flora because I think those are probably the most significant risks.  There’s one US study that found that when babies were exposed in labor to broad-spectrum antibiotics to prevent GBS, their risk of later serious bacterial infection was five times higher than that of babies that were not exposed to antibiotics.  And the bacteria infecting those babies were more likely to be resistant to ampicillin, which is the usual antibiotic given to prevent GBS.  So, there’s also a concern about how the antibiotics used to treat GBS affect the bacteria that first colonizes the newborn’s digestive tract, and we’ve talked on previous shows a little bit about this, how important the early colonization of the newborn’s gut is to the baby’s future health.  These bacteria come from the mother’s bowel and vagina during birth, assuming the baby is born vaginally, and it’s been shown that the types of bacteria that are first established in the baby’s gut, which is actually sterile until birth, will persist and then really significantly influence everything from gut health to immune function to susceptibility to allergy and asthma and even risk of obesity and metabolic syndrome later in childhood.  And there’s a neonatal pediatrician in the UK named Dr. Bedford Russell, and she’s pointed out that a lot of infants today are becoming colonized because of overuse or increasing use of antibiotics, that many infants today are becoming colonized by bacterial patterns that are probably unique in evolutionary history, meaning for a long, long period of time human babies that were born, they weren’t born with the same bacterial patterns because those would differ based on the parents’ bacterial patterns and the geographical location perhaps, the type of food that’s eaten, all of the things that can affect gut flora.  But never before in history until very recently have infants been born to mothers who’ve been given IV antibiotics, which creates a profound shift in the mothers’ gut flora and thus the babies’ gut flora.  And she said, “There is increasing evidence from experimental studies that the initial colonization of the intestine is a moment of pivotal importance in long-term health, playing a profound role in imprinting of immune and systemic homeostasis.”

There are a few studies that bear this out.  One big study found that children exposed to antibiotics at delivery were 20% more likely to wheeze in the first two years and 40% more likely to have a wheeze persisting to age 6 or 7.  Now, of course, that’s epidemiological data, it doesn’t prove causation, but there are several other studies that have shown things like babies born via C-section have different gut flora than babies born vaginially, and babies that are breastfed have different gut flora than babies given formula.  And then when they follow these babies and track changes in health status over time, several studies have shown that babies born via C-section and fed formula have increased risk for obesity, autoimmunity, allergies, asthma, etc.  And this is another hot topic in the research literature, and I suspect we’ll be seeing a lot more data on this.  In fact, I just saw a study two or three days ago that Stephan Guyenet tweeted out, and it was linking, epidemiologically again, babies born via C-section with future increased risk of obesity as early as preschool.  So we have to be careful drawing conclusions with that kind of research because there could be other differences between babies born via C-section and babies born vaginially such as the diet of their mothers or any other kind of lifestyle habits that mothers have, whether they’re breastfed subsequently or formula-fed, so there are a lot of different complicating factors, but I think there’s enough epidemiological research combined with understanding of plausible mechanisms and what we’re learning about how gut health contributes to all these various aspects of overall health that it would be unwise to ignore this data and just wait until we know with absolute certainty.

So, as is the case with raw milk and vaccination and homebirth, I avoid making specific recommendations because I think it’s a very personal question and there are a lot of factors to consider that go beyond what the data actually say, such as your own individual risk tolerance, your priorities, your values, what’s most important to you.  For example, some women having a homebirth , especially if they’re using a midwife rather than a nurse-midwife or if they’re in a situation where they don’t have access to IV antibiotics or don’t want to do that at home, that’s a consideration here.  If the way in which they give birth and where they deliver the baby is of primary importance, then that’s, of course, gonna need to be factored into this decision.  So, there are lots of variables that people have to consider themselves and work out, and it’s impossible for me to make a specific recommendation for that reason.  But what I can say is that if you test positive for GBS like Jessica did, there are some alternatives to antibiotics that midwives and people with a more natural health bent might employ, but I want to stress that these have not been tested in clinical trials and their effectiveness is unknown.  There’s a well-known midwife, Anne Frye, who writes textbooks on midwifery, and she suggests a few things for women who have tested positive for GBS and don’t want to go the antibiotic route.  One is to increase the intake of fermented foods in the diet.  Number two, you can take probiotic supplements orally and also implant them into the vagina.  You can take a garlic clove and score it and insert it into the vagina overnight and repeat with a fresh clove for at least four nights in a row.  Grapefruit seed extract can be taken orally and/or by douche.  There’s a product called FemCleanse that has grapefruit seed extract in it.  General immune support using Vitamin C, Selenium, Vitamin D, Echinacea, etc.

It’s also important to note that most of these natural supplements have not been and never will be tested for safety in pregnancy.  We discussed this when we talked about the situations in which clinical trials are impossible.  It’s unethical, obviously, to take two groups of women and give one group a bunch of supplements and see what happens with the pregnancy and the baby, so that study will never be done.  But that said, a lot of midwives do feel that these things that I just mentioned would be safe at the end of pregnancy, which is when they would be taken, just before birth, especially when you compare them to the potential risk of IV antibiotics.  But again, this is something that if a woman is considering doing this, they should really talk it over with their midwife if they’re using a midwife or their doctor if they’re using a doctor, and it’s a really personal decision.  Also there are studies that have shown that washing a laboring woman’s vagina with chlorhexidine can reduce GBS colonization in babies, but studies have not shown that chlorhexidine confers an overall protection from GBS infection.  That may be because the studies that have looked at that have had a very small sample size, and it’s possible that it just wasn’t big enough to demonstrate a statistically significant effect.  But Anne Frye suggests adding a tablespoon of Hibiclens, which has chlorhexidine in it, with one cup of water and then using that solution as a douche or to wipe the inside of the laboring woman’s vagina with cotton gauze every 6 hours until birth.  And then finally, if antibiotics are given, it’s definitely preferable to use penicillin because it will have less of an impact on the gut flora than some of the broader-spectrum antibiotics out there.  So, that’s what I know about GBS, and a good resource, if you want to learn more about it, is a book called Gentle Birth, Gentle Mothering by Sarah Buckley, who is a physician, a GP, in Australia, I believe, and she writes a lot about natural childbirth and the various tests and the pros and cons of testing and treatment for things like GBS.

Steve Wright:  Well, it was great question from Jessica, and I know that it helped a lot of mothers out there, what you just went over, Chris, and I’m sure it helped a lot of fathers, as well.

Chris Kresser:  Great, so I think we have time for maybe one question.

Steve Wright:  Oh no, only one.

Chris Kresser:  Beyond that one that we just answered!  Maybe two.

What to do about unwanted Synthroid side effects

Steve Wright:  All right, I’m gonna go into my hat here, and I’m gonna pull out this one from Susannah, and she asks:  “I’ve been taking Synthroid for four years.  I was found to have a TSH of 14,” and I’m guessing that was before she started the Synthroid.  “While I feel some better, I still feel tired, and I have unwanted weight gain.  My mouth is so dry at times I can barely swallow.  My last TSH was 1.3, my T4 was 2.3, and my T3 was 99.  Is there a way to take T4 straight so I don’t feel symptomatic?”

Chris Kresser:  Well, let me kind of not answer that question and answer another question, which is what else should be considered here that might be contributing to this lack of response to Synthroid, and what other considerations might be really important here in terms of improving not only thyroid health, but overall health?  We’ve talked about this a lot on the show, but in many cases, hypothyroidism is caused by Hashimoto’s, which is an autoimmune disease where the immune system attacks the thyroid gland.  And I’ve said often that the key in that situation is to address the immune dysregulation so that the immune system stops attacking the thyroid or at least that attack is slowed down and you can mitigate the loss of thyroid tissue that occurs over time.  The conventional approach to treating hypothyroidism is just to give thyroid hormone, and I do believe that that’s necessary in many cases with Hashimoto’s, but it’s only addressing the effect; it’s not addressing the cause of the problem.  And so what happens, a lot of people find themselves in Susannah’s position where they take thyroid hormone, and it may work for a little while.  Sometimes it doesn’t really work at all, which sounds like it’s true in her case, but in many cases it will work for a little while, but then they’ll have to keep increasing their dose over time or change to a different type of medication because the underlying problem hasn’t been addressed, and the immune attack against the thyroid continues unchecked, tissue continues to be destroyed, and tissue is where the thyroid hormone gets produced.  So if that immune attack isn’t stopped, there will just be a progressive decline of thyroid function over time, and you’ll need either higher doses or different drugs to be able to address it.  So the very first thing that needs to be done, and Susannah may have already done this, it’s not clear from her question, but she needs to have her thyroid antibodies tested, both her thyroid peroxidase, or TPO, and thyroglobulin, Tg.  And if those are elevated, then I would really recommend finding a practitioner who specializes in treating autoimmune thyroid disorders and taking steps to regulate and balance the immune system so that you can preserve as much of your thyroid function as possible over time.  And usually what I find with patients is once we start addressing their immune dysregulation, the medication starts working better and then they will very often need to take less medication because the dose that they were on, which was inadequate before, all of a sudden becomes even too much when their immune system is not attacking their thyroid gland.  So that’s really important.

And in terms of determining what thyroid medication is optimal, that’s a pretty big question too, and it depends on a number of factors.  Number one, it depends on the pattern of thyroid dysfunction.  So, if somebody has high TSH and low T4, taking something like Synthroid or levothyroxine, which is just synthetic T4, makes sense…or may make sense at least, because that T4 will be converted, presuming there’s no issue with T4-to-T3 conversion the T4 level will come up, and T4 will be converted to T3, and that will work well.  But if somebody has a problem converting T4 to T3, which many, many people, especially with Hashimoto’s, do because inflammation suppresses the conversion of T4 to T3, then taking Synthroid or levothyroxine may not work very well because it will increase T4 levels, but that T4 won’t be effectively converted into T3, so it’s not really addressing the main problem in that situation.  And then you have to consider things like fillers.  Some of the different thyroid medications have different fillers, and people with sensitive immune systems, like people with Hashimoto’s, can react to those fillers.  For example, a few years back, there was a change in Armour, and people who had been taking it for years all of a sudden started reacting to it.  And the initial thought was that they changed the ratio of T4:T3 that’s present in Armour, but that actually didn’t get changed; it’s always been the same.  What they did change were the fillers, and just from changing the fillers, a whole bunch of people who had had success with it before stopped having success with it, so that’s something to pay attention to with any thyroid medication, and some patients need to a specially compounded thyroid medication because they’re so sensitive to the fillers that are used in the commercial alternatives.  So, that’s a lot to consider, but it’s always important to figure out what the underlying cause of the problem is.  That’s an ongoing theme here, and it’s no less true in the case of hypothyroidism.

Steve Wright:  It’s a very complex topic, and I think you laid out a pretty good plan there, though, for Susannah and anybody else who has that problem.

Chris Kresser:  Great.  Well, I gotta wrap it up.  I gotta go be a dad.

Steve Wright:  OK, well, we heard her yelling for you already.

Chris Kresser:  That’s right!

Steve Wright:  So, we knew we were on borrowed time there.

Chris Kresser:  That was my wife coming to remind me that it’s my turn!

Steve Wright:  Awesome, Chris.  Well, thanks for the knowledge you shared this week, and we’ll be back at it again soon.

Chris Kresser:  Look forward to it!

Steve Wright:  OK, great.  Well, thanks for listening to the show today.  Please keep sending us your questions at ChrisKresser.com.  If you enjoyed the show today, it would really help us out if you could head over to iTunes and leave us a review.  Those reviews help get us exposure and help spread the message.  Thanks, and we’ll see you on the next episode.