http://www.thekitchn.com/feedburnermain
Easy but impressive. That might be our favorite way to describe a recipe. We don’t always want to spend hours in the kitchen fixing dinner, but we still want to serve something that will elicit contented sighs.
That’s where these 15 meals come in handy. They are all pretty foolproof to prepare, and look much more complicated than they actually are. Choose one for tonight and let the oohs and aahs roll in.
http://www.thekitchn.com/feedburnermain
(Image credit: Kaitlin Flannery)
Is your farmers market or grocery store exploding with zucchini right now? There’s a new breakfast recipe in town that will help you make the most of this seasonal staple. Zoats — zucchini oatmeal — is the latest internet breakfast sensation.
Now, shredded zucchini and oatmeal might not sound like the most appetizing thing in the world— trust me, I was very skeptical about the idea — but I played up the taste of zucchini bread in this recipe by adding cream cheese, vanilla extract, and brown sugar and it turned out great (if I do say so myself). It basically tastes like a healthier version of the your favorite zucchini loaf, and who wouldn’t want that?
http://www.thekitchn.com/feedburnermain
(Image credit: Jerrelle Guy)
Peanut butter and jelly is a comforting classic that hardly needs improving. Instead, these one-ingredient twists turn a lunch-box staple into something fun and unexpected. Are you read to liven up lunchtime?
http://www.thekitchn.com/feedburnermain
(Image credit: Brie Passano)
Bell peppers can be stuffed with just about anything, but this version is protein-packed, gluten-free, and even vegan … if you want to omit the cheese. The filling — made with canned black beans, corn, and quinoa — gets cooked with Southwestern spices, and is right at home inside sweet, slow-roasted summer bell peppers.
http://www.thekitchn.com/feedburnermain
(Image credit: Design Manifest)
From Apartment Therapy → Next Level Shiplap: Creative Ways to Take Wood Paneling Way Beyond Walls
http://www.thekitchn.com/feedburnermain
(Image credit: The Candid Appetite)
You already know we’re big fans of elote here at Kitchn, so when I found these Mexican street corn dogs, I knew had to share them with you. A cross between a corn dog and Mexican street corn, this is truly summer on a stick.
https://www.girlsgonestrong.com/
GGS friend and fellow research rock star, Krista Rompoliski, tackled the Truth About Birth Control and Weight Gain previously, presenting the various problems with the research (i.e. what constitutes “significant” weight gain) and how the type of hormone (estrogen or progesterone) in your birth control matters when it comes to weight gain and oral contraceptives.
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In her article, Krista showed that at the end of the day the research is inconclusive. Dig into the scientific literature, and you will find that most studies show no correlation between the Pill and significant weight gain.
But I know there are many of you, myself included, who did have a very frustrating weight gain of anywhere between five and 15 pounds upon starting on the Pill. So, what gives? Are we crazy, or is this a case in which we have to look far deeper than what the available research tells us?
Well, of course, you’re not crazy, although you may have felt like it on the Pill—but that’s a subject for another day!
Almost everyone tells us we shouldn’t have. Yet, we did. Why is that?
It’s important to remember that hormones will behave different depending on the other hormones in your unique mix, so it’s very hard to look at just any one hormone in isolation—especially if you have any existing hormonal imbalance. The introduction of a bigger dose of any hormone will shift your already unbalanced scales, and you will likely experience more symptoms (you might even feel like the entire list of symptoms on the package insert is talking specifically about you). Most of what I’m about to discuss below goes beyond simply estrogen in the Pill causing weight gain. In this article, I’m diving a little deeper into the reasons why someone might experience more trouble with estrogen in the Pill.
I wrote about this sometimes vague and misunderstood term for GGS in the past (check out part one and part two of that series). If a woman is already estrogen dominant the Pill can easily make her even more so. This happens for a couple of reasons.
First, the Pill shuts off ovulation (that’s how it prevents pregnancy) so the woman doesn’t make the normal progesterone from the corpus luteum (the post ovulatory follicle that develops after an egg is released). The adrenals produce some progesterone, so depending on her stress level and adrenals status, she make fare worse than others with her adrenal progesterone back-up plan. Some pills also contain progesterone, and these seem to be associated with less weight gain.
When a woman becomes estrogen dominant, estrogen dominates progesterone and she loses some of the balancing effects progesterone has against the stress hormone cortisol, which can increase fat storage (especially around the midsection).
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The more body fat a woman has, the more estrogen her body produces in that fat tissue. This happens through a process called aromatization, in which testosterone is converted to estrogen, quickly leading to an unfavorable hormone balance for fat loss: less testosterone and more estrogen. This process is turned on by blood sugar problems as insulin surges spur the aromatase enzyme.
Estrogen and progesterone have some complex interactions with the thyroid. On the Pill a woman is at least relatively estrogen dominant and lower in progesterone (because her normal ovulation is disrupted). Here’s how that affects the thyroid:
Progesterone normally increases the TPO (thyroid peroxidase enzyme) production of thyroid hormone. A decrease or a lack of thyroid hormone can lead to hypothyroidism. Pills that include progesterone (that’s most of them these days) could theoretically lessen the impact, but synthetic progestins don’t seem to behave in quite the same way as our natural progesterone in all tissues.
Estrogen will increase thyroid binding protein, the protein carrier that shuttles around thyroid hormones, takes them to their target destination, and drops them off. When too much thyroid protein is bound up by proteins, there isn’t as much free or available for action (on lab tests this shows up as lower free T4, lower free T3, or lower T3Uptake). In short, having too much estrogen can make you a bit hypothyroid by decreasing your free, active, hormone.
Will every woman on the Pill end up with low enough T3 to feel the effects? Not necessarily. A lowering of free T3 will always happen with oral contraceptives to some degree, but if thyroid hormone levels are stellar, this may not be enough to cause hypothyroid symptoms like depression, fatigue, and weight gain. However, if thyroid hormone levels were already borderline or even overtly low, the Pill can easily push it low enough to produce symptoms.
There’s so much we don’t yet understand about the increasingly complex effects our gut bacteria, or microbiome, has on our health and our hormones—but we do know it’s very important.
The research on the interactions between oral estrogens and the gut bacterial landscape is growing, and we now know a couple of things.
Estrogens appear to alter gut bacteria. If you talk to any functional medicine practitioner, they’ll tell you that nearly all women who are taking estrogen have imbalanced gut bacteria. To me, this doesn’t necessarily prove that the Pill causes this disruption directly. It may be the low thyroid effect (thyroid hormone is key for proper gut health) or it may be that there’s more happening that we don’t totally understand yet.
We do know that oral estrogens have been linked in pre-menopausal women to an increased risks for Crohn’s Disease (an autoimmune, inflammatory bowel disorder). Estrogen is known to have some effects on the gut barrier (intestinal lining), thus it appears to have a role in the development of intestinal hyperpermeability and intestinal inflammation. Perhaps the cause is estrogen receptors present in the gut, or a disruption in the gut flora. Or perhaps estrogen can trigger autoimmunity (more on that in a moment).
We also know that gut bacteria have a role in metabolizing hormones, including estrogen. So a woman who has a disrupted intestinal balance already may have more trouble getting rid of excess estrogen. This can make her more estrogen dominant or lead to more estrogen related side effects of the Pill, or perhaps lead to the intestinal inflammation I just mentioned.
How does this affect weight gain? We looked at how estrogen dominance can increase weight, but we also know that a diverse, healthy intestinal landscape is key in health and weight loss. Studies are showing us that the less varied and healthy our gut bacteria is, the more inflammation, insulin resistance and weight gain we experience over time.
I’ve seen things written like “the Pill destroys your gut bacteria, just like antibiotics.” I think it is likely untrue and the research does not show it “wiping out” our flora in the same way antibiotics clear everything out. It’s more likely that it has a complex role with thyroid hormone, a woman’s genetic predisposition to inflammation and autoimmunity, and the current health of her gut bacteria (which honestly, as is the case with most of us, might need quite a bit of work!).
We have to remember that when it comes to hormones, it’s rarely so straightforward.
More often, it’s a “which came first” issue. For example, gut imbalance and inflammation can certainly create acne and altered hormones. If this the reason a woman went on the Pill was to clear up her skin, get her PMS under control, and get her period more regular, she is likely to also be one of the women with worse weight gain and symptoms on the Pill.
Surges in estrogen, like starting the Pill, going through perimenopause, or pregnancy have been shown to trigger autoimmune flares on the thyroid (probably other autoimmune disease affected here as well).
If a woman has a predisposition to autoimmunity, any surge in estrogen can be a cause in tripping it to turn on. Family history needs to be considered when it comes to initiating any type of oral estrogen and if she does have Hashimoto’s, it’s important to recognize that the Pill can trigger a flare.
Flares happen all the time, and one of my prime concerns in my practice is decreasing that frequency and lessening the tissue destruction. When there is an increased attack on the thyroid, a bit of tissue is destroyed and—you guessed it—it makes the woman more hypothyroid, this can impact weight loss. Many women will need an uptick in their thyroid hormone dose when they start the Pill . Others will go from not being on thyroid medicine to needing it.
Again, this won’t happen with every woman, but we know it happens, and it’s one more thread in a web that can lead to weight gain in some women when they take oral contraceptives.
One reason for weight gain on the Pill may simply be increased calorie consumption. Estrogen and progesterone have complex interactions with leptin, ghrelin and neuropeptide Y—all of which can lead to feeling hungry. Female hormones also impact serotonin and GABA, brain chemicals that drive cravings. So it may be as simple as munching more overall, having a harder time getting satiated, or experiencing a shift in cravings and eating more sweets or starches.
It could be as simple as needing a multivitamin. The Pill creates a host of nutrient deficiencies including folic acid, B2, b6, B12, vitamin C, selenium, zinc, magnesium and vitamin E.
Many of us could shore up this problem with a high quality multivitamin/multimineral. However, if a deficiency already exists, gut issues are already present impacting absorption, and the woman is already depleted in nutrients that support hormone clearance by the liver, she of course would suffer from a host of symptoms related to nutrient deficiencies. This can include anxiety, depression, poor skin healing, low thyroid symptoms, anemias, etc.
If a woman was low estrogen to begin with, the Pill may indeed help her lose fat. Estrogen is crucial for lean muscle mass and has an important role in fat burning. So if she were low, the Pill may have been a good addition to her fat loss hormone equation.
Women who may be low in estrogen include those who have PCOS (likely those who are not getting many periods, if any, in a year), and women going through perimenopause or who have premature ovarian failure (which is often autoimmune, but can also be due to disruption in the brain-ovary axis). Low estrogen can also be the result of chronic stress or thyroid disorders.
What other issues do you have going on? These complex interactions can make you a better or worse candidate for the Pill.
Let’s say you have something like small intestinal bacterial overgrowth ( SIBO) or poor digestion, you don’t eat a lot of grains (i.e. following a low carb or Paleo diet, thus you may be low in B6), and you don’t take a multivitamin. Or you know that you have a MTHFR gene mutation impacting your folic acid status. You are likely going to have some trouble on the Pill. You won’t clear it well due to low B6 and folic acid, which affect a process called methylation. You will have altered liver clearance of the estrogens and will notice estrogen-dominant issues and possible weight gain.
Another scenario would be if you are borderline low T3 and start on the Pill, creating a selenium deficiency. Selenium is key for the conversion of T4 into the active thyroid hormone T3. Now you could easily be low enough T3 to suffer with low thyroid symptoms, and the Pill just tipped the scale enough for you to really feel the effect of it, including some weight gain. Remember that estrogen will also shift those levels of free T3 (the one you need), and together this may be enough to really push you into hypothyroidism.
See how quickly this gets complicated, and why you and your BFF won’t necessarily have the same response to the same pill? Or why the research is perhaps a little too lacking for these complex hormonal interactions you’ve got going on?
Where you start counts, too. If you’re already overweight, synthetic progestins in most pills seem to cause more weight gain. And if you did gain weight when you started taking the Pill, studies show you’re likely to keep gaining, or will have a hard time losing it. So the notion to “stick with it, and let it level out” doesn’t make sense in my experience (nor according some studies).
Finally, remember that the research repeatedly says that the Pill wasn’t associated with “significant weight gain.” That’s a bit subjective right? Two to three pounds will feel different to different women. And because it’s so complex, think about this: if you put on three pounds due to your response to the synthetic progestin, three pounds from your sluggish thyroid and two pounds from estrogen dominance related issues that’s now eight pounds. That may very well feel “significant”.
I love research. It is how medicine works, and that’s a good thing—but it’s not the only thing. We have to let each woman take a look at her bigger hormonal picture and see what makes sense for her. By all means, don’t ignore yourself because the data implies that what’s happening with you shouldn’t be happening, or because someone tells you it’s all in your head (argh, do I ever hate that line!).
The Pill isn’t evil but it’s also not benign.
Your hormonal balance is beautifully and insanely complex. Taking a hormone has profound and complex interactions throughout your body, from your brain to your gut.
Women with less complex issues will obviously do better when introducing the Pill. If you have hormonal imbalances already, it’s more likely to make those imbalances worse, it really doesn’t correct anything (besides low estrogen for some). It does have some clear upsides like great skin, a regular, predictable (and usually pretty light) cycle—and for some women with low estrogen, it can help with weight loss.
However, if you’re considering the Pill for other reason like acne, PMS, irregular or heavy cycles, the Pill is at best a band-aid and will make many hormonal issues (like PCOS) worse when you come off it. There are so many ways to get your bleeding, mood, cycle, and breakouts under control and actually fix or substantially correct your hormonal imbalances, rather than cover them up or stress your system more.
If contraception is not the reason, find out how to get to your root cause and start setting your hormones straight, clearing up your skin and getting your period under control. The Pill isn’t necessarily the wrong choice for every woman, but know that it’s not the only choice.
One thing we can’t argue with is that the Pill is a relatively convenient and very reliable way to avoid getting pregnant.
There are non-hormonal methods of contraception that range from not having to think about it at all (i.e. the non-hormone IUD Paraguard, not the ones which secretes hormone), to the ol’ standbys like the diaphragm, cervical cap, and condoms that require more thought and planning in the heat of the moment.
Not every woman will tolerate an IUD (some experience cramping and heavy bleeding), but if it works for you, it’s a great option. Again, I’m talking non-hormonal IUD here (i.e. the Paraguard). The others involve a little planning and some spermicide (again, not something every woman tolerates), but they don’t mess with your hormones. And let’s never forget, it’s OK to ask your partner to be in on the birth control conversation.
So many couples I talk to are certain they do not want children and need a reliable contraceptive method, but haven’t discussed vasectomy. It’s quick, fairly painless (I know a man might disagree, but let’s talk after he gives birth), and more easily reversible than tubal ligation or tubal coils (Essure), should anyone have a change of heart about having kids. Men are often a little skittish, understandably so, but it’s a very good option for many couples and no one’s hormones get mucked with.
Ah, the Pill and weight gain….not so simple, huh?
As you can see, while much of the available research doesn’t show a correlation between taking the Pill gaining weight, the effect it may have on your body depends on your unique hormone mix. Other things that can have an effect on your hormones and help you manage your weight include a smart training program and sound nutrition habits. If you’re looking for expert guidance to help design a program for you, we can help
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The post Why Did I Gain Weight on the Pill, If the Research Says That Shouldn’t Happen? appeared first on Girls Gone Strong.
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In this episode:
04:48 The basics of intestinal permeability
06:52 Is it a good idea to test for leaky gut?
09:34 Testing options for intestinal permeability
11: 50 The lactulose/mannitol test
15:59 The antigenic permeability screen
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Chris Kresser: Hey everybody, it’s Chris Kresser here, welcome to another episode of Revolution Health Radio. And we are going to switch things up a little bit. If you’ve been listening to this show for a while, you’ll know that I have cycled through a few different formats over the years. Initially I did single-topic episodes where we dive deep on a particular topic, then I did some Q&A shows where I would answer multiple questions from listeners. I’ve always done some interviews, and that’s of course what I’ve focused on over the past several months. It’s been almost exclusively an interview show. And I am going to now do some Q&As again.
In this case, we’ll just be answering one question per show. We’re going to continue with the interviews because I think those are really informative and I get a lot of great feedback about them, and I enjoy doing them myself. But we’re going to intersperse some Q&A episodes as well, at least for the next few months. And who knows what comes after that.
But let’s start with a question from Kent and let’s give a listen and I’ll come back and answer it.
Kent Langley: Hello, this is Kent Langley and I’m calling on behalf of some friends and family. I’ve read a lot of your articles over the years and listen to most of your podcasts. Thank you for the fine work. The question I have is really relatively simple, but I suspect that it doesn’t have a simple answer. Is there a direct and high-accuracy methodology for testing if you have a leaky gut? My online research hasn’t turned up much, and I thought I would ask. If the answer is no, could you please explain why? Thank you.
Chris Kresser: Okay, thanks again, Kent. That’s a really good question. It’s one that we get in various forms quite often and it’s something I’ve been talking about a lot lately in my clinician training program. I’d love to cover some of the highlights at least briefly in the show.
So before we dive into the nitty-gritty about testing for intestinal permeability, I just want to cover a few basics of what intestinal permeability is for those that aren’t as familiar with it, and then some general aspects about testing for this condition.
The intestinal barrier covers a surface area of about 400 m² and requires about 40 percent of the body’s energy expenditure, and that’s pretty remarkable when you consider that only 20 percent of the body’s energy expenditure is required by the brain. So this tells us that the gut barrier is really crucial. It plays an important role in human health and disease. It prevents against loss of water and electrolytes and the entry of antigens and microorganisms, so allergens, things that could provoke an immune response, as well as bacteria, fungi, parasites, things like that, it allows absorption of nutrients in the exchange of molecules between anything that we eat or put into our mouth and then the inside of our body.
Do you have leaky gut? Two tests to consider.
I think I’ve said this before, but if you really think about the gut, it’s essentially just a hollow tube that connects the mouth to the anus. And everything that is inside of the gut is technically outside of the body. It’s kind of hard to get your head around that, but it’s really the inside of the gut is not technically inside of the body. And in order for it to move in the body, anything that’s in the gut to move into the body has to cross that barrier. And that’s really what the barrier is there for, it’s, at a simple level, supposed to let in things that should get in and keep out things that shouldn’t, that should stay out. And when it’s working well, it does a good job of that. But when certain conditions are present, the barrier’s capability of doing that regulatory task breaks down, and then this is when all kinds of problems can happen.
So there are a lot of different things that can interfere with the gut, the function of the gut barrier. Diet is an obvious factor. Western inflammatory diet, lack of fermentable carbohydrates, and lack of fermented foods, infections and toxins, so bacterial, viral, parasitic infections, fungal overgrowth, heavy metals, mold, etc. Certain medications like proton pump inhibitors, antibiotics, or NSAIDs; lifestyle factors like chronic stress or sleep deprivation or inappropriate physical activity, like too little or too much; inadequate immune stimulation during our developmental period. This is known as the hygiene hypothesis. So hygiene and really clean environments have done a lot to reduce acute infections and saved a lot of lives in that process, but there’s a theory that these overly or these particularly sterilized environments have actually contributed to immune dysregulation because our immune systems aren’t properly stimulated when when we grow up in those kinds of environments. Which explains why autoimmune diseases are really quite rare in the developing world when compared to the incidents in the developed world.
Then there are other factors which we call endogenous factors, which means they’re just things that are going on inside of the body that can contribute to leaky gut like chronic inflammation, or SIBO, or gut-brain axis problems, where low levels of certain hormones like melanocyte-stimulating hormone, or MSH, which regulates gut permeability, and then there’s actually probably some genetic susceptibility to leaky gut. For example, one study showed that 70 percent of asymptomatic relatives of patients with celiac disease were positive for intestinal permeability when they were screened. So there does seem to be a genetic component.
So before we talk about the different types of testing that are available for intestinal permeability, we should actually take a step back and talk about whether it’s even a good idea to test for intestinal permeability and when we should test for it. So my opinion is that intestinal permeability is almost always caused by something else that’s further upstream, meaning that it comes before intestinal permeability and it’s the underlying cause of intestinal permeability. So it could be talking about any of the things that I mentioned just now: poor diet, gut infections, chronic stress, etc. And one of the key principles of functional medicine is that we want to get to the bottom of what is causing symptoms or even manifestations like intestinal permeability, and we want to remove or address those causes or triggers before we try to do anything about the symptom or the manifestation. And the more we can get to the root of the problem, the more effective the intervention will be and the longer term the result will be.
So if we’re just suppressing symptoms or dealing with manifestations of problems, it’s not only going to be less effective, this whatever we’re doing isn’t going to last for as long because we haven’t actually addressed the underlying cause. So with intestinal permeability, if you remove the triggers what’s causing leaky gut the first place—like you fix the diet, you treat the gut infections, the patient starts managing their stress—in many cases you won’t need to even address intestinal permeability because it will take care of itself. One of the amazing things about the cells in the gut is they regenerate every two to three days. And so if you remove the triggers that are causing the problem, then the cells can regenerate and the tight junctions can restore themselves and the intestinal permeability will go away.
So typically in our clinic, we’ll test and treat for SIBO, gut infections, other gut issues, we’ll correct the diet, we’ll address HPA axis dysregulation and screen for heavy metals and mold and other problems like that. And if the patient is still having problems that could be associated with leaky gut, at that point is when we’ll proceed to testing for intestinal permeability.
So if you look at the research, there are a number of different tests that have been used to define or identify intestinal permeability. And some of these are more common than others, but I’m just going to mention a few different ones and then I’ll tell you what we use in our practice and what I recommend.
So the first is the lactulose/mannitol permeability assay, and this uses molecules, sugars, long-chain sugars called oligosaccharides, and I’ll explain a little bit more about it in a moment.
The second is an antigenic permeability screen, and this looks at antibodies to particular antigens like lipopolysaccharides and then also antibodies to endogenous molecules like actomyosin and occludin and zonulin. So these are proteins that the body produces in the gut that help to regulate tight junction permeability and the structure of the gut and determine whether the gut is permeable or not.
The next marker that’s sometimes used in studies is called D-lactate or D-lactic acid. This is different than lactic acid that you may have heard about that can be high after exercise. This is a product of bacterial metabolism. So it’s produced in the gut. And when D-lactate levels are high, that in some studies has correlated pretty well with intestinal permeability. Butyrate, which is a short-chain fatty acid, has been investigated as a potential marker for intestinal permeability. When butyrate is low, that would be a sign of leaky gut. And then zonulin, as I just mentioned, is a protein that regulates the tight junctions in the gut. That’s being investigated as a marker for intestinal permeability.
But in terms of clinical practice and what’s readily available and what’s been most validated by the scientific research, the lactulose/mannitol test and the antigenic permeability screen, I think, are the two most useful tests.
With the lactulose/mannitol test, I’m not going to go into a lot of detail because it gets pretty geeky, but it essentially involves measuring levels of two sugars in the urine after the patient consumes those sugars orally. And these sugars have different molecular weights, and then you can look at the results and look at the ratio of those two sugars in the urine and that ratio can tell you whether the gut is permeable and allowing the larger sugar molecules that shouldn’t pass through the gut into the bloodstream or whether it’s doing its job and keeping those molecules out. And so that lactulose/mannitol test is available through labs like Genova Diagnostics, which is a pretty popular functional lab that offers this kind of testing. But there are some definite shortcomings of lactulose/mannitol testing. One of them is that the transport of lactulose or mannitol through the gut barrier is not actually or not necessarily an indicator of malfunction of the intestinal tight junctions. So in other words, a positive result doesn’t necessarily mean that there is intestinal permeability present.
There are a lot of factors that can influence the uptake of those sugars, like GI motility, use of medication like NSAIDs, the surface area of the intestine, gastric emptying, mucosal blood flow, etc., and so these variations can affect the result. But they don’t necessarily mean that the gut is permeable. The other thing is that some studies have shown that only really large molecules, larger than 5,000 daltons, can change the permeability of intestinal epithelial cells and then result in an inflammatory response in the body, which is really what we’re concerned with. And lactulose and mannitol are below 500 daltons, which means they’re much smaller than that, and that suggests that they may not be appropriate as challenge molecules for an intestinal permeability test. So that may have been a little more geeky than I intended it to be, but the takeaway is that the lactulose/mannitol test can give us some information about permeability. But it does have some limitations and it probably shouldn’t be used exclusively. It should maybe just be part of an overall workup that also uses the antigenic permeability test.
There are some ways to increase lactulose/mannitol testing accuracy. One of those is to avoid anything containing lactulose. One of the test molecules that’s used in the diet—and lactulose is not really in a lot of foods, but it’s found in heat-processed dairy and nondairy beverages like soy milk, for example, or some yogurts. You want to avoid mannitol for 24 hours prior to the test, and that’s found in brown seaweed, celery, carrot, coconut, cauliflower, cabbage, pineapple, lettuce, watermelon, pumpkin, squash, cassava, pea, asparagus, coffee, olives and berries, and chewing gum. So you’ll probably have to refer to the transcript for a list of those. You want to generally avoid dairy products for 24 hours before the test, and on the day of the test you want to just avoid drinking too much water, period. And those things can help increase the accuracy of the test. But as I said, it’s still potentially, there are some other issues with it that are more difficult to overcome. I think it’s useful, but it shouldn’t be used in isolation.
So the second test for leaky gut is called the antigenic permeability screen, and this was developed by Doctor Aristo Vojdani in Cyrex Labs. In large part, they developed the test because of the shortcomings of the lactulose/mannitol test that we just talked about. Since the lactulose and mannitol are small molecules that don’t necessarily initiate an immune response, Doctor Vojdani wanted to create a test that would better reflect pathological permeability of the gut, which again is really what we’re concerned with. So instead of using larger sugars, he decided to screen for antibodies to proteins and bacterial endotoxins, since those are the major concern when it comes to immunoreactivity. And we know that uptake of these kinds of antigens, proteins and bacterial endotoxins, plays a significant role in the pathogenesis of gastrointestinal and autoimmune disease. In other words, there are a lot of studies showing that inappropriate transfer of these proteins and endotoxins from the gut into the bloodstream initiates an inflammatory response that can contribute to autoimmune disease. And this explains the connection between leaky gut and autoimmune disease. Less than 10 percent of subjects with a genetic susceptibility to autoimmune disease actually progressed to having clinical autoimmune disease in their lifetime, and this suggests that environmental triggers like toxic chemicals and infections and dietary proteins are probably involved in the development of autoimmune disease.
So I’m not going to go into a lot of detail about exactly how this test works because it’s pretty complex, but it’s a blood test. The lactulose/mannitol test that we were talking about earlier is a urine test. This test is only offered by one lab that I know of right now, which is Cyrex Labs. It’s called Cyrex Array 2, and you can check it out at CyrexLabs.com. It needs to be ordered by a clinician. So unfortunately you can’t just order this on your own as a patient, and it is a blood test. And so they draw a blood sample and then they test for antibodies to lipopolysaccharide, they test IgM, IgG and IgA antibodies, which if positive is an indicator of gut permeability and dysbiosis, because lipopolysaccharide is produced by gram-negative bacteria. Those tend to be more pathogenic types of bacteria. Then they test for IgA antibodies to actomyosin, and if those are positive, that indicates epithelial cell damage and that would be an indicator of gut permeability. And then they screen for IgG, IgM, and IgA antibodies to occludin and zonulin. And those are proteins that regulate tight junction. And so if you get a positive result there, that’s an indicator that the tight junctions have been damaged.
And so there are different types of intestinal permeability, and that’s what these different markers give us information about. So those are the two main types of testing that I use in the clinic for intestinal permeability. I’ll say that I don’t actually find myself testing for intestinal permeability very often for the reasons that I mentioned. Typically we tend to look at the underlying cause of intestinal permeability and address that. And if we do a good job with that, in most cases, the intestinal permeability will resolve on its own. When we do test for permeability, we use these two different tests, and I also pay attention to D-lactate. D-lactate can be obtained by running a urine organic acids panel from a lab like Great Plains Labs or also Genova Diagnostics. And if D-lactate is very high then, and especially if Cyrex Array 2 or the lactulose/mannitol permeability tests are positive, I would think it very likely that intestinal permeability is present. So you kind of put together these various tests and along with looking at the history of symptoms and the more indicators you have pointing towards gut permeability, the more likely it is that it’s present. And that’s really the best that we can do from a testing perspective at this point.
Okay, so thanks again, Kent, for your question. Thanks everybody for listening, and I will talk to you soon. We did take a little bit of time off this summer and may have some time off coming up as well. So thanks for being patient in between episodes and hopefully we’ll be back with another episode soon. Thanks for listening.
http://chriskresser.com/
In this episode:
04:48 The basics of intestinal permeability
06:52 Is it a good idea to test for leaky gut?
09:34 Testing options for intestinal permeability
11: 50 The lactulose/mannitol test
15:59 The antigenic permeability screen
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Chris Kresser: Hey everybody, it’s Chris Kresser here, welcome to another episode of Revolution Health Radio. And we are going to switch things up a little bit. If you’ve been listening to this show for a while, you’ll know that I have cycled through a few different formats over the years. Initially I did single-topic episodes where we dive deep on a particular topic, then I did some Q&A shows where I would answer multiple questions from listeners. I’ve always done some interviews, and that’s of course what I’ve focused on over the past several months. It’s been almost exclusively an interview show. And I am going to now do some Q&As again.
In this case, we’ll just be answering one question per show. We’re going to continue with the interviews because I think those are really informative and I get a lot of great feedback about them, and I enjoy doing them myself. But we’re going to intersperse some Q&A episodes as well, at least for the next few months. And who knows what comes after that.
But let’s start with a question from Kent and let’s give a listen and I’ll come back and answer it.
Kent Langley: Hello, this is Kent Langley and I’m calling on behalf of some friends and family. I’ve read a lot of your articles over the years and listen to most of your podcasts. Thank you for the fine work. The question I have is really relatively simple, but I suspect that it doesn’t have a simple answer. Is there a direct and high-accuracy methodology for testing if you have a leaky gut? My online research hasn’t turned up much, and I thought I would ask. If the answer is no, could you please explain why? Thank you.
Chris Kresser: Okay, thanks again, Kent. That’s a really good question. It’s one that we get in various forms quite often and it’s something I’ve been talking about a lot lately in my clinician training program. I’d love to cover some of the highlights at least briefly in the show.
So before we dive into the nitty-gritty about testing for intestinal permeability, I just want to cover a few basics of what intestinal permeability is for those that aren’t as familiar with it, and then some general aspects about testing for this condition.
The intestinal barrier covers a surface area of about 400 m² and requires about 40 percent of the body’s energy expenditure, and that’s pretty remarkable when you consider that only 20 percent of the body’s energy expenditure is required by the brain. So this tells us that the gut barrier is really crucial. It plays an important role in human health and disease. It prevents against loss of water and electrolytes and the entry of antigens and microorganisms, so allergens, things that could provoke an immune response, as well as bacteria, fungi, parasites, things like that, it allows absorption of nutrients in the exchange of molecules between anything that we eat or put into our mouth and then the inside of our body.
Do you have leaky gut? Two tests to consider.
I think I’ve said this before, but if you really think about the gut, it’s essentially just a hollow tube that connects the mouth to the anus. And everything that is inside of the gut is technically outside of the body. It’s kind of hard to get your head around that, but it’s really the inside of the gut is not technically inside of the body. And in order for it to move in the body, anything that’s in the gut to move into the body has to cross that barrier. And that’s really what the barrier is there for, it’s, at a simple level, supposed to let in things that should get in and keep out things that shouldn’t, that should stay out. And when it’s working well, it does a good job of that. But when certain conditions are present, the barrier’s capability of doing that regulatory task breaks down, and then this is when all kinds of problems can happen.
So there are a lot of different things that can interfere with the gut, the function of the gut barrier. Diet is an obvious factor. Western inflammatory diet, lack of fermentable carbohydrates, and lack of fermented foods, infections and toxins, so bacterial, viral, parasitic infections, fungal overgrowth, heavy metals, mold, etc. Certain medications like proton pump inhibitors, antibiotics, or NSAIDs; lifestyle factors like chronic stress or sleep deprivation or inappropriate physical activity, like too little or too much; inadequate immune stimulation during our developmental period. This is known as the hygiene hypothesis. So hygiene and really clean environments have done a lot to reduce acute infections and saved a lot of lives in that process, but there’s a theory that these overly or these particularly sterilized environments have actually contributed to immune dysregulation because our immune systems aren’t properly stimulated when when we grow up in those kinds of environments. Which explains why autoimmune diseases are really quite rare in the developing world when compared to the incidents in the developed world.
Then there are other factors which we call endogenous factors, which means they’re just things that are going on inside of the body that can contribute to leaky gut like chronic inflammation, or SIBO, or gut-brain axis problems, where low levels of certain hormones like melanocyte-stimulating hormone, or MSH, which regulates gut permeability, and then there’s actually probably some genetic susceptibility to leaky gut. For example, one study showed that 70 percent of asymptomatic relatives of patients with celiac disease were positive for intestinal permeability when they were screened. So there does seem to be a genetic component.
So before we talk about the different types of testing that are available for intestinal permeability, we should actually take a step back and talk about whether it’s even a good idea to test for intestinal permeability and when we should test for it. So my opinion is that intestinal permeability is almost always caused by something else that’s further upstream, meaning that it comes before intestinal permeability and it’s the underlying cause of intestinal permeability. So it could be talking about any of the things that I mentioned just now: poor diet, gut infections, chronic stress, etc. And one of the key principles of functional medicine is that we want to get to the bottom of what is causing symptoms or even manifestations like intestinal permeability, and we want to remove or address those causes or triggers before we try to do anything about the symptom or the manifestation. And the more we can get to the root of the problem, the more effective the intervention will be and the longer term the result will be.
So if we’re just suppressing symptoms or dealing with manifestations of problems, it’s not only going to be less effective, this whatever we’re doing isn’t going to last for as long because we haven’t actually addressed the underlying cause. So with intestinal permeability, if you remove the triggers what’s causing leaky gut the first place—like you fix the diet, you treat the gut infections, the patient starts managing their stress—in many cases you won’t need to even address intestinal permeability because it will take care of itself. One of the amazing things about the cells in the gut is they regenerate every two to three days. And so if you remove the triggers that are causing the problem, then the cells can regenerate and the tight junctions can restore themselves and the intestinal permeability will go away.
So typically in our clinic, we’ll test and treat for SIBO, gut infections, other gut issues, we’ll correct the diet, we’ll address HPA axis dysregulation and screen for heavy metals and mold and other problems like that. And if the patient is still having problems that could be associated with leaky gut, at that point is when we’ll proceed to testing for intestinal permeability.
So if you look at the research, there are a number of different tests that have been used to define or identify intestinal permeability. And some of these are more common than others, but I’m just going to mention a few different ones and then I’ll tell you what we use in our practice and what I recommend.
So the first is the lactulose/mannitol permeability assay, and this uses molecules, sugars, long-chain sugars called oligosaccharides, and I’ll explain a little bit more about it in a moment.
The second is an antigenic permeability screen, and this looks at antibodies to particular antigens like lipopolysaccharides and then also antibodies to endogenous molecules like actomyosin and occludin and zonulin. So these are proteins that the body produces in the gut that help to regulate tight junction permeability and the structure of the gut and determine whether the gut is permeable or not.
The next marker that’s sometimes used in studies is called D-lactate or D-lactic acid. This is different than lactic acid that you may have heard about that can be high after exercise. This is a product of bacterial metabolism. So it’s produced in the gut. And when D-lactate levels are high, that in some studies has correlated pretty well with intestinal permeability. Butyrate, which is a short-chain fatty acid, has been investigated as a potential marker for intestinal permeability. When butyrate is low, that would be a sign of leaky gut. And then zonulin, as I just mentioned, is a protein that regulates the tight junctions in the gut. That’s being investigated as a marker for intestinal permeability.
But in terms of clinical practice and what’s readily available and what’s been most validated by the scientific research, the lactulose/mannitol test and the antigenic permeability screen, I think, are the two most useful tests.
With the lactulose/mannitol test, I’m not going to go into a lot of detail because it gets pretty geeky, but it essentially involves measuring levels of two sugars in the urine after the patient consumes those sugars orally. And these sugars have different molecular weights, and then you can look at the results and look at the ratio of those two sugars in the urine and that ratio can tell you whether the gut is permeable and allowing the larger sugar molecules that shouldn’t pass through the gut into the bloodstream or whether it’s doing its job and keeping those molecules out. And so that lactulose/mannitol test is available through labs like Genova Diagnostics, which is a pretty popular functional lab that offers this kind of testing. But there are some definite shortcomings of lactulose/mannitol testing. One of them is that the transport of lactulose or mannitol through the gut barrier is not actually or not necessarily an indicator of malfunction of the intestinal tight junctions. So in other words, a positive result doesn’t necessarily mean that there is intestinal permeability present.
There are a lot of factors that can influence the uptake of those sugars, like GI motility, use of medication like NSAIDs, the surface area of the intestine, gastric emptying, mucosal blood flow, etc., and so these variations can affect the result. But they don’t necessarily mean that the gut is permeable. The other thing is that some studies have shown that only really large molecules, larger than 5,000 daltons, can change the permeability of intestinal epithelial cells and then result in an inflammatory response in the body, which is really what we’re concerned with. And lactulose and mannitol are below 500 daltons, which means they’re much smaller than that, and that suggests that they may not be appropriate as challenge molecules for an intestinal permeability test. So that may have been a little more geeky than I intended it to be, but the takeaway is that the lactulose/mannitol test can give us some information about permeability. But it does have some limitations and it probably shouldn’t be used exclusively. It should maybe just be part of an overall workup that also uses the antigenic permeability test.
There are some ways to increase lactulose/mannitol testing accuracy. One of those is to avoid anything containing lactulose. One of the test molecules that’s used in the diet—and lactulose is not really in a lot of foods, but it’s found in heat-processed dairy and nondairy beverages like soy milk, for example, or some yogurts. You want to avoid mannitol for 24 hours prior to the test, and that’s found in brown seaweed, celery, carrot, coconut, cauliflower, cabbage, pineapple, lettuce, watermelon, pumpkin, squash, cassava, pea, asparagus, coffee, olives and berries, and chewing gum. So you’ll probably have to refer to the transcript for a list of those. You want to generally avoid dairy products for 24 hours before the test, and on the day of the test you want to just avoid drinking too much water, period. And those things can help increase the accuracy of the test. But as I said, it’s still potentially, there are some other issues with it that are more difficult to overcome. I think it’s useful, but it shouldn’t be used in isolation.
So the second test for leaky gut is called the antigenic permeability screen, and this was developed by Doctor Aristo Vojdani in Cyrex Labs. In large part, they developed the test because of the shortcomings of the lactulose/mannitol test that we just talked about. Since the lactulose and mannitol are small molecules that don’t necessarily initiate an immune response, Doctor Vojdani wanted to create a test that would better reflect pathological permeability of the gut, which again is really what we’re concerned with. So instead of using larger sugars, he decided to screen for antibodies to proteins and bacterial endotoxins, since those are the major concern when it comes to immunoreactivity. And we know that uptake of these kinds of antigens, proteins and bacterial endotoxins, plays a significant role in the pathogenesis of gastrointestinal and autoimmune disease. In other words, there are a lot of studies showing that inappropriate transfer of these proteins and endotoxins from the gut into the bloodstream initiates an inflammatory response that can contribute to autoimmune disease. And this explains the connection between leaky gut and autoimmune disease. Less than 10 percent of subjects with a genetic susceptibility to autoimmune disease actually progressed to having clinical autoimmune disease in their lifetime, and this suggests that environmental triggers like toxic chemicals and infections and dietary proteins are probably involved in the development of autoimmune disease.
So I’m not going to go into a lot of detail about exactly how this test works because it’s pretty complex, but it’s a blood test. The lactulose/mannitol test that we were talking about earlier is a urine test. This test is only offered by one lab that I know of right now, which is Cyrex Labs. It’s called Cyrex Array 2, and you can check it out at CyrexLabs.com. It needs to be ordered by a clinician. So unfortunately you can’t just order this on your own as a patient, and it is a blood test. And so they draw a blood sample and then they test for antibodies to lipopolysaccharide, they test IgM, IgG and IgA antibodies, which if positive is an indicator of gut permeability and dysbiosis, because lipopolysaccharide is produced by gram-negative bacteria. Those tend to be more pathogenic types of bacteria. Then they test for IgA antibodies to actomyosin, and if those are positive, that indicates epithelial cell damage and that would be an indicator of gut permeability. And then they screen for IgG, IgM, and IgA antibodies to occludin and zonulin. And those are proteins that regulate tight junction. And so if you get a positive result there, that’s an indicator that the tight junctions have been damaged.
And so there are different types of intestinal permeability, and that’s what these different markers give us information about. So those are the two main types of testing that I use in the clinic for intestinal permeability. I’ll say that I don’t actually find myself testing for intestinal permeability very often for the reasons that I mentioned. Typically we tend to look at the underlying cause of intestinal permeability and address that. And if we do a good job with that, in most cases, the intestinal permeability will resolve on its own. When we do test for permeability, we use these two different tests, and I also pay attention to D-lactate. D-lactate can be obtained by running a urine organic acids panel from a lab like Great Plains Labs or also Genova Diagnostics. And if D-lactate is very high then, and especially if Cyrex Array 2 or the lactulose/mannitol permeability tests are positive, I would think it very likely that intestinal permeability is present. So you kind of put together these various tests and along with looking at the history of symptoms and the more indicators you have pointing towards gut permeability, the more likely it is that it’s present. And that’s really the best that we can do from a testing perspective at this point.
Okay, so thanks again, Kent, for your question. Thanks everybody for listening, and I will talk to you soon. We did take a little bit of time off this summer and may have some time off coming up as well. So thanks for being patient in between episodes and hopefully we’ll be back with another episode soon. Thanks for listening.
http://www.thekitchn.com/feedburnermain
(Image credit: Marina’s NYC apartment, photographed for Apartment Therapy by Dylan Chandler)
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