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A New Study Has the Media Buzzing About Gluten. Again.

February 25, 2013 in For Babies, Paleo Philosophy, Practical Tips, Topics for Paleo Families

A new study in the journal Pediatrics has the gluten-free/celiac disease world buzzing (this article has been published on dozens of websites).  The study concludes that early introduction of small amounts of gluten while still breastfeeding reduces the risk of celiac disease.

The study looked at two cohorts of Swedish 12-year olds, the first were a group born in 1993 during an epidemic of celiac disease (during the epidemic, the incidence of celiac disease increased from 1 in 100 to 3.3 in 100, believed attributable to changes in government recommendations for the age of gluten introduction to 6 months old, combined with a concurrent increase in the gluten content of baby foods) and the second were a group born in 1997 after the epidemic (after the government revised their guidelines to lower the age of gluten introduction to 4 months and the amount of gluten in baby foods was reduced).  The study sought to determine the impact of breastfeeding in relation to gluten introduction on the future development of celiac disease.

The hypothesis of the study is well summarized in this statement from the discussion section.

“Oral tolerance to an antigen develops early in life, and celiac disease can be viewed as a failure to develop oral tolerance to gluten, or a later loss of this tolerance.  The development of oral tolerance is a complex immunologic process involving interactions between genetic factors and environmental and lifestyle exposures, such as bacterial gut colonization and infant feeding.”

And this idea is what has my inbox flooded with questions.  If oral tolerance for gluten develops early in life and breastfeeding helps with the development of oral tolerance, is it better to give our paleo babies some gluten now?  Will that help prevent celiac disease and other autoimmune diseases?

To answer this question, let me first summarize exactly what this paper shows about the relation between breastfeeding, gluten introduction and celiac disease.  Over 13000 children were enrolled in the study.  The incidence of celiac disease was 2.8 in 100 in the 1993 cohort versus 2.2 in 100 in the 1997 cohort.  The median age of gluten introduction was the same (5 months old) between both cohorts.  But, the infants in the 1997 cohort were breastfed an average of 2 months longer than the 1993 cohort (age of weaning increased from an average of 7 months to an average of 9 months between 1993 and 1997).  What this means is that the number of babies who were breastfed during and beyond gluten introduction was significantly larger in the 1997 cohort (number of babies breastfed beyond gluten introduction was 70% vs 78% in the 1993 and 1997 cohorts, respectively).  From this, the authors conclude that introducing gluten before weaning reduces the risk of celiac disease.

24GLUTEN-articleInlineThis is an interesting observation and I think that this Op Ed piece in the NY Times provides a possible explanation for the result that is not thoroughly discussed in the original paper:  it’s all about the gut microbiota.

The most current understanding of celiac disease (well summarized in this paper, which sadly requires a subscription to view) is that the development of celiac disease (and indeed all autoimmune diseases) relies on three factors:

  1. Genetic predisposition
  2. Environmental trigger (in the case of celiac disease, that trigger is gluten)
  3. A leaky gut and/or gut dysbiosis

All three of these factors work together to develop autoimmune disease.  In terms of celiac disease, the genetic predisposition is at least partially understood: 90% of celiacs have one of two variants of the HLA gene (either DQ8 or DQ2).  What you need to know about the HLA gene is that it (or more specifically the protein in encodes) is involved in antigen presentation to the adaptive immune system, and defects in this process seem to be permissive for autoantibody formation.  But, approximately 30% of us have one of these gene variants and only 1% of us develop celiac disease (it should be noted that these gene variants are linked to other autoimmune diseases as well as non-celiac gluten sensitivity, so it’s not like the other 29% of us are getting off easy).  The environmental trigger for celiac disease is dietary gluten (or more specifically the protein fraction of gluten, called gliadin).  So, what’s the wild card?  A leaky gut.  And the development of a leaky gut may be what determines the age of disease onset, which is highly variable.  Chance (or maybe previous infections or maybe gut dysbiosis, i.e., the wrong types of bacteria growing in the wrong numbers in the wrong part of the gut) may be what determines whether a person develops celiac disease versus another autoimmune disease versus other health problems linked to gluten.

A leaky gut can be caused by a wide variety of factors, including: diets rich in some types of lectin (like gluten) and saponins (especially glycoalkaloids), stress, and gut dysbiosis (especially bacterial overgrowths).  Gut dysbiosis itself can be caused by diets rich in processed foods, refined carbohydrates, some types of lectins (especially prolamins like gluten and agglutinins like wheat germ agglutinin) and saponins (especially glycoalkaloids), by some medications (such as PPIs and antibiotics) and by stress.  A leaky gut and gut dysbiosis go hand in hand and it is not known which comes first.

So, what is the link between breastfeeding and a leaky gut?  The link is really to gut dysbiosis (or lack thereof).  Studies show that breastfeeding is important for the establishment and growth of normal gut microorganisms.  In particular, breastmilk contains probiotics (from strains shown to be deficient in the guts of those with celiac disease) and for the duration of breastfeeding, the guts of babies are being constantly inoculated with these beneficial bacteria.  It is becoming increasingly recognized that the healthy diversity and relative amounts of gut microorganisms are intricately linked your health.  So, it’s no surprise that whatever factors contribute to healthy gut microorganisms in babies will protect them from disease.

So, let’s get back to the study.  It has one very big limitation relevant to this discussion.  It cannot separate whether the exact age of gluten introduction in babies who were breastfed longer has any effect on celiac risk.  This study definitely shows that breastfeeding longer decreases celiac risk.  But, the idea that this is because breastfeeding occurred during and beyond gluten introduction is speculative.  It certainly makes sense given other research on the link between gut microorganisms and disease risk that a healthy gut is important in celiac disease risk and that breastfeeding longer improves the health of the gut microorganisms.  But, this study just can’t tell you whether introduction of gluten early (and before weaning) is important.  If the reason breastfeeding is protective is because of its probiotic effects (it’s nutrient value would be another good reason), then it could be that it doesn’t matter when gluten is introduced (if ever) as long as the gut is healthy when you do.

From birth through adulthood, diet has a profound effect on the composition and relative quantities of your gut microorganisms (I explain this is detail in my book).  And healthy gut microorganisms have a profound protective effect on the integrity of the gut barrier and are essential modulators of the immune system (yes, I explain this in detail in my book as well).  The optimal diet in terms of gut and gut microorganism health seems to be a hunter/gatherer/gardener type diet, rich in plants (but not grains or legumes and nothing processed or refined) and wild or pastured meat and/or wild-caught fish (no surprise to us in the paleo community).   What is healthy nutrient-dense food for you just happens to be healthy food for your gut microorganisms.  And, while this is an oversimplification, if you feed your gut bacteria good food, they are healthy, and therefore you are healthy.

So, getting back to the question that is flooding my inbox:  does this paper mean you should feed your paleo babies a little gluten now so that they will develop immune tolerance?  This study does not allow us to conclusively say yes or no.  Certainly, this study does not prove its assertion that introducing small amounts of gluten into the diet very early and prior to weaning will increase immune tolerance and therefore protect your baby against ever developing celiac disease (although you can add this study to the bounty of scientific studies showing that breastfeeding is beneficial for your baby). It should also be noted that the health of the mother greatly affects the probiotic and nutrient content of the breastmilk.  It is unknown whether breastmilk is still protective in the context of obese mothers or mothers with chronic health conditions.

I believe that the best thing that you can do for your baby’s long term health (besides love and cherish them) is feed them nutrient-dense, nourishing foods that will help them have healthy guts and healthy gut microorganisms.  I do not believe that gluten consumption promotes a healthy gut or healthy gut microorganisms (and the science backs me up on this one—I reference a few hundred studies on this topic in my book).  But, I also don’t know whether, if you wait “too long” to introduce gluten, if some magical window of opportunity to develop immune tolerance against gluten will be missed (or how much gluten you would need to keep in the diet to maintain immune tolerance).  I also don’t know whether having immune tolerance against gluten is even a good thing in terms of overall long term health.  Science does not yet provide a clear answer.  So, with all of these ideas in mind, the decision will have to be yours and will have to be based on your own risk assessment.

Bengmark S. Gut microbiota, immune development and function. Pharmacol Res. 2013 Mar;69(1):87-113. doi: 10.1016/j.phrs.2012.09.002. Epub 2012 Sep 16.

Fasano A. Leaky gut and autoimmune diseases. Clin Rev Allergy Immunol. 2012 Feb;42(1):71-8. doi: 10.1007/s12016-011-8291-x.

Groschwitz KR and Hogan SP. Intestinal barrier function: molecular regulation and disease pathogenesis. J Allergy Clin Immunol. 2009 Jul;124(1):3-20; quiz 21-2. doi: 10.1016/j.jaci.2009.05.038.

Hascoët JM et al. Effect of formula composition on the development of infant gut microbiota. J Pediatr Gastroenterol Nutr. 2011 Jun;52(6):756-62. doi: 10.1097/MPG.0b013e3182105850.

Ivarsson A et al Epidemic of coeliac disease in Swedish children. Acta Paediatr. 2000 Feb;89(2):165-71.

Ivarsson A, Prevalence of Childhood Celiac Disease and Changes in Infant Feeding. Pediatrics. 2013 Feb 18. [Epub ahead of print] http://pediatrics.aappublications.org/content/early/2013/02/13/peds.2012-1015.long

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The Benefits of Probiotics –Teaser Excerpt from The Paleo Approach

February 12, 2013 in Gut Health, Supplements, The Paleo Approach Excerpts

The Paleo Approach by Sarah BallantyneThere are many topics that I am researching and writing about for the book that I’ve been meaning to write about for the blog for ages (the book just gives me a firm deadline).  I have decided take some of these topics (especially the more blog-sized ones) and publish them as teaser excerpts for the book (also because I think this information should be here too).

The book also contains a detailed (yet easy-to-follow) description of the components of the immune system, so when you read the book, you’ll already know why modulating Th1 versus Th2 versus regulatory T-cells is important and you’ll know what dendritic cells, antigen presentation and cytokines are. For a quick primer: Th1 and Th2 cells are over-activated in autoimmunity and cause damage (typically one or the other is over-activated).  Regulatory T-cells are supposed to keep all the other immune cells in check and suppress both over-activation of the immune system and autoimmunity (they tend to be deficient in autoimmune disease).  Cytokines are chemical messengers of inflammation.  Dendritic cells are a type of sentinel cell that detects foreign invaders.  Antigens are small sequences of amino acids on foreign invaders that are recognized by the immune system.   When a dendritic cell detects foreign invaders, they “show” the antigens to B-cells and T-cells (cells of the adaptive immune system).  Gut-Associated Lymphoid Tissue is the collection of immune cells and other tissues just inside the intestinal barrier in the gut.  Enterocytes are the cells that line the small intestine and form the barrier between inside the gut and outside the gut.

So, forgive the references to Chapters 2, 3, 8 and 12.  While you’ll have to wait until the book is out in September to read those sections, in the meantime, please enjoy this part of my section of probiotics (actually, probiotics are talked about in 4 separate sections-this section is from the chapter on healing foods).

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Consumption of probiotics, either as a supplement or in the form of unpasteurized fermented foods, can dramatically help modulate the immune system.  A vast number of scientific and clinical studies have evaluated the various effects of the commensal bacteria in the gut (those healthy gut bacteria) and/or probiotic supplement of specific bacterial strains on various aspects of the immune system.  The cliff notes?  It’s all good.

The exact mechanisms behind the many observed benefits of probiotics remain largely unknown.  This may be because different bacterial strains have different effects on the body and interact differently with the immune system.  For example, some probiotic strains stimulate production of cytokines (those chemical messengers of inflammation) that promote Th1 cell development (which may augment the immune system to help fight infection and prevent cancer).  Other probiotic strains stimulate production of cytokines that promote regulatory T-cell development, thereby providing that all important immune system modulation needed in autoimmune disease (see Chapter 2).  Yet other probiotic strains, including several lactobacillus strains, are beneficial both in diseases of compromised immune systems and diseases of excessively activated immune systems.

It has been shown that probiotics interact with dendritic cells during antigen presentation during the initiation of adaptive immune responses, meaning that probiotics are useful in preventing immune-related diseases (see Chapter 2).  However, they also affect the effector phase of adaptive immunity, so they can be used as a treatment for established immune-related diseases (this applies to both immune-related diseases like asthma and allergies but also autoimmune diseases).  In fact, probiotic supplementation has been shown to be beneficial in a variety of autoimmune conditions, including:  autoimmune myasthenia gravis, inflammatory bowel diseases, rheumatoid arthritis, multiple sclerosis, and autoimmune thyroid disease.

It used to be believed that probiotic supplementation and the consumption of unpasteurized fermented foods provided health benefits by re-inoculating the gut with beneficial strains of bacteria and yeast.  Having a healthier variety and types of gut microorganisms would then be responsible for the positive benefits of probiotic supplementation.  However, recent scientific research puts this explanation into doubt—at least in some cases.  A recent study of diarrhea-predominant Irritable Bowel Syndrome demonstrated that the administration of probiotic supplements did not to alter the composition of the gut microflora.  It’s important to emphasize that probiotic supplementation was still beneficial.  This implies that the benefits of probiotic consumption might be directly due to the interaction of those probiotic bacteria (and yeast) with the gut-associated lymphoid tissue (see Chapter 2) as it passes through the body, at least in some cases.

There are clearly still some situations where probiotic supplements do have profound effects on the gut microflora.  For example, studies have shown differences in the composition of the gut microflora after taking antibiotics in people who supplemented with probiotics compared to those who didn’t.  There may also be more impactful effects on those with bacterial overgrowths.  Probiotic microorganisms have the capability to affect the gut microflora through a variety of mechanisms, including: reducing the acidity in the intestinal lumen (the area in the middle of the “tube” that forms the gut), competition for nutrients, secretion of antimicrobial compounds by the probiotics themselves, stimulating the production of antimicrobial compounds by your cells, and preventing adhesion and interaction of other bacteria with gut epithelial cells.  In these ways, probiotics may help to “correct” gut dysbiosis.

Beyond restoring balance to the gut microflora and modulating the immune system, research has shown that administration of probiotics can have a direct effect on the tight junctions between enterocytes in the gut—resulting in decreased intestinal permeability.  So, taking a probiotic or eating food naturally rich in probiotic organisms can directly help heal a leaky gut.

As already mentioned in Chapter 3, what you eat has a profound effect on the types, relative quantities and location of different bacteria growing in your gut—this effect is largely independent of the benefits of consuming fermented foods or taking probiotic supplements.  However, consuming probiotics has the great potential to speed healing and modulate the immune system and should not be underrated in importance when dealing with autoimmune disease.

Some researchers are taking on the task of characterizing the precise effects of each probiotic strain on the human body (recall that there are approximately 35,000 of them among all humans).  Certainly some strains have already been isolated for their anti-inflammatory and immune modulatory properties, yet others for their abilities to improve the barrier function of the gut or the ability to reduce visceral hypersensitivity.  It is completely possible that in the future, probiotic supplements will be tailored to address specific health problems by providing specific strains known to counteract those issues.  However, until then, the best focus is on variety.

Because different probiotic strains have slightly (and sometimes vastly) different effects (which may also depend on your genetics, level of inflammation, and current gut health), the best way to ensure complete modulation/regulation of the immune system is to consume as many different probiotic strains as possible.  So, where do you get variety?  You actually get far more variety from fermented foods and soil than you do from most supplement available (that doesn’t mean that probiotic supplements aren’t useful—see chapter 8 for more information specific to probiotic supplements).  Every time you make a new batch of homemade sauerkraut, the probiotic organisms within it will be slightly different.

So, what are good food sources of probiotics?

  • Raw unpasteurized sauerkraut
  • Raw unpasteurized lactofermented vegetables (kimchee, beets, carrots, pickles)
  • Raw unpasteurized lactofermented fruits (green papaya, chutneys)
  • Raw unpasteurized lactofermented condiments (relishes, salsas)
  • Water kefir
  • Milk kefir grown in coconut milk
  • Kombucha
  • Beet Kvass

Some form of probiotic should be consumed every day.  It is typically understood that a small amount several times per day is more beneficial than a large amount at one sitting.  When you first start consuming probiotic foods, it’s a good idea to keep the amount very small (as little as 1 teaspoon) and see how you feel.  Some people with severe gut dysbiosis can have dramatic gastrointestinal symptoms from probiotics.  If one probiotic food doesn’t work for you, try another.  If none of them work for you, you may have more luck with a supplement or just might need more time to heal your gut before introducing probiotics.  It’s okay if you need to follow The Paleo Approach for a couple of weeks before adding probiotic foods (for more information, see the Troubleshooting section in Chapter 9).  The amount you eat at any given time can then be slowly increased over the course of several weeks.  And of course, you can skip ahead to Chapter 12 to start making probiotic foods in your own home.

An often underrated source of probiotics is soil.  Soil-based organisms (SBOs) have not been as extensively studied as the lactobacillus and bifidus genus of bacteria.  However, they are normal residents of a healthy gut, have been shown to be potent modulators of the immune system, and supplementation with SBOs has been shown to be beneficial in diabetes, chronic fatigue syndrome, insomnia and Irritable Bowel Syndrome.  Soil-based probiotic supplements are available (see Chapter 8 for more information).  You can also get exposure by playing in the dirt (a good excuse to take up gardening as a hobby!) and by growing your own vegetables organically (or buying locally-grown organic vegetables) and eating them without washing them.  Okay, you can rinse the big clumps of dirt off.

 

Barbara, G., et al., Mucosal permeability and immune activation as potential therapeutic targets of probiotics in irritable bowel syndrome, J Clin Gastroenterol. 2012 Oct;46 Suppl:S52-5

Bittner, A.C., et al., Prescript-assist probiotic-prebiotic treatment for irritable bowel syndrome: an open-label, partially controlled, 1-year extension of a previously published controlled clinical trial, Clin Ther. 2007 Jun;29(6):1153-60.

Chae, C.S., et al., Prophylactic effect of probiotics on the development of experimental autoimmune myasthenia gravis, PLoS One. 2012;7(12):e52119.

Corridoni D, et al., Probiotic bacteria regulate intestinal epithelial permeability in experimental ileitis by a TNF-dependent mechanism, PLoS One. 2012;7(7):e42067

Fooks LJ and Gibson GR Probiotics as modulators of the gut flora. Br J Nutr 2002 88(Suppl 1):S39–S49.

Gerritsen, J. et al., Intestinal microbiota in human health and disease: the impact of probiotics, Genes Nutr. 2011 August; 6(3): 209–240.

Kiseleva, E.P., et al., The role of components of Bifidobacterium and Lactobacillus in pathogenesis and serologic diagnosis of autoimmune thyroid disease, Benef Microbes. 2011 Jun;2(2):139-54.

Kobayashi T, et al.,  Probiotic upregulation of peripheral IL-17 responses does not exacerbate neurological symptoms in experimental autoimmune encephalomyelitis mouse models, Immunopharmacol Immunotoxicol. 2012 Jun;34(3):423-33

Le Bert, N., et al., DC priming by M. vaccae inhibits Th2 responses in contrast to specific TLR2 priming and is associated with selective activation of the CREB pathway, PLoS One. 2011 Apr 1;6(4):e18346

Michail, S. & Kenche, H., Gut microbiota is not modified by Randomized, Double-blind, Placebo-controlled Trial of VSL#3 in Diarrhea-predominant Irritable Bowel Syndrome, Probiotics Antimicrob Proteins. 2011 Mar;3(1):1-7

Ng SC, et al., Mechanisms of action of probiotics: recent advances. Inflamm Bowel Dis. 2009;15(2):300–310.

Ruemmele F.M., et al., Clinical evidence for immunomodulatory effects of probiotic bacteria, J Pediatr Gastroenterol Nutr. 2009 Feb;48(2):126-41.

Shida, K. & Nanno, M., Probiotics and immunology: separating the wheat from the chaff, Trends Immunol. 2008 Nov;29(11):565-73.

Shida K, et al., Flexible cytokine production by macrophages and T cells in response to probiotic bacteria: a possible mechanism by which probiotics exert multifunctional immune regulatory activities, Gut Microbes. 2011 Mar-Apr;2(2):109-14

Schiffer, C., et al., A strain of Lactobacillus casei inhibits the effector phase of immune inflammation, J Immunol. 2011 Sep 1;187(5):2646-55

Tlaskalová-Hogenová, H., et al., Commensal bacteria (normal microflora), mucosal immunity and chronic inflammatory and autoimmune diseases, Immunol Lett. 2004 May 15;93(2-3):97-108.

Tsilingiri K & Rescigno M., Postbiotics: what else?, Benef Microbes. 2012 Dec 27:69-75.

Soil-based organisms improve immune function: shift cytokine profile from TH2 to TH1, Posit Health News. 1998 Spring;(No 16):16-8

http://www.old-herborn-university.de/literature/books/OHUni_book_8_article_4.pdf

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How Long Does it Take the Gut to Repair after Gluten Exposure?

September 27, 2012 in FAQ, FAQ, Featured Posts, Gut Health

This is a very relevant question for those who are just embarking on their gluten-free journey.  But, it’s also extremely important for anyone who has been following a paleo/primal/gluten-free diet for a while, but has been inadvertently exposed to gluten.  It sometimes feels as though the longer we avoid gluten, the more sick we feel after accidentally eating some.  This is in large part because the body stops protecting itself from gluten (for example, there may be less mucus in the gut) so when we do consume some, we are defenseless.  It may also be because we forget how we used to feel and are so used to feeling so much healthier.  Whether you are new to paleo or have been eating this way for a while, a common question is:  how long does it take the gut to heal after gluten exposure? 

I have talked about the irritation, inflammation and damage to the lining of the small intestine that can be caused gluten (I promise I will go back and add references to this post soon) and I have mentioned that it can take up to 6 months for the body to fully heal after a single gluten exposure.  After delving into the research more thoroughly, I have discovered that this statement is simultaneously a gross understatement and an overstatement.  Just like the extent of damage that gluten causes varies from individual to individual (see this post for a little bit more on variability in tolerance), so does the length of time it takes to recover.  And it’s not as simple as the more damage you have, the longer it takes to recover.  There are factors that control how sensitive you are (genetics, overall health, diet, stress, nutritional-deficiencies, gut microflora) and there are factors that affect how quickly you heal (okay, it’s the same list of factors, but it’s more complicated than A+B=C).

The cells that line the gut, called enterocytes or gut epithelial cells are organized into hills and valleys (to help maximize the surface area of the gut), forming finger-like columns of cells called villi separated by valleys called crypts.  The enterocytes are constantly regenerating themselves (a pool or resident stem cells supplies the new enterocytes).  As the cells age, they migrate higher up the villi and are eventually shed into the gut to be redigested (yes, we are constantly cannibalizing ourselves).  This is called the “turnover” of the gut epithelium.  In the normal healthy gut, the enterocytes migrate to the top of the villi in in 1-4 days, meaning that all of the villi cells are replaced with new cells every 3-5 days (this gets slower as we age) 1,2,3.  The cells that migrate toward the bottom of the crypts have a longer lifespan of 2-3 weeks.  What does this mean?  A healthy person has an entirely new intestinal lining every 2-3 weeks.

Repairing the intestine following injury (whether that is caused by ingested toxins, infection, or some other injury) is a more involved and complex process that is tightly regulated and controlled by the body (for a detailed understanding of this process, see reference 4).  The healing time varies depending on the extent of injury and studies trying to understand the role of the resident stem cells of the gut show that repair of the crypt and villi structure of the intestinal wall after injury can take anywhere from 2 to 12 weeks (depending on whether the stem cells themselves are injured) in the absence of confounding factors 4,5.

What does this mean?  For healthy individuals without celiac disease or gluten sensitivity (where their bodies are producing antibodies against gluten), the damage to individual cells and the junctions between them that can be caused by gluten is relatively fast to heal, anywhere from a few days to 3 weeks.  For these healthy individuals, most of this time is likely asymptomatic.  Many people report symptoms that only last from a couple of hours to a couple of days after gluten exposure.  This also means that healthy individuals should be able to heal their guts completely after following a 30-day paleo challenge such as a Whole30.

For those with confounding factors, healing is slower. Confounding factors are numerous and include gluten sensitivity (where the body is producing antibodies against gluten which increases inflammation and slows healing), celiac disease (an autoimmune condition), uncontrolled inflammation in the gut (which could be caused by food allergies, food sensitivities or diseases such as Inflammatory Bowel Disease), nutritional deficiencies (which can be caused by having a very inflamed and damaged gut, but slows healing because not all of the raw materials needed to repair are available), gut dysbiosis (the wrong type, amount and/or location of microorganisms in the gut), infections, stress, body-wide inflammation, and chronically elevated insulin.

How much do these confounding factors slow healing?  The extreme end of the spectrum is those with Celiac Disease, an autoimmune condition triggered by gluten exposure.  One hallmark of Celiac Disease is a shortening or blunting of the intestinal villi which is observed by performing a biopsy of the small intestine (they are typically 3-5 times longer in healthy individuals than those with Celiac Disease).  For those with celiac disease, one study showed that only 66% of patients had a normal intestinal biopsy after 5 years on a gluten-free diet 6.  This means that even after 5 years, 34% of Celiac Disease sufferers had not recovered.  There are no good similar studies evaluating intestinal repair in people with non-celiac gluten-sensitivity, but medical professionals who specialize in treating gluten-sensitivity report time frames of approximately 1½-2 years 7.

It’s probably worth mentioning here that current reports suggest that both Celiac Disease and gluten-sensitivity are ridiculously underdiagnosed.  It is estimated that 1 in every 100 Americans suffer from Celiac Disease but only 5% are ever diagnosed 8.  This means that there is something like 2.5-3 million Americans with celiac disease that have no idea that they have it (when you extrapolate this statistic globally, it’s even scarier!).  Gluten intolerance is estimated to affect 15-20% of the population 9.  The take home message here?  Even if you have never been diagnosed with celiac disease or gluten intolerance, you may have one of these conditions which could be contributing to slowed intestinal repair after switching to a paleo diet or after accidental gluten exposure.

How much gluten can cause a problem?  This is highly individual.  For those with Celiac disease (whether confirmed or undiagnosed), even a minute amount of gluten can cause significant damage to the small intestine in the majority of sufferers 10.  Interestingly, a not unsubstantial percentage of these people (22%) will have significant damage to their small intestine but not suffer any gastrointestinal symptoms.  For healthy individuals, the threshold amount to suffer symptoms is highly variable.  Unfortunately, you don’t know until you test it on yourself.

So, how long does it take the gut to repair after gluten exposure?  Once again, like so many topics I cover on this blog, the answer is “it depends”.  For healthy individuals, healing likely takes only a couple of weeks.  For those with celiac disease (and perhaps autoimmune diseases in general), fully healing the lining of the small intestine may take years.  The rest of us can be anywhere in between.

1 Creamer B et al. “The turnover and shedding of epithelial cells–Part I The turnover in the gastro-intestinal tract”. Gut 1961 2: 110-116

2 Lipkin M et al. “Cell Proliferation Kinetics In The Gastrointestinal Tract Of Man. I. Cell Renewal In Colon And Rectum” J Clin Invest. 1963 June; 42(6): 767–776.

3 Godlewski MM et al “Into the Unknown–The Death Pathways in the Neonatal Gut Epithelium”  Current Pediatric Reviews. 2011. 7(4):337-345

4 Blikslager AT et al. “Restoration of Barrier Function in Injured Intestinal Mucosa” Physiol Rev 87:545-564, 2007.

5 Booth C and Potten CS “Gut instincts: thoughts on intestinal epithelial stem cells” J Clin Invest. 2000;105(11):1493–1499.

6 Rubio-Tapia A “Mucosal recovery and mortality in adults with celiac disease after treatment with a gluten-free diet.” Am J Gastroenterol. 2010 Jun;105(6):1412-20.

7 http://glutendoctors.blogspot.com/2010/04/healing-time-after-removing-gluten.html

8 Lohi S et al. “Increasing prevalence of coeliac disease over time.” Aliment Pharmacol Ther. 2007 Nov 1;26(9):1217-25.

9 http://www.gastroendonews.com/ViewArticle.aspx?d=In%2Bthe%2BNews&d_id=187&i=October%2B2010&i_id=672&a_id=16015

10 Lähdeaho ML et al. “Small- bowel mucosal changes and antibody responses after low- and moderate-dose gluten challenge in celiac disease.” BMC Gastroenterol. 2011 Nov 24;11:129.

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