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TPV Episode 33 Show Notes: Breastfeeding and First Foods

April 5, 2013 in Practical Tips, Show Notes

Our thirty-third show!
Ep. 33: Breastfeeding and First Foods

In this episode, Stacy and Sarah welcome Arsy from Rubies and Radishes, author of The Paleo Slow Cooker, to talk about breastfeeding and first foods. Discussed are such topics as handling food sensitivities in babies, how to deal with issues with milk supply, and why Stacy knows so much about this stuff.

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The Paleo View (TPV), Episode 33: Breastfeeding and First Foods

 

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The Link Between Gallbladder Disease and Gluten Sensitivity

December 1, 2012 in Beyond Paleo, Gut Health

(Created as a guest post for Paleo Parents.)

Celiac disease is estimated to affect approximately 1 in every 100 people, but only 5% of these people receive a positive diagnosis 1.  This is, in part, because celiac disease often doesn’t present with what are thought of as the classic symptoms (abdominal pain, bloating, intermittent diarrhea, weight loss).  In fact, more often, celiac disease presents as a collection of symptoms that many physicians don’t associate with the disease (irritability or depression, anemia, stomach upset, joint pain, muscle cramps, skin rash, mouth sores, dental and bone disorders such as osteoporosis, neuropathy, and/or micronutrient deficiency) 2.  However, the recognition and understanding of celiac disease is improving and more and more people with the disease are receiving positive diagnoses.

The same is not so true of gluten sensitivity, which includes immune reactions that are currently tested for (IgE, IgG or IgA antibody formation against gluten), immune reactions that are not currently tested for (IgM antibody formation, T-cell activation and/or immune complex formation), and non-immune reactions (increased zonulin production and/or gut dysbiosis resulting from deficiency of appropriate digestive enzymes).  Gluten intolerance (where antibodies are formed against gluten) is thought to affect upwards of 20-40% of the general population 3-4.  There are no estimates of the percentage of people who are sensitive to gluten in other ways.  Genetic tests (HLA-DQ, DR, etc.) exist but it is still unknown if current genetic tests accurately identify all individuals who are gluten sensitive 4.

A wider and wider range of health issues are being linked to gluten sensitivity and/or celiac disease.  This is a positive development in medical research because it is starting to bring more focus on how detrimental these grain proteins are in the human diet.  One such health issue is gallbladder disease, although the link between gallbladder disease and gluten sensitivity/celiac disease has not permeated through the public knowledge.  Because so many people are unaware that their gallbladder problems might be linked to gluten in their diets, it seemed like a good idea to write a post about this topic!

Let’s take a step backward and first talk about what exactly a gallbladder is.  The gallbladder is a little pear-shaped sac, nestled toward the front and a little underneath of the liver.  It has a very simple job:

  • store bile (which is produced by the liver) between meals
  • concentrate bile by reabsorbing water
  • release bile into the small intestine when there’s food that needs to be digested

Bile is composed of water, bile salts, bile pigments (products of red blood cell breakdown that are normally excreted in the bile), cholesterol, and various electrolytes.  Bile salts are the only components of bile that actually have a digestive function.  Bile salts are not the same as digestive enzymes (which are produced by the cells that line the stomach and by the pancreas).  Instead, bile salts aid the actions of digestive enzymes and enhance the absorption of fatty acids and fat-soluble vitamins.

The most important action of bile salts is that of an emulsifier.  In essence, bile salts break up fat globules in the small intestine into tiny droplets that are able to mix with water.  The enzymes that break fat up into fatty acids (lipases) can then perform their function more effectively.  Bile salts also aid in the absorption of fatty acids and cholesterol (some of the cholesterol released into the small intestine in the bile is reabsorbed).  Fat-soluble vitamins (such as A, D, E, K1 and K2) are also absorbed.

If the gallbladder is not functioning properly, fats cannot be properly digested (fats are essential for survival and health) and fat-soluble vitamins cannot be effectively absorbed, leading to micronutrient deficiencies.  Gallbladder health is critical for digestive health and overall health.

As is so often the case with research linking gluten sensitivity to other health complications, the research is strongest in the context of celiac disease.  Approximately 60% of celiac disease sufferers are known to have liver, gallbladder, and/or pancreatic conditions 5.  While some of these conditions may be a result of the malnutrition and/or directly linked to the gut damage that occurs in celiac disease, others are thought to share common genetic factors or have a common immunopathogenesis (i.e., the condition originates from the same immune system attacks on the small intestine also attacking these organs) 5.  Specifically, primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune forms of hepatitis or cholangitis are thought to have a common immune system/inflammation origin as celiac disease itself—and that means gluten.

What does this mean?  In celiac disease (and in non-celiac gluten sensitivity, albeit to a lesser extent or perhaps just in a slightly different way), gluten triggers an autoimmune response.  The body’s own immune system attacks the cells that line the small intestine, resulting in the characteristic shortening or pruning of the intestinal villi (microscopic, finger-like projections of small intestine wall tissue made of columns of gut epithelial cells).  As you can imagine, this creates a very leaky gut, which also stimulates the immune system, causes inflammation, and allows toxins and foreign proteins into the body.  In the majority of celiac disease patients, the immune system does not limit its attack to the cells that line the small intestine.  This is why second and even third autoimmune conditions are so common in celiac disease.

When you eat, the cells that line the duodenum (the first segment of the small intestine) detect the presence of fat and protein and react by releasing a hormone called cholecystokinin.  This hormone stimulates both the release of digestive enzymes from the pancreas and bile from the gallbladder.  It also signals to the stomach to slow down the speed of digestion so the small intestine can effectively digest the fats.  When the gut is damaged (whether from celiac disease or other gut pathology), the cells that line the small intestine (called enterocytes or gut epithelial cells) are less able to secrete cholecystokinin.  This means there is not enough signal to the gallbladder that it’s time to release bile salts into the duodenum.  Reduced cholecystokinin release is reported in celiac disease and may be one of the key causes of the gallbladder malfunction that occurs concomitantly with celiac 6-8.

Importantly for this discussion, the dominant gallbladder symptoms that might be caused by gluten sensitivity is cholecystitis (inflammation of the gallbladder) or malfunctioning gallbladder, and not gall stones (reported in 20% of elderly celiac patients, but only 2.5% of the more general celiac population).    The frequency of liver and gallbladder conditions suffered by celiac disease patients has allowed researchers to make the converse argument.  It is now recommended that those with unexplained liver and/or gallbladder symptoms be evaluated for celiac disease 9-11.  If you have been diagnosed with gallbladder disease (especially if it is not gall stones, but don’t rule out this possibility if it is), it is important to investigate gluten sensitivity or celiac disease as the possible cause.  No one has yet studied how frequently someone with gallstones actually has undiagnosed celiac disease (or gluten sensitivity) and there is a feeling within the celiac community that this may actually be quite frequent.

What if you test negative for celiac disease and gluten intolerance?  Unless you had the DNA test done for gluten sensitivity, these tests actually are embarrassingly inaccurate in the sense that the false negative rate is very high (false negative means that you do have celiac but the test showed that you don’t).  There are a variety of ways that false negatives can occur and no one likes to put a number on just how likely they are.  But, if you remember from the beginning of this post, these tests generally only test for antibody formation (and a biopsy only looks at one very small piece of your small intestine).  The best way to be sure that gluten is not the problem is to eliminate it completely from your diet for several months (those with celiac disease can take up to 5 years to heal from the damage caused by gluten 12).  It is not enough to eliminate gluten however, as antibodies that your body may have formed against gluten may also recognize proteins in other foods.  This means that even if you aren’t eating any gluten, your body still thinks that it is (see this post for a complete explanation and list of foods to avoid).

The take home message?  There is a strong link between gallbladder health and celiac disease.  In fact, a failing gallbladder may be your first symptom of celiac disease.  Of course, I believe that a grain-free, legume-free, dairy-free, refined sugar-free, modern vegetable oil-free diet is optimal for our health in every way; however, if you are suffering from gallbladder problems, then I recommend addressing your diet as soon as possible.  The earlier you adopt an anti-inflammatory diet that prioritizes gut health, the more likely you are to save your gallbladder.

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

2 http://www.mayoclinic.com/health/celiac-disease/DS00319/DSECTION=symptoms

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

4 http://www.glutenfreesociety.org/gluten-free-society-blog/the-many-heads-of-gluten-sensitivity/

5 Freeman HJ.” Hepatobiliary and pancreatic disorders in celiac disease.” World J Gastroenterol. 2006 Mar 14;12(10):1503-8. http://www.wjgnet.com/1007-9327/full/v12/i10/1503.htm

6 Masclee AA et al. “Gallbladder sensitivity to cholecystokinin in coeliac disease. Correlation of gallbladder contraction with plasma cholecystokinin-like immunoreactivity during infusion of cerulein.” Scand J Gastroenterol. 1991 Dec;26(12):1279-84. http://www.ncbi.nlm.nih.gov/pubmed/1763298

7 Fraquelli M et al “Gallbladder emptying and somatostatin and cholecystokinin plasma levels in celiac disease.” Am J Gastroenterol. 1999 Jul;94(7):1866-70.

8 Nousia-Arvanitakis S et al.  “Subclinical exocrine pancreatic dysfunction resulting from decreased cholecystokinin secretion in the presence of intestinal villous atrophy.” J Pediatr Gastroenterol Nutr. 2006 Sep;43(3):307-12. http://www.ncbi.nlm.nih.gov/pubmed/16954951

9 Biecker E et al “Autoimmune hepatitis, cryoglobulinaemia and untreated coeliac disease: a case report.” Eur J Gastroenterol Hepatol. 2003 Apr;15(4):423-7. http://www.ncbi.nlm.nih.gov/pubmed/12655265

10 Parfenov AI et al “Asymptomatic celiac disease in patient with chronic acalculous cholecystitis” Eksp Klin Gastroenterol. 2011;(3):122-4.

11 Galán Bertrand L et al. “Acute lithiasic cholecystitis as an exceptional presentation of celiac disease” An Pediatr (Barc). 2006 Jul;65(1):87-8. Spanish

12  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.

 

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The WHYs behind the Autoimmune Protocol: Eggs

June 23, 2012 in The WHYs of the AIP

Eggs are one of the most allergenic foods with approximately 2-3% of the population affected.  However, people are still surprised when I advertise an egg-free recipe or mention that I can’t eat eggs.  It’s not because I’m allergic but because I have an autoimmune disease and eggs are excluded on the Autoimmune Protocol.  Given that eggs are such an important staple for the paleo enthusiast (as a breakfast food, as a cheap protein, and as an ingredient in the vast majority of paleo baking recipes), I get asked “Why Eggs?” frequently. 

One of the main functions of the white of the egg is to protect the yolk against microbial attack while the embryo grows.   It achieves this worthy goal by using proteolytic enzymes (or proteases), enzymes that can cleave proteins into shorter chains of amino acids (typically rendering those proteins inactive/useless in the process).  There are many different types of proteolytic enzymes, each highly specialized to cleave a specific type of protein and/or in a specific place.  In particular, the proteolytic enzymes in egg whites are very good at cleaving proteins in the cell membranes of certain bacteria (specifically gram-negative bacteria, which I’ll come back to in a couple of paragraphs).  The specific protease in egg whites that those of us with autoimmune disease (or severe allergies or severely leaky guts) need to be concerned with is called lysozyme. 

I used to use lysozyme in the biology lab to break apart the membranes of bacteria (typically bacteria that I had engineered to grow specific DNA strands for me).  Lysozyme is specific for bacterial membranes, works very quickly, is very resistant to heat, is stable in very acidic environments (so it’s still active even after cooking eggs thoroughly and digestion!), and is really a pretty ingenious little enzyme (that’s me geeking out).  Humans also produce lysozyme as part of our normal defense mechanisms against bacterial infections.  It is present in our saliva, tears and mucus (including the mucus layers in the intestines).  So, if we already make our own lysozyme, why is it a problem in egg whites?

Lysozyme has the ability to form strong complexes with other proteins.  So, lysozyme from egg white typically passes through our digestive system in large complexes with other egg white proteins.  Many of the proteins present in egg whites are protease inhibitors (see this post for more information on how protease inhibitors can contribute to a leaky gut).  This means that the lysozyme/egg white protein complexes are resistant to digestion by our digestive enzymes (which are themselves proteases).  You might be wondering if lysozyme is still active if it is a protease and it is now bound to egg white protease inhibitors.  The answer is yes, it is still active.  The egg white protease inhibitors that are most likely to be bound to lysozyme are ovomucin and ovastatin, which are a trypsin inhibitors (trypsin is one of our main digestive enzymes), cystatin, which is a cysteine protease inhibitor, and ovoinhibitor, which is a serine protease inhibitor.  None of these inhibitors inhibit the activity of lysozyme.  And very importantly, as the lysozyme complex travels (largely intact) through the environment of our gut, lysozyme can also bind bacterial proteins from the bacteria normally present in our digestive tract (like the gram-negative E. coli!). 

Lysozyme has an unusual chemical property (it maintains a positive charge) that allows it to cross through the enterocytes by electrostatic attraction to negatively charged proteins imbedded in the enterocyte cell surface (proteoglycans).  Research confirms that consumed lysozyme gets into the circulation even in healthy individuals (even in conjunction with food intake, although the amount that enters the circulation is lower). 1,2,3Absorption of pure egg white lysozyme by itself into circulation is likely not problematic because lysozyme is an enzyme that the body naturally produces (unless it is absorbed in very high concentrations and then it can cause kidney damage).  The problem is the other proteins that piggyback on lysozyme across the gut enterocyte barrier.  It is this “leak” of other egg white proteins that is the reason why egg allergy is so common.  Any other proteins present in the digestive tract can potentially bind in the lysozyme complex and get helped across the gut and into the blood stream (or lymph).  And because lysozyme binds bacterial wall proteins, these are likely to “leak” across the gut enterocyte layer as well.  These foreign proteins are believed to contribute to a molecular mimicry response where the body, in its attempt to form antibodies against these foreign invaders, accidentally creates an antibody that also recognizes a normal protein in the human body. 

It’s also important to point out that the ability of lysozyme to cross the gut barrier (carrying potentially immunogenic proteins along with it) is a fairly small effect.  In normal, healthy individuals, lysozyme is not likely to cause significant damage to the healthy lining of the gut or cause a substantial immune response (although the effect of lysozyme is why Prof. Loren Cordain recommends limiting eggs to 6 per week).  In healthy individuals, pastured or omega-3 eggs can be an excellent, inexpensive source of protein, omega-3 fatty acids, lutein, zeaxanthin, choline, selenium, phosphorus, vitamin A, vitamin D and the B vitamins.  However, in the case of autoimmune disease, individuals are more sensitive and tend to have exaggerated immune and inflammatory responses to foreign proteins in the circulation.  These individuals are also more likely to form auto-antibodies in response to bacterial proteins that may enter into the circulation with lysozyme. 

You might notice here that this discussion was entirely related to egg white proteins.  Egg yolks are not likely to cause these issues.  However, if you are following the Autoimmune Protocol, I urge caution since egg yolks are a very common food sensitivity in those with leaky guts (note that this is different than being allergic to them).  I still recommend avoiding both egg white and yolk when you first adopt the Autoimmune Protocol.  But, of all of the foods that are restricted in this protocol, I think egg yolks are the most likely to be tolerated and many people can add them back in. 


1 Kondor-Koch C, et al.  Exocytotic pathways exist to both the apical and the basolateral cell surface of the polarized epithelial cell MDCK. Cell, 1985. 43(1): 297-306,

2 Hashida S, et al. Concentration of egg white lysozyme in the serum of healthy subjects after oral administration. Clin Exp Pharmacol Physiol. 2002.  29(1-2):79-83.

3 Nishikawa M, et. al. Electrical charge on protein regulates its absorption from the rat small intestine. Am J Physiol Gastrointest Liver Physiol. 2002.  282(4):G711-9.

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Challenge #2 Update: My Still Spirited but Much Healthier Kids

May 5, 2012 in 2012, About Sarah's Family

Over the past 6 months, I have successfully transitioned my daughters to a lacto-paleo diet.  I tackled this transition by finding great paleo substitutes for their favorites, gradually introducing new foods, and slowly phasing out the foods that we don’t eat anymore.  You can read about various aspects of my children’s transition to paleo in these posts:

and also about my general approach to the transition in this post:

How has going paleo improved their health?  Both girls had small patches of eczema that cleared up once their diet was gluten-free.  My youngest still gets very mild rashes from time to time, which I think might indicate a dairy sensitivity and I am also growing suspicious of strawberries (she got a very obvious rash after eating birthday cake so we know she is for sure gluten-sensitive).  I love that I don’t have to slather my girls in cortisone cream anymore!  I have also noticed that, since going gluten-free, both my daughters’ immune systems seem to be much stronger.  The last few colds that passed through our house were so minor as to be barely noticed.  We used to be sick all the time and catch absolutely everything that was going around.  Now, I’ve even started to not worry about exposure to other sick kids because for I finally have some confidence in their immune systems actually doing their job!  The most amazing accomplishment is that we were able to wean my oldest off of Miralax, which she had been on for the last three years (since she was 2!) for chronic constipation.  And this is saving a noticeable amount of money!  My oldest also seems to be sleeping a bit better and has better energy, but still seems lower energy than other kids her age.  We’ve had her tested for various deficiencies, all of which she doesn’t have, so it seems to be simply caused by not eating enough, or at least, not regulating her blood sugar well with what she is eating. 

Unfortunately, my youngest still has nighttime breathing issues which continue to be not fully diagnosed (and actually even less clear than they were before because now they continue after she awakes, so it doesn’t look like sleep apnea anymore).  We have taken her off the acid reflux medicine (it never did anything anyway!), which I think is progress in terms of ruling that out as a potential cause (I also disliked that she was on proton-pump inhibitors at all, so I am very pleased to have her off of them!).  We do know that she still has a laryngomalacia (a floppy epiglottis) and that her vocal cord bands are tight.  This may be the root cause of her breathing issues (in which case, she may grow out of it, but surgery is an option), which would be unrelated to diet.  We have another sleep study booked (her third!) to see whether or not she is still experiencing any obstructive sleep apnea and will proceed from there.

So, what are my goals with my kids?  I am proud of my girls (and myself) for making and accepting so many changes to their diets.  However, I have decided that I want to remove dairy products from their diet after all.  For my youngest, I am hoping it will fix whatever is causing her to gasp for air at night and hopefully put an end to the occasional rashes she gets.  For my oldest, I am hoping that removing these insulinogenic foods from her diet will help balance her blood sugar and hence her energy levels during the day.  I have actually already started the process.  We got my youngest used to drinking water instead of milk throughout the day (this was never an issue with my oldest who never did like to drink straight milk).  We no longer have cow’s milk in the house so that if they do want milk, it’s coconut milk.  And I have been experimenting with flavoring my own homemade coconut milk yogurt so that the girls will eat it.  I haven’t quite figured out what to do about cheese, except try to get used to not eating it.  My youngest doesn’t eat much, so this is mostly an issue for my oldest. 

When I think back to how my kids ate just 6 months ago, I am completely amazed at how much progress we have made.  I still have challenges ahead of me; but I can now say that I feel confident that I am feeding my children optimal nutrition and teaching them how to eat to stay healthy for their entire lives.  And that feels pretty good!

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