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What Exactly Does Food Intolerance Mean?

What Exactly Does Food Intolerance Mean?

Food intolerance is different than food allergy. Food intolerance is a non-specific, non-immune mediated reaction to specific foods.

According to one’s individual biochemistry and digestion, the digestive tract’s intestinal lining doesn’t recognize certain foods as nutritive, but rather as toxic or indigestible, responding with symptoms such as gas, bloating, abdominal pain, diarrhea, constipation, and many others. This also may be due to an enzyme deficiency.

Food intolerance is easily confused by the lay public with food allergies, which are immunologic in nature.

Food allergy can be potentially life threatening, inducing such reactions as anaphylactic shock, whereas food intolerances usually produce more chronic, in the background, low lying states

of inflammation. Food intolerance has to do with the body’s ability to sufficiently metabolize, digest, and absorb the nutrients from certain foods.

Though food intolerance is not immune mediated, the resulting inflammation is an immune response, characterized clinically by redness (rubor), heat (calor), swelling (tumor), and pain (dolor).

According to naturopathic doctors, inflammation is actually a compensatory, protective response on the part of the organism to reestablish normal balance in structure and function, to ward off “the bad guys,” or to resolve the underlying mechanisms or causes of the disease/state/condition.

The inflammatory response, in other words, is part of the body’s attempt to heal itself, and so should not be suppressed but rather worked with and supported. Unless, of course, a much more serious condition is at hand, such as the anaphylactic shock or severe IgE- mediated food allergy.

The dietary food intolerance evaluation is not a food allergy test or a lab, which classically measure IgG and IgE antibody titers that serve as biomarkers of the level of one’s individual response to certain foods as antigenic compounds.

In fact, this food intolerance assessment is a naturopathic, diagnostic tool, or rather, a functional evaluation that is evaluating the body’s ability to break down and absorb certain foods.

The foods listed above, in your results report, will likely irritate your intestinal lining and lead to symptoms of inflammation downstream, due to higher levels of toxicity in the blood (“toxemia”). These symptoms will be unique to each individual.

The only way to truly know how the foods listed below affect your digestive system is to remove them from your diet for a time. Knowledge empowers, and health is a journey, not a destination.

This information empowers you with more knowledge about what makes your body move in the direction of health and what makes it go against the trajectory- it’s up to you to determine what you want to do with it.

 

Two Reasons Dairy Could Be Driving Your Inflammation

Two Reasons Dairy Could Be Driving Your Inflammation

Dairy sensitivity is a commonly reported and documented ailment and complaint with symptoms including bloating and diarrhea, gas, indigestion, cramps, nasal congestion and heartburn, and just feeling off. (1)

Globally, dairy intolerance is the most common food intolerance in the world, said to be mainly due to lactose, the sugar found in milk, and shown to affect as much as 68% of the global population. (2) Dairy allergy, on the other hand, which has nothing to do with lactose, is especially common in children and infants, being an IgE-mediated, that is an allergenic and immunogenic reaction to cow’s milk. (3

Though it is widely acknowledged and accepted that dairy can cause a host of health complaints, it is not commonly known why this might be. Of course, it depends, to some degree, on the health and epigenetics of the individual and the environment to which their bodies and genes are exposed, but this article will discuss two biochemical reasons that dairy may be driving your inflammation. 

Reason #1: The Structure of Dairy Carbohydrates

One reason that dairy may be challenging to our health is based on the biochemistry of dairy carbohydrates. If you took biochemistry in school, you may recall that the structure of lactose bonds are composed of one molecule of D-galactose and one molecule of D-glucose linked by a beta-1,4-glycosidic bond (to form a single molecule), a bond which can only be broken with the enzyme lactase. (4)

Lactose is a disaccharide, meaning it’s composed of two sugars, and when the enzyme lactase cleaves the bond catalytically by acid hydrolysis, then you have two monosaccharides (a fancy word for a single molecule of sugar): galactose and glucose.

In other words, lactase converts a double molecule of sugar, lactose, to two single molecules, galactose and glucose. And without lactase, we cannot break down the lactose in dairy products. (5)

Grass-Fed Cows and Cellulose

We know that grass is what cows mainly eat, and grass is made up of a carbohydrate called cellulose. Fascinatingly, cellulose contains these same beta-1,4-glycosidic bonds but cellulose is indigestible to humans because of these bonds. (6)

Cellulose is composed of glucose monomers linked in unbranched chains joined by these bonds in a linear, fibrous structure. Unfortunately, humans don’t have any cellulase, which is made by bacteria in cows’ guts, to break down cellulose. 

Humans also don’t have four stomachs, like these ruminants, either: a rumen, reticulum, omasum, and abomasum. (7) Looking closely, the lactase-specific bond of lactose is similar in structure to the bonds in cellulose.

Reason #2: The Structure of Dairy Proteins

Out of the 12 most common genetic variants of cow, A1 and A2 are by far the most common. But they are both different in the single nucleotide polymorphisms in their dairy proteins (SNPs). There is something called the A1/A2 milk hypothesis. (8)

A little known fact is that A1 cows in the United States contain a histidine residue in the beta casein protein in their amino acid structure. Histidine is a precursor building block to histamine, which makes the symptoms of allergy much more likely. In other words, if your body has a bunch of histidine onboard, it might just go to town making histamine molecules. However, there is evidence that this isn’t the main reason that A1 cow milk consumption is associated with more problems. (9, 10)

Have you ever traveled over to Europe and eaten a ton of dairy, and noticed that you reacted much less severely to those foods? Or maybe you heard this story from a friend or family member, and found it to be curious? Well, here’s a possible reason why: 

The cows in Europe are mostly A2 cows, which produce dairy compounds that contain a proline residue, instead of histidine. In other words, from a biochemical perspective, the dairy of A2 cows in Europe are significantly more potentially hypoallergenic than the dairy of A1 cows in the US.

It has also been found that under normal digestive circumstances, an opiate-like protein called BCM-7 is released from A1 milk, however, not from A2 milk. This opiate-like protein appears to play a role in slowing gastric emptying and transit times, a well known side effect of opiate substances. It is not yet known to what degree this produces direct or indirect inflammatory responses. (11)

Conclusion

In summary, the problems that ensue for many when consuming dairy may be in part due to the biochemical conformation of carbohydrates and proteins and what our body is able to do or not do with them or in response to them. 

In other words, because the linkages in dairy carbohydrates are the same shape as the indigestible linkages in cellulose, dairy may to some degree be perceived by our bodies as grass-like in nature. 

Secondly, the histidine amino acid residues particularly prevalent in A1 cows which make up the majority of dairy products in the United States may lead to more histamine, and also to have opiate-like effects on the gastrointestinal tract which indirectly lead to inflammation.

If this is something you’re experiencing, or other food intolerances, remember to consult your naturopathic doctor, or your integrative medicine practitioner, regarding the role they may be playing in your life.

Resources

  1. Mishkin S. Dairy sensitivity, lactose malabsorption, and elimination diets in inflammatory bowel disease. Am J Clin Nutr. 1997 Feb;65(2):564-7. doi: 10.1093/ajcn/65.2.564. PMID: 9022546.
  2. Definition & facts for lactose intolerance. (2018, February 01). Retrieved March 10, 2021, from https://www.niddk.nih.gov/health-information/digestive-diseases/lactose-intolerance/definition-facts
  3. Flom JD, Sicherer SH. Epidemiology of Cow’s Milk AllergyNutrients. 2019;11(5):1051. Published 2019 May 10. doi:10.3390/nu11051051
  4. Study.com. (n.d.). Retrieved March 10, 2021, from https://study.com/academy/lesson/lactose-intolerance-and-the-major-disaccharides-definition-structure-examples.html
  5. Forsgård RA. Lactose digestion in humans: intestinal lactase appears to be constitutive whereas the colonic microbiome is adaptableAm J Clin Nutr. 2019;110(2):273-279. doi:10.1093/ajcn/nqz104
  6. Turning waste into food: Cellulose digestion. (n.d.). Retrieved March 10, 2021, from https://sites.dartmouth.edu/dujs/2011/02/03/turning-waste-into-food-cellulose-digestion/
  7. Digestive physiology of the cow. (n.d.). Retrieved March 10, 2021, from http://www.milkproduction.com/Library/Scientific-articles/Animal-health/Digestive-Physiology-of-the-Cow/#:~:text=The%20cow%20is%20a%20ruminant,omasum%3B%20and
  8. Sodhi M, Mukesh M, Kataria RS, Mishra BP, Joshii BK. Milk proteins and human health: A1/A2 milk hypothesisIndian J Endocrinol Metab. 2012;16(5):856. doi:10.4103/2230-8210.100685
  9. Truswell, A. S. (2005). The a2 milk case: A critical review. European Journal of Clinical Nutrition, 59(5), 623-631. doi:10.1038/sj.ejcn.1602104
  10. Brooke-Taylor S, Dwyer K, Woodford K, Kost N. Systematic Review of the Gastrointestinal Effects of A1 Compared with A2 β-CaseinAdv Nutr. 2017;8(5):739-748. Published 2017 Sep 15. doi:10.3945/an.116.013953
  11. Kamiński S, Cieslińska A, Kostyra E. Polymorphism of bovine beta-casein and its potential effect on human health. J Appl Genet. 2007;48(3):189-98. doi: 10.1007/BF03195213. PMID: 17666771.

A Natural Evidence-Based Approach to Allergies While Seeking the Root Cause

A Natural Evidence-Based Approach to Allergies While Seeking the Root Cause

Allergies arise when our immune system overreacts to what it perceives to be foreign intruders (allergens). The symptoms of allergies can range from mild to severe, and triggers include pollen, dust mites, pet and farm animal dander, insect bites and stings, mold, and even potentially medications.

Sometimes referred to as hypersensitivities, allergic reactions usually involve the skin, airways, and mucous membranes. This article will discuss some natural, evidence-based approaches to the treatment of allergies while working with a naturopathic doctor or other integrative medicine practitioner, such as a functional medicine doctor, in order to identify their underlying root causes.

The Role of Mast Cells in Allergy and Inflammation

Mast cells are a type of white blood cell rich in histamine granules famous for playing a significant role in causing the symptoms of allergy. (1) Mast cells live near blood vessels, releasing potent mediators of allergy and inflammation when activated.

When these cells degranulate, they can cause an allergic, inflammatory reaction characterized by redness, swelling, heat, and pain in the area of infection or trauma. (2)

Mast Cell Dysfunction and Histamine Intolerance

Mast cell dysfunction, and a related disorder, histamine intolerance, are implicated in many allergic and inflammatory conditions. But a discussion of these conditions in detail is best saved for another time.

Recent studies have shown how mast cells are critical to both arms of our immune system, the innate as well as the adaptive. (3)

But a root-cause approach begs the question: What is causing my symptoms of allergy? 

There are many answers to this question, such as food intolerance, the epigenetics of histamine intolerance, and a dysregulated HPA axis, but while a root-cause approach is being taken, it may be necessary to help stabilize the degranulation of these mast cells and their release of histamine without having to resort to the chronic use of conventional antihistamines, such as Zyrtec.

One naturopathic way to stabilize mast cells is by combining bioflavonoids, vitamin C, and bromelain.

The Anti-Inflammatory and Anti-Allergic Effects of Bioflavonoids

Inflammation plays a key role in allergy and asthma. Increasing scientific research points to the evidence of phenolic compounds, such as flavonoids, which exert an anti-inflammatory effect. (4)

Not only can flavonoids combat the mediators of allergy, but they also possess strong antioxidant properties. Numerous studies have shown that flavonoids can inhibit the onset as well as the development of chronic inflammatory disease. 

Flavonoids are rich in fruits, vegetables, and even legumes and cocoa.Bioflavonoids, on the other hand, are the most abundant type of polyphenol found in our diet. A famous polyphenol often found in natural antihistamine supplements is quercetin, a plant pigment found in red wine, berries, onions, apples, and even green tea. Also, because letting thy food be thy medicine is always a good thing, a person will benefit from incorporating diverse, polyphenol-rich foods into their diet whenever possible.

The Immune Enhances and Antioxidant Effects of Vitamin C

Our immune systems are highly complex and regulated by groups of immune cells, and as mentioned these cells can overreact when they perceive foreign substances, known as allergens.

Though its precise, multifactorial  mechanisms are still poorly understood, vitamin C has been shown to be an essential component in the management of allergic diseases. Chemical mediators in immediate hypersensitivity reactions are affected by the presence of ascorbic acid, as it has been shown to chelate with calcium and may control the release of mediators such as histamine. (5)

Vitamin C is also an antioxidant and can act as a free radical scavenger. Antimicrobial and natural killer cell activities are enhanced by Vitamin C. Vitamin C deficiency has been correlated with high levels of histamine in the blood, which is dangerous because high histamine, or histaminemia, has been shown to damage endothelial-dependent vasodilation. And because vasodilation lowers blood pressure and heart rate, this could easily lead to high blood pressure. (6, 7, 8)

The Anti-Inflammatory and Anti-Allergic Effects of Bromelain

Bromelain is a natural enzyme extracted from pineapple core and juice shown to have anti-inflammatory and anti-allergy activities, and shown (in mouse studies) to reduce the progression of allergic airway disease. This suggests that allergic sensitivity can be reduced. (9, 10)

Bioflavonoids, Vitamin C, and Bromelain in The Treatment of Mast Cell Dysfunction

In summary, while teasing out the root cause of allergic sensitivity with a naturopathic doctor or another integrative medicine practitioner, research indicates that the combination of bioflavonoids, Vitamin C, and bromelain can help stabilize mast cell degranulation. 

Of course, you should always consult your doctor first.

 

Resources

  1. da Silva EZ, Jamur MC, Oliver C. Mast cell function: a new vision of an old cell. J Histochem Cytochem. 2014 Oct;62(10):698-738. doi: 10.1369/0022155414545334. Epub 2014 Jul 25. PMID: 25062998; PMCID: PMC4230976.
  2. Bais S, Kumari R, Prashar Y, Gill NS. Review of various molecular targets on mast cells and its relation to obesity: A future perspective. Diabetes Metab Syndr. 2017 Dec;11 Suppl 2:S1001-S1007. doi: 10.1016/j.dsx.2017.07.029. Epub 2017 Jul 23. PMID: 28778429.
  3. Zhang T, Finn DF, Barlow JW, Walsh JJ. Mast cell stabilisers. Eur J Pharmacol. 2016 May 5;778:158-68. doi: 10.1016/j.ejphar.2015.05.071. Epub 2015 Jun 27. PMID: 26130122.
  4. Maleki SJ, Crespo JF, Cabanillas B. Anti-inflammatory effects of flavonoids. Food Chem. 2019 Nov 30;299:125124. doi: 10.1016/j.foodchem.2019.125124. Epub 2019 Jul 3. PMID: 31288163.
  5. Anogeianaki A, Castellani ML, Tripodi D, Toniato E, De Lutiis MA, Conti F, Felaco P, Fulcheri M, Theoharides TC, Galzio R, Caraffa A, Antinolfi P, Cuccurullo C, Ciampoli C, Felaco M, Cerulli G, Pandolfi F, Sabatino G, Neri G, Shaik-Dasthagirisaheb YB. Vitamins and mast cells. Int J Immunopathol Pharmacol. 2010 Oct-Dec;23(4):991-6. doi: 10.1177/039463201002300403. PMID: 21244748.
  6. Sharma SC, Wilson CW. The celluar interaction of ascorbic acid with histamine, cyclic nucleotides and prostaglandins in the immediate hypersensitivity reaction. Int J Vitam Nutr Res. 1980;50(2):163-70. PMID: 6156921.
  7. Shaik-Dasthagirisaheb YB, Varvara G, Murmura G, Saggini A, Caraffa A, Antinolfi P, Tete’ S, Tripodi D, Conti F, Cianchetti E, Toniato E, Rosati M, Speranza L, Pantalone A, Saggini R, Tei M, Speziali A, Conti P, Theoharides TC, Pandolfi F. Role of vitamins D, E and C in immunity and inflammation. J Biol Regul Homeost Agents. 2013 Apr-Jun;27(2):291-5. PMID: 23830380.
  8. BD, Y. (1970, January 01). Relationship between Vitamin C, Mast Cells and Inflammation. Retrieved February 01, 2021, from https://www.mendeley.com/catalogue/115cbf0e-8fb8-3bee-a492-f2a8bbb22135/
  9. Secor ER Jr, Carson WF 4th, Cloutier MM, Guernsey LA, Schramm CM, Wu CA, Thrall RS. Bromelain exerts anti-inflammatory effects in an ovalbumin-induced murine model of allergic airway disease. Cell Immunol. 2005 Sep;237(1):68-75. doi: 10.1016/j.cellimm.2005.10.002. Epub 2005 Dec 6. PMID: 16337164; PMCID: PMC2576519.
  10. Owoyele BV, Bakare AO, Ologe MO. Bromelain: A Review on its Potential as a Therapy for the Management of Covid-19. Niger J Physiol Sci. 2020 Jun 30;35(1):10-19. PMID: 33084621.

Is Food Allergy Testing Really the Answer?

Is Food Allergy Testing Really the Answer?

In alternative healthcare, food allergy panels are routinely ordered. An estimated 20% of the world believes it reacts adversely to specific foods (1), while as many as 15 million Americans suffer from food allergies (2).

Food reaction can be non-immune mediated, as in food intolerance or sensitivity, or immune mediated, as in food allergy, but there is confusion even among the medical establishment. Alternative food allergy tests usually measure serum IgG antibodies, while conventional allergy tests measure serum IgE antibodies.

Do IgG Antibodies Really Identify Food Intolerance or Sensitivity?

IgG antibodies represent a delayed as opposed to an immediate, immune-mediated food reaction (IgE), and are purported by some, though scientific evidence is scant (3), to identify food intolerance or sensitivity.

How can an immune-mediated food allergy test measure something that is non-immune mediated, such as an enzyme deficiency? And is the $300 to $700 of an IgG food intolerance panel worth the cost?

While Cyrex is the most well-known food allergy lab, Great Plains Laboratory and US Biotek are also reputable. While many alternative practitioners pay lip service to root-cause medicine, food allergy panels may reveal food reactivities which are more symptom than etiology.

Are Dietary Restrictions Revealed by Food Intolerance Testing Possible to Follow?

Routinely revealing long lists of common foods to which a person is producing high serum antibody loads (titers), patients are often placed on ultra-restrictive diets, such as low-FODMAPS (4), which can be difficult to follow, induce stress, and produce low compliance.

The question is: Why are IgG levels high for these specific foods? The answer seems to lie in increased intestinal permeability.

Increased Intestinal Permeability

The immune system, merely doing its job, generates antibody labels to all foods consumed, and because these now-offending foods are crossing the gut barrier into the bloodstream, it’s working overtime. Trained to attack any invader, the immune system begins to recognize the offending foods as antigens. Later on, overwhelmed by constant vigilance and hyperactivity, the body is triggered to begin attacking its own tissues (autoimmunity), as seen in Celiac disease where gliadin antibodies attack the intestinal lining. (5)

Antibody titers will be highest, naturally, to foods consumed most often and in the greatest quantities. When these foods are dietarily removed, antibody titers to said foods gradually lower and disappear. This is why testing for tissue transglutaminase auto-antibodies (tTG-IgA) in Celiac disease, e.g., must be done before going gluten-free. (6)

Leaky Gut, Gliadin Fractions in Gluten, and Zonulin

Increased intestinal permeability, aka leaky gut, will naturally increase food reactivity, and recent research indicates that gluten plays a key role. Gliadin fractions in gluten upregulate the protein zonulin which modulates gut mucosal barrier activity, thereby causing intercellular epithelial gap junctions to expand and produce leaky gut in the intestinal lining. (7) Bad gut bacteria or SIBO can also cause leaky gut, which can lead to metabolic endotoxemia. (8) Higher systemic inflammation results, measured by biomarkers, such as hs-CRP. (9)

The Physiology of the Intestinal Lining in the Small Intestine

The epithelial lining of the small intestine is like a cheesecloth one cell layer thick, just beneath which lies connective tissue called lamina propria. (10) When this cheesecloth stretches out, undigested food particles move from the lumen (tubular inside) of the small intestine into the bloodstream. (11)

When this cheesecloth tears, it takes 3 to 7 days for it to heal, during which many food stuffs supposed to be digesting end up permeating through the intestinal lining and ending up in the blood. (12) A slight degree of intestinal permeability is supposed to be happening, as this is the immune system’s way of sampling what is being eaten, to be on the lookout for infectious organisms. But when too much occurs, autoimmune disease can develop.

Attached to the GI tract’s epithelial cells are microvilli, finger-like projections that increase the surface area of the intestines and absorb vital nutrients, fatty acids, and glycerol from food. Interestingly, tiny arteries (arterioles) go to the top of each microvilli, and tiny veins (venules) go down. (An artery carries blood to something, whereas a vein carries blood away from something.) (13)

In the middle of these arterioles and venules are lymphatic capillaries (lacteals) which absorb dietary fats taken in through the microvilli. So, basically the microvilli and epithelial intestinal lining have a blood supply their own, which nourishes and regenerates them. These microvilli are also sloughed off every 7 days, but only pieces at a time. This is why a large portion of our fecal matter is made of dead skin-like tissue, such as sloughed microvilli. (14)

The Role of Stress in the Absorption of Nutrients in the Small Intestine

At the microvilli base is an A-V shunt or connection, that’s supposed to stay closed. But when it opens, blood naturally shunts across. If this is occurring, then the microvilli will not have the required blood supply and so they will be sloughed off, inducing temporary malabsorption syndrome. Without properly functioning microvilli, zero nutrient absorption will occur, and this can last up to a few days, or be chronic. (15)

Two hormones in particular will naturally open the A-V shunt. These are epinephrine (adrenaline) and norepinephrine, which are released during fight or flight. Chronic stress will cause the adrenal medullae to release these stress hormones into the blood, inducing malabsorption and causing energy levels to plummet. (16)

The Real Cause(s) of Food Intolerance/Sensitivity and Allergy

While following the restrictive recommendations gleaned from food allergy panels may lower or resolve some chronic symptoms initially or temporarily, the jury is still out as to whether they are financially feasible or lifestyle-amenable. There is growing evidence that increased intestinal permeability (17,18,19) and subsequent low-level, systemic inflammation, due to a compromised microbiome, the consumption of excess amounts of wheat, and chronic stress, needs to be addressed in order to resolve food allergies, particularly of the delayed IgG variety. Of course, ultimately it’s up to the patient and to their healthcare practitioner.

  1. Lomer, M. (2018). Review article: the aetiology, diagnosis, mechanisms and clinical evidence for food intolerance.
  2. “Facts and Statistics.” Food Allergy Research & Education, www.foodallergy.org/life-with-food-allergies/food-allergy-101/facts-and-statistics.
  3. Lavine, E. (2012). Blood testing for sensitivity, allergy or intolerance to foodCMAJ : Canadian Medical Association Journal184(6), 666–668. http://doi.org/10.1503/cmaj.110026
  4. Magge, S., & Lembo, A. (2012). Low-FODMAP Diet for Treatment of Irritable Bowel SyndromeGastroenterology & Hepatology8(11), 739–745.
  5. Meresse, B., Malamut, G., & Cerf-Bensussan, N. (2012). Celiac Disease: An Immunological JigsawImmunity,36(6), 907-919. doi:10.1016/j.immuni.2012.06.006
  6. Screening. (n.d.). Retrieved from https://celiac.org/celiac-disease/understanding-celiac-disease-2/diagnosing-celiac-disease/screening/
  7. Fasano, A. (2012). Zonulin, regulation of tight junctions, and autoimmune diseasesAnnals of the New York Academy of Sciences1258(1), 25–33. http://doi.org/10.1111/j.1749-6632.2012.06538.x
  8. Ferolla, S. M., Armiliato, G. N. A., Couto, C. A., & Ferrari, T. C. A. (2014). The Role of Intestinal Bacteria Overgrowth in Obesity-Related Nonalcoholic Fatty Liver DiseaseNutrients6(12), 5583–5599. http://doi.org/10.3390/nu6125583
  9. Tetzlaff, W. F., Meroño, T., Menafra, M., Martin, M., Botta, E., Matoso, M. D., … Brites, F. (2017). Markers of inflammation and cardiovascular disease in recently diagnosed celiac disease patientsWorld Journal of Cardiology9(5), 448–456. http://doi.org/10.4330/wjc.v9.i5.448
  10. Sollid, L. M., & Jabri, B. (2013). Triggers and drivers of autoimmunity: lessons from coeliac diseaseNature Reviews. Immunology13(4), 10.1038/nri3407. http://doi.org/10.1038/nri3407
  11. Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease(Ninth edition.). Philadelphia, PA: Elsevier/Saunders.
  12. O’Bryan, T. (2016). The Autoimmune Fix: How to Stop the Hidden Autoimmune Damage that Keeps you Sick, Fat, and Tired Before it Turns into Disease. Emmaus, PA: Rodale Books.
  13. Sauvanet, C., Wayt, J., Pelaseyed, T., & Bretscher, A. (2015). Structure, Regulation, and Functional Diversity of Microvilli on the Apical Domain of Epithelial CellsAnnual Review of Cell and Developmental Biology, 31(1), 593-621. doi:10.1146/annurev-cellbio-100814-125234
  14. Anatomy Of The Small Intestine. (n.d.). Retrieved from https://jonbarron.org/article/anatomy-small-intestine
  15. Tritz, G. J., & KCOM. (n.d.). Gastrointestinal Manifestations of Disease. Retrieved from https://www.atsu.edu/faculty/chamberlain/website/tritzid/gastro.htm
  16. Hasibeder, W. (2010). Gastrointestinal microcirculation: Still a mystery? British Journal of Anaesthesia, 105(4), 393-396. doi:10.1093/bja/aeq236
  17. Perrier, C., & Corthésy, B. (2010). Gut permeability and food allergiesClinical & Experimental Allergy, 41(1), 20-28. doi:10.1111/j.1365-2222.2010.03639.x
  18. Järvinen, K. M., Konstantinou, G. N., Pilapil, M., Arrieta, M., Noone, S., Sampson, H. A., . . . Nowak-Węgrzyn, A. (2013). Intestinal permeability in children with food allergy on specific elimination dietsPediatric Allergy and Immunology, 24(6), 589-595. doi:10.1111/pai.12106
    De Punder, K., & Pruimboom, L. (2015). Stress Induces Endotoxemia and Low-Grade Inflammation by Increasing Barrier PermeabilityFrontiers in Immunology6, 223. http://doi.org/10.3389/fimmu.2015.00223