Tag Archives: autoimmune

Celiac Disease, Gluten, and Children

Researchers posit introducing gluten at specific points of time during infancy development might be the key to celiac disease prevention. A few recent studies tested the hypothesis on an infant population who were genetically at risk for developing the disease.1

Celiac Disease - Diagram 1

Di Sabatino A, Corazza GR. Coeliac disease. Lancet. 2009;373:1480–1493.

For those unfamiliar, celiac disease is (very simply) defined as an autoimmune disorder, which is caused by a reaction to gliadin.2 Gliadin is a prolamine protein, which is found in wheat.3 Those with celiac disease are usually also sensitive to other proteins, which are chemically similar in structure.4, 5

Celiac Disease - Diagram 2

World J Gastroenterol. Nov 14, 2012; 18(42): 6036–6059.

Surprisingly, the researchers’ hypothesis was disproved.6 The studies exhibited that children developed the disease equally, regardless of the time frame of gluten introduction. Perhaps most surprisingly, breastfeeding didn’t seem to provide any protective benefits either, which is seemingly contradictory to earlier scientific findings.7

Celiac Disease - Diagram 3

BMC Pediatr. 2011; 11: 46.

Children with chronic illnesses are known to be more predisposed to emotional and behavioral problems.8 The above chart (MASC Tscore Mean) shows the increased rate of emotional and behavioral problems in children with celiac disease.9 Since the topic of gluten, celiac disease and children is a somewhat sensitive one, it is important for us to look at the likely cause of the disease.10 Causative, not correlative, mechanisms and reasons are, at the end of the day, what’s really important about scientific findings.11 What we seem to have learned from these very well conducted studies, is that celiac disease may be caused almost entirely by genetics.12

Celiac Disease Table 1

World J Gastroenterol. 2012 November 14; 18(42): 6036–6059.

Almost all people with celiac disease have one of 2 genes, DQ2 or DQ8.13 The above table shows the worldwide frequency and distribution of the genes.14 However, interestingly, about 33% of the population also has one of these genes – but they never develop the disease.15 This leads researchers to think that perhaps there are lifestyle and/or epigenetic factors at play, as well.16

Celiac Disease Diagram 3

J Clin Invest. 2011;121(6):2126-2132. doi:10.1172/JCI58109.

Genetic and diet-induced obesity are associated with alterations of (i) the composition and (ii) the functional properties of the gut microbiota. (A) Leptin-deficient ob/ob mice rapidly gain weight. Development of obesity correlates with a shift in the abundance of the 2 dominating divisions, the Bacteroidetes and the Firmicutes. Compared to lean ob/+ or +/+ littermates, obesity was associated with a 50% reduction in Bacteroidetes and a proportional division-wide increase in Firmicutes. Moreover, ob/ob mice showed an increase in environmental gene tags that matched Archaea, methanogenic microorganisms that might promote bacterial fermentation by removing one of its end products, namely hydrogen (H2). The metagenomic analysis of the obese gut microbiome revealed an increase in glycoside hydrolases, capable of breaking down otherwise indigestible alimentary polysaccharides. Furthermore, the obese microbiome showed enrichment for transport proteins and fermentation enzymes further processing breakdown products. As a consequence, ob/ob mice have an increased capacity to harvest energy from their diet. (B) The interrelationship between diet, intestinal microbial ecology, and energy homeostasis was investigated in a mouse model of diet-induced obesity.28 The microbiota of mice fed a high-fat/high-sugar prototypic Western diet was compared with the microbiota of mice receiving a low-fat/high-polysaccharide diet. Again, as in the ob/ob model, the Western diet was associated with an increased body weight, a lower relative abundance of Bacteroidetes, and a higher relative abundance of Firmicutes. However, unlike in the ob/ob model this shift was not division-wide. The overall diversity of the Western diet-associated gut microbiota dropped dramatically. The reason was a bloom in a single class of the Firmicutes—the Mollicutes. The Western diet gut microbiome was enriched for genes involved in import and fermentation of simple sugars and host glycans, enriched for genes for beta-fructosidases, and depleted for genes involved in motility. Gastroenterology Volume 136, Issue 5, Pages 1476–1483, May 2009 .

Tilg, Herbert et al. Gastroenterology. Volume 136 , Issue 5 , 1476 – 1483

One hypothesis is that changes may occur, in gut bacteria, before the disease develops.17 This means that things such as antibiotics, refined sugar, artificial colors, gluten and other artificial food elements may be causing detrimental changes in the microbiome.18 This would also mean that intervening with a probiotic might be one possible “fix.”19, 20 Above, we can see how changes in microbiota, sometimes brought upon by diet, affect many changes and processes in the body.21, 22

Prevalence of celiac disease worldwide. N/A: Not available.   World J Gastroenterol. Nov 14, 2012; 18(42): 6036–6059.

World J Gastroenterol. Nov 14, 2012; 18(42): 6036–6059.

Hypothetically, it would make sense that the recent rise in celiac disease could be due to our massive shift in diet.23 We have changed our diet, almost totally and completely, since the 1970s.24, 25 Obviously, our genome has not really had much time to adapt to these changes.26

Another interesting factor that has also changed since the 1970s is that children are exposed to fewer germs – and parents are much more vigilant about cleanliness.27 This theory of disease is nicknamed the “hygiene hypothesis.”28 With decreased exposure to harmful environmental elements, which our body then learns to defend itself against, children’s immune systems may be turning inward – attacking the body’s own tissue, instead.29, 30

Though the cause of celiac disease may be genetic, the only cure, as has long been known, is a gluten-free diet.31 On the diet, the small intestinal mucosal injury heals and gluten-induced symptoms and signs disappear.32 If you have children, the best course of action is a screening, to see if they may be at risk for celiac disease.33 This goes doubly if any family members have the disease, as the genetic risk factor makes the likelihood increase.34

However, regardless of your children’s potential risk for developing celiac disease, it is not a good idea to be eat gluten.35, 36 There are many downsides to gluten, and it has many negative effects on the body and mind.37, 38, 39, 40 In fact, one study showed that removing gluten from the diet reduced adiposity, inflammation and insulin resistance.41

Other studies have shown that in some individuals, gluten sensitivity was shown to manifest solely with neurological dysfunction, though this point is somewhat debatable.42, 43, 44 What is interesting, however we previously detailed, is that schizophrenics among others with mental disorders, seem to respond positively to the removal of gluten from the diet.45

As should be obvious by now, you can see the benefits in removing gluten and gluten-like compounds from your children’s diet. Therefore, a Paleo Diet, which is rich in nutrients and avoids problematic proteins like gluten, is the best course of action to take – for both children and adults. You will likely see a decrease in your blood pressure, improve your glucose tolerance and your lipid profile.46 These are all healthy, positive changes – whether you’re young or old.

REFERENCES

1. Lionetti E, Castellaneta S, Francavilla R, et al. Introduction of gluten, HLA status, and the risk of celiac disease in children. N Engl J Med. 2014;371(14):1295-303.

2. Rubio-tapia A, Murray JA. Celiac disease. Curr Opin Gastroenterol. 2010;26(2):116-22.

3. Thompson T. Wheat starch, gliadin, and the gluten-free diet. J Am Diet Assoc. 2001;101(12):1456-9.

4. Troncone R, Auricchio S, De vincenzi M, Donatiello A, Farris E, Silano V. An analysis of cereals that react with serum antibodies in patients with coeliac disease. J Pediatr Gastroenterol Nutr. 1987;6(3):346-50.

5. Hollén E, Högberg L, Stenhammar L, Fälth-magnusson K, Magnusson KE. Antibodies to oat prolamines (avenins) in children with coeliac disease. Scand J Gastroenterol. 2003;38(7):742-6.

6. Available at: http://www.bostonglobe.com/lifestyle/health-wellness/2014/10/05/studies-find-tactics-prevent-celiac-disease-newborns-don-work/zsbjwMAjdYOPFzRsDhriuO/story.html. Accessed October 12, 2014.

7. Norris JM, Barriga K, Hoffenberg EJ, et al. Risk of celiac disease autoimmunity and timing of gluten introduction in the diet of infants at increased risk of disease. JAMA. 2005;293(19):2343-51.

8. Hysing M, Elgen I, Gillberg C, Lundervold AJ. Emotional and behavioural problems in subgroups of children with chronic illness: results from a large-scale population study. Child Care Health Dev. 2009;35(4):527-33.

9. Mazzone L, Reale L, Spina M, et al. Compliant gluten-free children with celiac disease: an evaluation of psychological distress. BMC Pediatr. 2011;11:46.

10. Niewinski MM. Advances in celiac disease and gluten-free diet. J Am Diet Assoc. 2008;108(4):661-72.

11. Verhulst B, Eaves LJ, Hatemi PK. Correlation not causation: the relationship between personality traits and political ideologies. Am J Pol Sci. 2012;56(1):34-51.

12. Monsuur AJ, Wijmenga C. Understanding the molecular basis of celiac disease: what genetic studies reveal. Ann Med. 2006;38(8):578-91.

13. Castro-antunes MM, Crovella S, Brandão LA, Guimaraes RL, Motta ME, Silva GA. Frequency distribution of HLA DQ2 and DQ8 in celiac patients and first-degree relatives in Recife, northeastern Brazil. Clinics (Sao Paulo). 2011;66(2):227-31.

14. Gujral N, Freeman HJ, Thomson AB. Celiac disease: prevalence, diagnosis, pathogenesis and treatment. World J Gastroenterol. 2012;18(42):6036-59.

15. Szałowska-woźniak DA, Bąk-romaniszyn L, Cywińska-bernas A, Zeman K. Evaluation of HLA-DQ2/DQ8 genotype in patients with celiac disease hospitalised in 2012 at the Department of Paediatrics. Prz Gastroenterol. 2014;9(1):32-7.

16. Alegría-torres JA, Baccarelli A, Bollati V. Epigenetics and lifestyle. Epigenomics. 2011;3(3):267-77.

17. Nistal E, Caminero A, Herrán AR, et al. Differences of small intestinal bacteria populations in adults and children with/without celiac disease: effect of age, gluten diet, and disease. Inflamm Bowel Dis. 2012;18(4):649-56.

18. Kau AL, Ahern PP, Griffin NW, Goodman AL, Gordon JI. Human nutrition, the gut microbiome and the immune system. Nature. 2011;474(7351):327-36.

19. Tillisch K, Labus J, Kilpatrick L, et al. Consumption of fermented milk product with probiotic modulates brain activity. Gastroenterology. 2013;144(7):1394-401, 1401.e1-4.

20. Cryan JF, Dinan TG. Mind-altering microorganisms: the impact of the gut microbiota on brain and behaviour. Nat Rev Neurosci. 2012;13(10):701-12.

21. Tilg H, Moschen AR, Kaser A. Obesity and the microbiota. Gastroenterology. 2009;136(5):1476-83.

22. Tilg H, Kaser A. Gut microbiome, obesity, and metabolic dysfunction. J Clin Invest. 2011;121(6):2126-32.

23. Brown K, Decoffe D, Molcan E, Gibson DL. Diet-induced dysbiosis of the intestinal microbiota and the effects on immunity and disease. Nutrients. 2012;4(8):1095-119.

24. Hurt RT, Kulisek C, Buchanan LA, Mcclave SA. The obesity epidemic: challenges, health initiatives, and implications for gastroenterologists. Gastroenterol Hepatol (N Y). 2010;6(12):780-92.

25. Cordain L, Eaton SB, Sebastian A, et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005;81(2):341-54.

26. Tännsjö T. Should we change the human genome?. Theor Med. 1993;14(3):231-47.

27. Okada H, Kuhn C, Feillet H, Bach JF. The ‘hygiene hypothesis’ for autoimmune and allergic diseases: an update. Clin Exp Immunol. 2010;160(1):1-9.

28. Rook GA. Review series on helminths, immune modulation and the hygiene hypothesis: the broader implications of the hygiene hypothesis. Immunology. 2009;126(1):3-11.

29. Bloomfield SF, Stanwell-smith R, Crevel RW, Pickup J. Too clean, or not too clean: the hygiene hypothesis and home hygiene. Clin Exp Allergy. 2006;36(4):402-25.

30. Romagnani S. The increased prevalence of allergy and the hygiene hypothesis: missing immune deviation, reduced immune suppression, or both?. Immunology. 2004;112(3):352-63.

31. See J, Murray JA. Gluten-free diet: the medical and nutrition management of celiac disease. Nutr Clin Pract. 2006;21(1):1-15.

32. Mäki M. Celiac disease treatment: gluten-free diet and beyond. J Pediatr Gastroenterol Nutr. 2014;59 Suppl 1:S15-7.

33. Aggarwal S, Lebwohl B, Green PH. Screening for celiac disease in average-risk and high-risk populations. Therap Adv Gastroenterol. 2012;5(1):37-47.

34. Rubio-tapia A, Van dyke CT, Lahr BD, et al. Predictors of family risk for celiac disease: a population-based study. Clin Gastroenterol Hepatol. 2008;6(9):983-7.

35. Biesiekierski JR, Newnham ED, Irving PM, et al. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol. 2011;106(3):508-14.

36. Marziali M, Venza M, Lazzaro S, Lazzaro A, Micossi C, Stolfi VM. Gluten-free diet: a new strategy for management of painful endometriosis related symptoms?. Minerva Chir. 2012;67(6):499-504.

37. Drago S, El asmar R, Di pierro M, et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scand J Gastroenterol. 2006;41(4):408-19.

38. Gluten sensitivity as a neurological illness. Journal of Neurology, Neurosurgery & Psychiatry. 2002;72(5):560.

39. Hadjivassiliou M, Grünewald RA, Kandler RH, et al. Neuropathy associated with gluten sensitivity. J Neurol Neurosurg Psychiatr. 2006;77(11):1262-6.

40. Hadjivassiliou M, Grünewald RA, Lawden M, Davies-jones GA, Powell T, Smith CM. Headache and CNS white matter abnormalities associated with gluten sensitivity. Neurology. 2001;56(3):385-8.

41. Soares FL, De oliveira matoso R, Teixeira LG, et al. Gluten-free diet reduces adiposity, inflammation and insulin resistance associated with the induction of PPAR-alpha and PPAR-gamma expression. J Nutr Biochem. 2013;24(6):1105-11.

42. Hadjivassiliou M, Sanders DS, Grünewald RA, Woodroofe N, Boscolo S, Aeschlimann D. Gluten sensitivity: from gut to brain. Lancet Neurol. 2010;9(3):318-30.

43. Nijeboer P, Mulder C, Bouma G. [Non-coeliac gluten sensitivity: hype, or new epidemic?]. Ned Tijdschr Geneeskd. 2013;157(21):A6168.

44. Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology. 2013;145(2):320-8.e1-3.

45. Kraft BD, Westman EC. Schizophrenia, gluten, and low-carbohydrate, ketogenic diets: a case report and review of the literature. Nutr Metab (Lond). 2009;6(1):10.

46. Frassetto LA, Schloetter M, Mietus-synder M, Morris RC, Sebastian A. Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet. Eur J Clin Nutr. 2009;63(8):947-55.

Hidraenitis Suppurativa | The Paleo Diet

Hi Dr. Cordain,

I’m not sure if you remember me- I was one of the women who interviewed you last August at the Ancestral Health Symposium in LA.

The reason I’m writing you today is 1) to thank you and 2) to ask you some questions. When we spoke, I asked you about Hidradenitis Suppurativa (HS). You told me that you suspected it had an autoimmune connection, but didn’t have any more information to add. I suffered from HS for over 20 years, Stage II, so I was very motivated to get rid of it for good. Once you mentioned “autoimmunity,” I went on an autoimmune Paleo protocol and my HS disappeared. With experimentation, I found my trigger- potatoes. I never would have known, or even tried the AlP, had you not mentioned autoimmunity. For that, I thank you from the bottom of my heart. 3) I had a guest post on robbwolf.com about the issue (I’ve now been in clinical remission off medication for almost a YEAR) and am currently writing a book about it. My background is in Journalism, though, not science or any medical field, so I am quoting the hell out of your book, Robb Wolf’s book, and others.

1. I can’t find any documentation of HS being autoimmune in nature, except for what you told me in the hallway of the AHS building. Doctors currently treat it with antibiotics or don’t treat it at all. You did say when we spoke that you were going to look into it. Do you know of any medical literature that suggests that HS is autoimmune in nature?

2. When I experimented on myself by removing nightshades and went into remission, and then flared up when I reintroduced potatoes, did I not prove the autoimmune nature of HS in myself? I have been talking to other people who have been also putting their HS into remission by removing nightshades and it seems to be working across the board. Some have diagnosed wheat as their trigger, but the overwhelming majority of us have found nightshades to be the offender. I did do my elimination and reintroduction quite scientifically, but I’m not a scientist, so do my results “count” or are they just anecdotal?

3. You say that the white blood cells in our guts have become sensitized to proteins from bacteria or food or both. For people who have become sensitized to the bacteria, what options are available to them? Obviously antibiotics don’t work in this case, so would taking probiotics and something like Allimed (a garlic extract which has been shown to have antibacterial effects in the body) help? Since I didn’t have this particular problem, I would like to present options in my new book and help those who do. Obviously I am putting the dietary changes at the forefront of the treatment, but if those fail, then I would like to have another line of treatment, unless the dietary changes plus probiotics are enough if kept up in the long run (long enough to allow the gut to fully heal)?

That’s it! Thank you so much for your time and consideration. And thank you again for giving me the tools to change my life. I’ve had a few emails from people who say they want to kill themselves and I am driven to help them end their symptoms.

Cheers,

Tara Grant

Tara Grant has transformed from 235 pounds to 159 pounds since going Primal in 2009. Tara suffered a litany of serious health problems related to the Standard American Diet and repeated failures of western medicine to cure her. Empowered by the reclaiming of her health, Tara has made it her mission to inform and inspire others about Primal living. Her motto, “Empower. Enlighten. Evolve”, has been put into play in numerous ways! Her book, The Hidden Plague – A Comprehensive Guide to Surviving Hidradenitis Supprativa – details her struggle with this debilitating skin condition, and how sufferers can take matters into the own hands and heal naturally.

Tara is a veteran presenter of numerous PrimalCons, where she holds court detailing her Primal transformation from health to wellness. Tara is also a contributing writer for the Primal Blueprint Expert Certification program and is working with Carrie Sisson on her upcoming Primal Woman book. A dynamic speaker, Tara presents the Primal Transformation Seminar in numerous cities, and counsels individuals as a certified CHEK Holistic Life Coach. Tara holds a degree in Journalism from Carleton University in Ottawa, Canada and blogs regularly at www.primalgirl.com. She currently lives in Phoenix, Arizona with her husband Derek and their twin boys, Taylor and Gibson.

Dr. Cordain’s Response:

Hi Tara,

Let me dive into your questions. Specific white blood cells called dendritic cells process protein fragments (antigens) of gut bacteria and/or food antigens in a manner that may promote inflammation and autoimmunity in genetically susceptible people. When the gut becomes leaky, it allows these antigens to interact with dendritic cells and other immune system cells to set the stage for autoimmune diseases. Hence, dietary and environmental factors which promote a leaky gut need to be removed.

1. Nightshade plants contain a variety of compounds which promote a leaky gut, but also can be sources of immunological adjuvants (compounds used in vaccines to rev up the immune response).

2. Alpha tomatine in tomatoes has been demonstrated to be a powerful adjuvant.

3. Probiotics and Prebiotics represent good supplements for most people to promote and healthy gut flora and to reduce intestinal permeability. I know of one physician who healed his alopecia completely only after adopting Paleo and then adding probiotics. However, I also know of a few cases where probiotics may agitate the gut and make things worse.

4. Garlic has been used in traditional medicine for thousands of years to cure a variety of health problems. I haven’t examined the literature on the topic of autoimmunity and garlic, but garlic is a concentrated source of saponins which in most cases disrupt membrane function and can lead to a leaky gut.

In my most recent book, The Paleo Answer, I list all of the known dietary factors which promote a leaky gut.

Below are the references which led me to believe HS is a gut mediated autoimmune disease that has the potential to be improved or put into remission by contemporary Paleo diets – gluten free, dairy free, grain free, legume free, and nightshade free. In your case nightshades were the major triggering factor, and we believe it is because certain glycoalkaloids in tomatoes and potatoes may act to increase intestinal permeability and also contain certain immunological adjuvants (alpha tomatine in tomatoes) that up-regulate the immune response in genetically susceptible HLA haplotypes.

Good luck with your book!

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

References

1. Rambhatla PV, Lim HW, Hamzavi I. A systematic review of treatments for hidradenitis suppurativa. Arch
Dermatol. 2012 Apr;148(4):439-46 Epub 2011 Dec 19.

2. Nazary M, van der Zee HH, Prens EP, Folkerts G, Boer J. Pathogenesis and pharmacotherapy of
Hidradenitis suppurativa. Eur J Pharmacal. 2011 Dec 15;672(1-3):1-8. Epub 2011 Sep 14.

3.Dreno B, Khammari A, Brocard A, Moyse D, Blouin E, Guillet G, Leonard F, Knol AC. Hidradenitis
suppurativa: the role of deficient cutaneous innate immunity. Arch Dermatol. 2012 Feb;148(2):182-6.
Epub 2011 Oct 17.

4.Brocard A, Dreno B. Innate immunity: a crucial target for zinc in the treatment of inflammatory dermatosis. J Eur Acad Dermatol Venereal. 2011 Oct;25(10):1146-52. doi: 10.1111/j.1468-
3083.2010.03934.x. Epub 2011 Jan 24.

5. van der Zee HH, de Ruiter L, van den Broecke DG, Dik WA, Laman JD, Prens EP. Elevated levels of tumour necrosis factor (TN F)-a, interleukin (IL)-1[3 and IL-10 in hidradenitis suppurativa skin: a rationale for targeting TN F-a and IL-1[3. Br J Dermatol. 2011 Jun;164(6):1292-8. doi: 10.1111/j.1365-
2133.2011.10254.x. Epub 2011 May 17.

6. van der Zee HH, van der Woude CJ, Florencia EF, Prens EP. Hidradenitis suppurativa and inflammatory bowel disease: are they associated? Results of a pilot study. Br J Dermatol. 2010 Jan;162{1):195-7. Epub
2009 Aug 14.

7. van der Zee HH, Laman JD, de Ruiter L, Dik WA, Prens EP. Adalimumab (antitumour necrosis factor-a) treatment of hidradenitis suppurativa ameliorates skin inflammation: an in situ and ex vivo study. Br J
Dermatol. 2012 Feb;166(2):298-305.

8. Giamarellos-Bourboulis EJ, Antonopoulou A, Petropoulou C, Mouktaroudi M, Spyridaki E, Baziaka F,
Pelekanou A, Giamarellou H, Stavrianeas NG. Altered innate and adaptive immune responses in patients with hidradenitis suppurativa. Br J Dermatol. 2007 Jan;156(1):51-6.

9. Hunger RE, Surovy AM, Hassan AS, Braathen LR, Yawalkar N. Toll-like receptor 2 is highly expressed in lesions of acne inversa and colocalizes with C-type lectin receptor. Br J Dermatol. 2008 Apr;158(4) :691-7. Epub 2008 Jan 30.

10. Schlapbach C, Hanni T, Yawalkar N, Hunger RE. Expression ofthe IL-23/Th17 pathway in lesions of
hidradenitis suppurativa. JAm Acad Dermatol. 2011 Oct;65(4):790-8.

Hidradenitis Suppurativa | The Paleo Diet

Dear Professor Cordain,

I read very useful information on your website regarding the importance of nutrition for health, therefore I have a few questions and hope you will find time to provide the answers.

My fiance have been struggling with Hidradenitis Suppurativa (HS) for about 12 years. Doctors and antibiotics did not provide much help. The only thing that helped him about 10 years ago was his trip to Malaysia that resulted in total change of food (no bread, no meat – except fish, no diary, but a lot of turmeric).

Unfortunately, the illness returned about two years ago and has been getting worse. As a psychologist, and Ph.D. candidate in psychology, I know how stress can be related to this disease.

But, I also read on Internet (Primagirl Blog, more precisely), that The Paleo Diet can heal this disease, because it is always certain types of food that triggers it. I also found your name and information on your book there, therefore I decided to contact you.

I would really appreciate if you could help me with your advice. If you know what kind of food can trigger this disease, or if you can recommend something, I would strongly appreciate.

Thank you in advance.

Sincerely,

Alma

Dr. Cordain’s Response:

Hi Alma,

Abundant scientific evidence exists in Hidradenitis Suppurativa (HS) patients showing that pro-inflammatory cytokines (local hormones) are elevated in the blood are almost certainly involved in the skin lesions presenting in HS patients. Two major categories of circulating white blood cells (macrophages and dendritic cells) likely have become activated (sensitized) in the gut to specific gut proteins (either bacteria or food or both) and these gut borne cells then initiate an immune response which affects cells lining either the hair follicle or apocrine sweat glands in other parts of the body, particularly the groin and armpit areas. Hence, it seems likely that HS, although it presents clinically as a single disease, is actually at least two diseases, one in the hair follicle and one in the apocrine sweat glands, both likely to be autoimmune in nature. Women are more likely to have the form of HS involving the cells lining the hair follicle. To date, it has not been conclusively demonstrated that HS is autoimmune in nature. Nevertheless, work from our group as far back as 2002 and from Alessio Fasano’s group at the University of Maryland suggest that a key triggering event in most autoimmune diseases is a leaky gut.

My suggestion for all autoimmune patients is to restrict foods which are known to increase intestinal permeability. These food restrictions form the basis for the contemporary Paleo Diet, however for autoimmune patients a few more restrictions should be included.

General food restrictions for all Paleo Dieters include:

1. All cereal grains (wheat, rye, barley, oats, rice, corn, sorghum and millet). Wheat is probably the grain which should be avoided strictly because of its combination of antinutrients (wheat germ agglutinin, gliadin, thaumatin like proteins, and phytic acid) which have varying degrees of toxicity in humans.

2. All dairy products. The rationale for this food group restriction can be found in my new book, The Paleo Answer, in a single chapter I have written with hundreds of scientific references to support these conclusions.

3. All beans, legumes (including, green beans, soy, peas and peanuts). Again, I have extensively documented the rationale for these restrictions in The Paleo Answer.

4. All processed foods containing refined sugars, grains, vegetable oils and salt. The rationale for these restrictions can be found in all of my popular books and in my scientific writings which are available across the website.

An Elimination Diet

For Autoimmune patients including those with HS, I suggest restricting the following foods for a 30 day period to determine if symptoms improve. This strategy is called an “elimination diet” in which foods are removed from the diet and then added back in to determine if they are problematic.

1. All nightshades (potatotes, tomatoes, eggplants, tomatillos, tobacco and all capsaicin containing peppers [cayenne, serrano, jalapeno, paprika, habanera and all foods made with these- salsa, hot sauce, tomato pastes & sauces etc.]. The nightshade family of plants contain a variety of compounds which increase intestinal permeability. In potatoes, it is the glycoalkaloids (alpha solanine and alpha chaconine); in tomatoes it is alpha tomatine; in spicy peppers it is capsaicin. The scientific references showing how nightshade compounds increase intestinal permeability can be found in my new book, The Paleo Answer. In HS patients, smoking tobacco (a nightshade plant) has been shown to aggravate the disease symptoms in HS patients.

2. Alcohol (ethanol) found in beer wine and all alcoholic beverages increases intestinal permeability.

3. Aluminum hydroxide (alum) in antacids increases intestinal permeability.

4. Alfalfa sprouts contain high concentrations of compounds called saponins which increase intestinal permeability.

5. Psuedo grains (quinoa, amaranth) contain saponins which increase intestinal permeability in a dose dependent manner – meaning the more you consume the leakier the gut becomes. Chia seeds also likely increase intestinal permeability.

6. Oral contraceptives

7. NSAIDS (Nonsteroidal anti-inflammatory drugs) like aspirin and ibuprofen.

8. Egg whites contain a substance called lysozyme which increases intestinal permeability.

9. A foaming agent called Quillaja found in many brands of root beer increases intestinal permeability and potently stimulates the immune system.

10. In addition to peanuts, which are not a not at all, but a legume, tree nuts (almonds, walnuts, pecans, brazil nuts, etc.) are one of the most common allergenic foods. To date, tree nuts have been poorly studied for antinutrient content, and it is unclear if they increase intestinal permeability or adversely affect the immune system. This would be one of the last foods I suggest restricting.

Supplementation

Zinc supplementation (90 mg/day for 3 months) has been shown to reduce inflammation in HS patients. Supplements which improve intestinal integrity and which may reduce intestinal permeability include:

1. Probiotics

2. Prebiotics

3. Viamin D3

4. Fish oil (EPA and DHA)

5. Zinc

6. Medium chain triglycerides (Coconut Oil)

There are no guarantees that these food restrictions will improve symptoms or cure autoimmune diseases.

Nevertheless, I know of hundreds of anecdotal cases worldwide which demonstrate contemporary Paleo diets to be therapeutic in autoimmune patients. Together with my graduate students we are currently writing up a large case study involving nearly 100 autoimmune patients who have reported varying degrees of success in managing their conditions following The Paleo Diet.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

References

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Dermatol. 2012 Apr;148(4):439-46 Epub 2011 Dec 19.

2. Nazary M, van der Zee HH, Prens EP, Folkerts G, Boer J. Pathogenesis and pharmacotherapy of
Hidradenitis suppurativa. Eur J Pharmacal. 2011 Dec 15;672(1-3):1-8. Epub 2011 Sep 14.

3.Dreno B, Khammari A, Brocard A, Moyse D, Blouin E, Guillet G, Leonard F, Knol AC. Hidradenitis
suppurativa: the role of deficient cutaneous innate immunity. Arch Dermatol. 2012 Feb;148(2):182-6.
Epub 2011 Oct 17.

4.Brocard A, Dreno B. Innate immunity: a crucial target for zinc in the treatment of inflammatory dermatosis. J Eur Acad Dermatol Venereal. 2011 Oct;25(10):1146-52. doi: 10.1111/j.1468-
3083.2010.03934.x. Epub 2011 Jan 24.

5. van der Zee HH, de Ruiter L, van den Broecke DG, Dik WA, Laman JD, Prens EP. Elevated levels of tumour necrosis factor (TN F)-a, interleukin (IL)-1[3 and IL-10 in hidradenitis suppurativa skin: a rationale for targeting TN F-a and IL-1[3. Br J Dermatol. 2011 Jun;164(6):1292-8. doi: 10.1111/j.1365-
2133.2011.10254.x. Epub 2011 May 17.

6. van der Zee HH, van der Woude CJ, Florencia EF, Prens EP. Hidradenitis suppurativa and inflammatory bowel disease: are they associated? Results of a pilot study. Br J Dermatol. 2010 Jan;162{1):195-7. Epub
2009 Aug 14.

7. van der Zee HH, Laman JD, de Ruiter L, Dik WA, Prens EP. Adalimumab (antitumour necrosis factor-a) treatment of hidradenitis suppurativa ameliorates skin inflammation: an in situ and ex vivo study. Br J
Dermatol. 2012 Feb;166(2):298-305.

8. Giamarellos-Bourboulis EJ, Antonopoulou A, Petropoulou C, Mouktaroudi M, Spyridaki E, Baziaka F,
Pelekanou A, Giamarellou H, Stavrianeas NG. Altered innate and adaptive immune responses in patients with hidradenitis suppurativa. Br J Dermatol. 2007 Jan;156(1):51-6.

9. Hunger RE, Surovy AM, Hassan AS, Braathen LR, Yawalkar N. Toll-like receptor 2 is highly expressed in lesions of acne inversa and colocalizes with C-type lectin receptor. Br J Dermatol. 2008 Apr;158(4) :691-7. Epub 2008 Jan 30.

10. Schlapbach C, Hanni T, Yawalkar N, Hunger RE. Expression ofthe IL-23/Th17 pathway in lesions of hidradenitis suppurativa. JAm Acad Dermatol. 2011 Oct;65(4):790-8.

Cured My Esophagitis | The Paleo Diet

Dear Dr. Cordain,

I’m just sending a quick testimony to thank you for The Paleo Diet. It cured my esophagitis, which I had for 6 months straight, in less than 3 weeks. It seemed miraculous. I can even eat citrus and marinara sauce and drink coffee, tea, and wine again with absolutely no problems whatsoever. I discovered Paleo through Chris Kresser’s website when researching my health problems online.

I had been a vegetarian since the age of 10 and ate at least 80% grains, dairy and legumes since then. I’m now 29 and until last month I couldn’t understand why at my age I kept developing illnesses (colitis, esophagitis, and IBS, plus I was sleeping 10 hours at a time and still feeling tired.) I thought that perhaps I was doomed due to bad genes because these things run in my family on both sides (family members with Barrett’s Esophagus, Colostomy bags, Acid Reflux), but now I’m already all better! I’m totally healthy, full of energy, and as an added bonus, I lost a few pounds and am as skinny as I was as a teen. It happened so fast too! I can hardly believe it.

Thank you very much! I’m so happy to be off of medicine and symptom free! It is a huge relief.

Sincerely,

Sarah
Dr. Cordain’s Response:

Hi Sarah,

Congratulations upon your health successes with Paleo! Success stories like yours really are what this idea is all about — helping people to enjoy a better quality of life. Hopefully, others with similar conditions can benefit from your anecdotal experience.

Regards,

Loren Cordain, Ph.D., Professor Emeritus

Crohn's Disease | The Paleo Diet

Hello Dr. Cordain,

My husband has had Crohn’s disease for most of his life along with many surgeries. I have been advised to check out The Paleo Diet, but have noticed that it encourages eating leafy greens. Our problem is that he cannot eat any type of leafy greens or roughage, as much as he would love to, it would go right through him and cause him severe stomach pain. I am strongly considering trying this way of life (a lot of which we have already incorporated), but do not want to if its not feasible for my husbands health. Do you have any suggestions to help me along this path? Your response is greatly appreciated!

Thank you,

Katie Jenan

Dr. Cordain’s Response:

Hello Katie,

Many people have had success treating their Crohn’s disease symptoms with The Paleo Diet. Crohn’s disease is the result of autoimmune-based inflammation in the digestive system. The following foods should be avoided by those with Crohn’s disease:

  • All commonly consumed cereal grains, including wheat, rye, barley, oats, corn, and rice—note that rice is probably the least damaging grain.
  • All beans and legumes.
  • Potatoes and tomatoes.
  • All pseudo grains, including amaranth, quinoa, buckwheat, and chia seeds.

Almost all plant foods contain lectins, but most seem to be benign when it comes to our health, except for lectins in grains, legumes, and a few other foods that may enter our bloodstream and interact with most cells in our bodies, including those in our immune systems. I’ve written extensively about this in my book The Paleo Answer, a good place for you and your husband to start as you adopt the Paleo lifestyle.

If your husband has difficulty consuming leafy greens and other “roughage” he should completely eliminate these foods from his diet until his gut has healed completely. He will still be able to absorb all of the nutrients he needs without consuming vegetables. Many hunter-gatherer groups (Inuit, Inupiat) subsisted on diets with little to no plant matter, and their populations remained healthy and free of modern diseases. It would be beneficial to focus on consuming a diet rich in animal proteins and fats, bone broth, and fermented foods (kefir, sauerkraut, etc.) that will aid in healing the gut. If his system can handle it, fruit should also be consumed in moderation. Eventually, he could experiment with introducing thoroughly steamed or cooked veggies back into his diet if necessary. I wish you the best of luck treating his Crohn’s disease.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

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