In order answer this question, we need to know what AIP is…

AIP is paleo stacked with the avoidance of all the major allergens and some other devilish food products, making it likely one of the most restrictive diets on the planet.

NO grains, NO sugar, NO dairy, NO legumes, NO eggs, NO soy, NO nuts or seeds, NO vegetable oils, NO night shades, NO shellfish, NO mushrooms, NO coffee, NO Alcohol, and Absolutely NO processed food.

This framework invariably increases protein and fruit and vegetable intake, as well as fiber consumption dramatically, while limiting inflammatory omega 6 fatty acid consumption. It also eliminates pretty much the entire standard American diet, so it is not surprising that this diet results in significant weight loss and the improvement of health outcomes in the general population living the standard American life.

The paleo diet has been dismantled at length by Alan Aragon is many AARR editions, so I will not belabor this point. Instead, I will quote the December 2009, AARR.

“Based on the body of research, it’s clear that paleo dieting can have positive effects, but is yet to be proven superior to a macronutrient-matched comparison arm, let alone a macronutrient-matched, fiber-matched treatment in non-sedentary or athletic subjects.”

-Alan Aragon

This statement is still true in 2017. Although, a recent meta-analysis by Manheimer et al. [1] in AJCN concluded that, “The Paleolithic diet resulted in greater short-term improvements in metabolic syndrome components than did guideline based control diets.” But as indicated above, these dietary arms were far from equal, and these studies were carried out in sedentary, obese, and diabetic subjects, thus we know little to nothing about the effect of the paleo diet in fit, active, and lean individuals.

The paleo diet hypothesis is shot to shit from an ancestral standpoint; hunter-gather diets varied to extremes across the globe. But, the most dangerous aspect of the paleo diet is cutting out nearly every dense carbohydrate source (and whey) in an athletic population, who play and train inside higher intensities. As for the general population, some people can moderate, some people can’t, but black and white thinking can get us into trouble long-term [2].

 

Yet, is it at all feasible that this massively restrictive diet may benefit those with an autoimmune condition?

The largest AIP book in the popular press is The Paleo Approach: Reverse Autoimmune Disease and Heal Your Body by Dr. Sarah Ballantyne, who has Hashimoto’s Thyroiditis herself. This book is well-written and feels and reads like a textbook, but fails to cite inside the text, which makes it quite difficult to attain the author’s evidence for her written claims.

To break down the potential efficacy of AIP, we first have to ask a few questions.

 

What is an Autoimmune Disease?

An autoimmune disease is where the body’s immune system starts tagging its own tissue as foreign; this is considered a loss of self-tolerance. This results from a dysregulation of both cell mediated and humoral immunity. Those with autoimmunity show lower regulatory T-cell concentrations, as well as antibodies toward their own tissues [3]. Hashimoto’s Thyroiditis is the most common autoimmune condition, and it is estimated that 4-9.5% of the US population has Hashimoto’s. Interestingly, around 18% of the those without previously known thyroid disease had elevated thyroid antibodies [4]. The National Institutes of Health (NIH) puts the prevalence of autoimmune diseases at around 24 million and includes 24 diseases, while the American Autoimmune Association puts it at upwards of 50 million and includes 80 to 100 diseases. Other more common autoimmune diseases are: Type I Diabetes, Rheumatoid Arthritis, Celiac Disease, Addison’s Disease, Grave’s Disease, Pernicious Anemia, Scleroderma, Sjögren’s Syndrome, Multiple Sclerosis, Crohn’s Disease, Systemic Lupus Erythematosus.

Currently, if you are diagnosed with one of these diseases in the conventional medical model, there is little they can do for you. The usual course of action is to wait, and then if things get bad, they will start to suppress the immune system, and if possible, replace whatever function was lost (thyroid hormone, insulin, B12, etc). Per NIH, this results in a price tag of about 100 billion dollars per year in the US.

Thus, it makes sense that autoimmune patients are searching for alternatives and an answer to the question the conventional model never seems to ask…WHY?

 

Why did the immune system go haywire?

There are definitely unavoidable underlying genetic and environmental factors, but the largest factor under our control in regards to autoimmunity seems to be intestinal permeability laid out in the seminal work by Dr. Alessio Fasano [5-11]. The GI tract houses around 80% of the human immune system in what is called Gut Associated Lymphoid Tissue (GALT), and the average human eats three to five tons of food a year. But, why is this border so important?

“The intestinal barrier covers a surface of about 400 m2 and requires approximately 40% of the body’s energy expenditure. It prevents against loss of water and electrolytes and entry of antigens and microorganisms into the body while allowing exchange of molecules between host and environment and absorption of nutrients in the diet. Specialized adaptations of the mammalian intestinal mucosa fulfill two seemingly opposing functions: firstly to allow a peaceful co-existence with intestinal symbionts without eliciting chronic inflammation, and secondly to provide a measured inflammatory and defensive response according to the threat from pathogens”

-Bischoff et al. 2014 [12]

Interestingly, gluten, alcohol, and the standard American diet can all result in intestinal permeability [12, 13]. Pathogenic micro-organisms and changes to the microbiome have also been implicated in the pathogenesis of intestinal permeability [14, 15], which brings into play the development of oral tolerance as an infant [16] and the effects of stress, exercise, sleep, sun exposure, and circadian rhythms on the microbiome and potentially intestinal barrier function [17-20].

To summarize this idea, we can look to a figure from immunologist Dr. Aristo Vojdani’s [21].

 

Thus, the conglomeration of GI symptoms, autoimmunity, intestinal permeability, and large dietary proteins crossing over into circulation potentially activating an already dysregulated immune system is not something to be taken lightly, and the research in this area is constantly being published on a multitude of fronts.

Zopf et al. [22] found that 15-20% of the population is believed to have food intolerances, and the gold standard in identifying these intolerances is the elimination provocation method.  Thus, the Autoimmune Paleo diet may be start, but it certainly isn’t the end, and this ideology is highlighted by most of the present-day authors who have supplanted Cordain’s early work in regards to the paleo diet [23].

 

BUT, can foods cause your immune system to target its own tissues?

The answer here is yes. Gluten is the most well-known protein to cause such an autoimmune reaction in those with Celiac disease [8] and gluten has also been implicated in the pathogenesis of Type 1 Diabetes [9]. Also, in a retrospective analysis, those with NCGS and Celiac Disease were more likely to develop Hashimoto’s (29%) and show up positive for anti-nuclear antibodies (ANA) [24]. Conversely, only 5.5% of those with Hashimoto’s were found to have anti-gliadin antibodies [25]. Yet, testing in serum for an immune reaction to gluten contains its own limitations as there are many different epitopes of gliadin that the human immune system can react to, and serum testing of IgG and IgA antibodies against food as a whole is likely more of a measure of a loss of oral tolerance, which would already be expected in those with autoimmunity.

We have far less or no peer-reviewed literature in regards to all the other foods that are eliminated in Autoimmune Paleo Protocol. However, 90% of all IgE mediated food allergies are to eggs, milk, wheat, peanuts, fish, shellfish, tree nuts, and soy beans, and milk proteins have been found to be molecularly quite similar to gliadin [26]. It is now standard of care to temporarily remove dairy in those diagnosed with Celiac Disease [27].

The positives of regulating the immune system in an autoimmune patient are potentially vast, and every step should be taken to identify all environmental and lifestyle inflammatory triggers and avoid them.

The negatives of a restrictive diet like AIP are social, as well as the potential to develop disordered eating patterns and a black and white viewpoint of foods. These negatives are not to be taken lightly and need to be discussed with the patient. If the patient elects to pursue this dietary protocol, they need to be educated on the why, and the goal should be to eventually get them to a diet that is as least restrictive as possible, which will be highly individualized based on the patient. Also, if symptoms do not remarkably improve in three to four weeks of adopting AIP, further testing in regards to the gastrointestinal system may be warranted as autoimmune diseases have been correlated with gastrointestinal infections[28, 29].

In summary, the mechanism exists, but there is still a lot of work to done. There are currently no cures for autoimmunity, but doing everything within the patient’s power to naturally regulate the immune system could theoretically help slow the progression of the disease. Whether this chance, is worth changing one’s entire relationship with food is up to each individual.

REFERENCES:

  1. Manheimer EW, van Zuuren EJ, Fedorowicz Z, Pijl H: Paleolithic nutrition for metabolic syndrome: systematic review and meta-analysis. Am J Clin Nutr 2015, 102(4):922-932.
  2. Palascha A, van Kleef E, van Trijp HC: How does thinking in Black and White terms relate to eating behavior and weight regain? Journal of health psychology 2015, 20(5):638-648.
  3. Paust S, Cantor H: Regulatory T cells and autoimmune disease. Immunol Rev 2005, 204:195-207.
  4. Zaletel K, Gaberscek S: Hashimoto’s Thyroiditis: From Genes to the Disease. Curr Genomics 2011, 12(8):576-588.
  5. Fasano A: The Gut is Not Like Las Vegas. In.; 2014.
  6. Fasano A: Zonulin, regulation of tight junctions, and autoimmune diseases. Ann N Y Acad Sci 2012, 1258:25-33.
  7. Fasano A, Not T, Wang W, Uzzau S, Berti I, Tommasini A, Goldblum SE: Zonulin, a newly discovered modulator of intestinal permeability, and its expression in coeliac disease. Lancet 2000, 355(9214):1518-1519.
  8. Hollon J, Puppa EL, Greenwald B, Goldberg E, Guerrerio A, Fasano A: Effect of gliadin on permeability of intestinal biopsy explants from celiac disease patients and patients with non-celiac gluten sensitivity. Nutrients 2015, 7(3):1565-1576.
  9. Visser J, Rozing J, Sapone A, Lammers K, Fasano A: Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms. Ann N Y Acad Sci 2009, 1165:195-205.
  10. Watts TL, Fasano A: Modulation of intestinal permeability: a novel and innovative approach for the oral delivery of drugs, macromolecules and antigens. Biotechnol Genet Eng Rev 2000, 17:433-453.
  11. Fasano A, Catassi C: Current approaches to diagnosis and treatment of celiac disease: an evolving spectrum. Gastroenterology 2001, 120(3):636-651.
  12. Bischoff SC, Barbara G, Buurman W, Ockhuizen T, Schulzke JD, Serino M, Tilg H, Watson A, Wells JM: Intestinal permeability–a new target for disease prevention and therapy. BMC Gastroenterol 2014, 14:189.
  13. Purohit V, Bode JC, Bode C, Brenner DA, Choudhry MA, Hamilton F, Kang YJ, Keshavarzian A, Rao R, Sartor RB et al: Alcohol, intestinal bacterial growth, intestinal permeability to endotoxin, and medical consequences: summary of a symposium. Alcohol 2008, 42(5):349-361.
  14. Konig J, Wells J, Cani PD, Garcia-Rodenas CL, MacDonald T, Mercenier A, Whyte J, Troost F, Brummer RJ: Human Intestinal Barrier Function in Health and Disease. Clin Transl Gastroenterol 2016, 7(10):e196.
  15. Kelly JR, Kennedy PJ, Cryan JF, Dinan TG, Clarke G, Hyland NP: Breaking down the barriers: the gut microbiome, intestinal permeability and stress-related psychiatric disorders. Front Cell Neurosci 2015, 9:392.
  16. Vojdani A: Oral tolerance and its relationship to food immunoreactivities. Alternative therapies in health and medicine 2015, 21 Suppl 1:23-32.
  17. Luna RA, Foster JA: Gut brain axis: diet microbiota interactions and implications for modulation of anxiety and depression. Curr Opin Biotechnol 2015, 32:35-41.
  18. Clark A, Mach N: Exercise-induced stress behavior, gut-microbiota-brain axis and diet: a systematic review for athletes. J Int Soc Sports Nutr 2016, 13:43.
  19. Cronin O, Molloy MG, Shanahan F: Exercise, fitness, and the gut. Curr Opin Gastroenterol 2016, 32(2):67-73.
  20. Rosselot AE, Hong CI, Moore SR: Rhythm and bugs: circadian clocks, gut microbiota, and enteric infections. Curr Opin Gastroenterol 2016, 32(1):7-11.
  21. Vojdani A: Molecular mimicry as a mechanism for food immune reactivities and autoimmunity. Alternative therapies in health and medicine 2015, 21 Suppl 1:34-45.
  22. Zopf Y, Baenkler HW, Silbermann A, Hahn EG, Raithel M: The differential diagnosis of food intolerance. Dtsch Arztebl Int 2009, 106(21):359-369; quiz 369-370; 354 p following 370.
  23. O’Keefe JH, Jr., Cordain L: Cardiovascular disease resulting from a diet and lifestyle at odds with our Paleolithic genome: how to become a 21st-century hunter-gatherer. Mayo Clinic proceedings 2004, 79(1):101-108.
  24. Carroccio A, D’Alcamo A, Cavataio F, Soresi M, Seidita A, Sciume C, Geraci G, Iacono G, Mansueto P: High Proportions of People With Nonceliac Wheat Sensitivity Have Autoimmune Disease or Antinuclear Antibodies. Gastroenterology 2015, 149(3):596-603 e591.
  25. Akcay MN, Akcay G: The presence of the antigliadin antibodies in autoimmune thyroid diseases. Hepatogastroenterology 2003, 50 Suppl 2:cclxxix-cclxxx.
  26. Vojdani A, Kharrazian D, Mukherjee PS: The prevalence of antibodies against wheat and milk proteins in blood donors and their contribution to neuroimmune reactivities. Nutrients 2014, 6(1):15-36.
  27. Celiac Disease – Treatment Overview [http://www.webmd.com/digestive-disorders/celiac-disease/celiac-disease-treatment-overview]
  28. Bassi V, Santinelli C, Iengo A, Romano C: Identification of a correlation between Helicobacter pylori infection and Graves’ disease. Helicobacter 2010, 15(6):558-562.
  29. Patil AD: Link between hypothyroidism and small intestinal bacterial overgrowth. Indian J Endocrinol Metab 2014, 18(3):307-309.

 

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