Lots of things appear to increase intestinal permeability. I think a focus the gluten component of grains alone, without also considering the effect of grain prebiotics (like inulin and oligosaccharides) in improving microbiota and reducing intestinal permeability, is misleading.
For example, high saturated fat meals, high fructose diets, and alcohol all appear to increase intestinal permeability to endotoxins from gram-negative gut bacteria, in both human and animal studies. Given the close association of endotoxemia with chronic inflammation, oxidative stress and disease risk, these sorts of studies should be a core concern for students of longevity.
For SFAs and intestinal permeability, see:
Erridge, C., Attina, T., Spickett, C. M., & Webb, D. J. (2007). A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation. The American journal of clinical nutrition, 86(5), 1286-1292.
Ma, X., Hua, J., Mohamood, A. R., Hamad, A. R. A., Ravi, R., & Li, Z. (2007). A high‐fat diet and regulatory T cells influence susceptibility to endotoxin‐induced liver injury. Hepatology, 46(5), 1519-1529.
Ghoshal, S., Witta, J., Zhong, J., De Villiers, W., & Eckhardt, E. (2009). Chylomicrons promote intestinal absorption of lipopolysaccharides. Journal of lipid research, 50(1), 90-97.
Ghanim, H., Abuaysheh, S., Sia, C. L., Korzeniewski, K., Chaudhuri, A., Fernandez-Real, J. M., & Dandona, P. (2009). Increase in plasma endotoxin concentrations and the expression of toll-like receptors and suppressor of cytokine signaling-3 in mononuclear cells after a high-fat, high-carbohydrate meal implications for insulin resistance. Diabetes care, 32(12), 2281-2287.
Suzuki, T., & Hara, H. (2010). Dietary fat and bile juice, but not obesity, are responsible for the increase in small intestinal permeability induced through the suppression of tight junction protein expression in LETO and OLETF rats. Nutr Metab (Lond), 7(1), 19.
Rabot, S., Membrez, M., Bruneau, A., Gérard, P., Harach, T., Moser, M., ... & Chou, C. J. (2010). Germ-free C57BL/6J mice are resistant to high-fat-diet-induced insulin resistance and have altered cholesterol metabolism. The FASEB Journal, 24(12), 4948-4959.
Erridge, C. (2011). Diet, commensals and the intestine as sources of pathogen-associated molecular patterns in atherosclerosis, type 2 diabetes and non-alcoholic fatty liver disease. Atherosclerosis, 216(1), 1-6.
Laugerette, F., Vors, C., Géloën, A., Chauvin, M. A., Soulage, C., Lambert-Porcheron, S., ... & Michalski, M. C. (2011). Emulsified lipids increase endotoxemia: possible role in early postprandial low-grade inflammation. The Journal of nutritional biochemistry, 22(1), 53-59.
Pendyala, S., Walker, J. M., & Holt, P. R. (2012). A high-fat diet is associated with endotoxemia that originates from the gut. Gastroenterology, 142(5), 1100-1101.
Kim, K. A., Gu, W., Lee, I. A., Joh, E. H., & Kim, D. H. (2012). High fat diet-induced gut microbiota exacerbates inflammation and obesity in mice via the TLR4 signaling pathway. PLoS One, 7(10), e47713.
Harte, A. L., Varma, M. C., Tripathi, G., McGee, K. C., Al-Daghri, N. M., Al-Attas, O. S., ... & McTernan, P. G. (2012). High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects.Diabetes care, 35(2), 375-382.
Shrestha, U. K. (2012). High-fat diet is associated with endotoxemia and low-grade inflammation. Nepal Journal of Medical Sciences, 1(2), 62-63.
Laugerette, F., Furet, J. P., Debard, C., Daira, P., Loizon, E., Géloën, A., ... & Michalski, M. C. (2012). Oil composition of high-fat diet affects metabolic inflammation differently in connection with endotoxin receptors in mice.American Journal of Physiology-Endocrinology and Metabolism, 302(3), E374-E386.
Mani, V., Hollis, J. H., & Gabler, N. K. (2013). Dietary oil composition differentially modulates intestinal endotoxin transport and postprandial endotoxemia. Nutr Metab, 10(6).
Ghosh, S. S., Bie, J., Wang, J., & Ghosh, S. (2014). Oral supplementation with non-absorbable antibiotics or curcumin attenuates western diet-induced atherosclerosis and glucose intolerance in LDLR−/− mice–role of intestinal permeability and macrophage activation. PloS one, 9(9), e108577.
For high-fructose diets and intestinal permeability, see:
Bergheim, I., Weber, S., Vos, M., Krämer, S., Volynets, V., Kaserouni, S., ... & Bischoff, S. C. (2008). Antibiotics protect against fructose-induced hepatic lipid accumulation in mice: role of endotoxin. Journal of hepatology, 48(6), 983-992.
Thuy, S., Ladurner, R., Volynets, V., Wagner, S., Strahl, S., Königsrainer, A., ... & Bergheim, I. (2008). Nonalcoholic fatty liver disease in humans is associated with increased plasma endotoxin and plasminogen activator inhibitor 1 concentrations and with fructose intake. The Journal of Nutrition, 138(8), 1452-1455.
Spruss, A., Kanuri, G., Wagnerberger, S., Haub, S., Bischoff, S. C., & Bergheim, I. (2009). Toll‐like receptor 4 is involved in the development of fructose‐induced hepatic steatosis in mice. Hepatology, 50(4), 1094-1104.
Spruss, A., & Bergheim, I. (2009). Dietary fructose and intestinal barrier: potential risk factor in the pathogenesis of nonalcoholic fatty liver disease. The Journal of nutritional biochemistry, 20(9), 657-662.
Volynets, V., Spruss, A., Kanuri, G., Wagnerberger, S., Bischoff, S. C., & Bergheim, I. (2010). Protective effect of bile acids on the onset of fructose-induced hepatic steatosis in mice. Journal of lipid research, 51(12), 3414-3424.
Spruss, A., Kanuri, G., Stahl, C., Bischoff, S. C., & Bergheim, I. (2012). Metformin protects against the development of fructose-induced steatosis in mice: role of the intestinal barrier function. Laboratory Investigation, 92(7), 1020-1032.
Kavanagh, K., Wylie, A. T., Tucker, K. L., Hamp, T. J., Gharaibeh, R. Z., Fodor, A. A., & Cullen, J. M. (2013). Dietary fructose induces endotoxemia and hepatic injury in calorically controlled primates. The American journal of clinical nutrition, 98(2), 349-357.
For alcohol, see:
Bode, C., & Bode, J. C. (2005). Activation of the innate immune system and alcoholic liver disease: effects of ethanol per se or enhanced intestinal translocation of bacterial toxins induced by ethanol?. Alcoholism: Clinical and Experimental Research, 29(s2), 166S-171S.
Supplementation with the prebiotics inulin and oligofructose, selective feeds for beneficial bifidobacteria, appears to displace pathogenic strains in the gut, reduce intestinal permeability to endotoxins, or both.
Cani, P. D., Neyrinck, A. M., Fava, F., Knauf, C., Burcelin, R. G., Tuohy, K. M., ... & Delzenne, N. M. (2007). Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia. Diabetologia, 50(11), 2374-2383.
Cani, P. D., Bibiloni, R., Knauf, C., Waget, A., Neyrinck, A. M., Delzenne, N. M., & Burcelin, R. (2008). Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet–induced obesity and diabetes in mice. Diabetes, 57(6), 1470-1481.
Neyrinck, A. M., Van Hee, V. F., Piront, N., De Backer, F., Toussaint, O., Cani, P. D., & Delzenne, N. M. (2012). Wheat-derived arabinoxylan oligosaccharides with prebiotic effect increase satietogenic gut peptides and reduce metabolic endotoxemia in diet-induced obese mice. Nutrition & diabetes, 2(1), e28.
Dehghan, P., Gargari, B. P., Jafar-Abadi, M. A., & Aliasgharzadeh, A. (2013). Inulin controls inflammation and metabolic endotoxemia in women with type 2 diabetes mellitus: a randomized-controlled clinical trial. International journal of food sciences and nutrition, 65(1), 117-123.
Where do we get inulin and oligofructose in our diet? 25% comes from onions (and other Allium), and 70% comes from wheat.
Moshfegh, A. J., Friday, J. E., Goldman, J. P., & Ahuja, J. K. C. (1999). Presence of inulin and oligofructose in the diets of Americans. The Journal of nutrition, 129(7), 1407S-1411s.
All of the prebiotics that beneficially alter the gut microbiota (inulin, oligofructose, galacto-oligosaccharides and lactulose) are in the now maligned FODMAPS category. I fear that a premature demonization of FODMAPs, as with gluten, will worsen gut microbiota, intestinal permeability, and disease risk in the media susceptible.
Edited by Darryl, 23 October 2014 - 07:33 PM.