Dr. Jess Reed is Professor of Animal Nutrition at the University of Wisconsin-Madison. He received a PhD from Cornell in 1983. His 33 years of research has focused on the effects of phytochemicals in foods and forages on human and animal health and nutrition, including 6 years at the International Livestock Center for Africa where he studied the phyochemistry of tropical legume forages.
Starting in 1996, he began researching the effects of flavonoids in foods on human health, including cardiovascular disease, urinary tract infections and cancer. Reed has over 100 research publications in his field and a successful research program funded through competitive grants from NIH and USDA along with collaborative projects with the food and nutritional supplements industry. Dr. Reed also maintains an active outreach program in agricultural development with project experience in 20 countries.
Berry Tannins and Gut Health
Jess D. Reed, University of Wisconsin-Madison
Consumption of berries and other foods that contain tannins is associated with decreased risk of disease.  Tannins are oligomeric polyphenolic compounds that form multiple hydrogen bonds with proteins resulting in decreased protein activity, solubility and digestibility. Therefore, tannin-protein interactions modulate bioactivity of both molecules. Absorption of tannins from the gastrointestinal tract is low. Greater than 95% of tannins consumed are excreted in feces in complexes with proteins and polysaccharides from food or endogenous origins.
Research on the effects of tannins on protein digestion and metabolism indicates that tannins lower digestion and increase fecal excretion of protein.  However, in vitro and cell culture experiments indicate that tannins are bioactive in disease processes such as inflammation, microbial adherence and oxidation. Therefore, the health benefits of berry tannins may be a function of interactions in the gut and not a function of post absorptive effects.
The role of the gastrointestinal tract in health and disease is generally underappreciated although the gut is as important as the liver in metabolism. Enterohepatic circulation is central to absorption, excretion and metabolism of nutrients, drugs and polyphenols. The gut associated lymphoid tissue (GALT) is the largest immune tissue in the body and 50% of the body’s immunity originates in the gut.  GALT is also the largest compartment of the mucosal immune system and affects mucosal immunity in the lungs, urogenital tract, and mammary glands. GALT dysfunction is associated with chronic inflammatory diseases such as inflammatory bowl disease, Crohn’s disease as well as food allergies and colon cancer.
The gut is constantly exposed to microbial and food antigens but, under normal conditions, GALT response is characterized by B cell populations that home to mucosal tissues and produce secretory immunoglobulin A (sIgA).  Normal GALT continuously responds to luminal contents in this fashion without inducing a systemic response or local inflammation while protecting other mucosal surfaces from infection. The interaction between the GALT and systemic inflammatory processes that are associated with cancer and atherosclerosis is poorly understood. However, acute models of GALT dysfunction indicate that GALT plays a central role in modulating immune responses that lead to mortality and morbidity.[6-8]
In vitro and cell culture experiments indicate that tannins are bioactive in disease processes such as inflammation, microbial adherence and oxidation. Disease processes such as inflammation, microbial adherence and oxidation are mediated in the gut by protein interactions with gut epithelium and GALT. Activation of GALT cells may lead to a pro-inflammatory or anti-inflammatory immune response.  Gut macrophage and dendritic cells in the lamina propria and Peyer’s patches (PP) are the inductive cells of gut immunity.
The anti-adherence properties of tannins  may provide protection from enteric pathogens such as E. coli, Salmonella, Listeria, Heilicobacter pylor [11, 12], and peridontal pathogens. [13-15] The anti-oxidant propterties of tannins may prevent lipid oxidation in the gut, reducing oxidized lipoproteins in serum which are a causative factor in atherosclerosis and cardiovascular disease. [16-18] Therefore, the health benefits of berry tannins may be a function of gut level interactions with proteins and polysaccharides from the gut microbiota, endogenous secretions and food, and not a function of post absorptive effects.
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2. Reed, J.D., Nutritional Toxicology of Tannins and Related Polyphenols in Forage Legumes. Journal of animal science, 1995. 73(5): p. 1516-1528.
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11. Burger, O., et al., A high molecular mass constituent of cranberry juice inhibits Helicobacter pylori adhesion to human gastric mucus. Fems Immunology and Medical Microbiology, 2000. 29(4): p. 295-301.
12. Shmuely, H., et al., Effect of cranberry juice on eradication of Helicobacter pylori in patients treated with antibiotics and a proton pump inhibitor. Molecular Nutrition & Food Research, 2007. 51(6): p. 746-751.
13. Bodet, C., et al., Inhibition of periodontopathogen-derived proteolytic enzymes by a high-molecular-weight fraction isolated from cranberry. J Antimicrob Chemother, 2006.
14. Steinberg, D., et al., Effect of a high-molecular-weight component of cranberry on constituents of dental biofilm. Journal of Antimicrobial Chemotherapy, 2004. 54(1): p. 86-89.
15. Steinberg, D., et al., Cranberry high molecular weight constituents promote Streptococcus sobrinus desorption from artificial biofilm. International Journal of Antimicrobial Agents, 2005. 25(3): p. 247-251.
16. Staprans, I., et al., The role of dietary oxidized cholesterol and oxidized fatty acids in the development of atherosclerosis. Molecular Nutrition & Food Research, 2005. 49(11): p. 1075-1082.
17. McKay, D.L. and J.B. Blumberg, Cranberries (Vaccinium macrocarpon) and cardiovascular disease risk factors. Nutrition Reviews, 2007. 65(11): p. 490-502.
18. Reed, J., Cranberry flavonoids, atherosclerosis and cardiovascular health. Crit Rev Food Sci Nutr, 2002. 42(3 Suppl): p. 301-16.