dietary lectins
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2021 ◽  
Vol 135 ◽  
pp. 27-35
Author(s):  
Jaime Daniel Babot ◽  
Eloy Argañaraz-Martínez ◽  
María Quiroga ◽  
Sonia María Grande ◽  
María Cristina Apella ◽  
...  

Author(s):  
Jonathan M. Rhodes

The health benefits of fruit, vegetables and dietary fibre have been promoted for many years. Much of the supporting evidence is circumstantial or even contradictory and mechanisms underlying health benefits of specific foods are poorly understood. Colorectal cancer shows marked geographical differences in incidence, probably linked with diet, and explanations for this require knowledge of the complex interactions between diet, microbiota and the gut epithelium. Dietary fibres can act as prebiotics, encouraging growth of saccharolytic bacteria, but other mechanisms are also important. Some but not all soluble fibres have a ‘contrabiotic’ effect inhibiting bacterial adherence to the epithelium. This is particularly a property of pectins (galacturonans) whereas dietary fructans, previously regarded as beneficial prebiotics, can have a proinflammatory effect mediated via toxic effects of high butyrate concentrations. This also suggests that ulcerative colitis could in part result from potentially toxic faecal butyrate concentrations in the presence of a damaged mucus layer. Epithelial adherence of lectins, either dietary lectins as found in legumes, or bacterial lectins such as the galactose-binding lectin expressed by colon cancer-associated Fusobacterium nucleatum, may also be important and could be inhibitable by specific dietary glycans. Conversely, emulsifiers in processed foods may increase bacterial translocation and alter the microbiota thus promoting inflammation or cancer. Focusing on one condition is of limited value although in developing public health messages and growing evidence for impacts of dietary components on all-cause mortality is gaining more attention. We are only just starting to understand the complex interactions between food, the microbiota and health.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Steven R Gundry

All autoimmune diseases are highly associated with increased rates of coronary artery and vascular disease secondary to immune cell attack on epithelial cells. The causes of autoimmune disease (AID) seem to be multifactorial. However, the idea that derangement of the microbiome, breaches of the intestinal barrier (leaky gut) and introduction into the human diet of plant defense molecules such as lectins, which are capable of molecular mimicry, prompted our group to investigate the application of a lectin limited diet, coupled with probiotics and prebiotics (The Pant Paradox Protocol) to impact biomarker proven autoimmune disease activity in humans and their impact on endothelial biomarkers of inflammation. One hundred and two consecutive patients with immunoassay markers of autoimmune disease activity, i.e., RF, anti-CCP, ANA, Histone, etc, and signs and symptoms of RA, Lupus, Sjogrens, Crohns, Colitis, Scleroderma, Mixed Connective Tissue Disease, and biomarkers of endothelial inflammation, were enrolled into a program of elimination of major dietary lectins, consisting of all grains and pseudo grains, beans and legumes, peanuts, cashews, nightshades, squashes, and Casein A1 milk products (The Plant Paradox Program), supplemented with probiotics and prebiotics including resistant starches and polyphenol supplements. All pts initially low Vit D levels and low Omega 3 index and adiponectin levels above 16mg/dl. Biomarkers of inflammation, hs-CRP, TNF-alpha, IL-6, fibrinogen, myeloperoxidase and autoimmune markers were measured every 3 months. 95/102 patients achieved complete resolution of autoimmune markers and inflammatory markers within 9 months. The other 7/102 patients all had reduced markers, but incomplete resolution. 80/102 patients were weaned from all immunosuppressive and/or biologic medications without rebound. We conclude that a lectin limited diet, supplemented with pro and prebiotics, and polyphenols are capable of curing or putting into remission most autoimmune diseases.


2017 ◽  
Vol 5 (6) ◽  
pp. 212-222 ◽  
Author(s):  
Isaac W. Ofosu ◽  
William O. Ellis ◽  
Kwabena Nsiah ◽  
Ibok N. Oduro
Keyword(s):  

2014 ◽  
Vol 146 (5) ◽  
pp. S-90
Author(s):  
Luca Toti ◽  
Gregory M. Holmes ◽  
R. Alberto

Glycobiology ◽  
2010 ◽  
Vol 21 (4) ◽  
pp. 521-529 ◽  
Author(s):  
Manmohan Bajaj ◽  
Ashwini Hinge ◽  
Lalita S Limaye ◽  
Rajesh Kumar Gupta ◽  
Avadhesha Surolia ◽  
...  

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