Last week I threw down a challenge. Following on from the ruffling of many feathers regarding Jason Hawrelak’s report that dietary saturated fat increases uptake of endotoxins from the gut, I provided his reference list in support of this claim, effectively saying, “if you don’t like his findings, then make your own informed conclusions but make sure you read all the evidence first”. I offered a prize to everyone who made an attempt and a year’s free subscription to Update in Under 30, to the person who produced arguably the best summary.
I’ve said it before and I will say it again, and again, and again: Our professional community abounds with extraordinary individuals.
People’s response to this challenge proved that once again.
A huge congratulations 🙂 to everyone putting in the hard yards. Here are some key points from their reviews:
Consider the confounding issue of emulsifiers says Helen Bevilaqua, “The cream used in the study had Polysorbate 80 and Carrageenan in as food additives…( not mentioned in the study protocol….!!!). Poysorbate 80 is an emulsifier and surfactant and has been shown to induce low grade inflammation as reported in Nature by Benoit Chassaing of Georgia State University. https://www.nature.com/nature/j
While Silvia Pinca makes the very sensible point, “it is dangerous to draw conclusions for a general habitual diet. The meals tested were often unbalanced, with excessive fats and usually no carbohydrates (including no fibers) and no proteins. Trials with more balanced diets should be performed in order to reach conclusions on a recommended diet suitable for patients at risk of metabolic syndrome.”
And finally…to our ‘winner’ (please note everyone who contributed is a ‘winner’ as far as I’m concerned) Sarah Poulton, well this is what she comprehensively summised…check it out:
Endotoxin or lipopolysaccharide (LPS) is a cell wall component of gram-negative bacteria capable of triggering the release of inflammatory mediators, and promoting intestinal permeability.(1,2) A number of small-scale human studies have investigated the effects of saturated fat intake on LPS levels. The majority of available evidence pertains to post-prandial alterations to plasma LPS observed following a single meal with a high saturated fatty-acid (HSFA) content.(3,4)
Increased post-prandial plasma LPS has been observed following consumption of a HSFA meal in human subjects.(3,4) Endotoxic effects have also been noted from intake of a combined HSFA/high-carbohydrate meal, which induced increased plasma LPS concentration and inflammatory marker expression.(5) Furthermore, saturated fat intake has been compared to smoking for LPS alteration, with higher plasma LPS resulting from a single HSFA meal than smoking 3 cigarettes. Observations of this study are understandably limited to the endotoxin specific alterations following a single ingestion/exposure, and not indicative of the greater health effects of saturated fat consumption vs cigarette smoking.(6) The metabolic endotoxemia correlated with HSFA intake, may contribute to postprandial inflammation, endothelial activation, gastrointestinal barrier dysfunction, altered microbiota composition, and the development of atherosclerotic markers.(1,6,7,8)
Other dietary fats have been explored for their effects on LPS and inflammatory markers. Postprandial LPS decreased following consumption of a meal high in omega-3 polyunsaturated fatty acids (PUFA).(3)The available evidence infers that consumption of saturated fats should be limited, and omega-3 PUFA intake encouraged for minimisation of LPS release, inflammatory marker expression and regulation of gut microbiota.(9) Further studies are required to investigate the long term effects of repeated dietary consumption of low-moderate saturated fat intake on LPS levels, considering most studies to date explore HSFA intake after consumption of a single meal.
- Pendyala S, Walker JM, Holt PR. A high-fat diet is associated with endotoxemia that originates from the gut. Gastroenterology 2012;142(5):1100-1 e2.
- Deopurkar R, Ghanim H, Friedman J, Abuaysheh S, Sia CL, Mohanty P, et al. Differential effects of cream, glucose, and orange juice on inflammation, endotoxin, and the expression of Toll-like receptor-4 and suppressor of cytokine signaling-3. Diabetes Care 2010;33(5):991-7.
- Lyte JM, Gabler NK, Hollis JH. Postprandial serum endotoxin in healthy humans is modulated by dietary fat in a randomized, controlled, cross-over study. Lipids Health Dis 2016;15(1):186.
- Laugerette F, Vors C, Geloen A, Chauvin MA, Soulage C, Lambert-Porcheron S, et al. Emulsified lipids increase endotoxemia: possible role in early postprandial low-grade inflammation. J Nutr Biochem 2011;22(1):53-9.
- Ghanim H, Abuaysheh S, Sia CL, Korzeniewski K, Chaudhuri A, Fernandez-Real JM, et al. 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 2009;32(12):2281-7.
- Erridge C, Attina T, Spickett CM, Webb DJ. A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation. Am J Clin Nutr 2007;86(5):1286-92.
- Cani PD, Delzenne NM. The role of the gut microbiota in energy metabolism and metabolic disease. Curr Pharm Des 2009;15(13):1546-58.
- Lopez-Moreno J, Garcia-Carpintero S, Jimenez-Lucena R, Haro C, Rangel-Zuniga OA, Blanco-Rojo R, et al. Effect of Dietary Lipids on Endotoxemia Influences Postprandial Inflammatory Response. J Agric Food Chem 2017;65(35):7756-63.
- Candido FG, Valente FX, Grzeskowiak LM, Moreira APB, Rocha D, Alfenas RCG. Impact of dietary fat on gut microbiota and low-grade systemic inflammation: mechanisms and clinical implications on obesity. Int J Food Sci Nutr 2017:1-19.
Well done Sarah Poulton for going above and beyond, for reading all the articles and for providing us all with a stellar summary – we will be in contact today to organise your year’s free UU30 subscription!! 🙂