Diet Induced Inflammation and Hypertension: High Fat Diet’s link to Disease
Introduction. Heart disease caused by hypertension remains the number one cause of death in the United States and predictions made by the American Heart Association project a continuing rise in the ‘Hypertensive Crisis5. So too does obesity seem to rise at a parallel rate as hypertension—does a link between diet, inflammation, and hypertension exist? Studies show mice consumption of High Fat Diets (HFD) increases inflammation through changes in gut bacteria like Firmicutes and change the gut flora similarly as humans 1,2,3. Antibiotics may be a useful prophylactic treatment of hypertension. A tricyclic antibiotic, minocycline, stunts inflammatory changes in gut flora.1 Understanding the impact of diet on inflammation is essential to developing national health advisory guidelines to minimize hypertension. Methods. In the mouse models fed both a HFD and LFD, fecal matter was assessed at days 7 and 21 for bacterial changes1. Function of vagal nerve and solitary and dorsal nuclei were assessed via IB4-tags. In another study, mice were fed for 4, 8, 12, and 16 weeks on a HFD or LFD with or without 10% fructose (LFD, LFD + F, HFD, and HFD + F) 2 .Caloric intake, fasting glucose, cholesterol levels, and blood pressure were measured. Oxidative stress was measured using quantitative murine IL-6 sandwich ELISA 1-4. Human patients undergoing elective coronary angiography were assessed for metabolites of inflammatory pathways (trimethylamine-N-oxide (TMA/TMAO) and short chain fatty acids (SCFA) pathways) 1,4. Gut microbiota was measured in these patients 1-4. Result. Mice fed a HFD, compared to LFD, had significantly higher levels of inflammatory gut bacteria and decreased nervous and nuclei activity1. Minocycline decreased inflammation and hypertension1. High ratio of inflammatory bacteria (Firmicutes/Bacteriodes) was noted1. Mice fed a HFD+F solution had a significantly higher fat index, total cholesterol, low-density lipoprotein, fasting glucose, blood pressure, and fat index than other groups1-3. Levels of oxidative stress were measured to be significantly higher than other groups 2,3. Humans undergoing elective coronary artery angiography showed higher levels of TMAO, increased macrophage foam cells, increased aortic plaques, and hypertension (down-regulation of Olfr 78 and GP41 of the SCFA)4. Conclusion. Studies show that a HFD, compared to a LFD, increase gut inflammatory bacteria like Firmicytes and Bacteriodes and increases in hypertension1,-4. Further evidence shows that antibiotics like minocycline can minimize changes in diet that lead to increases in inflammatory markers TNF-a and IL-6 implicated in hypertension1-4.
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(2) Della Vedova MC, Muñoz MD, Santillan LD, Plateo-Pignatari MG, Germanó MJ, Rinaldi Tosi ME, Garcia S, Gomez NN, Fornes MW, Gomez Mejiba SE, Ramirez DC. A Mouse Model of Diet-Induced Obesity Resembling Most Features of Human Metabolic Syndrome. Nutr Metab Insights. 2016;9:93-102. PubMed [citation] PMID: 27980421, PMCID: PMC5140012
(3) Tang WH, Kitai T, Hazen SL. Gut Microbiota in Cardiovascular Health and Disease. Circ Res. 2017 Mar 31;120(7):1183-1196. doi: 10.1161/CIRCRESAHA.117.309715. Review. PubMed [citation] PMID: 28360349, PMCID: PMC5390330
(4) Noble EE, Hsu TM, Kanoski SE. Gut to Brain Dysbiosis: Mechanisms Linking Western Diet Consumption, the Microbiome, and Cognitive Impairment. Front Behav Neurosci. 2017;11:9. doi: 10.3389/fnbeh.2017.00009. PubMed [citation] PMID: 28194099, PMCID: PMC5277010
(5) American Heart Association. Heart Disease and Stroke Statistics 2017 At-a-Glance. (2017) Accessed online: https://www.heart.org/idc/groups/ahamah-public/@wcm/@sop/@smd/documents/downloadable/ucm_491265.pdf