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Atherosclerosis is a major pathology for cardiovascular diseases (CVDs). Clinically, the intermittent fasting (IF) has been observed to reduce the risk of CVDs. However, the effect of IF on the development of atherosclerosis has not been fully elucidated. Herein, we determined the protection of IF against high-fat diet–induced atherosclerosis in pro-atherogenic low-density lipoprotein receptor deficient (LDLR-/-) mice and the potentially involved mechanisms. The LDLR-/- mice were scheduled intermittent fasting cycles of 3-day HFD feeding ad libitum and 1 day fasting, while the mice in the control group were continuously fed HFD. The treatment was lasted for 7 weeks (∼12 cycles) or 14 weeks (∼24 cycles). Associated with the reduced total HFD intake, IF substantially reduced lesions in the en face aorta and aortic root sinus. It also increased plaque stability by increasing the smooth muscle cell (SMC)/collagen content and fibrotic cap thickness while reducing macrophage accumulation and necrotic core areas. Mechanistically, IF reduced serum total and LDL cholesterol levels by inhibiting cholesterol synthesis in the liver. Meanwhile, HFD-induced hepatic lipid accumulation was attenuated by IF. Interestingly, circulating Ly6Chigh monocytes but not T cells and serum c-c motif chemokine ligand 2 levels were significantly reduced by IF. Functionally, adhesion of monocytes to the aortic endothelium was decreased by IF via inhibiting VCAM-1 and ICAM-1 expression. Taken together, our study indicates that IF reduces atherosclerosis in LDLR-/- mice by reducing monocyte chemoattraction/adhesion and ameliorating hypercholesterolemia and suggests its potential application for atherosclerosis treatment.

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Background: Family history may inform individuals that they are at risk of gastric cancer (GC). However, it is too extensive to conduct intensive screening strategies for all individuals with family history of GC instead of average-risk screening. To establish more precise prevention strategies, accurate risk estimates are necessary for individuals with family history of GC. Methods: We searched PubMed, EMBASE and Cochrane for all relevant studies from their inception to May 21, 2020, for cohort and case-control studies investigating the association between family history of GC and its risk. Relative risk (RR) and 95% confidence interval (CI) were pooled from studies using random-effects or fixed effects. Results: The RR of GC was 2.08 (95% CI=1.86-2.34) in individuals with family history of GC according to twenty-nine case-control studies and 1.83 (95%CI=1.67-2.01) from six cohort studies. The increased risk was higher in individuals with sibling history of GC than those with parental history of GC (RR=3.18, 95% CI=2.12-4.79 vs. RR=1.66, 95% CI=1.46-1.89, P=0.021). For individuals with 2 or more first-degree relatives (FDRs) with GC, the RR was 2.81(95% CI=1.89-3.99). Subjects with both family history and Helicobacter pylori (H. pylori) infection confer a higher risk of GC (RR = 4.03, 95%CI=2.46-6.59). Conclusion: The RR of GC among FDRs is lower than in previous studies. However, the risk of GC is markedly increased in individuals having a sibling with GC, more than 2 FDRs with GC. Intensified screening and eradication therapy for H. pylori could be considered for these individuals.

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