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Background and Aims The effects of low‐level alcohol consumption on fatty liver disease and the potential for effect modification by obesity is uncertain. We investigated associations among low‐level alcohol consumption, obesity status, and the development of incident hepatic steatosis (HS), either with or without an increase in noninvasive liver fibrosis score category (from low to intermediate or high category). Approach and Results A total of 190,048 adults without HS and a low probability of fibrosis with alcohol consumption less than 30 g/day (men) and less than 20 g/day (women) were followed for up to 15.7 years. Alcohol categories of no, light, and moderate consumption were defined as 0, 1‐9.9, and 10‐29.9 g/day (10‐19.9 g/day for women), respectively. HS was diagnosed by ultrasonography, and the probability of fibrosis was estimated using the fibrosis‐4 index (FIB‐4). Parametric proportional hazards models were used to estimate multivariable‐adjusted hazard ratios (HRs) and 95% confidence intervals (CIs). A total of 43,466 participants developed HS, 2,983 of whom developed HS with an increase in FIB‐4 index (to intermediate or high scores). Comparing light drinkers and moderate drinkers with nondrinkers, multivariable‐adjusted HRs (95% CI) for incident HS were 0.93 (0.90‐0.95) and 0.90 (0.87‐0.92), respectively. In contrast, comparing light drinkers and moderate drinkers with nondrinkers, multivariable‐adjusted HRs (95% CI) for developing HS plus intermediate/high FIB‐4 were 1.15 (1.04‐1.27) and 1.49 (1.33‐1.66), respectively. The association between alcohol consumption categories and incident HS plus intermediate/high FIB‐4 was observed in both nonobese and obese individuals, although the association was stronger in nonobese individuals (P for interaction by obesity = 0.017). Conclusions Light/moderate alcohol consumption has differential effects on the development of different stages of fatty liver disease, which is modified by the presence of obesity.

Objective— We examined the association of cardiovascular health (CVH) metrics with the development and progression of coronary artery calcium (CAC) among apparently healthy adults. Approach and Results— This cohort study included 65 494 men and women 30 years of age and older free of cardiovascular disease at baseline who underwent a comprehensive exam including CAC scoring. CVH metrics were defined according to the American Heart Association Life’s Simple 7 metrics based on smoking, diet, physical activity, body mass index, blood pressure, total cholesterol, and fasting glucose. CVH scores range from 0 (all metrics considered unhealthy) to 7 (all metrics considered healthy). Participants were followed-up for a maximum of 6.6 years. Compared with participants with ideal CVH scores 0–1, the multivariable-adjusted difference in the change in geometric means of CAC scores over 5 years of follow-up were −0.40 (−0.62 to −0.19), −0.83 (−1.03 to −0.63), −1.06 (−1.25 to −0.86), −1.22 (−1.42 to −1.03), and −1.05 (−1.42 to −0.69) in participants with ideal CVH scores 2, 3, 4, 5, and 6–7, respectively. The inverse association between CVH scores and progression of CAC was observed both in participants with no CAC and in those with CAC detectable at baseline. Conclusions— A higher ideal CVH metrics score was strongly associated with a lower prevalence of CAC and with lower progression of CAC in males and females in a large cohort of healthy adults. Our findings suggest that maintaining a healthy life habits could help reduce the development and progression of subclinical atherosclerosis and ultimately prevent clinically cardiovascular event.