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We examined the association between parental and offspring <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> in the multigenerational Framingham Heart Study, which characterized <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> using computed tomography.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We performed multivariable logistic regression models adjusted for age, sex, alcohol use, and body mass index to generate the odds of <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> according to parental <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content>. We determined the proportion of participants with <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> according to parental <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> and the presence or absence of hypertension, diabetes, or obesity (<jats:styled-content style=\"fixed-case\">BMI<\/jats:styled-content> \u226530\u00a0kg\/m<jats:sup>2<\/jats:sup>). After excluding heavy alcohol use (n\u00a0=\u00a0126) and missing covariates (n\u00a0=\u00a01), 785 offspring with at least one parent were included.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Approximately 23% (183\/785) had at least one parent with <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> and 1.1% had two affected parents (9\/785). In adjusted models, participants with at least one parent with <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> had a nearly two\u2010fold increased odds of <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> compared to participants without a parental history of <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content> 1.86, 95% confidence interval 1.15\u20103.03). Among participants without hypertension, diabetes, or obesity, a higher proportion had <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> if they had a parental history of <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> compared to those without (16.1% vs 5.2%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.001). However, for participants with cardiometabolic risk factors, we did not observe a difference in <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> among those with and without parental <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> (30.3% vs 28.5%, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.78).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Individuals with a parental history of <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> are at increased risk for <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content>. Specifically, a parental history of <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> may be an important factor among those that are otherwise metabolically healthy.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.13956","type":"journal-article","created":{"date-parts":[[2018,9,4]],"date-time":"2018-09-04T14:34:19Z","timestamp":1536071659000},"page":"740-747","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["Parental non\u2010alcoholic fatty liver disease increases risk of non\u2010alcoholic fatty liver disease in offspring"],"prefix":"10.1111","volume":"39","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6131-3981","authenticated-orcid":false,"given":"Michelle T.","family":"Long","sequence":"first","affiliation":[{"name":"Section of Gastroenterology Boston Medical Center Boston University School of Medicine  Boston Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ellen 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