Non-alcoholic fatty liver disease and cardiovascular disease: assessing the evidence for causality
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Key result
Mendelian randomization studies of NAFLD susceptibility genes suggest that plasma lipids are an important mediator between non-alcoholic fatty liver disease and cardiovascular disease risk.
Why the study?
Although epidemiological studies show NAFLD is associated with CVD, it remains unknown whether NAFLD is an active contributor or an innocent bystander.
Design
Review
Authors
Discussion
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Implication
May guide anti-NAFLD therapies toward lipid effects; leaves open impact on cardiovascular outcomes.
PICO
P
Population
Non-alcoholic fatty liver disease and cardiovascular disease
E
Exposure / Comparator
Non-alcoholic fatty liver disease (NAFLD)
Genetic evidence suggests that plasma lipids are the primary mediators of the causal relationship between NAFLD and cardiovascular disease, highlighting the need for anti-NAFLD drugs to favorably affect lipid metabolism.
Limitations
- Risk of horizontal pleiotropy in Mendelian randomization studies since there is no gene that specifically encodes NAFLD
- Statistical power limitations requiring large cohorts due to small effect sizes of common gene variants
- Risk of pleiotropy in Mendelian randomization studies
- Statistical power limitations requiring large cohorts
Cite This Study
Brouwers et al. (2019) conducted a review in Non-alcoholic fatty liver disease and cardiovascular disease. Non-alcoholic fatty liver disease (NAFLD) was evaluated. Mendelian randomization studies of NAFLD susceptibility genes suggest that plasma lipids are an important mediator between non-alcoholic fatty liver disease and cardiovascular disease risk.
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