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High-quality diet, physical activity, and college education are associated with low risk of NAFLD among the US population
  June 2022
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Background and Aims

The effects of diet quality (DQ), physical activity (PA), and socioeconomic status (SES) on the risk of NAFLD are unclear. We examined the association among DQ, PA, SES, and NAFLD risk.
Approach and Results
This is a cross-sectional analysis of the National Health and Nutrition Examination Surveys, 2017-2018, which included 3589 participants with reliable information on vibration-controlled transient elastography (VCTE) measurements, 24-h dietary recalls, PA, and SES. DQ was assessed by the Healthy Eating Index (HEI)-2015. PA was determined by the Global Physical Activity Questionnaire. SES was assessed by the educational attainment and family poverty income ratio (PIR). Risk of NAFLD was considered by means of a composite outcome using VCTE measurements: non-NAFLD versus NAFLD without clinically significant fibrosis (CSF) versus NAFLD with CSF.
The NAFLD risk was lower in physically active (≥600 metabolic equivalent of task [MET] min/week) versus inactive participants (<600 MET min/week) (OR: 0.71, p = 0.043). A high-quality diet (HQD) (HEI > 56.64) was associated with a lower risk of NAFLD (OR: 0.58, p < 0.01) compared with a non-HQD.
The lowest NAFLD risk was observed in those physically active with HQD (OR: 0.43, p < 0.01). Body mass index and waist circumference significantly mediated the effect of DQ and PA on NAFLD risk.
Education (college or above) (OR: 0.65, p = 0.034), but not PIR, was associated with a reduced NAFLD risk. HQD and increased PA partially mediated the effect of education on NAFLD risk. The total effect of education on NAFLD risk mediated by DQ was 29% and by PA was 8%.
HQD, increased physical activity, and college education were associated with lower NAFLD risk in the US population.
In this nationally representative sample of US adults, we found that those who met PA recommendations or had the healthier diet were at reduced risk of NAFLD than those who did not. We identified an inverse and dose-dependent effect of DQ on NAFLD risk; higher HEI scores were associated with lower risks of NAFLD. Of note, HQD was linked with a 42% reduction in risk of NAFLD. We also noted that levels of PA of ≥ 600 MET min/week were associated with a 29% lower risk of NAFLD. Among adults physically active, those with PA levels of ≥ 8000 MET min/week displayed a 37% reduction in NAFLD risk. Among those physically active with a HQD, the risk of NAFLD was significantly reduced up to 57%. The benefits of a HQD along with increased PA extended to all racial/ethnic groups and both sexes. These results underscore the concept that improvements in DQ along with increased PA could significantly decrease the risk of NAFLD as compared with each lifestyle intervention separately.
Definition and assessment of hepatic steatosis and clinically significant fibrosis
In this study, we selected those controlled attenuation parameter (CAP) and liver stiffness measurement (LSM) cutoffs that have been developed and validated in the US population for detecting individuals with hepatic steatosis or clinically significant fibrosis (CSF; stages of fibrosis ≥2).[22] An optimal CAP cutoff of ≥285 dB/m (sensitivity of 80% and specificity of 77%) is indicative of hepatic steatosis, whereas an optimal LSM cutoff of ≥8.6 kPa (sensitivity of 66% and specificity of 80%) is suggestive of CSF.
A composite categorical (ordered) outcome, including (1) non-NAFLD (CAP < 285 dB/m) versus (2) NAFLD (CAP ≥ 285 dB/m) without CSF (LSM < 8.6 kPa) versus (3) NAFLD (CAP ≥ 285 dB/m) with CSF (LSM ≥ 8.6 kPa) was considered our primary outcome of interest. Two further composite secondary ordinal outcomes using LSM cutoffs at 90% sensitivity (≥5.6 kPa) and 90% specificity (≥6.5 kPa) for excluding or diagnosing CSF, respectively, were defined as follows: LSM ≥ 5.6 kPa: (1) non-NAFLD (CAP <2 85 dB/m) versus (2) NAFLD (CAP ≥ 285 dB/m) without CSF (LSM < 5.6 kPa) versus (3) NAFLD (CAP ≥ 285 dB/m) with CSF (LSM ≥ 5.6 kPa); and LSM ≥ 6.5 kPa: (1) non-NAFLD (CAP < 285 dB/m) versus (2) NAFLD (CAP ≥ 285 dB/m) without CSF (LSM < 6.5 kPa) versus (3) NAFLD (CAP ≥ 285 dB/m) with CSF (LSM ≥ 6.5 kPa).
Dietary assessment and HEI-2015 calculation
Dietary intakes used in these analyses were obtained using data from the two 24-h dietary recalls.[23] We used the latest iteration of the HEI (2015), which was created to assess alignment with the 2015-2020 US DGA, and to examine relationships between DQ and health-related outcomes.[4] It consists of 13 components that are scored based on energy-adjusted food and nutrient intakes. Of the 13 components, nine assess dietary adequacy (total fruits, whole fruits, total vegetables, greens and beans, whole grains, dairy, total protein foods, and fatty acids) and four assess moderation (refined grains, sodium, added sugar, and saturated fats).[11] For the adequacy components, higher scores are associated with higher levels of intake, whereas for the moderation components, higher scores are linked to lower levels of consumption. Seven components are each scored on a 0 to 10 scale, and the six other components are each scored on a 0 to 5 scale. The HEI components are summed to obtain the total score with a maximum of 100 points; higher scores indicate better DQ and therefore closer compliance with 2015-2020 DGA recommendations. Further information is provided in the Appendix.
PA assessment
Information on PA in NHANES has been self-reported by participants using the Global Physical Activity Questionnaire (GPAQ). It is a validated instrument for PA surveillance.[24] To explore dose-response effects of PA on risk of NAFLD, we created the following categories of total PA: <600, 600-7999, and ≥8000 metabolic equivalent of task (MET) min/week, based on previously published data.[25] We further classified PA into two levels: active (≥600 MET min/week) and inactive (<600 MET min/week). PA levels of ≥600 MET min/week have been consistently associated with substantial health benefits.[15] A more detailed description about the GPAQ and how the PA was calculated is stated in the Appendix.

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