Naveed Saleh, MD, MS, for MDLinx | August 08, 2018
Maintaining a healthy diet is correlated with lower accumulation of fat in the liver and lower risk for developing hepatic steatosis, according to a recent analysis of the Framingham Heart Study published in Gastroenterology. Moreover, the benefits of healthy eating are compounded in patients genetically predisposed to nonalcoholic fatty liver disease (NAFLD).
“Lifestyle modification, primarily a weight loss diet, is recommended for treatment of NAFLD,” wrote authors led by Jiantao Ma, PhD, Population Sciences Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD. “Available evidence also suggests that a healthy eating pattern, such as a Mediterranean diet, may favorably affect NAFLD independent of weight loss.”
In previous population-based studies, researchers have used the Mediterranean-style diet score (MDS) and the Alternative Healthy Eating Index (AHEI) score as proxies for diet quality. Improvements in these measures were significantly linked to reduced weight gain, heart disease, and death. Nevertheless, whether a long-term correlation between diet quality and fatty liver exists has yet to be determined.
Dr. Ma and colleagues set out to prospectively assess whether improved diet—as indicated by MDS and AHEI scores—are linked to lower liver fat accumulation, as well as whether improved diet alters genetic risk for NAFLD.
The researchers analyzed data from the second- and third-generation cohorts of the Framingham Heart Study—comprising middle-aged to elderly adults—gathered from two consecutive examinations. In total, 1,521 subjects were included in the analysis, with 610 participants from the second-generation cohort and 911 participants from the third-generation cohort.
Participants took the semiquantitative 126-item Harvard food frequency questionnaire to describe their dietary patterns during the year before each examination. The team obtained liver-phantom ratio (LPR) values from computed tomography (CT) to assess fat accumulation in the liver. These CTs were administered at baseline between 2002 and 2005 and during follow-up between 2008 and 2011. Because LPR values are inversely related to liver fat values, a higher LPR value indicates less liver fat.
During the primary analysis, the investigators analyzed associations between changes in MDS and AHEI diet scores (ie, the primary exposures) and change in LPR (ie, the primary outcome). The team conducted a sensitivity analysis controlling for various covariates, including body mass index (BMI), bariatric surgery, heart attack, stroke, and cancer.
During the secondary analysis, the authors analyzed the relationship between changes in MDS and AHEI diet scores and NAFLD genetic risk scores. These genetic risk scores were based on multiple single-nucleotide polymorphisms picked up during NAFLD genome-wide association studies. The investigators stratified subjects into low, medium, and high genetic risk groups for NAFLD. Furthermore, as with the primary analysis, a sensitivity analysis was performed to adjust for the same covariates.
Dr. Ma and coauthors observed that better diet quality between the baseline and follow-up exams was significantly linked to lower accumulation of liver fat in participants. These associations held up following sensitivity analysis for confounding variables and remained statistically significant. Adjusting for BMI, however, lessened the association.
Increases in diet scores (reflecting better diet) were correlated with decreased risk of participants’ developing increasingly advanced fatty liver or disease accompanied by higher liver enzymes.
Finally, higher genetic risk scores were significantly associated with fatty liver in participants with worse diet (ie, lower MDS and AHEI scores), but this association was not observed in subjects with ameliorated or stable diet scores.
“Compared with participants whose diet quality declined most over time (ie, the lowest quartile of longitudinal dietary score change), those whose diet improved the most (ie, the highest quartile) had approximately 80% less liver fat accumulation from base line to follow-up,” the authors wrote.
The researchers suggested that the associations discovered in this study were driven by increased intake of fruits, vegetables, nuts, legumes, whole grains, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), as well as decreased intake of red meat and foods containing trans-fat. Additionally, they suggested that the direct effects of diet on liver fat accumulation could be because diet controls patterns of overall adiposity.
One potential limitation of this study was that, due to technological advances, the investigators used an 8-slice CT scanner at baseline but a 64-slice CT scanner during follow-up exams.
“In an analysis of participants in the Framingham Heart Study, increasing diet quality, determined based on MDS and AHEI scores, is associated with less liver fat accumulation and reduced risk for new-onset fatty liver,” the authors concluded. “An improved diet is particularly important for individuals with a high genetic risk for NAFLD.”
This research was supported by the National Heart, Lung and Blood Institute’s Framingham Heart Study. Genotyping services were provided by Affymetrix.