Dataset Information

Sugar-sweetened beverage, diet soda, and fatty liver disease in the Framingham Heart Study cohorts.

ABSTRACT:

Background & aims

Non-alcoholic fatty liver disease affects ∼30% of US adults, yet the role of sugar-sweetened beverages and diet soda on these diseases remains unknown. We examined the cross-sectional association between intake of sugar-sweetened beverages or diet soda and fatty liver disease in participants of the Framingham Offspring and Third Generation cohorts.

Methods

Fatty liver disease was defined using liver attenuation measurements generated from computed tomography in 2634 participants. Alanine transaminase concentration, a crude marker of fatty liver disease, was measured in 5908 participants. Sugar-sweetened beverage and diet soda intake were estimated using a food frequency questionnaire. Participants were categorized as either non-consumers or consumers (3 categories: 1 serving/month to <1 serving/week, 1 serving/week to <1 serving/day, and ⩾1 serving/day) of sugar-sweetened beverages or diet soda.

Results

After adjustment for age, sex, smoking status, Framingham cohort, energy intake, alcohol, dietary fiber, fat (% energy), protein (% energy), diet soda intake, and body mass index, the odds ratios of fatty liver disease were 1, 1.16 (0.88, 1.54), 1.32 (0.93, 1.86), and 1.61 (1.04, 2.49) across sugar-sweetened beverage consumption categories (p trend=0.04). Sugar-sweetened beverage consumption was also positively associated with alanine transaminase levels (p trend=0.007). We observed no significant association between diet soda intake and measures of fatty liver disease.

Conclusion

In conclusion, we observed that regular sugar-sweetened beverage consumption was associated with greater risk of fatty liver disease, particularly in overweight and obese individuals, whereas diet soda intake was not associated with measures of fatty liver disease.

SUBMITTER: Ma J

PROVIDER: S-EPMC4827616 | biostudies-literature | 2015 Aug

REPOSITORIES: biostudies-literature

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Publications

Sugar-sweetened beverage, diet soda, and fatty liver disease in the Framingham Heart Study cohorts.

Ma Jiantao J Fox Caroline S CS Jacques Paul F PF Speliotes Elizabeth K EK Hoffmann Udo U Smith Caren E CE Saltzman Edward E McKeown Nicola M NM

Journal of hepatology 20150605 2

<h4>Background & aims</h4>Non-alcoholic fatty liver disease affects ∼30% of US adults, yet the role of sugar-sweetened beverages and diet soda on these diseases remains unknown. We examined the cross-sectional association between intake of sugar-sweetened beverages or diet soda and fatty liver disease in participants of the Framingham Offspring and Third Generation cohorts.<h4>Methods</h4>Fatty liver disease was defined using liver attenuation measurements generated from computed tomography in 2 ...[more]

PMID: 26055949

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Project description:BackgroundThe consumption of sugar-sweetened beverages (SSBs), which has increased substantially during the last decades, has been associated with obesity and weight gain.ObjectiveCommon genetic susceptibility to obesity has been shown to modify the association between SSB intake and obesity risk in 3 prospective cohorts from the United States. We aimed to replicate these findings in 2 large Swedish cohorts.DesignData were available for 21,824 healthy participants from the Malmö Diet and Cancer study and 4902 healthy participants from the Gene-Lifestyle Interactions and Complex Traits Involved in Elevated Disease Risk Study. Self-reported SSB intake was categorized into 4 levels (seldom, low, medium, and high). Unweighted and weighted genetic risk scores (GRSs) were constructed based on 30 body mass index [(BMI) in kg/m(2)]-associated loci, and effect modification was assessed in linear regression equations by modeling the product and marginal effects of the GRS and SSB intake adjusted for age-, sex-, and cohort-specific covariates, with BMI as the outcome. In a secondary analysis, models were additionally adjusted for putative confounders (total energy intake, alcohol consumption, smoking status, and physical activity).ResultsIn an inverse variance-weighted fixed-effects meta-analysis, each SSB intake category increment was associated with a 0.18 higher BMI (SE = 0.02; P = 1.7 × 10(-20); n = 26,726). In the fully adjusted model, a nominal significant interaction between SSB intake category and the unweighted GRS was observed (P-interaction = 0.03). Comparing the participants within the top and bottom quartiles of the GRS to each increment in SSB intake was associated with 0.24 (SE = 0.04; P = 2.9 × 10(-8); n = 6766) and 0.15 (SE = 0.04; P = 1.3 × 10(-4); n = 6835) higher BMIs, respectively.ConclusionsThe interaction observed in the Swedish cohorts is similar in magnitude to the previous analysis in US cohorts and indicates that the relation of SSB intake and BMI is stronger in people genetically predisposed to obesity.

Project description:BackgroundCeramides have been implicated in the pathogenesis of type 2 diabetes and cardiovascular disease. Limited data exist on how habitual dietary intake of foods that can alter hepatic lipid metabolism may influence circulating ceramide concentrations.ObjectivesWe investigated the cross-sectional association of cumulative sugar-sweetened beverage (SSB) consumption with concentrations of 3 circulating ceramides and ceramide ratios.MethodsWe examined participants from the Framingham Heart Study's Offspring Cohort who had 3 ceramides measured (n = 1561, mean age 66 y, 59% women). SSB consumption was measured 4 times over ∼14 y. Participants were categorized by cumulative SSB intake as nonconsumers (0 to <1 SSB serving/mo) and occasional (1 SSB serving/mo to <1 serving/wk), frequent (1 SSB serving/wk to <1 serving/d), and daily (≥1 SSB serving/d) consumers. Multivariable linear regression models were used to relate cumulative SSB consumption (independent variable) to blood concentrations of ceramides (C16:0, C22:0, and C24:0) and ceramide ratios (C22:0/C16:0 and C24:0/C16:0).ResultsIn adjusted models, more frequent cumulative SSB consumption was positively associated with concentrations of the C16:0 and C22:0 ceramides (Ptrend < 0.05). Compared with nonconsumers, daily consumers had 0.01 μg/mL (95% CI: 0.002, 0.017 µg/mL) and 0.06 µg/mL (95% CI: 0.018, 0.092 µg/mL) higher mean concentrations of the C16:0 and C22:0 ceramides, respectively. Results were consistent when modeling continuous cumulative SSB consumption per 1 serving/d. We observed effect modification by diabetes status in the relation between cumulative SSB consumption and concentrations of the C24:0 ceramide (Pinteraction = 0.014). In a stratified analysis, more frequent cumulative SSB consumption was positively associated with concentrations of the C24:0 ceramide only in individuals with prediabetes or diabetes (Ptrend = 0.001).ConclusionsOur study raises the possibility that higher concentrations of distinct ceramide species, previously associated with adverse metabolic health, may be one mechanism by which SSB consumption contributes to higher risk of cardiometabolic diseases.

Dataset Information

Sugar-sweetened beverage, diet soda, and fatty liver disease in the Framingham Heart Study cohorts.

Background & aims

Methods

Results

Conclusion

Publications

Sugar-sweetened beverage, diet soda, and fatty liver disease in the Framingham Heart Study cohorts.

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