By Vijay Kumar MalesuReviewed by Susha Cheriyedath, M.Sc.Sep 16 2024
Research reveals that consuming more soft drinks significantly raises the likelihood of developing liver disease, with men at greater risk, underscoring the need for dietary changes in Mexico.
Study: Soft drink consumption and increased risk of nonalcoholic fatty liver disease: Results from the health workers cohort study. Image Credit: BlueRingMedia / Shutterstock
In a recent study published in the journal Annals of Hepatology, a group of researchers evaluated the association between soft drinks (SD) consumption and the risk of nonalcoholic fatty liver disease (NAFLD) in a cohort of Mexican adults, primarily consisting of employees of the Mexican Social Security Institute (IMSS) and their relatives.
Background
NAFLD is the most prevalent liver condition, affecting 20-30% of the global population, with obesity and metabolic disorders being significant risk factors. In Mexico, elevated liver enzymes such as aspartate aminotransferase (AST), aminotransferase (ALT), and gamma-glutamyl transferase (GGT) are commonly used to assess NAFLD risk. NAFLD encompasses a spectrum of liver diseases, from simple steatosis to nonalcoholic steatohepatitis (NASH) (Severe NAFLD with liver inflammation and damage), which can progress to serious conditions. Recently, the terminology for liver diseases has evolved, introducing the term Metabolic Associated Steatotic Liver Disease (MASLD), which focuses on metabolic risk factors, while NAFLD excludes significant alcohol consumption and secondary causes of hepatic steatosis. SD are a key source of added sugars, contributing to NAFLD development. Further research is needed to clarify the causal relationship between SD consumption and NAFLD, particularly in diverse populations with varying lifestyles and risk factors.
About the study
The Health Workers Cohort Study (HWCS) began in 2004-2006 and included Mexican Social Security Institute (IMSS) employees and their relatives. For this analysis, adults aged 20 or older with ALT/AST levels and energy intake between 500-6500 kcal/day were eligible. From 2010-2012, 1,627 participants responded to a follow-up, with 186 new participants added. By 2016-2018, 1,012 individuals attended, with 1,412 included in the final analysis based on complete data from at least two waves.
ALT and AST levels were measured after 8-14 hours of fasting. NAFLD was assessed using the hepatic steatosis index (HSI), calculated from ALT/AST ratios, body mass index (BMI), with adjustments for sex and type 2 diabetes. SD consumption was determined through a validated food frequency questionnaire (FFQ) and classified into three categories: less than one serving/week, 1 to less than 3.5 servings/week, and 3.5 or more servings/week. It's important to note that diet/zero-calorie soft drinks were excluded from the analysis. Covariates such as age, smoking, physical activity, health status, and alcohol consumption were also collected.
Statistical analysis used fixed effects regression models to assess associations between SD consumption and NAFLD, adjusting for confounding factors. Additionally, generalized estimating equations (GEE) models were used to analyze the association further, combining within- and between-subject variations for a more robust assessment. Sex-stratified analyses were conducted to explore metabolic differences. The study adhered to ethical guidelines, with informed consent from participants and approval from the IMSS Institutional Review Board.
Study results
The final analytic sample for males consisted of participants with a median age of 44.8 years. The median SD intake was 3.1 servings per week, with 28.0% of males consuming 1 to <3.5 servings per week and 47.4% consuming ≥3.5 servings per week. For females, the sample size had a median age of 46.6 years, with 31.1% consuming 1 to <3.5 servings per week and 26.5% consuming ≥3.5 servings per week.
Among males, fixed-effects linear regression analysis indicated that higher SD consumption was associated with increased ALT levels in the crude model (β = 11.1; 95% CI: 3.2, 18.9). This association remained statistically significant even after adjusting for potential confounders (β = 11.1; 95% CI: 2.9, 19.3 for model 2 and β = 10.6; 95% CI: 2.5, 18.8 for model 3). After adjustment, males also demonstrated an increased risk of NAFLD, based on HSI levels, when SD consumption increased from low to high (β = 2.8; 95% CI: 0.5, 5.0). Age was positively associated with ALT, AST, truncal fat, and glucose in model 2, and truncal fat was linked to higher AST levels, while glucose was associated with increased HSI scores in model 3.
For females, while SD consumption was linked to higher AST, ALT, and NAFLD (as measured by HSI) in the crude model, the results were not statistically significant after adjustment. For example, HSI levels increased when SD consumption rose from low to high (β = 0.9; 95% CI: -0.2, 1.9). Similar to males, age was positively associated with ALT, AST, truncal fat, and glucose in model 2. Additionally, truncal fat was linked to higher ALT and HSI levels, and glucose was associated with elevated HSI scores.
Results from fixed-effects logistic regression models showed increased odds of high HSI when SD consumption rose from the lowest to the highest category. For instance, the odds of NAFLD increased by 39% (OR = 1.39; 95% CI: 0.98, 2.39) when SD intake rose from <1 serving/week to ≥3.5 servings/week. The generalized estimating equations (GEE) model yielded similar results, indicating a 42% higher risk of NAFLD (OR = 1.42; 95% CI: 1.15, 1.74) for the highest SD consumption category compared to the lowest across both sexes.
Conclusions
To summarize, the study found that higher SD intake is linked to elevated AST and ALT levels in males and an increased risk of NAFLD, as indicated by the HSI, in both sexes. However, after adjusting for confounders, the association was statistically significant only in males, reflecting sex differences in metabolism. The association was stronger in men, reflecting sex differences in metabolism. The results suggest that reducing SD consumption could help lower the risk of NAFLD, particularly in males. Further research is needed to generalize these findings to broader populations and to assess the impact of recent updates in liver disease terminology on clinical outcomes.
Journal reference: Edgar Denova-Gutiérrez, Berenice Rivera-Paredez, Amado D. Quezada-Sánchez, et al. Soft drink consumption and increased risk of nonalcoholic fatty liver disease: Results from the health workers cohort study, Annals of Hepatology, (2024), DOI- https://doi.org/10.1016/j.aohep.2024.101566, https://www.sciencedirect.com/science/article/pii/S1665268124003491