Sugar-sweetened beverages, low/no-calorie beverages, fruit juice and non-alcoholic fatty liver disease defined by fatty liver index: the SWEET project.


Journal

Nutrition & diabetes
ISSN: 2044-4052
Titre abrégé: Nutr Diabetes
Pays: England
ID NLM: 101566341

Informations de publication

Date de publication:
21 04 2023
Historique:
received: 18 08 2022
accepted: 06 04 2023
revised: 30 03 2023
medline: 25 4 2023
pubmed: 22 4 2023
entrez: 21 04 2023
Statut: epublish

Résumé

Sweetened beverage intake may play a role in non-alcoholic fatty liver disease (NAFLD) development, but scientific evidence on their role is limited. This study examined associations between sugar-sweetened beverages (SSB), low/no-calorie beverages (LNCB) and fruit juice (FJ) intakes and NAFLD in four European studies. Data for 42,024 participants of Lifelines Cohort, NQPlus, PREDIMED-Plus and Alpha Omega Cohort were cross-sectionally analysed. NAFLD was assessed using Fatty Liver Index (FLI) (≥60). Restricted cubic spline analyses were used to visualize dose-response associations in Lifelines Cohort. Cox proportional hazard regression analyses with robust variance were performed for associations in individual cohorts; data were pooled using random effects meta-analysis. Models were adjusted for demographic, lifestyle, and other dietary factors. Each additional serving of SSB per day was associated with a 7% higher FLI-defined NAFLD prevalence (95%CI 1.03-1.11). For LNCB, restricted cubic spline analysis showed a nonlinear association with FLI-defined NAFLD, with the association getting stronger when consuming ≤1 serving/day and levelling off at higher intake levels. Pooled Cox analysis showed that intake of >2 LNCB servings/week was positively associated with FLI-defined NAFLD (PR 1.38, 95% CI 1.15-1.61; reference: non-consumers). An inverse association was observed for FJ intake of ≤2 servings/week (PR 0.92, 95% CI: 0.88-0.97; reference: non-consumers), but not at higher intake levels. Theoretical replacement of SSB with FJ showed no significant association with FLI-defined NAFLD prevalence (PR 0.97, 95% CI 0.95-1.00), whereas an adverse association was observed when SSB was replaced with LNCB (PR 1.12, 95% CI 1.03-1.21). Pooling results of this study showed that SSB and LNCB were positively associated with FLI-defined NAFLD prevalence. Theoretical replacement of SSB with LNCB was associated with higher FLI-defined NAFLD prevalence. An inverse association was observed between moderate intake of FJ and FLI-defined NAFLD. Our results should be interpreted with caution as reverse causality cannot be ruled out.

Sections du résumé

BACKGROUND
Sweetened beverage intake may play a role in non-alcoholic fatty liver disease (NAFLD) development, but scientific evidence on their role is limited. This study examined associations between sugar-sweetened beverages (SSB), low/no-calorie beverages (LNCB) and fruit juice (FJ) intakes and NAFLD in four European studies.
METHODS
Data for 42,024 participants of Lifelines Cohort, NQPlus, PREDIMED-Plus and Alpha Omega Cohort were cross-sectionally analysed. NAFLD was assessed using Fatty Liver Index (FLI) (≥60). Restricted cubic spline analyses were used to visualize dose-response associations in Lifelines Cohort. Cox proportional hazard regression analyses with robust variance were performed for associations in individual cohorts; data were pooled using random effects meta-analysis. Models were adjusted for demographic, lifestyle, and other dietary factors.
RESULTS
Each additional serving of SSB per day was associated with a 7% higher FLI-defined NAFLD prevalence (95%CI 1.03-1.11). For LNCB, restricted cubic spline analysis showed a nonlinear association with FLI-defined NAFLD, with the association getting stronger when consuming ≤1 serving/day and levelling off at higher intake levels. Pooled Cox analysis showed that intake of >2 LNCB servings/week was positively associated with FLI-defined NAFLD (PR 1.38, 95% CI 1.15-1.61; reference: non-consumers). An inverse association was observed for FJ intake of ≤2 servings/week (PR 0.92, 95% CI: 0.88-0.97; reference: non-consumers), but not at higher intake levels. Theoretical replacement of SSB with FJ showed no significant association with FLI-defined NAFLD prevalence (PR 0.97, 95% CI 0.95-1.00), whereas an adverse association was observed when SSB was replaced with LNCB (PR 1.12, 95% CI 1.03-1.21).
CONCLUSIONS
Pooling results of this study showed that SSB and LNCB were positively associated with FLI-defined NAFLD prevalence. Theoretical replacement of SSB with LNCB was associated with higher FLI-defined NAFLD prevalence. An inverse association was observed between moderate intake of FJ and FLI-defined NAFLD. Our results should be interpreted with caution as reverse causality cannot be ruled out.

Identifiants

pubmed: 37085478
doi: 10.1038/s41387-023-00237-3
pii: 10.1038/s41387-023-00237-3
pmc: PMC10121594
doi:

Types de publication

Meta-Analysis Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

6

Subventions

Organisme : European Commission (EC)
ID : 774293
Organisme : European Commission (EC)
ID : 774293
Organisme : European Commission (EC)
ID : 774293
Organisme : European Commission (EC)
ID : 774293
Organisme : European Commission (EC)
ID : 774293
Organisme : European Commission (EC)
ID : 774293
Organisme : European Commission (EC)
ID : 774293
Organisme : European Commission (EC)
ID : 774293
Organisme : European Commission (EC)
ID : 774293
Organisme : European Commission (EC)
ID : 774293
Organisme : European Commission (EC)
ID : 774293
Organisme : European Commission (EC)
ID : 774293

Informations de copyright

© 2023. The Author(s).

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Auteurs

Novita D Naomi (ND)

Division of Human Nutrition and Health, Wageningen University and Research, Wageningen, the Netherlands.

Joy Ngo (J)

Nutrition Research Foundation, Barcelona Science Park, Barcelona, Spain.

Elske M Brouwer-Brolsma (EM)

Division of Human Nutrition and Health, Wageningen University and Research, Wageningen, the Netherlands.

Marion E C Buso (MEC)

Division of Human Nutrition and Health, Wageningen University and Research, Wageningen, the Netherlands.

Sabita S Soedamah-Muthu (SS)

Center of Research on Psychological Disorders and Somatic Diseases (CORPS) Department of Medical and Clinical Psychology, Tilburg University, Tilburg, the Netherlands.
Institute for Food, Nutrition and Health, University of Reading, Berkshire, UK.

Carmen Pérez-Rodrigo (C)

Nutrition Research Foundation, Barcelona Science Park, Barcelona, Spain.

Joanne A Harrold (JA)

Department of Psychology, University of Liverpool, Liverpool, UK.

Jason C G Halford (JCG)

Department of Psychology, University of Liverpool, Liverpool, UK.
School of Psychology, University of Leeds, Leeds, UK.

Anne Raben (A)

Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
Clinical Research, Copenhagen University Hospital - Steno Diabetes Center Copenhagen, Herlev, Denmark.

Johanna M Geleijnse (JM)

Division of Human Nutrition and Health, Wageningen University and Research, Wageningen, the Netherlands.

Lluis Serra-Majem (L)

Research Institute of Biomedical and Health Sciences (IUIBS), University of Las Palmas de Gran Canaria, Preventive Medicine Service, Centro Hospitalario Universitario Insular Materno Infantil (CHUIMI), Canarian Health Service, Las Palmas, Spain.
Centro de Investigación Biomédica en Red Fisiopatologia de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, Madrid, Spain.

Edith J M Feskens (EJM)

Division of Human Nutrition and Health, Wageningen University and Research, Wageningen, the Netherlands. edith.feskens@wur.nl.

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