Ultra-processed food consumption, plasma metabolite profile, and risk of all-cause and cause-specific mortality in a population-based cohort.

Metabolites Mortality NOVA classification Prospective cohort Ultra-processed food

Journal

Clinical nutrition (Edinburgh, Scotland)
ISSN: 1532-1983
Titre abrégé: Clin Nutr
Pays: England
ID NLM: 8309603

Informations de publication

Date de publication:
20 Oct 2024
Historique:
received: 24 07 2024
revised: 27 09 2024
accepted: 15 10 2024
medline: 30 10 2024
pubmed: 30 10 2024
entrez: 29 10 2024
Statut: aheadofprint

Résumé

Epidemiological evidence on ultra-processed food (UPF) and cause-specific mortality remains limited and mixed. Molecular mechanisms underlying UPF intake and mortality remain unexplored. This study aimed to evaluate the associations between UPF consumption, metabolic signatures, and all-cause, premature, and cause-specific mortality. This study included 27670 participants (mean age 58.1 years) from the Malmö Diet and Cancer (MDC) cohort study. Consumption of UPF was assessed using a food frequency questionnaire and a 7-day food diary. In a subset of the MDC (n = 879), the associations of UPF with 991 plasma metabolites were investigated. An elastic net regression model was used to establish the metabolic signature of UPF. Cox proportional hazards regression model was used to determine the association between UPF intake, metabolic signature, and mortality risk. During a median follow-up of 23.3 years, a total of 11333 participants died. UPF intake showed a nonlinear positive association with all-cause mortality, with more pronounced associations found in females (P Our results suggest that higher UPF intake is associated with increased risk of all-cause, premature, CVD, and respiratory disease mortality, with the association varying across sex for all-cause mortality. The plasma metabolic signature of UPF showed a positive association with all-cause mortality.

Sections du résumé

BACKGROUND & AIMS OBJECTIVE
Epidemiological evidence on ultra-processed food (UPF) and cause-specific mortality remains limited and mixed. Molecular mechanisms underlying UPF intake and mortality remain unexplored. This study aimed to evaluate the associations between UPF consumption, metabolic signatures, and all-cause, premature, and cause-specific mortality.
METHODS METHODS
This study included 27670 participants (mean age 58.1 years) from the Malmö Diet and Cancer (MDC) cohort study. Consumption of UPF was assessed using a food frequency questionnaire and a 7-day food diary. In a subset of the MDC (n = 879), the associations of UPF with 991 plasma metabolites were investigated. An elastic net regression model was used to establish the metabolic signature of UPF. Cox proportional hazards regression model was used to determine the association between UPF intake, metabolic signature, and mortality risk.
RESULTS RESULTS
During a median follow-up of 23.3 years, a total of 11333 participants died. UPF intake showed a nonlinear positive association with all-cause mortality, with more pronounced associations found in females (P
CONCLUSIONS CONCLUSIONS
Our results suggest that higher UPF intake is associated with increased risk of all-cause, premature, CVD, and respiratory disease mortality, with the association varying across sex for all-cause mortality. The plasma metabolic signature of UPF showed a positive association with all-cause mortality.

Identifiants

pubmed: 39471546
pii: S0261-5614(24)00380-7
doi: 10.1016/j.clnu.2024.10.023
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

184-193

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interest The authors declare no conflict of interest.

Auteurs

Yufeng Du (Y)

Department of Epidemiology and Statistics, School of Public Health, Lanzhou University, Lanzhou, Gansu, China; Nutritional Epidemiology, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden. Electronic address: yufeng.du@med.lu.se.

Shunming Zhang (S)

Nutritional Epidemiology, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden; School of Public Health, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.

Johanne Slørdal Schjølberg (JS)

Nutritional Epidemiology, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.

Deja Hadden (D)

Nutritional Epidemiology, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.

J Gustav Smith (JG)

Department of Cardiology, Clinical Sciences, Lund University and Skåne University Hospital, Lund, Sweden; Wallenberg Center for Molecular Medicine and Lund University Diabetes Center, Lund University, Lund, Sweden; Department of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University and Sahlgrenska University Hospital, Gothenburg, Sweden; Science for Life Laboratory, Gothenburg University, Gothenburg, Sweden.

Lu Qi (L)

Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA, USA; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.

Emily Sonestedt (E)

Nutritional Epidemiology, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden; Department of Food and Meal Science and the Research Environment MEAL, Faculty of Natural Science, Kristianstad University, Kristianstad, Sweden.

Yan Borné (Y)

Nutritional Epidemiology, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden. Electronic address: yan.borne@med.lu.se.

Classifications MeSH