Ben Schöttker1, Kai-Uwe Saum2, Eugène H J M Jansen3, Bernd Holleczek4, Hermann Brenner5. 1. Division of Clinical Epidemiology and Aging Research, German Cancer Research Center, Heidelberg, Germany Network Aging Research, University of Heidelberg, Heidelberg, Germany. 2. Division of Clinical Epidemiology and Aging Research, German Cancer Research Center, Heidelberg, Germany. 3. Centre for Health Protection, National Institute for Public Health and the Environment, Bilthoven, The Netherlands. 4. Saarland Cancer Registry, Saarbrücken, Germany. 5. Division of Clinical Epidemiology and Aging Research, German Cancer Research Center, Heidelberg, Germany Network Aging Research, University of Heidelberg, Heidelberg, Germany Division of Preventive Oncology, German Cancer Research Center, Heidelberg, Germany.
Abstract
BACKGROUND: imbalances in metabolic, inflammatory and redox homeostasis play an important role in the leading theories of age-related morbidity, but no large-scale epidemiological study has been conducted so far assessing their associations with total morbidity and multi-morbidity in the same model. METHODS: analyses were conducted in 2,547 participants of an established population-based cohort study from Germany. The participants' median age was 70 years (range: 57-84) and 51.9% were women. End points were total somatic morbidity and multi-morbidity, assessed by the Cumulative Illness Rating Scale-Geriatric version. RESULTS: overall, 251 study participants had multi-morbidity (9.9%). Except for the redox marker 'total thiol levels of proteins', all other assessed metabolic (obesity, diabetes, dyslipidaemia and hypertension), inflammatory (C-reactive protein) and oxidative stress markers (derivatives of reactive oxygen metabolites) were significantly associated with total somatic morbidity and multi-morbidity if assessed individually. If modelled jointly, effect estimates were attenuated but remained statistically significant for the outcome 'total morbidity' and for low weight, obesity, insufficiently controlled diabetes and derivatives of reactive oxygen metabolites with respect to the outcome 'multi-morbidity'. CONCLUSIONS: results from this large sample of older adults support hypotheses that relate imbalances in metabolic, inflammatory and redox homeostasis to age-related morbidity. Despite over adjustment for closely related metabolic, inflammatory and oxidative stress conditions in the full model, independent associations of the markers with total morbidity and/or multi-morbidity were observed. Therefore, adverse metabolic, inflammatory and oxidative stress conditions may all play important roles in the pathogenesis of age-related morbidity, which should be investigated further in future longitudinal studies.
BACKGROUND: imbalances in metabolic, inflammatory and redox homeostasis play an important role in the leading theories of age-related morbidity, but no large-scale epidemiological study has been conducted so far assessing their associations with total morbidity and multi-morbidity in the same model. METHODS: analyses were conducted in 2,547 participants of an established population-based cohort study from Germany. The participants' median age was 70 years (range: 57-84) and 51.9% were women. End points were total somatic morbidity and multi-morbidity, assessed by the Cumulative Illness Rating Scale-Geriatric version. RESULTS: overall, 251 study participants had multi-morbidity (9.9%). Except for the redox marker 'total thiol levels of proteins', all other assessed metabolic (obesity, diabetes, dyslipidaemia and hypertension), inflammatory (C-reactive protein) and oxidative stress markers (derivatives of reactive oxygen metabolites) were significantly associated with total somatic morbidity and multi-morbidity if assessed individually. If modelled jointly, effect estimates were attenuated but remained statistically significant for the outcome 'total morbidity' and for low weight, obesity, insufficiently controlled diabetes and derivatives of reactive oxygen metabolites with respect to the outcome 'multi-morbidity'. CONCLUSIONS: results from this large sample of older adults support hypotheses that relate imbalances in metabolic, inflammatory and redox homeostasis to age-related morbidity. Despite over adjustment for closely related metabolic, inflammatory and oxidative stress conditions in the full model, independent associations of the markers with total morbidity and/or multi-morbidity were observed. Therefore, adverse metabolic, inflammatory and oxidative stress conditions may all play important roles in the pathogenesis of age-related morbidity, which should be investigated further in future longitudinal studies.
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