Multimorbidity is highly prevalent and a major driver of premature mortality(1–5). While healthy lifestyle behaviours are known to reduce mortality risk in the general population(6,7), it remains unclear to what extent individuals with multimorbidity benefit from sustained lifestyle improvements. We aimed to evaluate the association between lifestyle and mortality risk in people with multimorbidity, and whether it varied across the specific multimorbidity patterns. This prospective study included 475,706 UK Biobank participants. A lifestyle score(8) according to nine risk factors (smoking, alcohol, physical activity, sleep, TV viewing, fruit and vegetable intake, oily fish, red meat, processed meat) was established and categorised as healthy and unhealthy lifestyle. Specific multimorbidity patterns were defined as metabolic (≥2 of diabetes, stroke, heart disease), cardio-renal (≥2 of diabetes, stroke, heart disease, kidney disease), and overall (≥2 of 43 conditions) multimorbidity(9). All-cause mortality was ascertained from death registries and hospital records. Cox proportional hazards models, with interaction terms, assessed associations between lifestyle and the outcome across multimorbidity types. Participants with missing covariates or implausible values of lifestyle risk factors were excluded. Models were adjusted for age, sex, ethnicity, deprivation, and BMI. All participants provided written informed consent(10). Among participants, 44.5% reported an unhealthy lifestyle, and 1.9%, 1.7% and 32.8% had cardiovascular, cardio-renal and overall multimorbidity, respectively. Compared with those without multimorbidity, hazard ratios (HRs) for all-cause mortality were 4.63 (95% CI, 4.30-4.98) for metabolic multimorbidity and 4.84 (95% CI,4.51-5.20) for cardio-renal multimorbidity. Compared with people without diseases and with healthy lifestyle, participants with cardio-renal multimorbidity and an unhealthy lifestyle had a markedly elevated risk of HR 6.65 (95% CI, 6.10–7.25) for all-cause mortality. Significant multiplicative and additive interactions between lifestyle and multimorbidity were observed for all-cause mortality in overall multimorbidity. Lifestyle behaviours substantially modify the mortality risk among people with multimorbidity. The greatest benefit is observed in cardio-renal multimorbidity. Targeted, cluster-specific lifestyle interventions could markedly reduce premature mortality and support precision prevention strategies in people with high multimorbidity burden.
Qi Zhang, B. Jani, Frederick K. Ho et al.· Proceedings of the Nutrition...· 0 citations
Abstract INTRODUCTION The associations of modifiable daily lifestyle variables (e.g., smoking, diet, alcohol intake, sedentary behavior, and physical activity) with structural brain atrophy, and interaction with apolipoprotein E (APOE) ε4 genetic risk, remain unclear. METHODS Among 3265 UK Biobank participants with repeated magnetic resonance imaging (MRI) data (mean follow‐up 2.6 years), we assessed the relations between lifestyle, APOE ε4 genotype, and volumetric changes in 15 structural brain phenotypes, using linear regression. RESULTS APOE ε4 presence showed greater atrophy by 25.1 mm3 in the left hippocampus (β: −0.115 standard deviations, 95% confidence interval [CI] [−0.192, −0.039] and 187.7 mm3 in frontal pole gray matter (β: −0.112, 95% CI [–0.186, −0.039]) (q < 0.05). Unfavorable lifestyle accelerated left hippocampal atrophy, and smoking increased white matter hyperintensity volumes (q > 0.05). No interactions were observed. DISCUSSION Our study reinforces the independent effect of APOE ε4 on longitudinal brain atrophy. Lifestyle may help preserve structural brain health, and our findings provide no evidence this varies by APOE ε4 genotype.
Yating You, Laura M. Lyall, Frederick K. Ho et al.· Alzheimer's & Dementia· 0 citations
Dementia is a major public health challenge, and Apolipoprotein E (APOE) ε4 is strongly associated with all-cause dementia, particularly Alzheimer's disease (AD). We aim to quantify the overall contribution of modifiable lifestyle, adiposity, socioeconomic status (SES), and health conditions occurring before dementia, to the association between ε4 genotype and the development of all-cause dementia, with AD examined as a major subtype. A population cohort study of 181,006 white UK Biobank participants aged ≥ 55 years at baseline was conducted, to examine the associations between APOE ε4 and all-cause dementia, and specifically AD, including modification and mediation role of lifestyle factors, adiposity, SES, and health conditions occurring before dementia. All risk factors, except for high alcohol intake, low diet quality, and phenotypic obesity, were associated with higher risk of all-cause dementia. The interaction contributions of lifestyle, adiposity, SES, and health conditions occurring before dementia varied by sex and dementia type. Low educational attainment had the strongest interaction effects with the association of APOE ε4 carriers and AD/all-cause dementia (up to 32.1%). In women, high deprivation level, abnormal sleep duration, anxiety, and depression showed interaction effects with APOE genotype (5-11.6%) as well. Phenotypic adiposity was associated with an increased risk of dementia among APOE ε4 non-carriers, but with a reduced risk among APOE ε4 carriers. Educational attainment explained a meaningful proportion of the APOE ε4 association with dementia. The strength of the association between APOE ε4 and dementia differed by risk factors and sex.
Mengrong Zhang, Frederick K. Ho, Jill P. Pell et al.· GeroScience· 0 citations
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