Healthy lifestyles and survival beyond age 100: Evidence from a national cohort of Chinese centenarians.

Introduction: Parkinson’s disease (PD) is the second most common neurodegenerative disease with largely unknown etiology. Evaluating the association between a healthy lifestyle with PD and genetic risk is necessary. Methods: The study included 438,241 participants from the UK Biobank, with lifestyle information collected via baseline questionnaires. Polygenic risk scores (PRS) were divided into quartiles. The healthy lifestyle, including alcohol consumption, body mass index, physical activity, sleep duration, sedentary time, social connections, and diet, was categorized into favorable (scoring 6–7), intermediate (scoring 4–5), and unfavorable (scoring ≤3) lifestyles. Results: During an average follow-up of 9.34 years, 2,996 cases were diagnosed with PD. Compared to participants with an unfavorable lifestyle, those with a favorable lifestyle had a significantly lower risk (hazard ratio [HR] 0.862, 95% CI: 0.753–0.986), whereas those with an intermediate lifestyle had no difference in PD risk. Regular physical activity, adequate sleep, and appropriate social connection were protective factors for the risk of PD (HR 0.839, 95% CI: 0.779–0.905; HR 0.921, 95% CI: 0.851–0.997; HR 0.790, 95% CI: 0.698–0.893). Subgroup analysis by PRS showed that adhering to a healthy lifestyle reduced the risk of PD in all subgroups except the low genetic risk (HR 0.673, 95% CI: 0.510–0.889; HR 0.774, 95% CI: 0.611–0.982; HR 0.769, 95% CI: 0.633–0.935). There was an interaction between high genetic risk and lifestyle scores and sleep duration (p = 0.015 and p = 0.024, respectively) and also between sex and sedentary time (p = 0.002). Conclusion: A healthy lifestyle was associated with a lower risk of PD, and it is important to identify the effect of genetic risk and sex on PD significantly influenced by lifestyle.

Association Between SES and Healthy Lifestyle With Depressive Symptoms in Older Adults: Evidence From 5 Prospective Cohort Studies.

Background: Many genetic variants have been associated with increased risk of breast cancer. In contrast, an overall healthy lifestyle has been associated with a reduced risk. However, the degree to which an overall healthy lifestyle may attenuate the impact of genetic variants on risk of breast cancer remains equivocal. In this study, we examined the association of a healthy lifestyle index (HLI) with risk of breast cancer by genetic risk groups. Methods: The study included 106,814 postmenopausal women of white descent aged 40 to 70 years who were enrolled in the UK Biobank cohort between 2006 and 2010. The HLI was based on a combination of diet, physical activity, smoking, alcohol consumption and anthropometry (ranging from 0 to 20, with the higher scores representing more favorable lifestyle). A polygenic risk score (categorized as low, intermediate and high) was generated as the sum of risk alleles weighted by the logOR of 117 breast cancer associated single nucleotide polymorphisms. A total of 1,949 incident invasive breast cancer cases were ascertained after a median follow-up of 5.7 years. Cox proportional hazards regression models were used to estimate the hazard ratios (HR) and 95% confidence intervals (CI) for the association of a healthy lifestyle risk score with risk of breast cancer by genetic risk groups. Results: Compared to women with an unfavorable lifestyle (lowest quartile), women with a favorable lifestyle (highest quartile) had a 32% reduced risk of invasive breast cancer (HR: 0.68: 0.59, 0.79). Women with high genetic risk (highest tertile) had an 86% increased risk of invasive breast cancer (1.86: 1.66, 2.08) compared to those with low genetic risk (lowest tertile). Compared with women who had an unfavorable lifestyle, a favorable lifestyle did not significantly reduce risk of invasive breast cancer among women with low genetic risk (0.80: 0.63-1.02), while women with a favorable lifestyle had 32% and 43% reduced risk of invasive breast cancer in the intermediate and high genetic risk categories, respectively (0.68: 0.53, 0.86 and 0.57; 0.44, 0.74, respectively). However, interaction between the genetic score and the lifestyle score did not achieve statistical significance (pinteraction=0.162). Conclusion: This study suggests that an overall healthy lifestyle may attenuate the impact of genetics on risk of breast cancer, particularly among women with intermediate and high genetic risk. Citation Format: Rhonda S. Arthur, Tao Wang, Thomas Rohan. The interplay between lifestyle-related factors and genetics with risk of invasive breast cancer among postmenopausal women from the UK Biobank [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 963.

Lower socioeconomic status (SES) is a risk factor for poor cognitive function, while a healthy lifestyle is associated with better cognitive function. We examined the complex relationship between SES and a healthy lifestyle and cognitive function among older Chinese adults. We used a national prospective cohort of the Chinese Longitudinal Healthy Longevity Survey (CLHLS) from 2008-18, aged 65 years and older with normal cognition at baseline. Participants were categorised into the favourable group if they had four to six healthy lifestyle factors and the unfavourable group for zero to three factors. SES was classified as higher and lower by assessing the socioeconomic vulnerability index (SEVI) with six components. Cognitive function was measured using the Mini-Mental State Examination (MMSE) scores and the standardised Z-scores. We applied the linear mixed effects and time-dependent Cox regression models to explore associations and further stratified the analysis by healthy lifestyles. A total of 6851 participants were included (the mean age was 80.87, 43.44% had a favourable lifestyle, and 49.29% had higher SES). Over the 10-year follow-up period, SES status and lifestyle profiles significantly affected the decline in the standardised Z-scores (P < 0.05). The higher SES group with favourable lifestyles exhibited a slower cognitive decline than those with lower SES (by 0.031 points per year, P < 0.05). The association was not observed in those in the unfavourable group (0.010 points per year, P > 0.05). During a follow-up, 25.06% of participants developed cognitive impairment (MMSE<18). We also observed a significant interaction between SES and healthy lifestyles (P < 0.05), with the corresponding associations of SES being more pronounced among participants with unfavourable lifestyles (hazard ratio (HR) = 0.821; 95% confidence interval (CI) = 0.701-0.960) than those with favourable lifestyles (HR = 1.006; 95% CI = 0.844-1.200). A healthy lifestyle may attenuate the adverse impacts of lower SES on cognitive function among older adults. This study might provide important information for protecting cognitive function, especially in low- and middle-income countries.

It remains unclear whether the benefits of adhering to a healthy lifestyle outweigh the effects of high genetic risk on cognitive decline. We examined the association of combined lifestyle factors and genetic risk with changes in cognitive function and six specific dimensions of cognition among older adults from the Chinese Longitudinal Healthy Longevity Survey (1998–2018, n = 18,811, a subset of 6301 participants with genetic information). Compared to participants with an unfavorable lifestyle, those with a favorable lifestyle showed a 46.81% slower rate of cognitive decline, with similar results across most cognitive domains. High genetic risk was associated with a 12.5% faster rate of cognitive decline. Individuals with a high genetic risk and a favorable lifestyle have slower cognitive decline than those with a low genetic risk and an unfavorable lifestyle. These data suggest that the benefits of a favorable lifestyle outweigh genetic factors, and therefore that adhering to a favorable lifestyle may offset the genetic risk for accelerated cognitive decline.

BackgroundAlthough studies have demonstrated that both lifestyles and subjective well-being (SWB) are associated with mortality risk, the joint effects of a healthy lifestyle and SWB on the risk of mortality are unclear. This study aimed to explore the combined impact of lifestyles and SWB on total mortality among the older Chinese population.MethodsData were obtained from the Chinese Longitudinal Healthy Longevity Survey conducted from 2002 to 2018. A total of 13,282 participants aged ≥ 65 years were included. SWB was measured by an eight-item tool covering life satisfaction, optimism, conscientiousness, anxiety, loneliness, personal control, feeling useless, and happiness. A total healthy lifestyle score was calculated by summing across five lifestyle factors (smoking, drinking, exercise, dietary diversity and body mass index), ranging from 0 to 5, and was categorized into the following groups: healthy (4–5 points), intermediate (2–3 points) and unhealthy (0–1 point). Cox proportional regression analyses were carried out adjusting for demographic characteristics and other potential confounders.ResultsIn total, 8549 (64.4%) deaths were reported during the follow-up period. Compared with the higher healthy lifestyle score, the hazard ratios (HRs) for all-cause mortality for the intermediate and unhealthy lifestyle scores were 1.11 (1.04–1.17) and 1.17 (1.09–1.26), respectively, independent of SWB. A similar relationship between SWB and total mortality was observed, independent of lifestyle factors. The participants who had worse SWB experienced a 1.19 (1.14–1.25) higher risk of total mortality in comparison with those who had better SWB after adjusting for lifestyles. Combinations of unhealthy lifestyle scores and poor SWB were associated with an increased risk of total mortality, and the highest risk was found among participants with a healthy lifestyle score of 0–1 and worse SWB (HR = 1.41, 95% CI = 1.28–1.55).ConclusionsA stronger risk of total mortality was found when worse SWB and unhealthy lifestyle occurred together, suggesting that a comprehensive approach to healthy lifestyle and SWB might be a potential strategy to improve longevity.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12877-025-06345-2.

To evaluate modifiable lifestyle-genetic susceptibility interactions with the risk of developing radiographic axial spondyloarthritis (r-axSpA). This study included 382,035 individuals without r-axSpA at baseline in the UK Biobank. A combined lifestyle score consisting of 6 factors and a polygenic risk score (PRS) using r-axSpA-associated genetic loci was constructed for each participant. Participants were further classified into 3 categories (unfavorable, intermediate, or favorable lifestyle) based on their score. Cox proportional hazards regression models were applied to evaluate the associations of lifestyle and PRS with risk of developing r-axSpA. Moreover, the association between lifestyle score and r-axSpA mediated by systemic inflammation was estimated. During a median follow-up period of 13.57 years, 694 patients with r-axSpA were diagnosed. With unfavorable lifestyle as the reference group, intermediate lifestyle (hazard ratio [HR] 0.67, 95% CI 0.57-0.80) and favorable lifestyle (HR 0.62, 95% CI 0.49-0.78) were associated with a decreased risk of developing r-axSpA. For the combined effect of lifestyle and PRS, participants with unfavorable lifestyle and high genetic risk had the highest risk of developing r-axSpA (HR 2.18, 95% CI 1.47-3.23) compared to those with favorable lifestyle and low genetic risk. However, no evidence of addictive and multiplicative interaction was observed. Further, mediation analyses revealed that the inverse association between healthy lifestyle score and the risk of developing r-axSpA was in part mediated by systemic inflammation, which ranged from 0.20% for neutrophil-to-high-density lipoprotein cholesterol ratio to 10.29% for C-reactive protein. Our study suggested that adherence to a favorable lifestyle significantly reduced the risk of developing r-axSpA by attenuating the systemic inflammatory response, which was independent of genetic susceptibility to r-axSpA.

Visual impairment, encompassing low visual acuity and visual field loss, significantly impacts the older adult population worldwide, leading to increased disability and mortality risks. Recent studies suggest a strong association between visual impairment and anxiety, particularly among older adults. This study aims to explore the relationship between visual impairment and anxiety symptoms in older adult individuals in China, and to investigate potential mediating factors. Data for this study were derived from the 2018 Chinese Longitudinal Healthy Longevity Survey (CLHLS), including 11,702 participants aged 65 and older. Visual impairment was assessed through self-reported visual function, while anxiety symptoms were measured using the 7-item Generalized Anxiety Disorder scale (GAD-7). Additional assessments included sleep quality and duration, exercise status, and dietary diversity. Logistic regression models and mediation analysis were employed to explore associations and mediating effects. The findings indicate that visual impairment is significantly associated with increased anxiety symptoms among the older adult (OR = 1.51, 95% CI: 1.32-1.72, p < 0.001). Mediation analysis revealed that sleep quality, dietary diversity score (DDS), and plant-based DDS significantly mediated the relationship between visual impairment and anxiety. In contrast, sleep duration, exercise, and animal-based DDS did not show significant mediating effects. Visual impairment is a crucial predictor of anxiety symptoms in the older adult. Improving sleep quality and promoting a diverse plant-based diet may mitigate anxiety symptoms in this population. Interventions targeting these areas could enhance the mental health and quality of life of older adult individuals with visual impairment.

With population ageing, multimorbidity has become a major public health concern. Although healthy lifestyles are associated with reduced risks of single chronic diseases and mortality, their relationship with multimorbidity patterns among older Chinese remains insufficiently explored. Data from 16,820 participants aged 60 and older, from the 2008-2018 waves of the China Longitudinal Healthy Longevity Survey (CLHLS), were analyzed. Participants were categorized into three lifestyle groups (favorable, average, and unfavorable) based on five modifiable lifestyle factors: social engagement, physical activity, smoking, drinking, and diet. Disease progression was assessed using multimorbidity networks, and all-cause mortality was analyzed with Cox proportional hazards models. Compared to an unfavorable lifestyle, a favorable lifestyle was associated with a lower risk of all-cause mortality (HR = 1.63, 95% CI: 1.50-1.77). Among the five lifestyle factors, social engagement showed the strongest association with mortality (HR for inactive vs. active engagement = 1.36, 95% CI: 1.29-1.43). Multimorbidity networks revealed that individuals with favorable lifestyles exhibited denser, more interconnected disease networks, while those with unfavorable lifestyles showed more streamlined, linear disease progressions, primarily driven by hypertension, cardiovascular disease, and dementia. A favorable lifestyle was linked to lower mortality and more complex multimorbidity networks, likely due to longer survival and the accumulation of chronic conditions. These findings underscore the need for interventions to reduce premature mortality and manage multimorbidity in aging populations.

Genetic Risk, Incident Depression, and the Benefits of Adhering to a Healthy Lifestyle: A Prospective Analysis of the UK Biobank Cohort

This study explored the associations of genetic susceptibility and adherence to a healthy lifestyle with incident coronary heart disease (CHD) and stroke in individuals with hypertension. This study included 258 531 European descendants with hypertension at baseline from UK Biobank. Genetic risk of CHD and stroke was estimated using polygenic risk scores derived from 300 and 87 single-nucleotide polymorphisms, respectively. Lifestyle scores were calculated based on 4 lifestyle components (no obesity, no current smoking, regular physical activity and healthy diet). Cox regression with age as the underlying timescale was fit for incident CHD (n = 7470) and stroke (n = 5015), separately. A favourable lifestyle (3-4 lifestyle components) was associated with 37% and 30% lower hazards of CHD (95% confidence intervals, 32-42%) and stroke (23-37%), compared with an unfavourable lifestyle (0-1 lifestyle component), at all levels of genetic risk. Evidence of interaction between genetic susceptibility and lifestyle adherence was found for stroke (P = 0.036): no evidence of interaction for CHD (P = 0.524). A favourable lifestyle at high genetic risk had lower 12-year absolute risk of CHD and stroke, compared with an unfavourable lifestyle at low-to-intermediate genetic (exception: an unfavourable lifestyle at low CHD genetic risk). Adhering to a healthy lifestyle is associated with lower CHD and stroke risk regardless of genetic risk among individuals with hypertension. Risk of CHD and stroke for those at high genetic risk but adhering to a healthy lifestyle was generally lower than for those at low-to-intermediate genetic risk but adhering to an unhealthy lifestyle.

Association of Genetic Risk and Lifestyle Factors with Incident Depression: A Prospective Analysis of the UK Biobank Cohort

To prospectively evaluate the association between modifiable lifestyle factors and peripheral artery disease (PAD) among individuals with type 2 diabetes (T2D). We included 14,543 individuals with T2D from the UK Biobank. We defined a weighted healthy lifestyle score using nonsmoking, regular physical activity, high-quality diet, moderate alcohol consumption, optimal waist-to-hip ratio, and adequate sleep duration, and categorized into unfavorable, intermediate, and favorable lifestyles. We created a genetic risk score (GRS) using 19 single nucleotide polymorphisms previously found to be associated with PAD. We modeled the association between lifestyle score and PAD, overall and stratified by PAD genetic susceptibility. After a median 13.5 years of follow-up, 628 incident cases of PAD were documented. A linear inverse association between the weighted lifestyle score and PAD was observed, with a hazard ratio (HR) (95% CI) of 0.27 (0.19, 0.38) for favorable compared with unfavorable lifestyle (Ptrend < 0.0001). An estimated 58.3% (45.0%, 69.1%) of PAD in this population could be potentially avoidable if all participants attained a favorable lifestyle. Moreover, the PAD GRS was associated with increased PAD risk (HR [95% CI] per SD increment: 1.13 [1.03, 1.23]). A favorable lifestyle was able to partially mitigate the excess risk of PAD associated with higher GRS, albeit as a nonsignificant interaction. Several biomarkers in the lipid metabolism, hepatic/renal function, and systemic inflammation pathways collectively explained 13.3% (8.5%, 20.1%) of the association between weighted lifestyle score and PAD. A favorable lifestyle was associated with lower risk of PAD among individuals with T2D, independent of genetic predisposition to PAD.

BackgroundBoth genetic factors and lifestyle play a critical role in colorectal cancer (CRC), but the extent to which an increased genetic risk can be offset by a healthy lifestyle remains...

Lipoprotein (a) [Lp(a)] is associated with coronary artery disease (CAD). However, the role of healthy lifestyle against the risk of CAD with consideration of high Lp(a) levels remains unclear. This study examined 4512 participants who underwent serum Lp(a) level assessment at Kanazawa University Hospital from 2008 to March 2016. Their lifestyle habits were examined based on four questionnaires regarding dietary pattern, exercise habits, smoking status and body weight. Logistic regression analyses were performed to identify the association between healthy lifestyle and CAD independent of Lp(a) levels. The Lp(a) levels were significantly associated with CAD (odds ratio [OR]: 1.12, 95% confidence interval [CI]: 1.08-1.17, p = 1.3 × 10-7 per 10 mg/dL). Under these circumstances, the lifestyle risk score was also significantly associated with CAD (OR: 1.24, 95% CI: 1.12-1.36, p = 2.4 × 10-8 ). Compared with patients with a favourable lifestyle who have Lp(a) levels of <30 mg/dL, those with an intermediate or unfavourable lifestyle were at higher risk for CAD (OR: 1.11, 95% CI: 1.02-1.20, p = 0.003 and OR: 1.40, 95% CI: 1.16-1.54, p = 3.6 × 10-5 , respectively). Further, patients with a favourable, intermediate or unfavourable lifestyle who have Lp(a) levels of ≥30 mg/dL were at high risk for CAD (OR: 1.21, 95% CI: 1.08-1.34, p = 0.0014; OR: 1.31, 95% CI: 1.14-1.48, p = 1.2 × 10-4 ; and OR: 1.81, 95% CI: 1.44-2.18, p = 2.2 × 10-7 , respectively). Healthy lifestyle was associated with a lower risk of CAD regardless of Lp(a) levels.