Background
Previous studies suggest that outdoor sunlight exposure was associated with a lower risk of Parkinson’s disease (PD). However, the interaction of genetic predisposition and the potential role of lifestyle risk factors in mediating this association remains unclear from prospective evidence.
Methods
A cohort study based on the UK Biobank enrolled participants between 2006 and 2010, with the latest follow-up in November 2022. In the prospective population-based study 375,599 UK adults aged 37–73 years were enrolled. The outdoor light time was assessed using a questionnaire survey to investigate how many hours were spent outdoors on typical summer and winter days. New-onset PD was identified through linkage with inpatient hospitalization and death registers. Multivariate Cox proportional hazard regression models were used. The polygenic risk score (PRS) for PD comprised 44 single-nucleotide variants. The mediation analysis of lifestyle risk factors and vitamin D on this association was performed.
Results
A total of 375,599 participants (mean age, 56.8 years; 46.3% males) were included, and 2,824 individuals were first-ever diagnosed with PD. Compared with the individuals with shorter outdoor light time, those with longer time in summer (HR 0.77; 95% CI, 0.68–0.88), in winter (HR 0.85; 95% CI, 0.75–0.96), and on average (HR 0.83; 95% CI, 0.73–0.93), were prone to have lower PD risk. There was a joint association between outdoor light time and genetic predisposition in PD incidence, and higher genetic risk of PD could be modifiably decreased through longer outdoor light exposure. In mediation analyses, physical activities mainly explained 15.83% on average, while the mediating effects of sleep patterns (2.71%) and vitamin D (4.91%) were relatively mild of the association between outdoor light time and PD, respectively.
Conclusion
In this cohort study, a longer duration of outdoor sunlight exposure was associated with a lower risk of PD, and was more pronounced in individuals with high genetic risk. This association was partly mediated by physical activity, sleep patterns, and vitamin D. These findings highlight the potential of promoting regular outdoor activities as a practical strategy to mitigate PD risk, especially among genetically susceptible individuals.
Supplementary Information
The online version contains supplementary material available at 10.1186/s41043-025-00992-2.
Keywords: Parkinson’s disease, Sunlight, Cohort study, Genetic predisposition, Vitamin D, Sleeping habits
Highlights
Whether outdoor light exposure is associated with a lower risk of PD and the potential mediating factors in a prospective cohort of UK adults.
Longer outdoor light exposure linearly reduced PD risk, and more significant in high genetic predisposition individuals.
Increasing outdoor light exposure may be a potentially modifiable lifestyle factor that could reduce the risk of developing PD.
Supplementary Information
The online version contains supplementary material available at 10.1186/s41043-025-00992-2.
Introduction
Parkinson’s disease (PD) is the second most common neurodegenerative disease in the world and is characterised by bradykinesia, rigidity, postural instability, and resting tremor [1]. In 2021, the global estimates show over 11.77 million individuals living with PD, and 25.2 million people were projected to be living with PD worldwide in 2050, representing the fastest-increasing disease among all neurological disorders [2–4]. Importantly, PD is a progressive disease with limited therapeutic effectiveness, suggesting the importance of prevention [5].
Growing evidence has suggested that moderate outdoor light was beneficial for promoting health [6–8]. Experimental studies have shown that sunlight exposure influences neurobehavioral functions via its effects on the hypothalamus [9]. Recent evidence also links sunlight to dopamine transporters (DAT), with PD patients showing higher DAT availability in the left caudate nucleus in association with prolonged sunlight exposure, suggesting daylight may modulate dopaminergic neurotransmission [10]. However, prospective evidence exploring the association between outdoor light exposure and the risk of PD remains limited, and small sample sizes in previous studies may restrict the generalizability of their findings. Although both genetic and environmental factors contribute to PD development [11–13], the role of genetic predisposition in the link between outdoor light exposure and PD risk remains uncertain. Furthermore, previous studies revealed that outdoor light exposure has a crucial effect on vitamin D status, sleep circadian rhythms, and physical activity—all of which are closely associated with PD. However, the mediating effects and proportions of them are unclear [14–17].
Given that, the study utilized long-term UK Biobank data to examine the association between outdoor sunlight and incident PD in summer, winter, and on average. Additionally, the potential interaction and joint association of genetic predisposition were explored. Furthermore, physical activity, sleep patterns, and vitamin D levels were evaluated as potential mediators to elucidate the underlying mechanisms linking outdoor light exposure to PD development.
Methods
Study population
The UK Biobank is a large population-based cohort study that recruited approximately half a million participants aged 40–69 years from 2006 to 2010 across England, Scotland, and Wales. Each participant completed touchscreen questionnaires, underwent a physical examination, and provided biological samples [18, 19]. The UKB was approved by the North West Multi-Centre Research Ethics Committee. This research has been carried out using the UKB resource under application number 68307.
For the current analyses, we excluded individuals who subsequently withdrew from the study (n = 1,432), those diagnosed with PD (n = 944) at baseline, and those with disqualified data on time spent in outdoor light (n = 45,233) [8]. Participants with incomplete genetic information (n = 10,338), those displaying non-conforming sex in phenotypic and genetic data (n = 314), and individuals not of European descent (n = 68,634) were also excluded from the analysis. Fig. (S1): Following these exclusions, 375,599 participants were included in the main analysis.
Ascertainment of outcomes
Participants with Parkinson’s disease were identified using the algorithm recommended by the UK Biobank [20]. Table (S1): Detailed definitions of PD based on International Classification of Diseases, Tenth Revision (ICD-10) codes. Disease information was obtained from hospital admission electronic health records and death registers through linkages. We calculated the follow-up time from baseline to PD diagnosis, death, loss to follow-up, or censorship, whichever occurred first.
Assessment of time spent in outdoor light
The duration of outdoor light during typical daylight in summer or winter was recorded using an electronic questionnaire at baseline [8, 21]. Participants were asked, ‘In a typical day in summer or winter, how many hours do you spend outdoors?’ They could enter a specific number or choose from pre-set options including ‘less than an hour a day’, ‘do not know’, or ‘prefer not to answer’. A moderate correlation was observed between summer and winter outdoor light exposure, as per Pearson’s correlation analysis (r = 0.64, P < 0.001). Furthermore, to derive a singular measure of outdoor light exposure, we calculated the average time based on summer and winter data.
Assessment of covariates
Structured questionnaires were used to assess several possible confounding variables: sociodemographic characteristics (age, sex, ethnicity, education, and occupation), socioeconomic status (Townsend Deprivation Index), lifestyle factors (physical activity, sleep pattern, smoking, alcohol consumption, and usual diet), comorbidities (hypertension, dyslipidaemia, cardiovascular disease, and cancer) at the time of recruitment, vitamin D supplementation, vitamin D levels, and outdoor environmental-related variables (use of sun/UV protection and PM2.5). Physical activity, including moderate and vigorous-intensity activities, was evaluated as the metabolic equivalent of task (MET) minutes per week and was categorised as < 10 MET-h/week or ≥ 10 MET-h/week [22]. We defined healthy diet using the following items: total fruit and vegetable intake > 4.5 pieces or servings/week, total fish intake > 2 times/week, and processed meat intake ≤ 2 times per week and red meat intake ≤ 5 times per week, with meeting at least two items considered healthy [23]. The healthy sleep pattern score was generated based on a combination of chronotype, sleep duration, insomnia, snoring, and excessive daytime sleepiness [24]. Additionally, we included the PD-polygenic risk score (PRS), a genotyping array, and the first 10 principal components of ancestry as covariates [25].
Assessment of polygenic risk score
The PRS showed the association between genotype and risk of PD by score points and was composed of 44 single nucleotide polymorphisms (SNPs), which were associated with the incidence of PD in white participants [26]. Table (S2): Details regarding these SNPs were provided. Moreover, details on genotyping and quality control can be found online [27]. We constructed the weighted PRS of PD based on 44 SNPs using the following formula:
 |
Fig. (S2): Exhibited a normal distribution of PRS-PD. Table (S3): Revealed a higher score signifying increased genetic susceptibility to PD. Participants were classified as having low (quintile 1), intermediate (quintiles 2 to 4), or high (quintile 5) genetic risk for each outcome.
Statistical analysis
Sample characteristics were reported as mean ± standard deviations, medians (interquartile ranges), and numbers variables. Differences between groups were compared using the Student’s t-test, Wilcoxon test, or chi-squared test when appropriate.
Cox proportional hazard models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between the time spent outdoors and the incident PD. Schoenfeld residuals were used to test the proportional hazards assumption, and no violations were observed. In model 1, we adjusted for age and sex. Model 2 (full model) was further adjusted for education, TDI, BMI, outdoor environmental-related variables, lifestyle factors, comorbidities, PRS, the first ten principal components of ancestry, and genotype measurement batch. To investigate the dose-response association, a restricted cubic spline model with three knots (at the 10th, 50th, and 90th percentiles) was employed [28]. The missing values of the covariates were imputed and analysed using multiple imputations with five imputations (SAS PROC MI and PROC MIANALYZE).
To assess the interaction and joint association between outdoor light time and PRS on the risk of PD, we treated participants with a low PRS and long outdoor light time as the reference group to conduct a joint analysis, and multiplicative interactions were assessed by likelihood ratio tests [29].
Stratified analyses and interactions were performed to examine the association according to age, sex, BMI, and occupation. Fig. (S3): A directed acyclic graph explaining the relationship between the exposures, the outcome, and the covariates. Mediation analysis was performed to evaluate the proportional contribution of physical activity, sleep patterns, and vitamin D to the association between outdoor light time and PD risk (SAS PROC CAUSALMED). In the sensitivity analysis, we repeated the analyses after excluding individuals who died or developed PD within 2 years of follow-up and used the Fine-Gray subdistribution hazard model [30]. To test the robustness of the results, total physical activity, sleep patterns, and vitamin D levels were further adjusted.
All analyses were performed using SAS version 9.4 (SAS Institute, Cary, NC, USA) and R software (version 4.3.1; R Foundation for Statistical Computing). A two-sided p < 0.05 was considered statistically significant.
Results
Characteristics of the study population
A total of 375,599 participants (mean age, 56.8 years; 173688 males, 46.3%) with a median follow-up of 13.7 years (interquartile range: 13.13–14.31) were included in this prospective study, and 2,824 individuals were first-ever diagnosed with PD. Table (1): Baseline demographics and characteristics according to outdoor light hours. Overall, individuals with longer outdoor light exposure times (> 3 h/day in summer; >2 h/day in winter; >2.5 h/day on average) tended to be older, male, retired, current smokers, have lower education levels, and have a higher genetic risk of PD.
Table 1.
Baseline characteristics of participants
| Characteristics | Outdoor light time in summer | Outdoor light time in winter | Outdoor light time on average | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| < 2 h/day | 2 to 3 h/day | > 3 h/day | P | < 1 h/day | 1 to 2 h/day | > 2 h/day | P | < 1.5 h/day | 1.5 to 2.5 h/day | > 2.5 h/day | P | |
| No. of participants | 48,668 | 146,765 | 180,166 | 71,832 | 218,953 | 84,814 | 70,375 | 141,577 | 163,647 | |||
| Age (years), mean (SD) | 54.2 ± 7.5 | 55.8 ± 7.9 | 58.5 ± 7.8 | < 0.001 | 55.0 ± 7.7 | 56.8 ± 8.0 | 58.7 ± 7.9 | < 0.001 | 54.3 ± 7.6 | 56.1 ± 8.0 | 58.6 ± 7.8 | < 0.001 |
| Female (%) | 28,347 (58.3) | 84,660 (57.7) | 88,904 (49.4) | < 0.001 | 45,634 (63.5) | 121,957 (55.7) | 34,320 (40.5) | < 0.001 | 42,383 (60.2) | 81,824 (57.8) | 77,704 (47.5) | < 0.001 |
| Townsend deprivation index, median (IQR) | -2.27 (-3.74 to -0.27) | -2.41 (-3.79 to -0.13) | -2.39 (-3.74 to -0.03) | < 0.001 | -2.51 (-3.85 to -0.25) | -2.43 (-3.79 to -0.15) | -2.14 (-3.60 to -0.49) | < 0.001 | -2.40 (-3.81 to -0.04) | -2.44 (-3.80 to -0.18) | -2.33 (-3.70 to 0.12) | < 0.001 |
| College or University degree (%) | 22,349 (46.1) | 54,921 (37.6) | 41,998 (23.6) | < 0.001 | 28,506 (39.9) | 74,674 (34.3) | 16,090 (19.2) | < 0.001 | 31,126 (44.4) | 51,547 (36.6) | 36,595 (22.6) | < 0.001 |
| Smoking status (%) | < 0.001 | < 0.001 | < 0.001 | |||||||||
| Never | 29,394 (60.5) | 84,444 (57.7) | 91,060 (50.7) | 41,884 (58.5) | 121,183 (55.5) | 41,831 (49.5) | 42,396 (60.4) | 80,441 (56.9) | 82,061 (50.3) | |||
| Previous | 14,955 (30.8) | 49,052 (33.5) | 68,429 (38.1) | 23,072 (32.2) | 76,858 (35.2) | 32,506 (38.5) | 21,886 (31.2) | 48,041 (34.0) | 62,509 (38.4) | |||
| Current | 4225 (8.7) | 12,942 (8.8) | 20,017 (11.2) | 6705 (9.4) | 20,376 (9.3) | 10,103 (12.0) | 5957 (8.5) | 12,783 (9.1) | 18,444 (11.3) | |||
| Alcohol consumption (%) | < 0.001 | < 0.001 | 0.374 | |||||||||
| Never/special occasions only | 9204 (18.9) | 23,046 (15.7) | 29,984 (16.7) | 12,552 (17.5) | 34,126 (15.6) | 15,556 (18.4) | 12,359 (17.6) | 21,929 (15.5) | 27,946 (17.1) | |||
| No more than 2 times/week | 17,876 (36.8) | 55,169 (37.6) | 67,168 (37.3) | 27,104 (37.7) | 81,193 (37.1) | 31,916 (37.7) | 26,236 (37.3) | 52,903 (37.4) | 61,074 (37.3) | |||
| More than 2 times/week | 21,566 (44.3) | 68,500 (46.7) | 82,922 (46.0) | 32,148 (44.8) | 103,554 (47.3) | 37,286 (44.0) | 31,756 (45.1) | 66,692 (47.1) | 74,540 (45.6) | |||
| Body mass index (kg/m2), mean (SD) | 27.3 ± 5.2 | 27.2 ± 4.7 | 27.5 ± 4.6 | < 0.001 | 27.5 ± 5.2 | 27.2 ± 4.6 | 27.7 ± 4.5 | < 0.001 | 27.3 ± 5.1 | 27.2 ± 4.7 | 27.5 ± 4.5 | < 0.001 |
| Occupation (%) | < 0.001 | < 0.001 | < 0.001 | |||||||||
| retired | 7326 (15.1) | 39,381 (26.9) | 81,935 (45.7) | 15,787 (22.1) | 74,867 (34.3) | 37,988 (45.0) | 11,869 (16.9) | 41,720 (29.6) | 75,053 (46.1) | |||
| others | 41,161 (84.9) | 106,786 (73.1) | 97,441 (54.3) | 55,790 (77.9) | 143,182 (65.7) | 46,416 (55.0) | 58,258 (83.1) | 99,276 (70.4) | 87,854 (53.9) | |||
| PM2.5 (ug/m3), mean (SD) | 10.01 ± 1.07 | 9.93 ± 1.03 | 9.88 ± 1.02 | < 0.001 | 9.90 ± 1.01 | 9.91 ± 1.03 | 9.94 ± 1.05 | < 0.001 | 9.96 ± 1.05 | 9.92 ± 1.02 | 9.89 ± 1.03 | < 0.001 |
| Dietary pattern (%) | < 0.001 | < 0.001 | < 0.001 | |||||||||
| unhealthy | 25,425 (52.2) | 67,690 (46.1) | 77,732 (43.1) | 37,118 (51.7) | 96,850 (44.2) | 36,879 (43.5) | 36,420 (51.7) | 64,311 (45.4) | 70,116 (42.8) | |||
| healthy | 23,243 (47.8) | 79,075 (53.9) | 102,434 (56.9) | 34,714 (48.3) | 122,103 (55.8) | 47,935 (56.5) | 33,955 (48.3) | 77,266 (54.6) | 93,531 (57.2) | |||
| Vitamin D supplementation (%) | 2038 (4.2) | 5439 (3.7) | 6441 (3.6) | < 0.001 | 2737 (3.8) | 8277 (3.8) | 2904 (3.4) | < 0.001 | 2799 (4.0) | 5310 (3.8) | 5809 (3.6) | < 0.001 |
| Use of sun/UV protection (%) | 0.04 | < 0.001 | < 0.001 | |||||||||
| Never/rarely | 4127 (8.5) | 10,214 (7.0) | 15,497 (8.6) | 5159 (7.2) | 15,557 (7.1) | 9122 (10.8) | 5374 (7.6) | 9661 (6.8) | 14,803 (9.1) | |||
| Sometimes | 16,026 (32.9) | 48,724 (33.2) | 59,470 (33.0) | 22,971 (32.0) | 71,920 (32.9) | 29,329 (34.6) | 23,049 (32.8) | 46,660 (33.0) | 54,511 (33.3) | |||
| Most of the time | 18,190 (37.4) | 57,147 (39.0) | 63,951 (35.5) | 27,784 (38.7) | 83,907 (38.3) | 27,597 (32.6) | 27,065 (38.5) | 55,261 (39.0) | 56,962 (34.8) | |||
| Always | 9471 (19.5) | 30,062 (20.5) | 40,836 (22.7) | 15,266 (21.3) | 46,665 (21.3) | 18,438 (21.7) | 14,008 (19.9) | 29,439 (20.8) | 36,922 (22.6) | |||
| Do not go out in sunshine | 837 (1.7) | 576 (0.4) | 352 (0.2) | 632 (0.9) | 852 (0.4) | 281 (0.3) | 861 (1.2) | 518 (0.4) | 386 (0.2) | |||
| Genetic risk category (%) | < 0.001 | 0.003 | < 0.001 | |||||||||
| Lower | 9867 (20.3) | 29,603 (20.2) | 35,649 (19.8) | 14,595 (20.3) | 43,768 (20.0) | 16,756 (19.8) | 14,312 (20.3) | 28,411 (20.1) | 32,396 (19.8) | |||
| Intermediate | 29,308 (60.2) | 87,837 (59.8) | 108,215 (60.1) | 43,049 (59.9) | 131,341 (60.0) | 50,970 (60.1) | 42,336 (60.2) | 84,817 (59.9) | 98,207 (60.0) | |||
| Higher | 9493 (19.5) | 29,325 (20.0) | 36,302 (20.2) | 14,188 (19.8) | 43,844 (20.0) | 17,088 (20.1) | 13,727 (19.5) | 28,349 (20.0) | 33,044 (20.2) | |||
| Hypertension (%) | 22,981 (47.2) | 75,450 (51.4) | 107,742 (59.8) | < 0.001 | 35,752 (49.8) | 118,429 (54.1) | 51,992 (61.3) | < 0.001 | 33,649 (47.8) | 74,009 (52.3) | 98,495 (60.2) | < 0.001 |
| Dyslipidaemia (%) | 4616 (9.5) | 15,529 (10.6) | 25,796 (14.3) | < 0.001 | 7426 (10.3) | 25,891 (11.8) | 12,624 (14.9) | < 0.001 | 6662 (9.5) | 15,446 (10.9) | 23,833 (14.6) | < 0.001 |
| Cardiovascular disease (%) | 3275 (6.7) | 10,267 (7.0) | 17,525 (9.7) | < 0.001 | 5326 (7.4) | 17,077 (7.8) | 8664 (10.2) | < 0.001 | 4680 (6.7) | 10,138 (7.2) | 16,249 (9.9) | < 0.001 |
| Cancer (%) | 3432 (7.1) | 11,008 (7.5) | 14,909 (8.3) | < 0.001 | 5395 (7.5) | 17,262 (7.9) | 6692 (7.9) | 0.008 | 5034 (7.2) | 10,892 (7.7) | 13,423 (8.2) | < 0.001 |
IQR, interquartile range; SD, standard deviation; MET, metabolic equivalent
Association of time spent in outdoor light with PD
In the fully adjusted model, individuals with longer outdoor light exposure, compared with those with shorter exposure (< 2 h/day in summer, < 1 h/day in winter, and < 1.5 h/day on average), demonstrated a lower risk of PD. Specifically, the risk was 23% lower in summer (HR 0.77; 95% CI, 0.68–0.88), 15% lower in winter (HR 0.85; 95% CI, 0.75–0.96), and 17% lower on average (HR 0.83; 95% CI, 0.73–0.93), following adjustment for covariates. Table (2): Per 1 h increase in outdoor light time the risk of PD is decreased by 4%, 4%, and 6% in summer, winter, and on average, respectively (All p < 0.001). Fig. (S4): Restricted cubic spline analyses showed the significant linear relationship between outdoor light time and PD in summer, winter, and on average after adjustment (All p < 0.001).
Table 2.
Association between time spent in outdoor light and incident parkinson’s disease
| Time spent in outdoor light | Events / Total | Model 1a | Model 2b | Per 1 h increase in outdoor light time | P Value | ||
|---|---|---|---|---|---|---|---|
| HR (95% CI) | P Value | HR (95% CI) | P Value | ||||
| Summer | 0.96 (0.94, 0.97) | < 0.001 | |||||
| < 2 h/day | 298 / 48,668 | 1.00 (Ref.) | 1.00 (Ref.) | ||||
| 2 to 3 h/day | 1012 / 146,765 | 0.89 (0.78, 1.01) | 0.072 | 0.91 (0.80, 1.03) | 0.141 | ||
| > 3 h/day | 1514 / 180,166 | 0.76 (0.67, 0.86) | < 0.001 | 0.77 (0.68, 0.88) | < 0.001 | ||
| Winter | 0.96 (0.93, 0.98) | < 0.001 | |||||
| < 1 h/day | 417 / 71,832 | 1.00 (Ref.) | 1.00 (Ref.) | ||||
| 1 to 2 h/day | 1660 / 218,953 | 0.98 (0.88, 1.09) | 0.693 | 0.99 (0.89, 1.11) | 0.905 | ||
| > 2 h/day | 747 / 84,814 | 0.86 (0.76, 0.97) | 0.012 | 0.85 (0.75, 0.96) | 0.010 | ||
| Average | 0.94 (0.92, 0.97) | < 0.001 | |||||
| < 1.5 h/day | 403 / 70,375 | 1.00 (Ref.) | 1.00 (Ref.) | ||||
| 1.5 to 2.5 h/day | 1022/ 141,577 | 0.97 (0.86, 1.09) | 0.608 | 0.99 (0.88, 1.11) | 0.802 | ||
| > 2.5 h/day | 1399 / 163,647 | 0.82 (0.73, 0.92) | < 0.001 | 0.83 (0.73, 0.93) | 0.001 | ||
Abbreviation: HR, hazard ratio; 95% CI, 95% confidence interval
a. Model 1 was adjusted for age and sex
b. Model 2 was adjusted for age, sex, education, Townsend deprivation index, smoking status, alcohol consumption, body mass index, occupation, dietary pattern, vitamin
D supplementation, use of sun/UV protection, PM2.5, baseline hypertension, dyslipidaemia, cancer, cardiovascular disease, PRS, first 10 principal components of ancestry, and genotype measurement batch. HR: hazard ratio; CI: confidence interval
Genetic predisposition of the association of time spent in outdoor light with PD
Figure (1): The joint association between PRS, outdoor light time, and the incidence of PD was analysed. Participants with shorter outdoor light time and high PRS had the highest risk of PD in summer (HR 2.48; 95% CI, 1.93–3.19), winter (HR 2.13; 95% CI, 1.65–2.76), and on average (HR 2.27; 95% CI, 1.80–2.86), respectively. The higher genetic risk of PD could be modifiably decreased through longer outdoor light exposure. And the reverse relationship between outdoor light and PD was more pronounced in individuals with higher genetic predisposition. There were no genetic multiplicative interactions in the longitudinal association between outdoor sunlight duration and the incidence of PD (all p interaction > 0.05). In the stratified analyses, studies were categorised according to BMI, sex, age, and occupation. Tables (S4-S6): The interactions of outdoor light time and PD were more pronounced in women and older adults in summer and winter (p interaction < 0.05). The results were consistent across individuals with normal weight, overweight, or obese, as well as in different occupational groups.
Fig. 1.
Risk of incident Parkinson’s disease according to genetic risk and time spent in outdoor light. Adjusted for age, sex, education, Townsend deprivation index, smoking status, alcohol consumption, body mass index, occupation, dietary pattern, vitamin D supplementation, use of sun/UV protection, PM2.5, baseline hypertension, dyslipidaemia, cancer, cardiovascular disease, first 10 principal components of ancestry, and genotype measurement batch. HR: hazard ratio; CI: confidence interval
The mediating effect of lifestyle and vitamin D
In the mediation analyses, physical activity proportions mediated 13.50%, 25.96%, and 15.83% of the associations between time spent in outdoor light and incident PD in summer, winter, and on average, respectively. Table (3): The proportions mediated by vitamin D were 4.67%, 6.19%, and 4.91%, respectively, and those by sleep patterns were 2.05%, 4.32%, and 2.71%, respectively (All p < 0.05).
Table 3.
Mediation analysis to evaluate whether physical activities, sleep patterns, and vitamin D mediated the associations of the time spent in outdoor light with parkinson’s disease risk
| Time spent in outdoor light | Total Physical activities | P Value | Vitamin D | P Value | Sleep patterns | P Value | |||
|---|---|---|---|---|---|---|---|---|---|
| Proportion mediated, % (95% CI) | Proportion mediated, % (95% CI) | Proportion mediated, % (95% CI) | |||||||
| Summer | 13.50 (2.58, 24.42) | 0.015 | 4.67 (0.23, 9.11) | 0.039 | 2.05 (0.75, 3.36) | 0.002 | |||
| Winter | 25.96 (3.96, 47.96) | 0.021 | 6.19 (0.06, 12.31) | 0.048 | 4.32 (1.06, 7.58) | 0.009 | |||
| Average | 15.83 (2.00, 29.11) | 0.025 | 4.91 (0.19, 9.63) | 0.041 | 2.71 (0.97, 4.46) | 0.002 | |||
Adjusted for age, sex, education, Townsend deprivation index, smoking status, alcohol consumption, body mass index, occupation, dietary pattern, vitamin D supplementation, use of sun/UV protection, PM2.5, baseline hypertension, dyslipidaemia, cancer, cardiovascular disease, PRS, first 10 principal components of ancestry, and genotype measurement batch. CI: confidence interval
The sensitivity analysis
Table (S7): In the sensitivity analysis, significant associations between outdoor light time and PD remained in summer and on average after further adjusting for total physical activity, sleep patterns, and vitamin D levels. Table (S8): Excluding individuals who developed PD within the first 2 years of follow-up and adjusting for competing risk using the Fine-Gray model did not alter the assessment of the association between outdoor light time and PD risk.
Discussion
In this large prospective cohort study, we demonstrated that time spend outdoors light was associated with PD risk, and the linear relationship was significant in summer, winter, and on average. Additionally, physical activities, sleep patterns, and vitamin D partially mediated this association. The reverse relationship between outdoor light and PD was more pronounced in individuals with higher genetic predisposition.
To our knowledge, few prospective studies have reported the association between outdoor light and PD risk. And no study focused on the joint association of genetic predisposition in the correlation of outdoor light time and incident PD. A Danish case-control study reported that participants with work outdoors have a lower risk for PD [31]. However, the study population was limited to 23,101 male participants, and outdoor work duration served as a proxy for sunlight exposure rather than providing specific measurements of sun exposure time. A previous observational study from a French cohort reported a decreased risk of PD in participants with longer Ultraviolet B (UV-B) exposure [32]. Although 69,010 people with PD were included in this study, only UV-B exposure was estimated because of its biological role in vitamin D synthesis, which might overlook the effects of other components of sunlight on the incidence of PD. Previous studies found spending 1.5 h/day on average in outdoor light was associated with a lower risk of dementia and depression, while below or above this time was associated with a higher risk of those neurological diseases [8, 33]. Another study revealed that each additional hour spent outdoors sunlight was associated with lower risk of low mood, neuroticism, and insomnia symptoms [21]. These findings demonstrated different effects of outdoor sunlight on neurological diseases and mental health, which was greatly meaningful for us to explore the optimal outdoor light time for minimizing the risk of PD.
Parkinson’s disease (PD) is a neurodegenerative disorder influenced by genetic and environmental factors [13]. The outdoor sunlight exposure was associated with a lower risk of PD [34]. However, the potential genetic and environmental mechanisms remain unclear. Our study comprehensively analyzed the protective role of outdoor light exposure against PD from both genetic and environmental perspectives, adding to the understanding of the potential mechanisms underlying PD development and progression. Given that vitamin D, sleep patterns, and physical activity are linked to sunlight exposure, these factors may play essential roles in the association between outdoor light time and PD [14–17]. Several cross-sectional studies have shown that vitamin D deficiency is common in adults with PD, and exposed to sunlight can protect against PD through the synthesis of vitamin D [35–37], which has been reported to play various roles in normal brain physiology and processes, including regulation of synaptic plasticity and dopaminergic neurotransmission [38]. Consistent with our mediation analyses, vitamin D partially mediated the association between time spent outdoors and PD risk. Additionally, sunlight exposure regulates sleep and circadian rhythms via the suprachiasmatic nuclei, which transmit the light information to a network of clocks to synchronize physiological processes [39]. A UK Biobank study confirmed that reduced daytime light exposure is a risk factor for sleep and circadian outcomes [21]. The circadian system, crucial in regulating reactive oxygen species homeostasis, influences PD development through melatonin secretion, impacting the brain’s antioxidant defence and triggering PD development [40]. Consequently, circadian rhythm disruption could hasten PD-related pathology, elucidating the link between sunlight exposure, sleep patterns, and PD in our analysis [41]. Physical activity is well established as being strongly associated with the prognosis of PD [42, 43]. Individuals with more outdoor light time may engage in regular physical activity over time, which helps to improve gait speed, muscle strength, and fitness in patients with PD [44]. Furthermore, our mediation analysis revealed a significant mediating effect of physical activity on the association between outdoor sunlight exposure and PD risk, particularly during the winter season.
In addition to environmental factors, genetic predisposition plays a critical role in the development of PD [45]. Previous GWAS have identified over 90 risk variants, collectively accounting for approximately 22% of PD heritability [46]. Compared to individual risk loci, the PRS calculated as the weighted sum of risk alleles based on their effect sizes provides a more robust measure of genetic susceptibility [47]. Notably, a PRS derived from PD-associated SNPs has been associated with faster motor and cognitive decline, suggesting its potential utility in capturing both disease risk and progression across multiple domains [48]. Both PRS and outdoor sunlight are important factors in PD development. To address this key knowledge gap, we investigated the interaction between genetic predisposition (PRS) and outdoor sunlight exposure, revealing their combined effect on PD risk.
The stratified analyses revealed that the relationship between outdoor sunlight exposure and PD was more significant among older and female participants, and this age tendency is consistent with the previous study [32]. Some reasons might explain our findings that females are more likely to be affected by temperature and have fewer clothes with more skin exposed compared to males [49]. Older adults are more susceptible to PD due to age-related changes [13]. The beneficial effects of outdoor light in older adults may be attenuated due to reduced skin thickness and age-related declines in serum 25(OH)D levels [50].
Increasing outdoor light exposure might be a simple, accessible, non-pharmacological method to protect against PD in community settings. Nevertheless, excessive sunlight is linked to skin cancer, diabetes, and dementia [7, 8, 51]. These findings advance our understanding of the sunlight exposure and PD association and may inform clinical practice through evidence-based recommendations for optimal outdoor exposure duration in older adults.
This study benefits from a large sample size and extended follow-up capturing critical PD development phases. Furthermore, leveraging the well-characterized UK Biobank cohort enabled comprehensive confounder adjustment, including PD genetic susceptibility. However, several limitations should be acknowledged. First, due to the observational design, causal inference is limited, and reverse causality may be present. Second, potential recall bias arises from self-reported outdoor light exposure, and a single measurement may not accurately capture long-term exposure levels. Third, as the study population consisted predominantly of individuals of European descent, and given that outdoor light intensity and duration vary geographically, the generalizability of these findings to other regions and ethnic groups requires further investigation. Fourth, while accounting for numerous confounders, some crucial factors influencing PD onset remain unaddressed, such as the intensity of sunlight. Additionally, PD diagnosis relied on hospital admissions and death records, possibly overlooking early PD stages.
Conclusions
Longer outdoor light exposure (> 3 h/day in summer, > 2 h/day in winter, and > 2.5 h/day on average) was associated with a lower risk of PD, with a more pronounced effect observed among individuals with higher genetic susceptibility. In addition, physical activity, sleep patterns, and vitamin D partially mediated this favorable association. Further studies are warranted to confirm these findings and clarify the underlying mechanisms.
Electronic supplementary material
Below is the link to the electronic supplementary material.
Acknowledgements
We thank all participants in the UKB study and all those involved in the UKB study construction.
Abbreviations
- BMI
Body mass index
- CIs
Confidence intervals
- DAT
Dopamine transporters
- HRs
Hazard ratios
- ICD-10
International Classification of Diseases, Tenth Revision
- MET
Metabolic equivalent of task
- PD
Parkinson’s disease
- PRS
Polygenic risk score
- SNPs
Single nucleotide polymorphisms
- TDI
Townsend Deprivation Index
- UV-B
Ultraviolet B
Author contributions
Y.H. developed the methodology, curated the data, conducted the investigation, validated the results, drafted the original manuscript and reviewed the article. S.T. developed the methodology, performed formal analysis, utilized software tools, and drafted the original manuscript. K.Q. created visualizations, contributed to the writing of the original manuscript, and reviewed and edited the article. Y.H. S.T. and K.Q. contributed equally. J.X. curated data and contributed to methodology. A.P. supervised the project and provided resources. G.L. administered the project, provided resources, and validated the results. Y.L. conceptualized the study, supervised the project, administered project tasks, and acquired funding. All authors read and approved the final manuscript as submitted.
Funding
This work was supported by the National Nature Science Foundation of China (82470896 and 82070830), the Noncommunicable Chronic Diseases-National Science and Technology Major Project (No. 2023ZD0508300), and the National Key Research and Development Program of Hubei province (2022BCA036).
Data availability
Data is available on application to the UKB at http://www.ukbiobank.ac.uk/register-apply.
Declarations
Ethics approval and consent to participate
All participants in the UK Biobank provided informed consent at the time of recruitment, allowing their data to be used for a wide range of research purposes. We adhere to the terms and conditions set by the UK Biobank in the use of this data. The UKB was approved by the North West Multi-Centre Research Ethics Committee (Ref: 11/NW/0382).
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Yumei Huang, Shufan Tian and Kangli Qiu contributed equally to this work.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
Data is available on application to the UKB at http://www.ukbiobank.ac.uk/register-apply.