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Written by ︱ Gao Xu, edited by Liu Shuzhen ︱ Wang Sizhen Aging is a gradual and progressive degeneration of the integrity of biological systems, which is believed to be caused by accumulative changes at the cellular level[1]
.
Studies have found that aging is accompanied by a decline in sleep quality, especially in middle-aged and elderly people [2]
.
However, the causal relationship between sleep and accelerated aging remains controversial
.
Elucidating the causal relationship between aging and sleep has been greatly limited by the lack of precise measurements of aging
.
People of the same age may not have the same aging-related symptoms, and some may experience age-related decline faster than others [1]
.
In addition, biological aging is a complex process involving multiple organs and systems, and a single aging-related biomarker may not fully describe the overall situation of an individual's aging process [3]
.
Therefore, biological age, such as KDM-biological age and phenotypic age (PhenoAge), has been proposed and explored for a long time
.
The gap between biological age and chronological age, known as age accelerations, has been shown to be highly correlated with aging-related health outcomes and mortality [4]
.
Air pollution, especially fine particulate matter (PM2.
5), is an important environmental exposure that may accelerate aging and affect sleep quality [5, 6]
.
However, as the causal relationship between sleep and aging remains unclear, it has not been possible to elucidate whether sleep (or biological aging levels) can modulate the effects of air pollution on the other
.
On April 14, 2022, Xu Gao's team from Peking University School of Public Health published a paper entitled "Role of sleep quality in the acceleration of biological aging and its potential for preventive interaction on air pollution insults: Findings from the UK in the journal Aging Cell.
Biobank cohort" research paper exploring the causal relationship between sleep and aging, revealing that good sleep quality can slow the acceleration of biological aging caused by air pollution
.
The study obtained a sleep index by scoring self-reported snoring, work and rest time, daytime sleepiness, sleep duration, insomnia, and difficulty getting out of bed
.
KDM-biological age and phenotypic age were estimated using well-established algorithms, and the residual from chronological age was defined as age acceleration
.
After controlling for potential confounders, the authors first observed a significant negative association between sleep index and mean KDM-biological age acceleration and phenotypic age acceleration
.
For each unit increase in sleep index, KDM-biological age acceleration and phenotypic age acceleration decreased by 0.
104 and 0.
119 years, respectively, and further analysis found a significant dose-response relationship between them (Fig.
1)
.
In this step of the analysis, the authors finally verified that the age-accelerated rise was due to lower sleep quality using Mendelian randomization using sleep index and genetic risk score for biological age
.
The results suggest that poor sleep quality accelerates biological age
.
Figure 1 The relationship between sleep index and average age acceleration and the best fit curve (Source: Gao X, et al.
, Aging Cell, 2022) Based on the found causal relationship between sleep and biological age, the authors further observed five The combined effect of annual average exposure levels of various air pollutants (including PM2.
5, PMcoarse, PM10, NO2, NOx) and sleep on the acceleration of age, and whether sleep quality mediates the effect of air pollution on the acceleration of biological age, the The study found that PM2.
5, NO2 and sleep index have a combined effect on the average KDM-biological age acceleration and phenotypic age acceleration.
With the decrease of sleep index and the increase of pollutant concentration, the two age accelerations have a significant increasing trend.
(Figure 2)
.
The results suggest that people with low sleep quality and exposure to high concentrations of pollutants have a higher age acceleration
.
Figure 2 The joint relationship between sleep index and air pollution level and the acceleration of biological age (Source: Gao X, et al.
, Aging Cell, 2022) Figure 3 The regulatory effect of sleep quality on the acceleration of biological age caused by air pollution (Source: Gao X, et al.
, Aging Cell, 2022) Since sleep is a factor that can be manipulated, the study further analyzed the potential moderating effect of sleep quality on air pollution-induced age acceleration
.
The authors found that sleep quality can improve the acceleration of biological age caused by air pollution (P < 0.
001) (Figure 3), and PM2.
5 and NO2 have a significant nonlinear relationship with the two types of biological age acceleration.
PM2.
5 and sleep quality The effects on the two accelerated changes in biological age were distinct (Figures 4 and 5)
.
The results suggest that better sleep quality can improve the accelerated aging caused by air pollution
.
Figure 4 The best fitting curve of sleep quality to the biological age acceleration caused by PM2.
5 (Source: Gao X, et al.
, Aging Cell, 2022) Figure 5 The best fitting curve of sleep quality to the biological age acceleration caused by NO2 Combination curve (Source: Gao X, et al.
, Aging Cell, 2022) Conclusion and discussion, inspiration and prospect of the article In summary, this study uses two relatively mature biological age algorithms in a large sample of middle-aged and elderly people.
Computational biological age, comprehensively evaluated sleep quality by synthesizing six sleep behaviors, and revealed the causal relationship between sleep quality and aging through causal inference test of Mendelian randomization, and found for the first time that better sleep quality can delay biological Aging, and sleep and air pollution have separate and combined effects on biological aging, better sleep quality may slow the accelerated effect of air pollution on aging
.
This study not only provides exploratory evidence for the effects of sleep on aging, but also highlights the importance of high-quality sleep as an intervention to mitigate the accelerated effects of long-term air pollution exposure on human aging
.
To validate the findings of this study and further identify the underlying biological mechanisms, the authors believe that more cohort studies with more detailed aging assessments and comprehensive clinical measures of sleep quality are warranted in the future
.
Link to the original text: https://onlinelibrary.
wiley.
com/doi/10.
1111/acel.
13610 Gao Xu Corresponding author (photo provided by: Gao Xu's team) Gao Xu, Ph.
D.
, Department of Labor and Environmental Hygiene, School of Public Health, Peking University Assistant professor, associate researcher, doctoral supervisor
.
He is mainly engaged in epidemiological research on environmental exposure and elderly health based on population big data, using epigenetics, combined with other multi-omics data (genome, metabolome, microbiome, etc.
)
.
At present, he has published more than 40 SCI papers in international authoritative journals such as Nature Aging, American Journal of Respiratory and Critical Care Medicine, Journal of Hazardous Materials, Environment International, International Journal of Epidemiology and European Journal of Epidemiology, and serves as the director of Current Environmental Health Reports and Editorial Board Member of The Innovation Journal
.
Team postdoctoral recruitment webpage (recruiting): https://sph.
pku.
edu.
cn/info/1031/5586.
htm Selected articles from previous issues [1] Neuron's heavy review︱ Sheng Zuhang's team focuses on the maintenance and maintenance of axon mitochondria The important role of energy supply in neurodegenerative diseases and post-neural repair [2] Cell Death Dis︱ Kong Hui et al.
Reveal the role of P2X7/NLRP3 inflammasome pathway in early diabetic retinopathy [3] Sci Adv︱ Liu Xingguo/Tian Mei's team discovered a new mechanism of mitochondrial clearance in drug-induced Parkinson's syndrome【4】Front Aging Neurosci︱Gut preparation can affect postoperative delirium by changing the composition of flora【5】Mol Psychiatry︱C/EBPβ revealed by Ye Keqiang’s group /AEP signaling pathway mediates atherosclerosis and its induced Alzheimer's disease【6】Neurosci Bull viewpoint article︱Mechanism of flexible allocation of limited working memory resources under multitasking【7】Nat Commun︱Temperature cycle drives biological clock A New Mechanism of Gene Evolution: Timless Polymorphism [8] Nat Commun︱ For the first time! Structural analysis of the twisted dimer of transthyretin in the vitreous of human eye【9】Cereb Cortex︱left brain vs right brain: the functional lateralization mechanism of the medial temporal lobe in creative assessment【10】Cereb Cortex︱Jin Haiyang et al.
All-or-No Neural Mechanisms of Classification: Evidence from N170 Academic Conference/Lecture/Symposium Recommendation [1] Registration starts︱ Follow-up workshop: What is driving our decision-making? 【1】Academic seminar︱2022 Mini-Symposium for Brain Sciences high-quality scientific research training course recommendation【1】Symposium on patch clamp and optogenetics and calcium imaging technology May 14-15 Tencent conference 【2】Scientific research skills︱4 2018 Near-infrared Brain Function Data Analysis Class (Online: 2022.
4.
18~4.
30) References (swipe up and down to read) 1.
Ferrucci L, Levine ME, Kuo PL, Simonsick EM (2018) Time and the Metrics of Aging.
Circulation research 123(7):740-4.
https://doi.
org/10.