The researchers used data of almost half a million British participants in the United Kingdom to assess the influence of 164 environmental factors and genetic risk scores for 22 major diseases on aging, diseases linked to the age and premature death. The study is published in Nature medicine.
Key results:
- The environmental factors explained 17% of the variation in the risk of death, against less than 2% explained by the genetic predisposition (as we currently understand);
- Of the 25 independent environmental factors identified, smoking, socioeconomic status, physical activity and living conditions have had the most impact on mortality and biological aging;
- Smoking was associated with 21 diseases; Socioeconomic factors such as household income, ownership and employment status were associated with 19 diseases; and physical activity was associated with 17 diseases;
- 23 identified factors can be modified;
- Exhibitions have been shown at the start of life, including body weight and maternal smoking around birth, influence aging and the risk of premature death 30 to 80 years later;
- Environmental exhibitions have had a greater effect on lung, heart and liver disease, while genetic risk has dominated dementia and breast cancer.
https://www.youtube.com/watch?v=mhqe2k59iso“> Video by Cornelia and Austin Paper February 19
Professor Cornelia Van DuijnSt Cross professor of epidemiology at Oxford HEALTH Population And the main author of the article, said that “our research demonstrates the deep impact of the health of exhibitions which can be modified either by individuals or by policies aimed at improving socioeconomic conditions, to reduce smoking or promote physical activity.
“While genes play a key role in brain conditions and certain cancers, our results highlight the opportunities to alleviate the risks of chronic lung, heart and liver disease which are the main causes of disability and died worldwide. The exhibitions of the first lives are particularly important because they show that environmental factors accelerate aging early in life, but amply leave the opportunity to prevent lasting diseases and premature death.
The authors used a unique measurement of aging (A new “aged clock”) To monitor how people get older using blood protein levels. This has enabled them to link environmental exhibitions which predict early mortality with organic aging. It has previously been shown that this measure detects age -related changes, not only to British biobank, but also in two other Chinese and Finland cohort studies.
Dr Austin ArgentiriMain author of the study at Oxford Population Health and Research Fellow at Massachusetts General Hospital, said that “our approach to the exhibition has allowed us to quantify the relative environment and genetics contributions to aging, providing the overview The most complete on the date of the environment and the lifestyle leading to aging and premature death. These results highlight the potential advantages of concentration of concentration on our environments, our socio-economic contexts and our behaviors for the prevention of many diseases related to premature age and death.
Professor Bryan Williams, in scientific chief and doctor of the British Heart Foundation, added that “your income, your postal code and your history should not determine your chances of living a long and healthy life. But this pioneer study reinforces that it is the reality of too many people.
“We have long known that risk factors such as smoking have an impact on our heart and circulatory health, but this new research underlines how great the opportunity is to influence our chances of developing health problems, Including cardiovascular disease and death prematurely. We urgently need daring actions of the government to target over-the -ior obstacles to good health with which too many people in the United Kingdom face.
Research shows that if many identified individual exhibitions played a small role in premature death, the combined effect of these multiple exhibitions together during life (called Exposome) explained a large proportion of variation in premature mortality. The information of this study is paid to integrated strategies to improve the health of aging populations by identifying key combinations of environmental factors that shape the risk of premature death and many current diseases related to age simultaneously.
Professor Van Duijn said that “Environmental Health Studies have tended to focus on individual exhibitions based on a specific hypothesis. Although this approach has had many successes, the method has not always given reproducible and reliable results. Instead, we have followed an approach to the “without hypothesis” exhibition and studied all the exhibitions available to find the main engines of the disease and death.
“ We have taken a big step forward to understand how to provide precise evidence on the causes and consequences of age -related diseases by combining new calculation methods with clinical and epidemiological knowledge to explore the interaction between several Exhibitions. In a constantly evolving environment, it is essential that we combine these techniques with new progress in intelligent technology to monitor the lifestyle and the environment, as well as with biological data, to understand the impact of the environment over time. There are still many questions to answer related to diet, lifestyle and exposure to new pathogens (such as bird flu and COVVI-19) and chemicals (think of pesticides and plastics), and the impact of environmental and genetic factors in different populations.
The study was led by researchers from Oxford HEALTH Population in collaboration with researchers from Psychiatric departments And Anthropology at the University of Oxford; General Hospital of Massachusetts and Broad Institute, Boston; The University of Amsterdam; University of Erasmus, Rotterdam; and the University of Montpellier. Technical support was provided by the Biobank team from China Kadoorie.
Paper. ‘Integrate environmental and genetic architectures of aging and mortality‘. can be ready in Nature medicine.