Developmental Biology - Obesity|
Obesity Risks Different For Men and Women
Obesity causes a higher risk of type 2 diabetes in women, but COPD and chronic kidney disease in men...
People who carry around unhealthy amounts of weight don't just have heart disease and diabetes to worry about. Cecilia Lindgren of the University of Oxford along with her colleagues, report their new findings in a study published October 24th in PLOS Genetics.
Obesity is implicated in two thirds of the leading causes of death from non-communicable diseases worldwide, however the risk of certain diseases differs for men and women.
As rates of obesity continue to grow worldwide, scientists have begun to suspect that excess weight might lead to or exacerbate other causes of death besides heart disease and type 2 diabetes. To identify these additional causes of death made worse by obesity, researchers performed an analysis that explores cause-and-effect relationships using genes and 3 obesity measurements from 228,466 women and 195,041 men in the UK Biobank.
Their analysis shows that obesity contributes to a laundry list of health problems including coronary artery disease, type 1 and 2 diabetes, stroke, chronic obstructive pulmonary disease, lung cancer, non-alcoholic fatty liver disease, chronic liver disease and kidney failure.
While obesity causes type 2 diabetes in both women and men, women experienced a higher risk of type 2 diabetes when compared to men, while men face a greater risk of chronic obstructive pulmonary disease and chronic kidney disease.
"This study shows just how harmful carrying excess weight can be to human health. And, that women and men may experience different diseases as a result," explains first author, Jenny Censin.
Michael Holmes, who supervised the work along with Cecilia Lindgren, adds:
"Given the compelling evidence of harm that arises as a consequence of obesity across a broad range of diseases resulting in death — our findings highlight a critical need for public health measures to stem the obesity tide."
Overall, the study finds obesity causes or contributes to the majority of leading causes of death worldwide not linked to infectious disease. The impacts of obesity however, manifest differently in men and women, findings that have potential implications for the design of public health strategies, suggesting different preventative measures targeted at men and women may be warranted.
Obesity traits are causally implicated with risk of cardiometabolic diseases. It remains unclear whether there are similar causal effects of obesity traits on other non-communicable diseases. Also, it is largely unexplored whether there are any sex-specific differences in the causal effects of obesity traits on cardiometabolic diseases and other leading causes of death. We constructed sex-specific genetic risk scores (GRS) for three obesity traits; body mass index (BMI), waist-hip ratio (WHR), and WHR adjusted for BMI, including 565, 324, and 337 genetic variants, respectively. These GRSs were then used as instrumental variables to assess associations between the obesity traits and leading causes of mortality in the UK Biobank using Mendelian randomization. We also investigated associations with potential mediators, including smoking, glycemic and blood pressure traits. Sex-differences were subsequently assessed by Cochran’s Q-test (Phet). A Mendelian randomization analysis of 228,466 women and 195,041 men showed that obesity causes coronary artery disease, stroke (particularly ischemic), chronic obstructive pulmonary disease, lung cancer, type 2 and 1 diabetes mellitus, non-alcoholic fatty liver disease, chronic liver disease, and acute and chronic renal failure. Higher BMI led to higher risk of type 2 diabetes in women than in men (Phet = 1.4×10-5). Waist-hip-ratio led to a higher risk of chronic obstructive pulmonary disease (Phet = 3.7×10-6) and higher risk of chronic renal failure (Phet = 1.0×10-4) in men than women. Obesity traits have an etiological role in the majority of the leading global causes of death. Sex differences exist in the effects of obesity traits on risk of type 2 diabetes, chronic obstructive pulmonary disease, and renal failure, which may have downstream implications for public health.
Obesity is increasing globally and has been linked to major causes of death, such as diabetes and heart disease. Still, the causal effects of obesity on other leading causes of death is relatively unexplored. It is also unclear if any such effects differ between men and women. Mendelian randomization is a method that explores causal relationships between traits using genetic data. Using Mendelian randomization, we investigated the effects of obesity traits on leading causes of death and assessed if any such effects differ between men and women. We found that obesity increases the risks of heart disease, stroke, chronic obstructive pulmonary disease, lung cancer, diabetes, kidney disease, non-alcoholic fatty liver disease and chronic liver disease. Higher body mass index led to a higher risk of type 2 diabetes in women than in men, whereas a higher waist-hip ratio increased risks of chronic obstructive pulmonary disease and chronic kidney disease more in men than in women. In summary, obesity traits are causally involved in the majority of the leading causes of death, and some obesity traits affect disease risk differently in men and women. This has potential implications for public health strategies and indicates that sex-specific preventative measures may be needed.
Jenny C. Censin, Sanne A. E. Peters, Jonas Bovijn, Teresa Ferreira, Sara L. Pulit, Reedik Mägi, Anubha Mahajan, Michael V. Holmes and Cecilia M. Lindgren.
Computation used the Oxford Biomedical Research Computing (BMRC) facility, a joint development between the Wellcome Centre for Human Genetics and the Big Data Institute supported by Health Data Research UK and the NIHR Oxford Biomedical Research Centre. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health.
The authors thank the UK Biobank (application 11867; http://www.ukbiobank.ac.uk/).
JCC is funded by an NDM Prize Studentship (17/18_MSD_1108275) from the Oxford Medical Research Council Doctoral Training Partnership (Oxford MRC DTP; https://www.medsci.ox.ac.uk) and the Nuffield Department of Clinical Medicine (https://www.ndm.ox.ac.uk/), University of Oxford. SAEP is supported by a UK Medical Research Council Skills Development Fellowship (MR/P014550/1). JB is supported by funding from the Rhodes Trust (https://www.rhodeshouse.ox.ac.uk/), Clarendon Fund (https://www.ox.ac.uk/) and the Medical Sciences Doctoral Training Centre (https://www.medsci.ox.ac.uk/), University of Oxford. TF is supported by the NIHR Biomedical Research Centre, Oxford. SLP was funded by a Veni Fellowship (016.186.071; ZonMW; https://www.nwo.nl/) from the Dutch Organization for Scientific Research, Nederlandse Organisatie voor Wetenschappelijk Onderzoek (NWO) during the course of the study. MVH works in a unit that receives funding from the Medical Research Council (MRC; https://mrc.ukri.org/) and is supported by a British Heart Foundation Intermediate Clinical Research Fellowship (FS/18/23/33512; https://www.bhf.org.uk/) and the National Institute for Health Research Oxford Biomedical Research Centre (https://oxfordbrc.nihr.ac.uk). CML is supported by the Li Ka Shing Foundation (https://www.lksf.org/), WT-SSI/John Fell funds (https://researchsupport.admin.ox.ac.uk/), the National Institute for Health Research Biomedical Research Centre, Oxford (https://oxfordbrc.nihr.ac.uk/), Widenlife (H2020-TWINN-2015-692065; https://cordis.europa.eu/), and National Institute of Health (NIH; 5P50HD028138-27; https://www.nih.gov/). Computation used the Oxford Biomedical Research Computing (BMRC) facility, a joint development between the Wellcome Centre for Human Genetics and the Big Data Institute supported by Health Data Research UK and the NIHR Oxford Biomedical Research Centre, and with financial support provided by the Wellcome Trust Core Award Grant Number 203141/Z/16/Z. The funders had not role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.
SLP has, since the writing of the article, started working for Vertex. MVH has collaborated with Boehringer Ingelheim in research, and in accordance with the policy of the Clinical Trial Service Unit and Epidemiological Studies Unit (University of Oxford), did not accept any personal payment. CML has collaborated with Novo Nordisk and Bayer in research, and in accordance with the policy of University of Oxford, did not accept any personal payment.
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