Korte stevige wandeling elke dag kan er al voor zorgen dat je betere gezondheid houdt en 17 procent minder risico loopt op hart- en vaatziektes en 7 procent minder kanker.

1 maart 2023: Bron: BMJ

Uit een meta-analyse van totaal 196 studies, een zogeheten PROSPERO registratie blijkt samengevat dat mensen die elke dag een korte stevige wandeling maken (75 minuten per week) dit het risico op het krijgen van een hart- en vaatziekte en kanker vermindert en de kans op vroegtijdig overlijden ook vermindert. Volgens onderzoekers van de University of Cambridge kan een op de tien voortijdige overlijdens voorkomen worden door dagelijks een minuut of elf te bewegen. In deze meta-analyse onderzochten de onderzoekers van Cambridge universiteit in totaal meer dan 30 miljoen mensen wereldwijd.

De verschillen en aantoonbaar bewezen in losse studies was het grootst voor sterfte door alle oorzaken, maar ook sterfte aan hart- en vaatziektes en kanker gaven een duidelijk minder risico in relatie tot veel of weinig dagelijks wandelen / bewegen. De kans op een hartinfarct kan tot 17 procent kleiner worden, de kans op kanker gemiddeld 7 procent.

"Je moet jezelf voelen bewegen. Je hart gaat sneller slaan, zonder dat je buiten adem raakt", zegt hoofdonderzoeker Søren Brage.
Onder alle mensen die in de praktijk te weinig bewogen, had zelfs een op de zes voortijdige overlijdens voorkomen kunnen worden als diegene wél de minimaal aanbevolen hoeveelheid beweging had gehaald.

Het volledige studierapport is gratis in te zien. Klik op de titel van het abstract:

Non-occupational physical activity and risk of cardiovascular disease, cancer and mortality outcomes: a dose–response meta-analysis of large prospective studie.

http://orcid.org/0000-0001-5947-2617Leandro Garcia1,2,
http://orcid.org/0000-0003-3718-7502Matthew Pearce1,
Ali Abbas1,
Alexander Mok1,3,
http://orcid.org/0000-0002-7086-1047Tessa Strain1,
Sara Ali4,
Alessio Crippa5,
Paddy C Dempsey1,6,
Rajna Golubic1,7,
http://orcid.org/0000-0003-1946-9848Paul Kelly8,
Yvonne Laird9,10,
Eoin McNamara1,11,
Samuel Moore4,
Thiago Herick de Sa12,
Andrea D Smith1,13,
Katrien Wijndaele1,
James Woodcock1,
http://orcid.org/0000-0002-1265-7355Soren Brage1

Correspondence to Dr Soren Brage, MRC Epidemiology Unit, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK; soren.brage@mrc-epid.cam.ac.uk

Abstract

Objective To estimate the dose–response associations between non-occupational physical activity and several chronic disease and mortality outcomes in the general adult population.

Design Systematic review and cohort-level dose-response meta-analysis.

Data sources PubMed, Scopus, Web of Science and reference lists of published studies.

Eligibility criteria Prospective cohort studies with (1) general population samples >10 000 adults, (2) ≥3 physical activity categories, and (3) risk measures and CIs for all-cause mortality or incident total cardiovascular disease, coronary heart disease, stroke, heart failure, total cancer and site-specific cancers (head and neck, myeloid leukaemia, myeloma, gastric cardia, lung, liver, endometrium, colon, breast, bladder, rectum, oesophagus, prostate, kidney).

Results 196 articles were included, covering 94 cohorts with >30 million participants. The evidence base was largest for all-cause mortality (50 separate results; 163 415 543 person-years, 811 616 events), and incidence of cardiovascular disease (37 results; 28 884 209 person-years, 74 757 events) and cancer (31 results; 35 500 867 person-years, 185 870 events). In general, higher activity levels were associated with lower risk of all outcomes. Differences in risk were greater between 0 and 8.75 marginal metabolic equivalent of task-hours per week (mMET-hours/week) (equivalent to the recommended 150 min/week of moderate-to-vigorous aerobic physical activity), with smaller marginal differences in risk above this level to 17.5 mMET-hours/week, beyond which additional differences were small and uncertain. Associations were stronger for all-cause (relative risk (RR) at 8.75 mMET-hours/week: 0.69, 95% CI 0.65 to 0.73) and cardiovascular disease (RR at 8.75 mMET-hours/week: 0.71, 95% CI 0.66 to 0.77) mortality than for cancer mortality (RR at 8.75 mMET-hours/week: 0.85, 95% CI 0.81 to 0.89). If all insufficiently active individuals had achieved 8.75 mMET-hours/week, 15.7% (95% CI 13.1 to 18.2) of all premature deaths would have been averted.

Conclusions Inverse non-linear dose–response associations suggest substantial protection against a range of chronic disease outcomes from small increases in non-occupational physical activity in inactive adults.

PROSPERO registration number CRD42018095481.

What is already known

Higher levels of physical activity are associated with lower rates of premature death and chronic disease outcomes.
The shape of the dose–response association has been more difficult to determine and has not been established for a range of chronic diseases.
Accurate estimation of the dose–response association between physical activity and disease outcomes is needed to assess the disease burden of physical inactivity and the potential impact of changes to population levels of physical activity.

What are the findings?

Our findings suggest an appreciably lower risk of mortality, cardiovascular diseases and cancers from the equivalent of 75 min/week or less of moderate-intensity aerobic physical activity (ie, half the recommended minimum levels).
Our results include the first dose–response meta-analysis of nine site-specific cancers: bladder, esophageal, gastric cardia, head and neck, kidney, liver, lung, myeloid leukaemia and myeloma.
One in 10 premature deaths could have been prevented if everyone achieved even half the recommended level of physical activity.

Ethics statements

Patient consent for publication

Acknowledgments

We thank the authors of original articles who replied to our request for additional information about their analyses: Professor Alejandro Arrieta, Dr Michael Cook, Professor Ulf Ekelund, Professor Edward Giovannucci, Professor Reza Malekzadeh, Dr Jessica Morris, Dr Neil Murphy, Dr Mahdi Nalini, Dr Nicole Niehoff, Dr Tom Nilsen, Dr Annlia Paganini-Hill, Dr Song-Yi Park, Professor Louise Russell and Professor Wei Zheng. We also thank the IT team of the MRC Epidemiology Unit (University of Cambridge) for setting up the server to host the online results.

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Data supplement 1

Footnotes

Twitter @LGComplexity, @tessastraining, @narrowboat_paul, @SorenBrage
LG, MP, AA, AM and TS contributed equally.
JW and SB contributed equally.
Contributors Conception and design: LG, MP, AM, TS, JW, SB. Data acquisition: LG, MP, AM, TS, SA, PCD, RG, PK, YL, EM, SM, THdS, ADS, KW. Statistical analysis: LG, MP, AA, AC, JW, SB. Software: AA. Interpretation of data: LG, MP, AM, TS, PCD, RG, PK, YL, EM, THdS, ADS, KW, JW, SB. Drafting of the manuscript: LG, MP, AM, TS, SA, JW, SB. Critical revision of the manuscript: all authors. All authors approved the submitted version and agreed to be accountable for all aspects of the work.
Funding LG, AA and JW were supported by METAHIT, an MRC Methodology Panel project (MR/P02663X/1). AA, MP and JW have received funding from the European Research Council (ERC) under the Horizon 2020 Research and Innovation Programme (grant agreement 817754) (this material reflects only the authors’ views and the Commission is not liable for any use that may be made of the information contained therein). LG, AA and JW were supported by the Centre for Diet and Activity Research (CEDAR), a UKCRC Public Health Research Centre of Excellence funded by the British Heart Foundation, Cancer Research UK, Economic and Social Research Council, Medical Research Council, the National Institute for Health Research (NIHR) and the Wellcome Trust (MR/K023187/1). PCD was supported by a National Health and Medical Research Council of Australia Research Fellowship (no: 1142685). RG was supported by a Gates Cambridge Scholarship. MP and SB were supported by the NIHR Biomedical Research Centre, Cambridge (IS-BRC-1215-20014). AM was supported by the National Science Scholarship from Singapore, A*STAR. THdS was supported by the São Paulo Research Foundation (2012/08565-4 and 2013/25624-7) and the National Council for Scientific and Technological Development (200358/2014-6 and 402648/2015-3). MP, TS, PCD, KW and SB were supported by UK Medical Research Council (MC_UU_12015/3, MC_UU_00006/4).
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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