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Physical activity and mortality among Norwegian women – the Norwegian Women and Cancer Study

Physical activity and mortality among Norwegian women – the Norwegian Women and Cancer Study Clinical Epidemiology Dovepress open access to scientific and medical research Open Access Full Text Article O rig in AL rE s EA r C h Physical activity and mortality among norwegian women – the norwegian Women and Cancer study Kristin Benjaminsen Borch Background: Physical activity (PA) and its relationship with all-cause mortality suggest a strong and consistent inverse association. This study prospectively investigated the associa- Tonje Braaten tion between PA level and mortality among participants of the Norwegian Women and Cancer Eiliv Lund 1,2,3,4 (NOWAC) Study. Elisabete Weiderpass Methods: A total of 66,136 NOWAC participants were followed-up until December 31st 2008. Department of Community PA level and possible confounding factors were obtained through a self-administered question- Medicine/University of Tromsø, Tromsø, n orway; Department naire at enrolment. Cox proportional hazards regression was used to calculate adjusted relative of Medical Epidemiology and risks (RRs) and 95% confidence intervals (CIs) for all-cause, cardiovascular disease (CVD) and Biostatistics, Karolinska institutet, 3 cancer mortality and PA levels defined from 1 to 10 on a global scale. stockholm, sweden; Cancer registry of n orway, Oslo, n orway; Folkhälsan Results: PA levels 1–4 were associated with a significantly increased risk of all-cause mor - r esearch Centre, s amfundet tality (level 1 RR = 2.35; 95% CI: 1.94–2.84, level 2 RR = 1.71; 95% CI: 1.45–2.00, level 3 Folkhälsan, helsinki, Finland RR = 1.30; 95% CI: 1.14–1.49, level 4 RR = 1.07; 95% CI: 0.95–1.22), compared with PA level 5. CVD mortality risk increased in PA levels 1–3 (level 1 RR = 3.50; 95% CI: 2.41–5.10, level 2 RR = 1.50; 95% CI: 0.99–2.25, level 3 RR = 1.12; 95% CI: 0.79–1.60) as did cancer mortality risk (RR = 1.32; 95% CI: 0.96–1.81, RR = 1.48; 95% CI: 1.19–1.84, RR = 1.26; 95% CI: 1.06–1.50, respectively). The magnitude of the associations was consistent across strata of age, smoking, and body mass index. The population attributable fractions for PA levels 1–4 were: all-cause mortality, 11.5%; CVD mortality, 11.3%; cancer mortality, 7.8%. Conclusion: There is a significant trend of increased risk of all-cause, CVD and cancer mortal- ity in relation to low PA levels among Norwegian women. Keywords: physical activity, mortality, cardiovascular disease, cancer, Norway, women Introduction Physical activity (PA) and its relationship with mortality have been investigated in 1–9 several studies and a strong and consistent inverse association between PA and 10 11 all-cause mortality has been suggested. National and international public health recommendations for PA are based on evidence linking a physically active lifestyle to reduced mortality. One review on PA and all-cause mortality concluded that there is an inverse dose-response relationship between total amount of PA and all-cause mortality and another review suggested that physically active men and women have a 34% lower Correspondence: Kristin Benjaminsen Borch premature mortality risk. In a study of Norwegian and Swedish women below the Department of Community Medicine/ age of 60 years, PA at baseline substantially reduced all-cause mortality. It has not University of Tromsø, 9037 Tromsø, norway been convincingly documented whether this is also applicable to specific causes of Tel +47 776 45443 death such as cardiovascular disease (CVD) and cancer, and the degree to which PA Fax +47 776 44831 Email kristin.benjaminsen.borch@uit.no independently contributes to mortality risk has not been explored thoroughly. submit your manuscript | www.dovepress.com Clinical Epidemiology 2011:3 229–235 Dovepress © 2011 Borch et al, publisher and licensee Dove Medical Press Ltd. This is an Open Access article http://dx.doi.org/10.2147/CLEP.S22681 which permits unrestricted noncommercial use, provided the original work is properly cited. Borch et al Dovepress The aim of the present study was therefore to investigate and outcomes from objective measures of a combined sensor what impact PA level has on all-cause mortality in middle- monitoring heart rate and movement, and appeared valid to aged women, to specify the relative risk (RR) of death due rank PA in a Norwegian population of women. to CVD and cancer, and to calculate the population attribut- able fraction (PAF) of all-cause, CVD and cancer mortality Covariates among women in Norway. Information collected at cohort enrolment included age; duration of education; height; weight; smoking history Methods (including smoking status: current, former, never; duration and quantity of cigarettes smoked/day); alcohol consump- study population tion (grams/day); detailed information on dietary habits and The Norwegian Women and Cancer (NOWAC) Study is a intake of certain food items which was used to calculate total population-based prospective cohort study which enrolled energy intake (Kcal/day); parity; use of oral contraceptives or the first participants in 1991. A more detailed description of postmenopausal hormone therapy (HT); age at menarche; and the cohort and design of the NOWAC Study has previously 16–18 14 15 age at menopause. History of heart failure, myocardial been described, as has external validity. Briefly, from infarction, angina pectoris, diabetes mellitus, fibromyalgia, 1991–1997 a random sample of women aged 30–70 years rheumatism and hypertension were self-reported. Information was drawn from the National Population Register in Norway on cancer diagnosis before cohort enrolment was obtained and invited to participate in the study. All women received a through linkages to the database of the Cancer Registry of letter of invitation requesting informed consent and a com- Norway. prehensive eight-page self-administered questionnaire. Of those invited, 102,540 women (57%) completed and returned Follow-up the questionnaire. Due to study logistics, the first enrolment Person-years were calculated from the start of follow-up was divided into 24 mailings over 7 years. For the present until the date of emigration, death, or end of the study analysis, we collected baseline information from the women period (December 31st 2008), whichever occurred first. who answered the first mailing in 1996–1997 (37,899 women), We obtained information on date of emigration and death and those who answered a second mailing in 1998 (46,965 from the National Population Register. Cause of death was women), for a total of 84,864 women. We excluded 53 women obtained from the National Register for Causes of Death, with a reported date of emigration or death that was before and categorized into specific causes of death: CVD deaths the date of recruitment. We excluded 8137 women with miss- (ICD-10: I00-I99), including stroke, coronary heart disease, ing information on PA level at cohort enrolment and another and other vascular causes; cancer deaths (ICD-10: C00-D48) 10,538 women due to lack of information on other covariates and other-cause deaths (from causes other than CVD and examined. Hence 66,136 women were eligible for inclusion cancer). The combination of the aforementioned categories in our present analysis. The Regional Ethical Committee and was classified as all-cause mortality. the Norwegian Data Inspectorate approved the study. Assessment of PA level statistical analysis PA level at age 14 years, 30 years and at the time of cohort Characteristics of the study population are presented as means enrolment were assessed by self-report on a scale of 1 to 10. and standard deviations, and frequency tabulations over the PA was den fi ed in the questionnaire as follows: “By physical different PA levels. Cox proportional hazards regression, activity we mean activity both at work and outside work, at with follow-up time as the time scale, was used to calculate home, as well as training/exercise and other physical activ- adjusted hazard ratios (HRs) (interpreted as estimates of ity, such as walking, etc. Please mark the number that best RRs) and corresponding 95% confidence intervals (CIs), describes your level of physical activity; 1 being very low which were used to examine the association between PA level and 10 being very high”. The PA scale used for this study and all-cause, CVD and cancer mortality. The proportional refers to the total amount of PA, including different domains, hazard assumption was checked using Schoenfeld residuals frequencies, durations and intensities in one global score, and Kaplan–Meier plots, which suggested no evidence of and have been recently validated. A moderate but significant deviation from proportionality. The initial survival analyses (P , 0.001) Spearman’s rank correlation coefficient was were done by PA level adjusted for age and further built up found, in the range of 0.36 to 0.46, between the PA scale in multivariate models, with covariates added in a backward submit your manuscript | www.dovepress.com Clinical Epidemiology 2011:3 Dovepress Dovepress Physical activity and mortality among women stepwise manner to take possible confounders into account. equation: PAF = (P (RR - 1)/1 + P (RR - 1)), where P is e e e Additional analyses were conducted separately by age group, the proportion of the exposed population, and RR is the risk body mass index (BMI) and history of CVD, diabetes mel- estimate for the exposed compared to the unexposed popula- litus or prevalent cancer to determine whether associations tion in the final multivariate proportional hazards regression were stronger in these subgroups. The analyses were repeated model, including all aforementioned covariates. The cut-off excluding women with CVD, diabetes mellitus or prevalent point a priori for the exposed population was set at PA level 4 cancer to minimize the potential effect of reverse causality. PA or less, which divided the study population in two: exposed level at baseline was entered into the Cox regression models (PA levels 1–4) and unexposed (PA levels 5–10). Analyses as a categorical variable with 10 categories, in order to ree fl ct were conducted using STATA version 11.0, special edition the study scale. PA level 5 (moderate PA level) in the study (StataCorp, Lakeway Drive, College Station, TX). scale was used as the reference category, compared to PA Results levels 1–4 (low PA levels), and 6–10 (high PA levels). Characteristics of the study population at cohort enrol- Covariates examined in the multivariate Cox regression ment and mortality during follow-up are given in Table 1. models were age (40–49, 50–59, $ 60 years); BMI (weight in During 705,980 person-years of follow-up from 1996 to kilograms divided by height in centimeters squared, , 18.5, December 31st 2008, 2572 deaths were reported. The mean 18.5–24, 25–29, $ 30) with the second category as the refer- age of the participants at baseline was 50.5 years (standard ence; height (cm); total energy intake (Kcal/day). Smoking deviation, 41–70 years) (Table 1). status (never, former, current), smoking duration (years) and Self-reported PA level and health-related characteristics quantity smoked (pack-years = the total number of years a of study women are shown in Table 2 by PA level. Almost smoker smoked 20 cigarettes/day) were combined in the 30% of the women reported low PA levels (levels 1–4), and analysis as one variable (age at start $ 20 years and current women who reported moderate to high PA levels (levels 5–10) smoker, age at start $ 20 years and former smoker, age at tended to be leaner and had a higher total energy intake. start , 20 years, 0–19 pack-years and current smoker, age at Women with a PA level of 1 were more often current smokers start , 20 years and former smoker, and finally $ 20 pack- compared to women with moderate to high PA levels. CVD years, age at start , 20 years and current smoker). Duration was reported by 13% of study women, and this proportion of education (0–9, 10–12 and $ 13 years) and menopausal was lower among women reporting moderate to high PA status at enrolment (postmenopausal yes/no) were further levels compared with those who reported low PA levels. included. Baseline information on menopausal status was A similar pattern was observed for diabetes mellitus, which available for 50,875 women, and the remaining women was reported by 1.5% of study women. A total of 4.2% of were either perimenopausal (N = 6730), hysterectomized women were diagnosed with cancer before cohort enrolment, at ,  53 years of age (N = 2150), HT users ,  53 years of and there was a higher percentage of prevalent cancer among age (N = 5477) or had missing information (N = 1828). Use women with a PA level of 1 (Table 2). of HT was registered as ever or never, and self-reported Survival analysis of all-cause mortality with adjustments disease (yes/no to any of the following: heart failure, myo- for different covariates showed a significantly increased cardial infarction, angina pectoris, diabetes mellitus, fibro- myalgia, rheumatism or hypertension) was also included in order to analyze each disease as a separate covariate. Table 1 Characteristics of the study population at baseline and Alcohol intake was divided into four categories (none, mortality during follow-up – The norwegian Women and Cancer study low = 0.1–3.9 grams/day, medium = 4.0–10.0 grams/day and high intake . 10.0 grams/day) with low intake as refer- Characteristics number of women 66,136 ence category, and information on age at first birth (, 20, Mean age at entry (sD), years 50.5 (6.55) 20–25, . 25 years) and parity (0, 1, 2, $ 3 children) was Mean person-years of follow-up (sD) 10.70 (1.48) combined into one variable. Total person-years at risk 705,980 number of deaths in the follow-up period 2572 PAF was interpreted as the proportional reduction in the number of deaths by cause average population mortality risk that would occur if low CVD 401 PA levels were eliminated from the population, assuming Cancer 1584 that the distribution of the adjustment variables remained Other causes 587 unchanged. PAF was estimated using the following Abbreviations: sD, standard deviation; CVD, cardiovascular disease. submit your manuscript | www.dovepress.com Clinical Epidemiology 2011:3 Dovepress Borch et al Dovepress Table 2 Physical activity (PA) level and health-related characteristics according to PA level at cohort enrolment in 1996–1998 among 66,136 women from the norwegian Women and Cancer study Characteristics PA level 1 2 3 4 5 6 7 8 9 10 n 949 2421 5810 9713 16,862 12,021 9828 5489 1896 1147 PA level, % 1.43 3.7 8.8 14.7 25.5 18.2 14.9 8.3 2.9 1.73 Age, mean (years) 53.6 52 51.3 50.9 50.5 50 49.8 50 50.5 51.4 Duration of education, mean (years) 10.4 11.3 11.8 12 11.9 12 12.3 11.9 11.5 10.8 BMi, mean (kg/m ) 26.6 26.5 25.8 25.3 24.6 24.1 23.7 23.5 23.4 23.5 height, mean (cm) 165.1 165.9 165.9 166 166.2 166.3 166.4 166.1 166.2 165.6 Weight, mean (kg) 72.7 72.9 71.1 69.7 68 66.7 65.7 65 64.7 64.6 Current smoker (%) 44.9 39.4 34.5 32.5 32.3 30 28.6 30.9 32.3 36.7 Alcohol consumption (grams/day) 3.0 2.9 3.4 3.3 3.2 3.3 3.4 3.2 3.0 2.6 Total energy intake, mean (Kcal/day) 1472 1515 1548 1592 1626 1661 1686 1713 1738 1758 nulliparous (%) 9.5 10.0 9.5 9.0 8.1 7.7 7.8 9.1 7.5 8.4 First birth, mean age (years) 23.5 24 23.9 23.9 24 24 23.8 23.5 23.3 23.9 hormone therapy use at enrolment (%) 36.8 35.6 33.8 32.5 32.1 30.1 29.3 27.9 29.6 26.7 Postmenopausal at enrolment (%) 74.7 65.2 58.8 56.5 54.0 49.5 48.4 50.5 53.0 57.8 Cardiovascular disease (%) 27.8 23.3 18.7 16.4 13.2 11.3 10.4 10.3 9.3 11.2 Diabetes mellitus (%) 4.6 3.7 2.3 1.5 1.5 1.3 0.9 1.0 1.2 2.3 Cancer (%) 7.1 6.0 5.2 4.4 4.4 3.7 3.6 3.4 3.6 4.5 a b Notes: Among those who had children; Postmenopausal status based on 50,875 women, excluded from this category were 6291 women classified as perimenopausal, 2150 with hysterectomy , 53 years of age and 5477 hormone therapy users , 53 years of age; Self-reported cardiovascular diseases defined as heart failure, myocardial infarction, angina pectoris, and hypertension; information on cancer diagnosis before cohort enrolment obtained from the Cancer registry of norway. risk of mortality for women with low PA levels (level 1 prevalent cancer, did not signic fi antly change the results (data RR = 2.35; 95% CI: 1.94–2.84, level 2 RR = 1.71; 95% CI: not shown) and these participants were therefore retained in 1.45–2.00, level 3 RR = 1.30; 95% CI: 1.14–1.49, level 4 the n fi al analysis. Survival analysis was conducted in strata of RR = 1.07; 95% CI: 0.95–1.22), compared with women with age, BMI and history of CVD, diabetes mellitus and cancer. a moderate PA level (Table 3). The association between PA No evidence of a differential effect of PA level on mortality level and all-cause mortality showed a significant overall according to age, BMI, or history of included disease was trend (P , 0.001) of reduced mortality risk in women with found, indicating that the increased mortality risk found in moderate to high PA levels compared to women with low PA the main survival analyses are independent of these factors levels. However, the shape of the association seemed non- (data not shown). linear; more like an L-shape, indicating no additive effect on The proportion of the population with low PA levels mortality beyond the moderate PA level (Figure 1). was 29% with an adjusted RR of 1.45 (95% CI: 1.34–1.57) CVD mortality risk for women with a PA level of 1 was for all-cause mortality, 1.44 (95% CI: 1.17–1.76) for CVD found to be 3.5 times higher (95% CI: 2.41–5.10) than for mortality and 1.29 (95% CI: 1.16–1.43) for cancer mortality women with a moderate PA level (Table 3). PA levels of 2, for the exposed compared to the unexposed population. Our 3 and 4 separately showed an increased risk as well (though results showed that 11.5% of all-cause mortality, 11.3% of not significant), albeit not as high as for PA level 1 (Table 3). CVD mortality and 7.8% of cancer mortality was attributable The overall trend for CVD mortality risk in women with low to low PA levels. PA levels was significant (P , 0.001). The results indicated a significant trend (P = 0.002) of increased risk of cancer Discussion mortality for women with decreasing PA levels. Separate We found a significant trend of reduced all-cause mortality results for PA levels 1, 2 and 3 were RR = 1.32 (95% CI: with increasing PA level, although the shape of the inverse 0.96–1.81), 1.48 (95% CI: 1.19–1.84) and 1.26 (95% CI: association was non-linear and more L-shaped, with no 1.06–1.50), respectively. additional effect beyond the moderate PA level of 5. Women Participants with self-reported diseases or prevalent reporting low PA levels (ie, PA levels 1–4) had a signifi- cancer at baseline were included and adjusted for in the cantly increased risk of all-cause mortality, with a stronger main analytical model. The results of sensitivity analyses association for CVD than for cancer-related mortality. after exclusion of all women with CVD, diabetes mellitus, or Separate subgroup analyses indicated that the findings were submit your manuscript | www.dovepress.com Clinical Epidemiology 2011:3 Dovepress 1 Dovepress Physical activity and mortality among women Table 3 Relative risks (RRs) and 95% confidence intervals (CIs) All cause mortality of the association between physical activity (PA) level and all- CVD mortality Cancer mortality cause, cardiovascular disease and cancer mortality among 66,136 women from the norwegian Women and Cancer study PA level N of Age-adjusted Multivariate deaths RR (95% CI) RR (95% CI) All-cause mortality 1 139 3.17 (2.64–3.82) 2.35 (1.94–2.84) 0246 3579810 2 203 2.04 (1.74–2.39) 1.71 (1.45–2.00) Self-reported physical activity level 3 321 1.40 (1.22–1.60) 1.30 (1.14–1.49) 4 402 1.09 (0.96–1.23) 1.07 (0.95–1.22) Figure 1 Multivariate relative risks (rrs) of all cause, CVD and cancer mortality and 5 621 1.0 1.0 physical activity (PA) level. 6 342 0.80 (0.70–0.93) 0.83 (0.73–0.95) Abbreviation: CVD, cardiovascular disease. 7 276 0.81 (0.70–0.93) 0.86 (0.75–0.99) 8 170 0.87 (0.74–1.03) 0.89 (0.75–1.06) follow-up time, and the evaluation of cause-specic fi mortality. 9 54 0.76 (0.58–1.00) 0.76 (0.58–1.01) 20 21,22 The study information on HT use and dietary habits are 10 44 0.94 (0.69–1.28) 0.86 (0.63–1.17) considered valid. The NOWAC cohort is representative of P for trend ,0.001 ,0.001 Cardiovascular disease mortality the Norwegian female population in the studied age groups, 1 44 6.04 (4.21–8.66) 3.50 (2.41–5.10) and there was no major selection bias that would invalidate 2 32 2.10 (1.37–3.08) 1.50 (0.99–2.25) a PAF calculation. 3 46 1.31 (0.92–1.86) 1.12 (0.79–1.60) Despite the different methods that exist to measure PA 4 60 1.10 (0.78–1.49) 1.00 (0.72–1.39) 5 92 1.0 1.0 level, a substantial amount of evidence from observational 6 48 0.77 (0.5–1.09) 0.83 (0.58–1.17) studies confirms an inverse relationship between low PA 7 40 0.80 (0.55–1.17) 0.89 (0.61–1.30) 2,12,23,24 levels and increased mortality risk in women. Our 8 29 1.01 (0.67–1.55) 1.07 (0.71–1.63) 9 5 0.47 (0.19–1.15) 0.47 (0.19–1.15) findings are in line with these observations for all-cause, 10 5 0.70 (0.28–1.71) 0.62 (0.25–1.53) CVD and cancer mortality. Our observations suggested that P for trend ,0.001 ,0.001 the relationship is non-linear, with the greatest benefit to be Cancer mortality had by changing from a PA level of 1 to any level between 2 1 43 1.60 (1.17–2.19) 1.32 (0.96–1.81) 2 105 1.67 (1.35–2.08) 1.48 (1.19–1.84) and 5, which has also been confirmed in other studies. 3 192 1.32 (1.11–1.57) 1.26 (1.06–1.50) Physical inactivity is considered the fourth leading cause 4 252 1.07 (0.91–1.25) 1.07 (0.91–1.25) of death worldwide. In our study, assuming causality, 5 399 1.0 1.0 the PAF for low PA levels among women was 11.5% for 6 234 0.85 (0.73–1.00) 0.88 (0.75–1.03) 7 188 0.85 (0.72–1.01) 0.90 (0.76–1.07) all-cause, 11.3% for CVD and 7.8% for cancer mortality, 8 111 0.88 (0.72–1.09) 0.92 (0.74–1.13) which is substantial. For modifiable factors like PA level, 9 37 0.82 (0.58–1.14) 0.84 (0.60–1.17) PAF is useful for the planning of public health strategies 10 23 0.78 (0.51–1.18) 0.75 (0.49–1.15) and interventions. The Nurses’ Health study in the United P for trend ,0.001 ,0.002 States found a PAF of 17% for all-cause, 28% for CVD and Notes: Data are adjusted in the multivariate model for age at cohort enrolment, body mass index, height, smoking status, years of smoking, amount of smoking, alcohol 9% for cancer mortality among women reporting a duration intake, menopausal status, age at first birth, parity, hormone therapy use, cardiovascular disease diabetes mellitus and prevalent cancer. r eference level for body mass index is of PA of less than 30 minutes per day. In a global health normal weight and for alcohol intake the reference category is low intake. Duration of report the estimated PAF of mortality was 8% for physical education in years and total energy intake was tested in the model, but not included in the final analytical model as they did not change the risk estimates. All levels of PA inactivity in high-income countries. However, underestima- from the study scale, 1 being the lowest PA level, and 10 being the highest. tion is likely as PA level measures were limited. Our results indicated a significant, but weaker trend in the association independent of age, BMI and history of CVD, diabetes between PA and cancer mortality than CVD mortality. Cancer mellitus, or cancer. PAF calculation showed that 11.5% of develops over several years before symptoms appear and are all-cause deaths, 11.3% of CVD deaths and 7.8% of cancer diagnosed. This suggests that duration of follow-up is critical deaths were attributable to low PA levels. and must be of a certain length to capture the magnitude Strengths of our study include the prospective design, of an association. Among environmental risk factors for the large sample size, relatively high response rates, almost cancer incidence, lifestyle factors such as tobacco use, poor complete follow-up (99.9%) with almost 11 years of mean nutrition, obesity and physical inactivity, which we adjusted submit your manuscript | www.dovepress.com Clinical Epidemiology 2011:3 Dovepress Multivariate RR 0.5 1 2 4 Borch et al Dovepress for in our study, account for about one-third of all cancers. Disease or preliminary stages of a disease may inhibit We further adjusted for hormone use (oral contraceptives and a person’s ability to be physically active, meaning that part HT) and reproductive factors. Furthermore, our findings are of the observed association between PA level and mortality in line with several other studies that suggested an association may be due to confounding or reverse causation. Restricting 28–30 between reduced cancer mortality and PA level. the analysis to women without a history of disease would Our study has some limitations. PA level in our study have entailed exclusion of almost 12,000 women, and was self-reported and assessed at baseline only. Changes therefore we retained and adjusted for this information, in in PA level over time could introduce bias. Therefore the addition to performing a sensitivity analysis excluding them. interpretation of our results should take into consideration The effect of PA on mortality remained consistent both in the possibility of changes in behaviour over time: if anything the sensitivity analysis and the stratified analysis according PA levels decrease with age, and therefore our results are to CVD disease, diabetes mellitus and prevalent cancer. probably underestimates of the true PAF. Measurement errors Thus, it is unlikely that our results might be due to low PA are inevitable and self-report is a crude measure of PA level, levels explaining prevalent disease, but more probably that which necessarily entails some degree of misclassification. prevalent diseases are explaining low PA levels. Residual A known problem of self-reporting of a desirable behaviour confounding can never be excluded in non-randomized like PA is the tendency to report levels that are higher than studies, however, other prospective studies support our one really has. However, the size of the NOWAC cohort findings. limits the use of other more accurate measures such as Despite the limitations of this study, and the existence of accelerometer or heart rate monitors. The results from our a possible spurious component in the relationship between PA validation study indicated that the scale of 10 PA levels levels and mortality, the benefits of being physically active is suff icient to differentiate between levels of the total are biologically plausible. An increase from low PA levels amount of PA. Although the challenge of equating different up to a moderate PA level would entail an 11.5% reduction total amounts of PA to the different PA levels on the scale in all-cause mortality in women in Norway. PAF estimates remains, the 10 categories represent ordered levels of the depend on RRs and the proportion of exposure in a given total amount of PA which have a strong predictive value in population, which has to be considered when generalizing relation to mortality. Studies have shown that a higher total to other populations where low PA levels could differ. Our volume of PA is clearly associated with decreased all-cause study design cannot determine a causal association, but our 12,34 mortality. Total volume of PA refers to energy expenditure results indicate a significant trend of reduced mortality risk related to activity quantified by duration and frequency. If with increasing PA levels, which suggests such an associa- total volume of PA is the main contributor in the relationship tion. The results of the present study suggest that PA level between mortality and PA, it stands to reason that our global is an important lifestyle behaviour to target in public health score, which includes frequency, intensity and duration of PA strategies. to deduce PA levels, is appropriate for use in the estimation of the magnitude of a given effect. Acknowledgments A weakness of our study is the reliance on self-report The authors thank the NOWAC Study staff and participants for all covariates examined. This could introduce misclas- for their invaluable contributions to this study. sification error, thereby affecting our estimates. However, in the NOWAC Study information on the use of HT and Author contributions 21,22 dietary habits, including alcohol habits, have been vali- KBB carried out the statistical analysis and drafted the dated with good results. Furthermore, information on parity manuscript. TB contributed to the statistical analysis and and duration of education has been compared to national interpretation of the data. EL is the principal investigator and registers with no statistically significant differences found. designed the NOWAC Study. EW contributed with planning Self-reported information on height and weight has not yet of the data analysis, interpretation of the data and critical been validated in the NOWAC Study, but ongoing research revision of the manuscript. All authors read and approved (unpublished) indicates a limited extent of misclassification the final manuscript. bias. Despite certain limitations, self-reporting methods are considered adequate to deal with large sample sizes, practical Disclosure to administer, and less expensive. The authors report no conflicts of interest in this work. submit your manuscript | www.dovepress.com Clinical Epidemiology 2011:3 Dovepress Dovepress Physical activity and mortality among women 18. Skeie G, Hjartåker A, Lund E. Diet among breast cancer survivors and References healthy women. The Norwegian Women and Cancer Study. Eur J Clin 1. Besson H, Ekelund U, Brage S, et al. Relationship between subdomains Nutr. 2006;60(9):1046–1054. of total physical activity and mortality. Med Sci Sports Exerc. 2008; 19. Rockhill B, Newman B, Weinberg C. Use and misuse of population 40(11):1909–1915. attributable fractions. Am J Public Health. 1998;88(1):15–19. 2. Oguma Y, Sesso HD, Paffenbarger RS Jr, Lee IM. 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Clinical Epidemiology Dovepress Publish your work in this journal Clinical Epidemiology is an international, peer-reviewed, open access reviews, risk & safety of medical interventions, epidemiology & bio- journal focusing on disease and drug epidemiology, identification of statical methods, evaluation of guidelines, translational medicine, health risk factors and screening procedures to develop optimal preventative policies & economic evaluations. The manuscript management system initiatives and programs. Specific topics include: diagnosis, prognosis, is completely online and includes a very quick and fair peer-review treatment, screening, prevention, risk factor modification, systematic system, which is all easy to use. Submit your manuscript here: http://www.dovepress.com/clinical-epidemiology-journal submit your manuscript | www.dovepress.com Clinical Epidemiology 2011:3 Dovepress http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical Epidemiology Pubmed Central

Physical activity and mortality among Norwegian women – the Norwegian Women and Cancer Study

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Abstract

Clinical Epidemiology Dovepress open access to scientific and medical research Open Access Full Text Article O rig in AL rE s EA r C h Physical activity and mortality among norwegian women – the norwegian Women and Cancer study Kristin Benjaminsen Borch Background: Physical activity (PA) and its relationship with all-cause mortality suggest a strong and consistent inverse association. This study prospectively investigated the associa- Tonje Braaten tion between PA level and mortality among participants of the Norwegian Women and Cancer Eiliv Lund 1,2,3,4 (NOWAC) Study. Elisabete Weiderpass Methods: A total of 66,136 NOWAC participants were followed-up until December 31st 2008. Department of Community PA level and possible confounding factors were obtained through a self-administered question- Medicine/University of Tromsø, Tromsø, n orway; Department naire at enrolment. Cox proportional hazards regression was used to calculate adjusted relative of Medical Epidemiology and risks (RRs) and 95% confidence intervals (CIs) for all-cause, cardiovascular disease (CVD) and Biostatistics, Karolinska institutet, 3 cancer mortality and PA levels defined from 1 to 10 on a global scale. stockholm, sweden; Cancer registry of n orway, Oslo, n orway; Folkhälsan Results: PA levels 1–4 were associated with a significantly increased risk of all-cause mor - r esearch Centre, s amfundet tality (level 1 RR = 2.35; 95% CI: 1.94–2.84, level 2 RR = 1.71; 95% CI: 1.45–2.00, level 3 Folkhälsan, helsinki, Finland RR = 1.30; 95% CI: 1.14–1.49, level 4 RR = 1.07; 95% CI: 0.95–1.22), compared with PA level 5. CVD mortality risk increased in PA levels 1–3 (level 1 RR = 3.50; 95% CI: 2.41–5.10, level 2 RR = 1.50; 95% CI: 0.99–2.25, level 3 RR = 1.12; 95% CI: 0.79–1.60) as did cancer mortality risk (RR = 1.32; 95% CI: 0.96–1.81, RR = 1.48; 95% CI: 1.19–1.84, RR = 1.26; 95% CI: 1.06–1.50, respectively). The magnitude of the associations was consistent across strata of age, smoking, and body mass index. The population attributable fractions for PA levels 1–4 were: all-cause mortality, 11.5%; CVD mortality, 11.3%; cancer mortality, 7.8%. Conclusion: There is a significant trend of increased risk of all-cause, CVD and cancer mortal- ity in relation to low PA levels among Norwegian women. Keywords: physical activity, mortality, cardiovascular disease, cancer, Norway, women Introduction Physical activity (PA) and its relationship with mortality have been investigated in 1–9 several studies and a strong and consistent inverse association between PA and 10 11 all-cause mortality has been suggested. National and international public health recommendations for PA are based on evidence linking a physically active lifestyle to reduced mortality. One review on PA and all-cause mortality concluded that there is an inverse dose-response relationship between total amount of PA and all-cause mortality and another review suggested that physically active men and women have a 34% lower Correspondence: Kristin Benjaminsen Borch premature mortality risk. In a study of Norwegian and Swedish women below the Department of Community Medicine/ age of 60 years, PA at baseline substantially reduced all-cause mortality. It has not University of Tromsø, 9037 Tromsø, norway been convincingly documented whether this is also applicable to specific causes of Tel +47 776 45443 death such as cardiovascular disease (CVD) and cancer, and the degree to which PA Fax +47 776 44831 Email kristin.benjaminsen.borch@uit.no independently contributes to mortality risk has not been explored thoroughly. submit your manuscript | www.dovepress.com Clinical Epidemiology 2011:3 229–235 Dovepress © 2011 Borch et al, publisher and licensee Dove Medical Press Ltd. This is an Open Access article http://dx.doi.org/10.2147/CLEP.S22681 which permits unrestricted noncommercial use, provided the original work is properly cited. Borch et al Dovepress The aim of the present study was therefore to investigate and outcomes from objective measures of a combined sensor what impact PA level has on all-cause mortality in middle- monitoring heart rate and movement, and appeared valid to aged women, to specify the relative risk (RR) of death due rank PA in a Norwegian population of women. to CVD and cancer, and to calculate the population attribut- able fraction (PAF) of all-cause, CVD and cancer mortality Covariates among women in Norway. Information collected at cohort enrolment included age; duration of education; height; weight; smoking history Methods (including smoking status: current, former, never; duration and quantity of cigarettes smoked/day); alcohol consump- study population tion (grams/day); detailed information on dietary habits and The Norwegian Women and Cancer (NOWAC) Study is a intake of certain food items which was used to calculate total population-based prospective cohort study which enrolled energy intake (Kcal/day); parity; use of oral contraceptives or the first participants in 1991. A more detailed description of postmenopausal hormone therapy (HT); age at menarche; and the cohort and design of the NOWAC Study has previously 16–18 14 15 age at menopause. History of heart failure, myocardial been described, as has external validity. Briefly, from infarction, angina pectoris, diabetes mellitus, fibromyalgia, 1991–1997 a random sample of women aged 30–70 years rheumatism and hypertension were self-reported. Information was drawn from the National Population Register in Norway on cancer diagnosis before cohort enrolment was obtained and invited to participate in the study. All women received a through linkages to the database of the Cancer Registry of letter of invitation requesting informed consent and a com- Norway. prehensive eight-page self-administered questionnaire. Of those invited, 102,540 women (57%) completed and returned Follow-up the questionnaire. Due to study logistics, the first enrolment Person-years were calculated from the start of follow-up was divided into 24 mailings over 7 years. For the present until the date of emigration, death, or end of the study analysis, we collected baseline information from the women period (December 31st 2008), whichever occurred first. who answered the first mailing in 1996–1997 (37,899 women), We obtained information on date of emigration and death and those who answered a second mailing in 1998 (46,965 from the National Population Register. Cause of death was women), for a total of 84,864 women. We excluded 53 women obtained from the National Register for Causes of Death, with a reported date of emigration or death that was before and categorized into specific causes of death: CVD deaths the date of recruitment. We excluded 8137 women with miss- (ICD-10: I00-I99), including stroke, coronary heart disease, ing information on PA level at cohort enrolment and another and other vascular causes; cancer deaths (ICD-10: C00-D48) 10,538 women due to lack of information on other covariates and other-cause deaths (from causes other than CVD and examined. Hence 66,136 women were eligible for inclusion cancer). The combination of the aforementioned categories in our present analysis. The Regional Ethical Committee and was classified as all-cause mortality. the Norwegian Data Inspectorate approved the study. Assessment of PA level statistical analysis PA level at age 14 years, 30 years and at the time of cohort Characteristics of the study population are presented as means enrolment were assessed by self-report on a scale of 1 to 10. and standard deviations, and frequency tabulations over the PA was den fi ed in the questionnaire as follows: “By physical different PA levels. Cox proportional hazards regression, activity we mean activity both at work and outside work, at with follow-up time as the time scale, was used to calculate home, as well as training/exercise and other physical activ- adjusted hazard ratios (HRs) (interpreted as estimates of ity, such as walking, etc. Please mark the number that best RRs) and corresponding 95% confidence intervals (CIs), describes your level of physical activity; 1 being very low which were used to examine the association between PA level and 10 being very high”. The PA scale used for this study and all-cause, CVD and cancer mortality. The proportional refers to the total amount of PA, including different domains, hazard assumption was checked using Schoenfeld residuals frequencies, durations and intensities in one global score, and Kaplan–Meier plots, which suggested no evidence of and have been recently validated. A moderate but significant deviation from proportionality. The initial survival analyses (P , 0.001) Spearman’s rank correlation coefficient was were done by PA level adjusted for age and further built up found, in the range of 0.36 to 0.46, between the PA scale in multivariate models, with covariates added in a backward submit your manuscript | www.dovepress.com Clinical Epidemiology 2011:3 Dovepress Dovepress Physical activity and mortality among women stepwise manner to take possible confounders into account. equation: PAF = (P (RR - 1)/1 + P (RR - 1)), where P is e e e Additional analyses were conducted separately by age group, the proportion of the exposed population, and RR is the risk body mass index (BMI) and history of CVD, diabetes mel- estimate for the exposed compared to the unexposed popula- litus or prevalent cancer to determine whether associations tion in the final multivariate proportional hazards regression were stronger in these subgroups. The analyses were repeated model, including all aforementioned covariates. The cut-off excluding women with CVD, diabetes mellitus or prevalent point a priori for the exposed population was set at PA level 4 cancer to minimize the potential effect of reverse causality. PA or less, which divided the study population in two: exposed level at baseline was entered into the Cox regression models (PA levels 1–4) and unexposed (PA levels 5–10). Analyses as a categorical variable with 10 categories, in order to ree fl ct were conducted using STATA version 11.0, special edition the study scale. PA level 5 (moderate PA level) in the study (StataCorp, Lakeway Drive, College Station, TX). scale was used as the reference category, compared to PA Results levels 1–4 (low PA levels), and 6–10 (high PA levels). Characteristics of the study population at cohort enrol- Covariates examined in the multivariate Cox regression ment and mortality during follow-up are given in Table 1. models were age (40–49, 50–59, $ 60 years); BMI (weight in During 705,980 person-years of follow-up from 1996 to kilograms divided by height in centimeters squared, , 18.5, December 31st 2008, 2572 deaths were reported. The mean 18.5–24, 25–29, $ 30) with the second category as the refer- age of the participants at baseline was 50.5 years (standard ence; height (cm); total energy intake (Kcal/day). Smoking deviation, 41–70 years) (Table 1). status (never, former, current), smoking duration (years) and Self-reported PA level and health-related characteristics quantity smoked (pack-years = the total number of years a of study women are shown in Table 2 by PA level. Almost smoker smoked 20 cigarettes/day) were combined in the 30% of the women reported low PA levels (levels 1–4), and analysis as one variable (age at start $ 20 years and current women who reported moderate to high PA levels (levels 5–10) smoker, age at start $ 20 years and former smoker, age at tended to be leaner and had a higher total energy intake. start , 20 years, 0–19 pack-years and current smoker, age at Women with a PA level of 1 were more often current smokers start , 20 years and former smoker, and finally $ 20 pack- compared to women with moderate to high PA levels. CVD years, age at start , 20 years and current smoker). Duration was reported by 13% of study women, and this proportion of education (0–9, 10–12 and $ 13 years) and menopausal was lower among women reporting moderate to high PA status at enrolment (postmenopausal yes/no) were further levels compared with those who reported low PA levels. included. Baseline information on menopausal status was A similar pattern was observed for diabetes mellitus, which available for 50,875 women, and the remaining women was reported by 1.5% of study women. A total of 4.2% of were either perimenopausal (N = 6730), hysterectomized women were diagnosed with cancer before cohort enrolment, at ,  53 years of age (N = 2150), HT users ,  53 years of and there was a higher percentage of prevalent cancer among age (N = 5477) or had missing information (N = 1828). Use women with a PA level of 1 (Table 2). of HT was registered as ever or never, and self-reported Survival analysis of all-cause mortality with adjustments disease (yes/no to any of the following: heart failure, myo- for different covariates showed a significantly increased cardial infarction, angina pectoris, diabetes mellitus, fibro- myalgia, rheumatism or hypertension) was also included in order to analyze each disease as a separate covariate. Table 1 Characteristics of the study population at baseline and Alcohol intake was divided into four categories (none, mortality during follow-up – The norwegian Women and Cancer study low = 0.1–3.9 grams/day, medium = 4.0–10.0 grams/day and high intake . 10.0 grams/day) with low intake as refer- Characteristics number of women 66,136 ence category, and information on age at first birth (, 20, Mean age at entry (sD), years 50.5 (6.55) 20–25, . 25 years) and parity (0, 1, 2, $ 3 children) was Mean person-years of follow-up (sD) 10.70 (1.48) combined into one variable. Total person-years at risk 705,980 number of deaths in the follow-up period 2572 PAF was interpreted as the proportional reduction in the number of deaths by cause average population mortality risk that would occur if low CVD 401 PA levels were eliminated from the population, assuming Cancer 1584 that the distribution of the adjustment variables remained Other causes 587 unchanged. PAF was estimated using the following Abbreviations: sD, standard deviation; CVD, cardiovascular disease. submit your manuscript | www.dovepress.com Clinical Epidemiology 2011:3 Dovepress Borch et al Dovepress Table 2 Physical activity (PA) level and health-related characteristics according to PA level at cohort enrolment in 1996–1998 among 66,136 women from the norwegian Women and Cancer study Characteristics PA level 1 2 3 4 5 6 7 8 9 10 n 949 2421 5810 9713 16,862 12,021 9828 5489 1896 1147 PA level, % 1.43 3.7 8.8 14.7 25.5 18.2 14.9 8.3 2.9 1.73 Age, mean (years) 53.6 52 51.3 50.9 50.5 50 49.8 50 50.5 51.4 Duration of education, mean (years) 10.4 11.3 11.8 12 11.9 12 12.3 11.9 11.5 10.8 BMi, mean (kg/m ) 26.6 26.5 25.8 25.3 24.6 24.1 23.7 23.5 23.4 23.5 height, mean (cm) 165.1 165.9 165.9 166 166.2 166.3 166.4 166.1 166.2 165.6 Weight, mean (kg) 72.7 72.9 71.1 69.7 68 66.7 65.7 65 64.7 64.6 Current smoker (%) 44.9 39.4 34.5 32.5 32.3 30 28.6 30.9 32.3 36.7 Alcohol consumption (grams/day) 3.0 2.9 3.4 3.3 3.2 3.3 3.4 3.2 3.0 2.6 Total energy intake, mean (Kcal/day) 1472 1515 1548 1592 1626 1661 1686 1713 1738 1758 nulliparous (%) 9.5 10.0 9.5 9.0 8.1 7.7 7.8 9.1 7.5 8.4 First birth, mean age (years) 23.5 24 23.9 23.9 24 24 23.8 23.5 23.3 23.9 hormone therapy use at enrolment (%) 36.8 35.6 33.8 32.5 32.1 30.1 29.3 27.9 29.6 26.7 Postmenopausal at enrolment (%) 74.7 65.2 58.8 56.5 54.0 49.5 48.4 50.5 53.0 57.8 Cardiovascular disease (%) 27.8 23.3 18.7 16.4 13.2 11.3 10.4 10.3 9.3 11.2 Diabetes mellitus (%) 4.6 3.7 2.3 1.5 1.5 1.3 0.9 1.0 1.2 2.3 Cancer (%) 7.1 6.0 5.2 4.4 4.4 3.7 3.6 3.4 3.6 4.5 a b Notes: Among those who had children; Postmenopausal status based on 50,875 women, excluded from this category were 6291 women classified as perimenopausal, 2150 with hysterectomy , 53 years of age and 5477 hormone therapy users , 53 years of age; Self-reported cardiovascular diseases defined as heart failure, myocardial infarction, angina pectoris, and hypertension; information on cancer diagnosis before cohort enrolment obtained from the Cancer registry of norway. risk of mortality for women with low PA levels (level 1 prevalent cancer, did not signic fi antly change the results (data RR = 2.35; 95% CI: 1.94–2.84, level 2 RR = 1.71; 95% CI: not shown) and these participants were therefore retained in 1.45–2.00, level 3 RR = 1.30; 95% CI: 1.14–1.49, level 4 the n fi al analysis. Survival analysis was conducted in strata of RR = 1.07; 95% CI: 0.95–1.22), compared with women with age, BMI and history of CVD, diabetes mellitus and cancer. a moderate PA level (Table 3). The association between PA No evidence of a differential effect of PA level on mortality level and all-cause mortality showed a significant overall according to age, BMI, or history of included disease was trend (P , 0.001) of reduced mortality risk in women with found, indicating that the increased mortality risk found in moderate to high PA levels compared to women with low PA the main survival analyses are independent of these factors levels. However, the shape of the association seemed non- (data not shown). linear; more like an L-shape, indicating no additive effect on The proportion of the population with low PA levels mortality beyond the moderate PA level (Figure 1). was 29% with an adjusted RR of 1.45 (95% CI: 1.34–1.57) CVD mortality risk for women with a PA level of 1 was for all-cause mortality, 1.44 (95% CI: 1.17–1.76) for CVD found to be 3.5 times higher (95% CI: 2.41–5.10) than for mortality and 1.29 (95% CI: 1.16–1.43) for cancer mortality women with a moderate PA level (Table 3). PA levels of 2, for the exposed compared to the unexposed population. Our 3 and 4 separately showed an increased risk as well (though results showed that 11.5% of all-cause mortality, 11.3% of not significant), albeit not as high as for PA level 1 (Table 3). CVD mortality and 7.8% of cancer mortality was attributable The overall trend for CVD mortality risk in women with low to low PA levels. PA levels was significant (P , 0.001). The results indicated a significant trend (P = 0.002) of increased risk of cancer Discussion mortality for women with decreasing PA levels. Separate We found a significant trend of reduced all-cause mortality results for PA levels 1, 2 and 3 were RR = 1.32 (95% CI: with increasing PA level, although the shape of the inverse 0.96–1.81), 1.48 (95% CI: 1.19–1.84) and 1.26 (95% CI: association was non-linear and more L-shaped, with no 1.06–1.50), respectively. additional effect beyond the moderate PA level of 5. Women Participants with self-reported diseases or prevalent reporting low PA levels (ie, PA levels 1–4) had a signifi- cancer at baseline were included and adjusted for in the cantly increased risk of all-cause mortality, with a stronger main analytical model. The results of sensitivity analyses association for CVD than for cancer-related mortality. after exclusion of all women with CVD, diabetes mellitus, or Separate subgroup analyses indicated that the findings were submit your manuscript | www.dovepress.com Clinical Epidemiology 2011:3 Dovepress 1 Dovepress Physical activity and mortality among women Table 3 Relative risks (RRs) and 95% confidence intervals (CIs) All cause mortality of the association between physical activity (PA) level and all- CVD mortality Cancer mortality cause, cardiovascular disease and cancer mortality among 66,136 women from the norwegian Women and Cancer study PA level N of Age-adjusted Multivariate deaths RR (95% CI) RR (95% CI) All-cause mortality 1 139 3.17 (2.64–3.82) 2.35 (1.94–2.84) 0246 3579810 2 203 2.04 (1.74–2.39) 1.71 (1.45–2.00) Self-reported physical activity level 3 321 1.40 (1.22–1.60) 1.30 (1.14–1.49) 4 402 1.09 (0.96–1.23) 1.07 (0.95–1.22) Figure 1 Multivariate relative risks (rrs) of all cause, CVD and cancer mortality and 5 621 1.0 1.0 physical activity (PA) level. 6 342 0.80 (0.70–0.93) 0.83 (0.73–0.95) Abbreviation: CVD, cardiovascular disease. 7 276 0.81 (0.70–0.93) 0.86 (0.75–0.99) 8 170 0.87 (0.74–1.03) 0.89 (0.75–1.06) follow-up time, and the evaluation of cause-specic fi mortality. 9 54 0.76 (0.58–1.00) 0.76 (0.58–1.01) 20 21,22 The study information on HT use and dietary habits are 10 44 0.94 (0.69–1.28) 0.86 (0.63–1.17) considered valid. The NOWAC cohort is representative of P for trend ,0.001 ,0.001 Cardiovascular disease mortality the Norwegian female population in the studied age groups, 1 44 6.04 (4.21–8.66) 3.50 (2.41–5.10) and there was no major selection bias that would invalidate 2 32 2.10 (1.37–3.08) 1.50 (0.99–2.25) a PAF calculation. 3 46 1.31 (0.92–1.86) 1.12 (0.79–1.60) Despite the different methods that exist to measure PA 4 60 1.10 (0.78–1.49) 1.00 (0.72–1.39) 5 92 1.0 1.0 level, a substantial amount of evidence from observational 6 48 0.77 (0.5–1.09) 0.83 (0.58–1.17) studies confirms an inverse relationship between low PA 7 40 0.80 (0.55–1.17) 0.89 (0.61–1.30) 2,12,23,24 levels and increased mortality risk in women. Our 8 29 1.01 (0.67–1.55) 1.07 (0.71–1.63) 9 5 0.47 (0.19–1.15) 0.47 (0.19–1.15) findings are in line with these observations for all-cause, 10 5 0.70 (0.28–1.71) 0.62 (0.25–1.53) CVD and cancer mortality. Our observations suggested that P for trend ,0.001 ,0.001 the relationship is non-linear, with the greatest benefit to be Cancer mortality had by changing from a PA level of 1 to any level between 2 1 43 1.60 (1.17–2.19) 1.32 (0.96–1.81) 2 105 1.67 (1.35–2.08) 1.48 (1.19–1.84) and 5, which has also been confirmed in other studies. 3 192 1.32 (1.11–1.57) 1.26 (1.06–1.50) Physical inactivity is considered the fourth leading cause 4 252 1.07 (0.91–1.25) 1.07 (0.91–1.25) of death worldwide. In our study, assuming causality, 5 399 1.0 1.0 the PAF for low PA levels among women was 11.5% for 6 234 0.85 (0.73–1.00) 0.88 (0.75–1.03) 7 188 0.85 (0.72–1.01) 0.90 (0.76–1.07) all-cause, 11.3% for CVD and 7.8% for cancer mortality, 8 111 0.88 (0.72–1.09) 0.92 (0.74–1.13) which is substantial. For modifiable factors like PA level, 9 37 0.82 (0.58–1.14) 0.84 (0.60–1.17) PAF is useful for the planning of public health strategies 10 23 0.78 (0.51–1.18) 0.75 (0.49–1.15) and interventions. The Nurses’ Health study in the United P for trend ,0.001 ,0.002 States found a PAF of 17% for all-cause, 28% for CVD and Notes: Data are adjusted in the multivariate model for age at cohort enrolment, body mass index, height, smoking status, years of smoking, amount of smoking, alcohol 9% for cancer mortality among women reporting a duration intake, menopausal status, age at first birth, parity, hormone therapy use, cardiovascular disease diabetes mellitus and prevalent cancer. r eference level for body mass index is of PA of less than 30 minutes per day. In a global health normal weight and for alcohol intake the reference category is low intake. Duration of report the estimated PAF of mortality was 8% for physical education in years and total energy intake was tested in the model, but not included in the final analytical model as they did not change the risk estimates. All levels of PA inactivity in high-income countries. However, underestima- from the study scale, 1 being the lowest PA level, and 10 being the highest. tion is likely as PA level measures were limited. Our results indicated a significant, but weaker trend in the association independent of age, BMI and history of CVD, diabetes between PA and cancer mortality than CVD mortality. Cancer mellitus, or cancer. PAF calculation showed that 11.5% of develops over several years before symptoms appear and are all-cause deaths, 11.3% of CVD deaths and 7.8% of cancer diagnosed. This suggests that duration of follow-up is critical deaths were attributable to low PA levels. and must be of a certain length to capture the magnitude Strengths of our study include the prospective design, of an association. Among environmental risk factors for the large sample size, relatively high response rates, almost cancer incidence, lifestyle factors such as tobacco use, poor complete follow-up (99.9%) with almost 11 years of mean nutrition, obesity and physical inactivity, which we adjusted submit your manuscript | www.dovepress.com Clinical Epidemiology 2011:3 Dovepress Multivariate RR 0.5 1 2 4 Borch et al Dovepress for in our study, account for about one-third of all cancers. Disease or preliminary stages of a disease may inhibit We further adjusted for hormone use (oral contraceptives and a person’s ability to be physically active, meaning that part HT) and reproductive factors. Furthermore, our findings are of the observed association between PA level and mortality in line with several other studies that suggested an association may be due to confounding or reverse causation. Restricting 28–30 between reduced cancer mortality and PA level. the analysis to women without a history of disease would Our study has some limitations. PA level in our study have entailed exclusion of almost 12,000 women, and was self-reported and assessed at baseline only. Changes therefore we retained and adjusted for this information, in in PA level over time could introduce bias. Therefore the addition to performing a sensitivity analysis excluding them. interpretation of our results should take into consideration The effect of PA on mortality remained consistent both in the possibility of changes in behaviour over time: if anything the sensitivity analysis and the stratified analysis according PA levels decrease with age, and therefore our results are to CVD disease, diabetes mellitus and prevalent cancer. probably underestimates of the true PAF. Measurement errors Thus, it is unlikely that our results might be due to low PA are inevitable and self-report is a crude measure of PA level, levels explaining prevalent disease, but more probably that which necessarily entails some degree of misclassification. prevalent diseases are explaining low PA levels. Residual A known problem of self-reporting of a desirable behaviour confounding can never be excluded in non-randomized like PA is the tendency to report levels that are higher than studies, however, other prospective studies support our one really has. However, the size of the NOWAC cohort findings. limits the use of other more accurate measures such as Despite the limitations of this study, and the existence of accelerometer or heart rate monitors. The results from our a possible spurious component in the relationship between PA validation study indicated that the scale of 10 PA levels levels and mortality, the benefits of being physically active is suff icient to differentiate between levels of the total are biologically plausible. An increase from low PA levels amount of PA. Although the challenge of equating different up to a moderate PA level would entail an 11.5% reduction total amounts of PA to the different PA levels on the scale in all-cause mortality in women in Norway. PAF estimates remains, the 10 categories represent ordered levels of the depend on RRs and the proportion of exposure in a given total amount of PA which have a strong predictive value in population, which has to be considered when generalizing relation to mortality. Studies have shown that a higher total to other populations where low PA levels could differ. Our volume of PA is clearly associated with decreased all-cause study design cannot determine a causal association, but our 12,34 mortality. Total volume of PA refers to energy expenditure results indicate a significant trend of reduced mortality risk related to activity quantified by duration and frequency. If with increasing PA levels, which suggests such an associa- total volume of PA is the main contributor in the relationship tion. The results of the present study suggest that PA level between mortality and PA, it stands to reason that our global is an important lifestyle behaviour to target in public health score, which includes frequency, intensity and duration of PA strategies. to deduce PA levels, is appropriate for use in the estimation of the magnitude of a given effect. Acknowledgments A weakness of our study is the reliance on self-report The authors thank the NOWAC Study staff and participants for all covariates examined. This could introduce misclas- for their invaluable contributions to this study. sification error, thereby affecting our estimates. However, in the NOWAC Study information on the use of HT and Author contributions 21,22 dietary habits, including alcohol habits, have been vali- KBB carried out the statistical analysis and drafted the dated with good results. Furthermore, information on parity manuscript. TB contributed to the statistical analysis and and duration of education has been compared to national interpretation of the data. EL is the principal investigator and registers with no statistically significant differences found. designed the NOWAC Study. EW contributed with planning Self-reported information on height and weight has not yet of the data analysis, interpretation of the data and critical been validated in the NOWAC Study, but ongoing research revision of the manuscript. All authors read and approved (unpublished) indicates a limited extent of misclassification the final manuscript. bias. Despite certain limitations, self-reporting methods are considered adequate to deal with large sample sizes, practical Disclosure to administer, and less expensive. The authors report no conflicts of interest in this work. submit your manuscript | www.dovepress.com Clinical Epidemiology 2011:3 Dovepress Dovepress Physical activity and mortality among women 18. Skeie G, Hjartåker A, Lund E. Diet among breast cancer survivors and References healthy women. The Norwegian Women and Cancer Study. Eur J Clin 1. Besson H, Ekelund U, Brage S, et al. Relationship between subdomains Nutr. 2006;60(9):1046–1054. of total physical activity and mortality. Med Sci Sports Exerc. 2008; 19. Rockhill B, Newman B, Weinberg C. Use and misuse of population 40(11):1909–1915. attributable fractions. Am J Public Health. 1998;88(1):15–19. 2. Oguma Y, Sesso HD, Paffenbarger RS Jr, Lee IM. 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