Objective To examine the relation between body mass index (kg/m 2 ) and cancer incidence and mortality. Design Prospective cohort study. Participants 1.2 million UK women recruited into the Million Women Study, aged 50-64 during 1996-2001, and followed up, on average, for 5.4 years for cancer incidence and 7.0 years for cancer mortality.

SummaryBackgroundWomen born around 1940 in countries such as the UK and USA were the first generation in which many smoked substantial numbers of cigarettes throughout adult life. Hence, only in the 21st century can we observe directly the full effects of prolonged smoking, and of prolonged cessation, on mortality among women in the UK.MethodsFor this prospective study, 1·3 million UK women were recruited in 1996–2001 and resurveyed postally about 3 and 8 years later. All were followed to Jan 1, 2011, through national mortality records (mean 12 woman-years, SD 2). Participants were asked at entry whether they were current or ex-smokers, and how many cigarettes they currently smoked. Those who were ex-smokers at both entry and the 3-year resurvey and had stopped before the age of 55 years were categorised by the age they had stopped smoking. We used Cox regression models to obtain adjusted relative risks that compared categories of smokers or ex-smokers with otherwise similar never-smokers.FindingsAfter excluding 0·1 million women with previous disease, 1·2 million women remained, with median birth year 1943 (IQR 1938–46) and age 55 years (IQR 52–60). Overall, 6% (66 489/1 180 652) died, at mean age 65 years (SD 6). At baseline, 20% (232 461) were current smokers, 28% (328 417) were ex-smokers, and 52% (619 774) were never-smokers. For 12-year mortality, those smoking at baseline had a mortality rate ratio of 2·76 (95% CI 2·71–2·81) compared with never-smokers, even though 44% (37 240/85 256) of the baseline smokers who responded to the 8-year resurvey had by then stopped smoking. Mortality was tripled, largely irrespective of age, in those still smoking at the 3-year resurvey (rate ratio 2·97, 2·88–3·07). Even for women smoking fewer than ten cigarettes per day at baseline, 12-year mortality was doubled (rate ratio 1·98, 1·91–2·04). Of the 30 most common causes of death, 23 were increased significantly in smokers; for lung cancer, the rate ratio was 21·4 (19·7–23·2). The excess mortality among smokers (in comparison with never-smokers) was mainly from diseases that, like lung cancer, can be caused by smoking. Among ex-smokers who had stopped permanently at ages 25–34 years or at ages 35–44 years, the respective relative risks were 1·05 (95% CI 1·00–1·11) and 1·20 (1·14–1·26) for all-cause mortality and 1·84 (1·45–2·34) and 3·34 (2·76–4·03) for lung cancer mortality. Thus, although some excess mortality remains among these long-term ex-smokers, it is only 3% and 10% of the excess mortality among continuing smokers. If combined with 2010 UK national death rates, tripled mortality rates among smokers indicate 53% of smokers and 22% of never-smokers dying before age 80 years, and an 11-year lifespan difference.InterpretationAmong UK women, two-thirds of all deaths of smokers in their 50s, 60s, and 70s are caused by smoking; smokers lose at least 10 years of lifespan. Although the hazards of smoking until age 40 years and then stopping are substantial, the hazards of continuing are ten times greater. Stopping before a...

SummaryBackgroundMenarche and menopause mark the onset and cessation, respectively, of ovarian activity associated with reproduction, and affect breast cancer risk. Our aim was to assess the strengths of their effects and determine whether they depend on characteristics of the tumours or the affected women.MethodsIndividual data from 117 epidemiological studies, including 118 964 women with invasive breast cancer and 306 091 without the disease, none of whom had used menopausal hormone therapy, were included in the analyses. We calculated adjusted relative risks (RRs) associated with menarche and menopause for breast cancer overall, and by tumour histology and by oestrogen receptor expression.FindingsBreast cancer risk increased by a factor of 1·050 (95% CI 1·044–1·057; p<0·0001) for every year younger at menarche, and independently by a smaller amount (1·029, 1·025–1·032; p<0·0001), for every year older at menopause. Premenopausal women had a greater risk of breast cancer than postmenopausal women of an identical age (RR at age 45–54 years 1·43, 1·33–1·52, p<0·001). All three of these associations were attenuated by increasing adiposity among postmenopausal women, but did not vary materially by women's year of birth, ethnic origin, childbearing history, smoking, alcohol consumption, or hormonal contraceptive use. All three associations were stronger for lobular than for ductal tumours (p<0·006 for each comparison). The effect of menopause in women of an identical age and trends by age at menopause were stronger for oestrogen receptor-positive disease than for oestrogen receptor-negative disease (p<0·01 for both comparisons).InterpretationThe effects of menarche and menopause on breast cancer risk might not be acting merely by lengthening women's total number of reproductive years. Endogenous ovarian hormones are more relevant for oestrogen receptor-positive disease than for oestrogen receptor-negative disease and for lobular than for ductal tumours.FundingCancer Research UK.

Previous studies have reported inconsistent results on the effect of anthropometric and lifestyle factors on the risk of developing glioma or meningioma tumours. A prospective cohort of 1.3 million middle-aged women was used to examine these relationships. During 7.7 million women-years of follow-up, a total of 1563 women were diagnosed with a primary incident central nervous system tumour: 646 tumours were classified as glioma and 390 as meningioma. Our results show that height is related to the incidence of all central nervous system tumours with a risk of about 20% per 10 cm increase in height (relative risk ¼ 1.19, 95% CI ¼ 1.10 -1.30 per 10 cm increase in height, Po0.001): the risks did not differ significantly between specified glioma and meningioma. Body mass index (BMI) was also related to central nervous system tumour incidence, with a risk of about 20% per 10 kg m À2 increase in BMI (relative risk ¼ 1.17, 95% CI ¼ 1.03 -1.34 per 10 kg m À2 increase in BMI, P ¼ 0.02). Smoking status, alcohol intake, socioeconomic level, parity, age at first birth, and oral contraceptive use were not associated with the risk of glioma or meningioma tumours. In conclusion, for women in the United Kingdom, the incidence of glioma or meningioma tumours increases with increasing height and increasing BMI. British Journal of Cancer (2008) Keywords: body mass index; glioma; height; meningioma; women Primary brain and central nervous system cancers are relatively rare and represent approximately 2% of all cancers diagnosed in the United Kingdom. However, due to a poor prognosis, they are responsible for 7% of the years of life lost from cancer before the age of 70 years (Cancer Research UK, 2007). Very little is known about the aetiology of central nervous system tumours, but environmental factors are thought to play a role (McKinney, 2004;Connelly and Malkin, 2007).The two most common types of central nervous system tumour are glioma and meningioma (Claus et al, 2005). Gliomas arise from glial cells, are found predominantly in the brain and to a lesser extent in the spinal cord or other parts of the central nervous system, and represent more than 70% of all brain tumours (Ohgaki and Kleihues, 2005). Gliomas are typically histologically malignant, can be either slow or fast growing, and are more frequently diagnosed in men than in women. Meningiomas arise from the arachnoidal cells of the leptomeninges (the pia mater and arachnoid mater of the meninges) (Sanson and Cornu, 2000), are also more frequently found in the brain than elsewhere in the central nervous system, and represent more than 20% of all brain tumours (Longstreth et al, 1993). Meningiomas are typically benign (490%) and slow growing. The risk of meningioma increases with age (Sanson and Cornu, 2000), and they are more frequently diagnosed in women (Sanson and Cornu, 2000;Perry et al, 2007).There are few well-established risk factors for glioma and meningioma tumours among adults; while exposure to ionizing radiation and rare inherited genetic conditions such as n...

SummaryBackgroundPublished findings on breast cancer risk associated with different types of menopausal hormone therapy (MHT) are inconsistent, with limited information on long-term effects. We bring together the epidemiological evidence, published and unpublished, on these associations, and review the relevant randomised evidence.MethodsPrincipal analyses used individual participant data from all eligible prospective studies that had sought information on the type and timing of MHT use; the main analyses are of individuals with complete information on this. Studies were identified by searching many formal and informal sources regularly from Jan 1, 1992, to Jan 1, 2018. Current users were included up to 5 years (mean 1·4 years) after last-reported MHT use. Logistic regression yielded adjusted risk ratios (RRs) comparing particular groups of MHT users versus never users.FindingsDuring prospective follow-up, 108 647 postmenopausal women developed breast cancer at mean age 65 years (SD 7); 55 575 (51%) had used MHT. Among women with complete information, mean MHT duration was 10 years (SD 6) in current users and 7 years (SD 6) in past users, and mean age was 50 years (SD 5) at menopause and 50 years (SD 6) at starting MHT. Every MHT type, except vaginal oestrogens, was associated with excess breast cancer risks, which increased steadily with duration of use and were greater for oestrogen-progestagen than oestrogen-only preparations. Among current users, these excess risks were definite even during years 1–4 (oestrogen-progestagen RR 1·60, 95% CI 1·52–1·69; oestrogen-only RR 1·17, 1·10–1·26), and were twice as great during years 5–14 (oestrogen-progestagen RR 2·08, 2·02–2·15; oestrogen-only RR 1·33, 1·28–1·37). The oestrogen-progestagen risks during years 5–14 were greater with daily than with less frequent progestagen use (RR 2·30, 2·21–2·40 vs 1·93, 1·84–2·01; heterogeneity p<0·0001). For a given preparation, the RRs during years 5–14 of current use were much greater for oestrogen-receptor-positive tumours than for oestrogen-receptor-negative tumours, were similar for women starting MHT at ages 40–44, 45–49, 50–54, and 55–59 years, and were attenuated by starting after age 60 years or by adiposity (with little risk from oestrogen-only MHT in women who were obese). After ceasing MHT, some excess risk persisted for more than 10 years; its magnitude depended on the duration of previous use, with little excess following less than 1 year of MHT use.InterpretationIf these associations are largely causal, then for women of average weight in developed countries, 5 years of MHT, starting at age 50 years, would increase breast cancer incidence at ages 50–69 years by about one in every 50 users of oestrogen plus daily progestagen preparations; one in every 70 users of oestrogen plus intermittent progestagen preparations; and one in every 200 users of oestrogen-only preparations. The corresponding excesses from 10 years of MHT would be about twice as great.FundingCancer Research UK and the Medical Research Council.

SummaryBackgroundPoor health can cause unhappiness and poor health increases mortality. Previous reports of reduced mortality associated with happiness could be due to the increased mortality of people who are unhappy because of their poor health. Also, unhappiness might be associated with lifestyle factors that can affect mortality. We aimed to establish whether, after allowing for the poor health and lifestyle of people who are unhappy, any robust evidence remains that happiness or related subjective measures of wellbeing directly reduce mortality.MethodsThe Million Women Study is a prospective study of UK women recruited between 1996 and 2001 and followed electronically for cause-specific mortality. 3 years after recruitment, the baseline questionnaire for the present report asked women to self-rate their health, happiness, stress, feelings of control, and whether they felt relaxed. The main analyses were of mortality before Jan 1, 2012, from all causes, from ischaemic heart disease, and from cancer in women who did not have heart disease, stroke, chronic obstructive lung disease, or cancer at the time they answered this baseline questionnaire. We used Cox regression, adjusted for baseline self-rated health and lifestyle factors, to calculate mortality rate ratios (RRs) comparing mortality in women who reported being unhappy (ie, happy sometimes, rarely, or never) with those who reported being happy most of the time.FindingsOf 719 671 women in the main analyses (median age 59 years [IQR 55–63]), 39% (282 619) reported being happy most of the time, 44% (315 874) usually happy, and 17% (121 178) unhappy. During 10 years (SD 2) follow-up, 4% (31 531) of participants died. Self-rated poor health at baseline was strongly associated with unhappiness. But after adjustment for self-rated health, treatment for hypertension, diabetes, asthma, arthritis, depression, or anxiety, and several sociodemographic and lifestyle factors (including smoking, deprivation, and body-mass index), unhappiness was not associated with mortality from all causes (adjusted RR for unhappy vs happy most of the time 0·98, 95% CI 0·94–1·01), from ischaemic heart disease (0·97, 0·87–1·10), or from cancer (0·98, 0·93–1·02). Findings were similarly null for related measures such as stress or lack of control.InterpretationIn middle-aged women, poor health can cause unhappiness. After allowing for this association and adjusting for potential confounders, happiness and related measures of wellbeing do not appear to have any direct effect on mortality.FundingUK Medical Research Council, Cancer Research UK.

This paper describes the current wireless telecommunications infrastructure deployment regulations in Colombia. It also refers to the possible effects that this infrastructure could cause to the country`s health and environment. similarly, the results obtained show a comparison between the Argentina's current regulations, one of the most relevant researches carried out and the Colombian case. finally, some recommendations are proposed that can be considered in the project of regulations applicable in Colombia for the ensuring purpose that the non-ionizing radiation generated by wireless communications systems do not have effects on health and the environment. ResumenDescribe las actuales regulaciones colombianas para la instalación de infraestructuras de telecomunicaciones inalámbricas. También se refiere a los posibles efectos de esta infraestructura sobre la salud de la población y el medioambiente del país. Además, muestra los resultados de una comparación entre las actuales regulaciones de Argentina y el caso colombiano. Finalmente, se proponen algunas recomendaciones que pueden considerarse en A regulations' survey for the wireless telecommunications deployment in Colombia el proyecto regulatorio aplicable a Colombia, con el propósito de asegurar que la radiación no ionizada generada por los sistemas inalámbricos de comunicaciones no afecte la salud y el medioambiente.Palabras clave: Regulación de telecomunicaciones, Radiación no ionizante (RNI), Comunicaciones y salud, Polución visual, Instalación de infraestructura. ResumoDescreve as atuais regulamentações colombianas para a instalação de infraestruturas de telecomunicações sem fio. Também se refere aos possíveis efeitos desta infraestrutura sobre a saúde da população e o meio ambiente do país. Além disso, mostra os resultados de uma comparação entre as atuais regulamentações da Argentina e o caso colombiano. Finalmente, propõem-se algumas recomendações que podem considerar-se no projeto regulatório aplicável à Colômbia, com o propósito de assegurar que a radiação não ionizada gerada pelos sistemas sem fio de comunicações não afete a saúde e o meio ambiente.Palavras chave: Regulamentação de telecomunicações, Radiação não ionizante (RNI), Comunicações e saúde, Poluição visual, Instalação de infraestrutura.

Hip fracture risk is known to increase with physical inactivity and decrease with obesity, but there is little information on their combined effects. We report on the separate and combined effects of body mass index (BMI) and physical activity on hospital admissions for hip fracture among postmenopausal women in a large prospective UK study. Baseline information on body size, physical activity, and other relevant factors was collected in 1996-2001, and participants were followed for incident hip fractures by record linkage to National Health Service (NHS) hospital admission data. Cox regression was used to calculate adjusted relative risks of hip fracture. Among 925,345 postmenopausal women followed for an average of 6.2 years, 2582 were admitted to hospital with an incident hip fracture. Hip fracture risk increased with decreasing BMI: Compared with obese women (BMI of 30þ kg/m 2 ), relative risks were 1.71 [95% confidence interval (CI) 1.47-1.97)] for BMI of 25.0 to 29.9 kg/m 2 and 2.55 (95% CI 2.22-2.94) for BMI of 20.0 to 24.9 kg/m 2 . The increase in fracture risk per unit decrease in BMI was significantly greater among lean women than among overweight women ( p < .001). For women in every category of BMI, physical inactivity was associated with an increased risk of hip fracture. There was no significant interaction between the relative effects of BMI and physical activity. For women who reported that they took any exercise versus no exercise, the adjusted relative risk of hip fracture was 0.68 (95% CI 0.62-0.75), with similar results for strenuous exercise. In this large cohort of postmenopausal women, BMI and physical activity had independent effects on hip fracture risk. ß