IJE vol.34 no.1 © International Epidemiological Association 2005; all rights reserved.
Article |
The Midspan studies
1 Public Health and Health Policy, Division of Community Based Sciences, University of Glasgow, Glasgow G12 8RZ, Scotland, UK
2 General Practice and Primary Care, Division of Community Based Sciences, University of Glasgow, Glasgow G12 9LX, Scotland, UK
3 Robertson Centre for Biostatistics, University of Glasgow, Glasgow G12 8QQ, Scotland, UK
4 Department of Social Medicine, University of Bristol, Bristol, UK
5 Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI, USA
* Correspondence: Public Health and Health Policy, Division of Community Based Sciences, University of Glasgow, 1 Lilybank Gardens, Glasgow G12 8RZ, Scotland, UK. E-mail: c.l.hart{at}udcf.gla.ac.uk
Accepted 6 September 2004
 |
How did the study come about? |
|---|
 Top How did the study... What does it cover,...Who is in the...What has been measured?What is attrition like?What has it found?What are the main...Can I get hold...References |
|---|
The use of large-scale epidemiological studies for public health research was pioneered in Scotland by Victor Hawthorne in the 1960s (Figure 1). The Midspan studies (so called because they were centred around the ‘midspan’ of life; http://www.gla.ac.uk/faculties/medicine/midspan; Figure 2) originated in the post-war drive to control pulmonary tuberculosis using mass miniature radiography. The availability of a well-established and effective method of examining large numbers of apparently healthy volunteers suggested the extension of the screening examination to detect a much wider range of chronic disease and disability. Midspan is the name given to four separate occupational and general population cohort studies based in Scotland, which used Hawthorne's methodology.
|
|
The first study, incorporating the Main and Tiree study, received funding from the Board of Management for Glasgow Northern Hospitals and the Western Regional Hospital Board. It was developed in conjunction with the Whitehall study of civil servants in the Greater London area. The second study, the Collaborative study, was undertaken as part of an international co-operative study by the European office of the WHO on the prevention of ischaemic heart disease and hypertension and was funded by the Scottish Home and Health Department. The third study, the Renfrew/Paisley study, a general population cohort, was supported by the Renfrewshire King Edward Memorial Trust and the Scottish Home and Health Department. In the 1990s, the most recent study, the Family study (Figure 3), moved on to study the offspring of couples who had taken part in the Renfrew/Paisley study, and was funded by the NHS Cardiovascular Research and Development Programme and the Wellcome Trust.
|
|
What does it cover, and how has this changed? |
|---|
|
TopHow did the study...What does it cover,...Who is in the...What has been measured?What is attrition like?What has it found?What are the main...Can I get hold...References |
|---|
The general aim of these studies was to develop an evidence base for the detection and control of cardiorespiratory risks and diseases in whole populations in addition to improving the detection and control of tuberculosis. The idea was to pursue the precept that a small reduction in large numbers of, say, mild asymptomatic hypertensives, would have a bigger impact on the overall health of a total population than treating the relatively small numbers of those with overt disease. Cohort studies were needed to identify and measure the risks of dying from coronary artery disease, cardiovascular diseases, lung and other cancers, and respiratory disease—the main causes of excess mortality in west-central Scotland compared with the rest of Scotland, and in Scotland compared with England and Wales.
The Tiree survey investigated (and confirmed) the local belief that blood pressure was higher on the island than on the mainland (Figure 4).1
|
As the cohorts have matured, focus has changed from analyses of cardiorespiratory disease risk in relation to risk factors assessed in middle age to consideration of life course influences on adult health. More recently, it has been possible to trace the adult offspring of some of the 4067 married couples who took part in the Renfrew/Paisley study, for studies of intergenerational trends and familial aggregation of cardiorespiratory risk, disease, and associated behaviours.
|
Who is in the sample and how often have they been followed up? |
|---|
|
TopHow did the study...What does it cover,...Who is in the...What has been measured?What is attrition like?What has it found?What are the main...Can I get hold...References |
|---|
|
|
What has been measured? |
|---|
|
TopHow did the study...What does it cover,...Who is in the...What has been measured?What is attrition like?What has it found?What are the main...Can I get hold...References |
|---|
|
|
What is attrition like? |
|---|
|
TopHow did the study...What does it cover,...Who is in the...What has been measured?What is attrition like?What has it found?What are the main...Can I get hold...References |
|---|
About half of the members of the early cohorts were rescreened a few years after the initial screening (48% of Main, 46% of Collaborative, and 55% of Renfrew/Paisley). All cohorts were flagged for mortality with the General Register Office and we are informed of the small number of participants who emigrate.
|
What has it found? |
|---|
|
TopHow did the study...What does it cover,...Who is in the...What has been measured?What is attrition like?What has it found?What are the main...Can I get hold...References |
|---|
Key findings and key publications
Population screening
The feasibility of the mass screening examination in healthy populations in a timely and cost-efficient manner was first described and demonstrated by Hawthorne and others.1–3 Compared with previous studies in the UK, men in the Renfrew/Paisley study had shorter stature, higher blood pressure, a higher proportion of smokers continuing to smoke, lower forced expiratory volume in 1 s (FEV1), more angina (Rose questionnaire), higher breathlessness on effort, and more chronic bronchitis.4 Compared with Renfrew/Paisley men, Renfrew/Paisley women had higher plasma cholesterol, lower FEV1, fewer ever smokers, and higher breathlessness on effort. Compared with the Whitehall study, the Collaborative and Renfrew/Paisley cohorts had higher mortality rates, but these could be explained by the higher levels of smoking, poorer socioeconomic status, lower FEV1, and shorter stature in the cohorts from the west of Scotland.5
Blood pressure
The Renfrew/Paisley study made a major contribution to the debate about whether a substantial reduction of diastolic blood pressure could lead to a significant decrease in mortality.6 It was found that two blood pressure measurements are better than one for indicating stroke risk.7
Cholesterol
Cholesterol was not a good indicator of all-cause mortality, although there was a positive and close relationship with coronary heart disease (CHD).8 There was no relationship between cholesterol and overall stroke.9 However, there was a significant inverse relationship between cholesterol and haemorrhagic stroke, and a J shaped relationship between cholesterol and ischaemic stroke.
Smoking
The prevalence of respiratory symptoms increased with the number of cigarettes smoked and smokers had a mortality rate twice that of never smokers.10 The Renfrew/Paisley cohort provided the first opportunity to examine the characteristics of a population group in Scotland in relation to their cigarette smoking habits in an area which at that time had the highest lung cancer incidence rate in the world.11 Compared with other cohorts, the lung cancer rates were higher at all levels of cigarette smoking. Using linked data for participants living in the same household, the Renfrew/Paisley cohort was the first UK study to show the deleterious effects of passive smoking both in terms of reduced FEV1, increased symptomatology and poorer lung cancer and CHD mortality among passive smokers.12
Coronary heart disease
Coronary mortality in a representative population sample of women was examined and similarities with the known coronary risk factors found among men were established in women.13 Another study examining the consistency of coronary risk factors for both men and women, for both coronary disease and for stroke, highlighted similarities and differences.14 CHD mortality rates over 15 yr were quadrupled in people with two or more of Rose questionnaire angina, a previous history of CHD, and/or ECG evidence of ischaemia.15 Risk–mortality relationships were similar in men and women, with women having coronary events 15 yr later than men. ‘Visible risk’ (obesity and smoking) was a good predictor of CHD mortality.16 ‘Unexplained’ CHD deaths in men at low visible risk were rare and usually associated with less visible risk factors. ‘Unwarranted survivals’ (i.e. despite being at high visible risk) were usually associated with more favourable profiles of less visible risk factors. ‘Exceptions to the rule’ should not distract from the message that the differences in survival between high and low visible risk groups are dramatic.
Stroke
Blood pressure, smoking, cardiothoracic ratio, pre-existing heart disease, and diabetes were positively related to stroke mortality in 20 yr and height and FEV1 were inversely related.17 Stroke mortality rates in former smokers were similar to never smokers. Women's stroke mortality rates were similar to men's, unlike CHD mortality where women had lower rates than men. Risk factors for stroke in men and women had similar relationships with stroke incidence (measured by hospital admissions data), as with stroke mortality.18 Poorer socioeconomic circumstance was associated with greater stroke risk, with early life circumstances being of particular importance.19
Respiratory disease
Impaired lung function was a major clinical indicator of mortality risk in men and women for a wide range of diseases, in addition to respiratory disease, an observation also found in lifelong non-smokers.20 The effect of maternal and paternal smoking (documented over 20 yr previously) on lung function in more than 2000 adult offspring was estimated.21 There was a graded inverse association between maternal smoking and offspring FEV1, independent of offspring smoking, and no effect of paternal smoking on offspring FEV1. The Family study has also provided the first evidence that maternal smoking synergizes with personal smoking to increase airflow limitation and chronic obstructive pulmonary disease risk (Figure 5).22 Identical questions answered by parents and their adult offspring showed a 2-fold increase in the prevalence of asthma between the mid-1970s and the mid-1990s, against the background of a rising prevalence of atopy.23
|
Cancer
The main interest has been in lung cancer because of its high incidence locally. Analyses have established a higher risk per cigarette smoked generally in the population compared with other major cohort studies,11 an increased link with social class not explained purely by the amount smoked,24 and relationships with a range of variables, mostly respiratory, indicating an increased susceptibility to the effects of cigarette smoke.20,25 Increasing non-linear risks of lung cancer with increasing tar levels have been demonstrated.26 Repudiation of an underlying cancer risk in relation to blood pressure at a population level has been important in understanding varying cancer risks in some hypertensive patients.27,28
Qualitative studies about heart disease
Lay people may differ from health professionals in their perception of a family history of heart disease.29 Working class men required a greater number of relatives to be affected before they perceived that they had a family history. Participants did not always regard themselves as being at risk if they felt different from affected relatives. CHD was perceived to be a male disease, with women remaining invisible in discourses about heart disease.30 CHD was seen as a ‘good way to go’, compared with a painful and lingering death.31
Alcohol
There was no relationship between mortality from CHD and alcohol consumption, after adjustments for potential confounders.32 Drinkers of over 35 units per week had double the risk of stroke mortality compared with non-drinkers. All-cause mortality was higher in men drinking 22 units per week or more.
Haemostasis
Use of hormone replacement therapy (HRT) tablets was associated with increased levels of some clotting factors (Factor IX, activated protein resistance, and C-reactive protein) and reduced levels of others (tissue plasminogen activator, plasminogen activator inhibitor). Transdermal HRT (i.e. ‘patches’) was not associated with these changes.33 There was a negative association between birthweight and C-reactive protein in adulthood.34
Early origins
Lower birthweight of offspring was associated with higher parental mortality from all causes and from cardiovascular disease.35 This elevated mortality was not explained by a range of social, environmental, behavioural, and physiological risk factors. The strength of the association was greater than expected from the degree of concordance of birthweights across generations. Birthweight was positively associated with leg length, trunk length, and total height.36 Behavioural risk factors (cigarette smoking and recreational physical exercise) were more strongly associated with adult social circumstances than with childhood circumstances.37 Physiological risk factors (diastolic blood pressure, cholesterol, and FEV1) were associated to varying degrees with both childhood and adult circumstances. Having more siblings was related to adulthood disease risk, which could be explained by confounding risk factors, with the exception of stomach cancer mortality and haemorrhagic stroke.38
Height
Taller people and those with good FEV1 experienced a reduced risk of CHD.39 Leg length, an indicator of pre-pubertal nutritional status, was the component of height most strongly associated with risk. Height and FEV1 may both be markers of childhood exposures that influence growth and CHD risk. Greater height was associated with reduced risk of CHD, stroke, and respiratory death.40 Lung function was an important mediator of the association between height and cardiorespiratory mortality. Greater height was associated with increased risk of several cancers unrelated to smoking. The association between height and cancer may reflect the influence of calorie intake during childhood. There was a strong inverse relationship between height and haemorrhagic stroke and a weak, non-significant relationship with ischaemic stroke.41
Social class and life course
Individual (social class) and area-based (deprivation category) socioeconomic measures were independently associated with risk factors, morbidity, and mortality.42 Health and risk of premature death were determined by socioeconomic factors acting throughout life.43 Mortality from stroke and stomach cancer was particularly dependent on social circumstances in childhood, whereas mortality from CHD and respiratory disease was dependent on social circumstances in both adulthood and childhood.44 Mortality from accidents and violence and from lung cancer was mainly dependent on factors acting in adulthood. Socioeconomic and behavioural factors produced a cumulative influence on cardiovascular disease mortality risk.45 Childhood and adulthood social class, smoking, and heavy drinking explained about two thirds of the population burden of cardiovascular disease mortality in the west of Scotland. Occupational social class and education were both strongly associated with mortality.46 Social environment in adulthood was the key determinant of smoking behaviour. Occupational social class was more strongly associated with overall mortality and non-cardiovascular mortality than was the educational measure. The educational measure was more strongly associated with cardiovascular than with other causes of death.
Stress and psychosocial factors
Stress in day-to-day life, measured by the Reeder stress index, was related in the expected direction to behavioural risk factors, such as smoking, alcohol drinking, and lack of exercise—the more the stress, the worse the risk factor profile.47 This indicates that the stress measure correctly indexed the experience of stress. However, when these data were collected—in the early 1970s—people in more favourable social circumstances reported higher levels of stress. This confounding led to stress being apparently protective with respect to later mortality.48 People who reported high levels of stress also reported more adverse experiences with respect to other health measures, such as chest pain. This led to an apparent association between stress and angina—which was also reflected in hospital admissions, since people who go to the doctor complaining of chest pain are more likely to be admitted to hospital for suspected CHD—but the association was in the other direction with objective measures of CHD—ECG ischaemia and CHD mortality.49 This demonstrates how reporting tendency can seriously compromise the interpretations of studies relating stress to fully subjective or partly subjective health outcomes. Persistent short sleep duration was associated with elevated all-cause and cardiovascular disease mortality.50
Hospital admissions
About 79% of the Renfrew/Paisley cohort experienced at least one acute hospital stay.51 A high proportion of acute hospital bed days were required close to the time of death. For non-survivors, 42% of all acute episodes (55% of bed days) took place during the 12 months before death. Those who were at higher risk of admission were the older members of the cohort (especially men), those with low FEV1, smokers, those who were underweight or obese, the small number with abnormal levels of blood sugar, those with high blood pressure, and those who lived in the most deprived areas. Preventive programmes which have an impact on these determinants of ill health may be useful in reducing hospital admission rates.
|
What are the main strengths and weaknesses? |
|---|
|
TopHow did the study...What does it cover,...Who is in the...What has been measured?What is attrition like?What has it found?What are the main...Can I get hold...References |
|---|
The major strengths of the Midspan studies were the very large numbers of participants and the inclusion of women, at a time when other UK epidemiological studies included only men. An unplanned consequence of the Renfrew/Paisley study, as a general population study with high response rates in a defined area, was the inclusion of many married couples and the possibility of a subsequent family study. General goodwill, study loyalty, and the support of local family doctors made this a reality. Having occupational as well as general population cohorts in a similar location was another strength. The Collaborative study data were particularly suited for life course studies as information was collected on socioeconomic factors in childhood and early adulthood. A salient feature of the whole enterprise has been continued follow-up either by re-examination or more comprehensively, by linkage to NHS mortality, cancer, and other morbidity registers. Midspan has continued to attract the interest and participation of researchers from many disciplines and centres, whose achievements are given in the main list of references.
A major weakness has been the lack of core funding. Midspan has been funded by a series of short-term grants. Continuity remains uncertain. Different variables were introduced and dropped between studies, depending on current interests. It would have been preferable to have some of the variables that were collected only in the Collaborative study also collected in the other studies, in particular the life course, stress, and alcohol variables. Although the 1996 study stored blood samples for future use, no samples were stored for the original studies. Blood samples were collected from surviving parents of the Family study participants in 2001, but only 556 samples were obtained, limiting future genetic studies.
|
Can I get hold of the data and where can I find out more? |
|---|
|
TopHow did the study...What does it cover,...Who is in the...What has been measured?What is attrition like?What has it found?What are the main...Can I get hold...References |
|---|
The data are available to experienced teams of researchers who have applied and been granted permission by the Midspan Steering Committee to use the data for a specific research proposal. Such work is conducted in collaboration with the Midspan team.
For further details on how to apply for access to the data see—Procedure for Requests for Use of MIDSPAN Data in the Research section of the Midspan website: http://www.gla.ac.uk/faculties/medicine/midspan/.
A complete list of Midspan publications is available at International Journal of Epidemiology online.
|
Acknowledgments |
|---|
All the participants, study workers and researchers in the studies are thanked for their contributions to Midspan. We would also like to thank local organizations and the many grant awarding bodies that have supported the studies over the years.
|
References |
|---|
|
TopHow did the study...What does it cover,...Who is in the...What has been measured?What is attrition like?What has it found?What are the main...Can I get hold...References |
|---|
1 Hawthorne VM, Gillis CR, Lorimer AR, Calvert FR, Walker TJ. Blood pressure in a Scottish island community. BMJ 1969; 4:654.[Web of Science]
2 Hawthorne VM, Gillis CR, Maclean DS. Monitoring health in Scotland. Int J Epidemiol 1972; 1:369–74.
3 Hawthorne VM, Greaves D, Beevers DG. Blood pressure in a Scottish town. BMJ 1974; 3:600–03.
4 Hawthorne VM, Watt GCM, Hart CL, Hole DJ, Davey Smith G, Gillis CR. Cardiorespiratory disease in men and women in urban Scotland: baseline characteristics of the Renfrew/Paisley (Midspan) study population. Scott Med J 1995; 40:102–07.[Web of Science][Medline]
5 Davey Smith G, Shipley MJ, Hole DJ et al. Explaining male mortality differentials between the west of Scotland and the south of England. J Epidemiol Community Health 1995; 49:541.
6 Isles CG, Hole DJ. Is there a J curve distribution for diastolic blood pressure? Clin Exp Hypertens 1992; A14:139–49.
7 Hart CL, Hole DJ, Davey Smith G. Are two really better than one? Empirical examination of repeat blood pressure measurements and stroke risk in the Renfrew/Paisley and Collaborative studies. Stroke 2001; 32:2697–99.
8 Isles CG, Hole DJ, Gillis CR, Hawthorne VM, Lever AF. Plasma cholesterol, coronary heart disease, and cancer in the Renfrew and Paisley survey. BMJ 1989; 298:920–24.
9 Hart CL, Hole DJ, Davey Smith G. The relation between cholesterol and haemorrhagic or ischaemic stroke in the Renfrew/Paisley study. J Epidemiol Community Health 2000; 54:874–75.
10 Hawthorne VM, Fry JS. Smoking and health: the association between smoking behaviour, total mortality, and cardiorespiratory disease in west central Scotland. J Epidemiol Community Health 1978; 32:260–66.
11 Gillis CR, Hole DJ, Hawthorne VM. Cigarette smoking and male lung cancer in an area of very high incidence. II. Report of a general population cohort study in the west of Scotland. J Epidemiol Community Health 1988; 42:44–48.
12 Hole DJ, Gillis CR, Chopra C, Hawthorne VM. Passive smoking and cardiorespiratory health in a general population in the west of Scotland. BMJ 1989; 299:423–27.
13 Isles CG, Hole DJ, Lever AF. Relation between coronary risk and coronary mortality in women of the Renfrew and Paisley survey: comparison with men. Lancet 1992; 339:702–06.[CrossRef][Web of Science][Medline]
14 Isles CG, Hole DJ, Lever AF, Hawthorne VM. Risk factors for coronary disease and stroke in men and women. QJM 1996; 89:343–49.
15 Hart CL, Watt GCM, Davey Smith G, Gillis CR, Hawthorne VM. Pre-existing ischaemic heart disease and ischaemic heart disease mortality in women compared with men. Int J Epidemiol 1997; 26:508–15.
16 McConnachie A, Hunt K, Emslie C, Hart CL, Watt GCM. ‘Unwarranted survivals’ and ‘anomalous deaths’ from coronary heart disease: prospective survey of general population. BMJ 2001; 323:1487–91.
17 Hart CL, Hole DJ, Davey Smith G. Risk factors and 20 year stroke mortality in men and women in the Renfrew/Paisley study in Scotland. Stroke 1999; 30:1999–2007.
18 Hart CL, Hole DJ, Davey Smith G. Comparison of risk factors for stroke incidence and stroke mortality in 20 years of follow-up in men and women in the Renfrew/Paisley study in Scotland. Stroke 2000; 31:1893–96.
19 Hart CL, Hole DJ, Davey Smith G. Influence of socioeconomic circumstances in early and later life on stroke risk among men in a Scottish cohort study. Stroke 2000; 31:2093–97.
20 Hole DJ, Watt GCM, Davey Smith G, Hart CL, Gillis CR, Hawthorne VM. Impaired lung function in men and women : findings from the Renfrew and Paisley prospective population study. BMJ 1996; 313:711–15.
21 Upton MN, Watt GCM, Davey Smith G, McConnachie A, Hart CL. Permanent effects of maternal smoking on offsprings' lung function. Lancet 1998; 352:53.[CrossRef][Web of Science][Medline]
22 Upton M, Davey Smith G, McConnachie A, Hart C, Watt G. Maternal and personal cigarette smoking synergize to increase airflow limitation in adults. Am J Respir Crit Care Med 2004; 169:479–87.
23 Upton M, McConnachie A, McSharry C et al. Intergenerational 20 year trends in the prevalence of asthma and hay fever in adults: the Midspan family study surveys of parents and offspring. BMJ 2000; 321:88–92.
24 Hart CL, Hole DJ, Gillis CR, Davey Smith G, Watt GCM, Hawthorne VM. Social class differences in lung cancer mortality: risk factor explanations using two Scottish cohort studies. Int J Epidemiol 2001; 30:268–74.
25 Hole DJ, Gillis CR, Hawthorne VM. Which smokers develop lung cancer? Lung Cancer 1988;4(Suppl.):A5.[CrossRef]
26 Tang J-L, Morris JK, Wald NJ, Hole D, Shipley M, Tunstall-Pedoe H. Mortality in relation to tar yield of cigarettes: a prospective study of four cohorts. BMJ 1995; 311:1530–33.
27 Hole DJ, Gillis CR, McCallum IR et al. Cancer risk of hypertensive patients taking calcium antagonists. J Hypertens 1998; 16:119–24.[CrossRef][Web of Science][Medline]
28 Lever AF, Hole DJ, Gillis CR et al. Do inhibitors of angiotensin-I-converting enzyme protect against risk of cancer? Lancet 1998; 352:179–84.[CrossRef][Web of Science][Medline]
29 Hunt K, Emslie C, Watt G. Lay constructions of a family history of heart disease: potential for misunderstandings in the clinical encounter? Lancet 2001; 357:1168–71.[CrossRef][Web of Science][Medline]
30 Emslie C, Hunt K, Watt GCM. Invisible women? The importance of gender in lay beliefs about heart problems. Sociol of Health Illn 2001; 23:203–33.[CrossRef]
31 Emslie C, Hunt K, Watt GCM. ‘I'd rather go with a heart attack than drag on’; lay images of heart disease and the problems they present for primary and secondary prevention. Coron Health Care 2001; 5:25–32.[CrossRef]
32 Hart CL, Davey Smith G, Hole DJ, Hawthorne VM. Alcohol consumption and mortality from all causes, coronary heart disease and stroke: results from a prospective cohort study of Scottish men with 21 years of follow up. BMJ 1999; 318:1725–29.
33 Lowe GDO, Upton MN, Rumley A, McConnachie A, O'Reilly DSJ, Watt GCM. Different effects of oral and transdermal hormone replacement therapies on factor IX, APC resistance, t-PA, PAI and C-reactive protein. Thromb Haemost 2001; 86:550–56.[Web of Science][Medline]
34 Sattar N, McConnachie A, O'Reilly DSJ et al. Inverse association between birth weight and C-reactive protein concentrations in the Midspan Family study. Arterioscler Thromb Vasc Biol 2004; 24:583–87.
35 Davey Smith G, Hart C, Ferrell C et al. Birth weight of offspring and mortality in the Renfrew and Paisley study: prospective observational study. BMJ 1997; 315:1189–93.
36 Gunnell D, Davey Smith G, McConnachie A, Greenwood R, Upton MN, Frankel S. Separating in-utero and postnatal influences on later disease. Lancet 1999; 354:1526–27.[Web of Science][Medline]
37 Blane D, Hart CL, Smith GD, Gillis CR, Hole DJ, Hawthorne VM. Association of cardiovascular-disease risk-factors with socioeconomic position during childhood and during adulthood. BMJ 1996; 313:1434–38.
38 Hart CL, Davey Smith G. Relation between number of siblings and adult mortality and stroke risk: 25 year follow up of men in the Collaborative study. J Epidemiol Community Health 2003; 57:385–91.
39 Gunnell D, Whitley E, Upton M, McConnachie A, Davey Smith G, Watt G. Associations of height, leg length, and lung function with cardiovascular risk factors in the Midspan Family study. J Epidemiol Community Health 2003; 57:141–46.
40 Davey Smith G, Hart CL, Upton M et al. Height and risk of death among men and women: aetiological implications of associations with cardiorespiratory disease and cancer mortality. J Epidemiol Community Health 2000; 54:97–103.
41 McCarron P, Hart CL, Hole DJ, Davey Smith G. The relation between adult height and haemorrhagic and ischaemic stroke in the Renfrew/Paisley study. J Epidemiol Community Health 2001; 55:404–05.
42 Davey Smith G, Hart CL, Watt G, Hole D, Hawthorne VM. Individual social class, area-based deprivation, cardiovascular disease risk factors and mortality : the Renfrew and Paisley study. J Epidemiol Community Health 1998; 52:399–405.[Abstract]
43 Davey Smith G, Hart C, Blane D, Gillis C, Hawthorne V. Lifetime socioeconomic position and mortality: prospective observational study. BMJ 1997; 314:547–52.
44 Davey Smith G, Hart CL, Blane D, Hole D. Adverse socioeconomic conditions in childhood and cause specific adult mortality: prospective observational study. BMJ 1998; 316:1631–35.
45 Davey Smith G, Hart C. Life-course socioeconomic and behavioral influences on cardiovascular disease mortality: the Collaborative study. Am J Public Health 2002; 92:1295–98.
46 Davey Smith G, Hart C, Hole D et al. Education and occupational social class: which is the more important indicator of mortality risk? J Epidemiol Community Health 1998; 52:153–60.[Abstract]
47 Heslop P, Davey Smith G, Carroll D, Macleod J, Hyland F, Hart CL. Perceived stress and coronary heart disease risk factors: the contribution of socio-economic position. Br J Health Psychol 2001; 6:167–78.[CrossRef][Web of Science][Medline]
48 Macleod J, Davey Smith G, Heslop P, Metcalfe C, Carroll D, Hart C. Are the effects of psychosocial exposures attributable to confounding? Evidence from a prospective observational study on psychological stress and mortality. J Epidemiol Community Health 2001; 55:878–84.
49 Macleod J, Davey Smith G, Heslop P, Metcalfe C, Carroll D, Hart CL. Psychological stress and cardiovascular disease: empirical demonstration of bias in a prospective observational study of Scottish men. BMJ 2002; 324:1247–51.
50 Heslop P, Davey Smith G, Metcalfe C, Macleod J, Hart CL. Sleep duration and mortality: the effect of short or long sleep duration on cardiovascular and all-cause mortality in working men and women. Sleep Med 2002; 3:305–14.[CrossRef][Medline]
51 Hanlon P, Walsh D, Whyte B, Scott S, Lightbody P, Gilhooly M. Hospital use by an ageing cohort: an investigation into the association between biological, behavioural and social risk markers and subsequent hospital utilization. J Public Health Med 1998; 20:467–76.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  J E Ferrie, A Singh-Manoux, M Kivimaki, J Mindell, E Breeze, G D. Smith, and M J Shipley Cardiorespiratory risk factors as predictors of 40-year mortality in women and men Heart, August 1, 2009; 95(15): 1250 - 1257. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||