 |
|
Association of Childhood Socioeconomic Status With Subsequent Coronary Heart Disease in Physicians
Michelle M. Kittleson, MD, PhD;
Lucy A. Meoni, ScM;
Nae-Yuh Wang, PhD;
Audrey Y. Chu, BS;
Daniel E. Ford, MD, MPH;
Michael J. Klag, MD, MPH
Arch Intern Med. 2006;166:2356-2361.
ABSTRACT
Background Adult socioeconomic status (SES) is an independent risk factor for the development of coronary heart disease (CHD), but whether low childhood SES has an effect in adults who have achieved high SES is unknown.
Methods We examined the risk of CHD and mortality associated with low childhood SES in 1131 male medical students from The Johns Hopkins Precursors Study, a prospective cohort of graduates of The Johns Hopkins University School of Medicine from 1948 to 1964 with a median follow-up of 40 years.
Results Of 1131 subjects, 216 (19.1%) were from low-SES families. Medical students from low-SES families were slightly older at graduation (26.8 vs 26.2 years; P = .004) and gained more weight over time (P = .01). Low childhood SES conferred a 2.40-fold increased hazard of developing CHD on or before age 50 years (95% confidence interval, 1.21-4.74) but not at older ages. The impact of low SES on early CHD was not reduced by adjusting for other CHD risk factors, including body mass index, cholesterol level, amount of exercise, depression, coffee drinking, smoking, hypertension, diabetes mellitus, and parental CHD history. Low childhood SES did not confer an increased risk of all-cause mortality.
Conclusions Low childhood SES is associated with an increased incidence of CHD before age 50 years among men with high adulthood SES. This risk is not mediated by traditional risk factors for CHD. These findings highlight the importance of childhood events on the development of CHD early in adulthood and the persistent effects of low SES.
INTRODUCTION
Despite advances in medical and surgical care, coronary heart disease (CHD) remains the primary cause of morbidity and mortality in the United States.1 In addition to traditional risk factors such as older age, male sex, cigarette smoking, hypertension, diabetes mellitus, and hypercholesterolemia, low socioeconomic status (SES) is a consistent, moderately strong predictor of CHD risk.2-7 Individuals with low SES have poorer health outcomes compared with high-SES populations,2-10 and the health care community has been challenged to eliminate this disparity.11
Most studies of the effect of childhood SES on CHD in adulthood have focused on middle-aged or older populations; in these studies, no distinction was made between early vs late onset of CHD.12-29 Because most cardiovascular risk factors are more prevalent at older ages, the effects of childhood SES may play less of a role in the development of CHD at older ages.
The Johns Hopkins Precursors Study measures physicians' health outcomes over their lifetime and provides a unique opportunity to prospectively examine the effects of childhood SES on the development of CHD before and after middle age and to adjust for traditional risk factors measured throughout adult life. It also provides the results of a natural experiment: do physicians who are born into low-SES families but who have high levels of adulthood SES, medical knowledge, and access to high-quality health care have optimal health care outcomes? We hypothesized that the risk of poor health outcomes, particularly CHD presenting at a young age, would be greater in physicians with low childhood SES compared with those who grew up in a high-SES family.
METHODS
STUDY POPULATION
The Johns Hopkins Precursors Study was designed and initiated by Caroline Bedell Thomas, MD, in 1947 to identify precursors for cardiovascular disease. It is an ongoing, longitudinal cohort study of 1337 former medical students at The Johns Hopkins University School of Medicine in the classes of 1948 to 1964. Excluded from this analysis were the small number of women (n = 121), men of non-European ancestry (n = 36), those who did not answer the questions about parental occupation (n = 56), and those who were unavailable for follow-up (n = 15), leaving 1131 white male medical students for analysis of incident CHD (some individuals met >1 exclusion criterion).
DATA COLLECTION
At baseline during medical school, each participant provided a detailed medical history and underwent physical examination, including measurement of blood pressure, height, and weight. After medical school, follow-up data were collected using annual mailed questionnaires. In general, yearly response rates exceeded 70% and, during any 5-year interval, at least 85% of participants responded at least once. In addition, ongoing mortality surveillance is conducted by review of alumni records and obituaries and by periodic National Death Index searches. A committee of internists (including M.J.K. and D.E.F.) reviews copies of the death certificates, medical records, and self-reports to assign disease outcomes and assess cause of death.
MEASURE OF CHILDHOOD SES
Childhood SES was defined on the basis of the subject's father's occupation as reported from a 10-item checklist on a medical school questionnaire, derived from the occupations listed on the 1950 census of the population.30 A subject was classified as having a low childhood SES if he reported that his father was a farmer, laborer, service worker, clerical worker, sales worker, machine operator, or craftsman. A subject was classified as having a high childhood SES if he reported that his father was a professional (such as an accountant, banker, scientist, engineer, or lawyer), manager, or physician. In sensitivity analyses, alternate definitions of childhood SES were based on the mother’s, as well as the father’s, occupation. Socioeconomic status was also categorized as a 3-level variable: low (farmers, machine operators, service workers, and laborers), middle (clerical workers, sales workers, and craftsmen), and high (professionals, physicians, and managers).
COVARIATES
Information about other risk factors for CHD was also collected at baseline and during follow-up using annual questionnaires and medical records. Starting with the class of 1949, nonfasting serum cholesterol level was measured during medical school.31 Physical activity was assessed during medical school and follow-up using the question, "How much physical training have you had in the past month?" Possible responses were "none," "little," "moderate," and "much." Parental history of premature CHD was defined as development of CHD before age 55 years in a participant's father or before age 65 years in his mother. Prevalence of CHD in parents was assessed at baseline and throughout follow-up.32
Body mass index (BMI) was defined as weight in kilograms divided by the square of height in meters. Number of cigarettes smoked per day was categorized as follows: 0, 1 to 10, 11 to 20, 21 to 39, and 40 or more. Participants indicated their current coffee intake based on 8 possible responses ranging from 0 to 7 or more cups a day.
Hypertension was defined as a blood pressure of 160/105 mm Hg or greater on 1 annual questionnaire, 140/90 mm Hg on at least 2 readings at least 1 week apart, or pharmacologic treatment of hypertension. Type 2 diabetes mellitus was defined as report of pharmacologically treated diabetes on a single questionnaire, report of nonpharmacologically treated diabetes on 2 or more questionnaires, physician diagnosis of diabetes in medical records, or report of a fasting plasma glucose level of at least 140 mg/dL (7.8 mmol/L) or a nonfasting plasma glucose level of at least 200 mg/dL (11.1 mmol/L).33 Incidence of clinical depression was measured on the mailed surveys with direct questions concerning the occurrence of depression and associated treatment.34
OUTCOME MEASURES
The primary dependent variable for this analysis was the incidence of CHD occurring on or before age 50 years. Secondary dependent variables were all CHD (incident events, fatal and nonfatal) occurring at any age, CHD mortality, and total mortality. Coronary heart disease was defined as myocardial infarction, sudden death, angina pectoris, chronic ischemic heart disease, and other coronary disease requiring coronary bypass surgery or percutaneous coronary intervention.
STATISTICAL ANALYSIS
Follow-up began at graduation from medical school and continued through December 31, 2001. Baseline characteristics for physicians from low- and high-SES families were summarized and compared using means and t tests for continuous variables and percentages and  2 tests for categorical variables. Kaplan-Meier methods and the log-rank test were used to compare the time to event for incident CHD and mortality between physicians with low and high childhood SES. Proportional hazards models were used to assess the impact of possible CHD risk factors on the relationship between childhood SES and CHD. These factors were serum cholesterol level and exercise during medical school and the presence of parental history of premature CHD and of hypertension, diabetes mellitus, depression, smoking, coffee drinking, and BMI as time-dependent covariates. Follow-up was truncated at age 50 years in models used to assess the effects of covariates on incidence at or before age 50 years. The relatively few CHD events at and before age 50 years limited our ability to adjust for multiple variables simultaneously. Thus, bivariate models were used to determine whether the effect of childhood SES on CHD was mediated through other CHD risk factors. The proportionality of hazards was confirmed with log-log plots and by examining the Schoenfeld residuals.35 A 2-tailed P .05 was considered statistically significant. All statistical analyses were carried out with commercially available software (Stata Release 8.0; StataCorp, College Station, Tex).
RESULTS
BASELINE CHARACTERISTICS
The baseline characteristics of the 1131 men in this study assessed during medical school are given in Table 1. Of 1131 subjects, 216 (19.1%) were from low-SES families. Medical students from low-SES families were slightly older at graduation (26.8 vs 26.2 years; P = .004), and there was no difference in other CHD risk factors at the time of medical school graduation, including BMI, serum cholesterol levels, cigarette smoking, amount of exercise, or family history of premature CHD.
|
|
|
|
Table 1. Baseline Characteristics According to Childhood SES in 1131 White Male Medical School Graduates in The Johns Hopkins Precursors Study*
|
|
|
CHANGES IN CARDIOVASCULAR DISEASE RISK FACTORS OVER TIME
Body mass index increased over time in physicians from both low-SES and high-SES families (Table 2). Physicians from low-SES families, however, had a significantly higher mean BMI at ages 40 to 49, 50 to 59, and 60 to 69 years. While the rates of cigarette smoking decreased in both groups over time, physicians from low-SES families had higher smoking rates in each decade, although the differences were not statistically significant.
|
|
|
|
Table 2. BMI and Cigarette Smoking During Follow-up by Childhood SES in 1131 White Male Medical School Graduates in The Johns Hopkins Precursors Study*
|
|
|
The mean age of developing hypertension and diabetes mellitus was similar in the 2 groups. Physicians from low-SES families developed hypertension 1 year earlier than did physicians from high-SES families, with a mean (SD) age at onset of 54.1 (13.3) vs 55.0 (13.0) years, although this difference was not significant. There was no difference in the age at onset of diabetes mellitus, with a mean age of 57 years in both groups.
CHILDHOOD SES AND RISK OF CHD
Median follow-up time in this analysis was 40 years, yielding 43 160 person-years of observation. During this period, 217 men experienced CHD events. The incidence of CHD from age 40 to age 75 years was consistently greater in men from lower childhood SES backgrounds than in those from higher SES families (Figure). During the entire follow-up, differences in incidence between the groups did not achieve a conventional level of statistical significance (P = .11; Figure), but the incidence of CHD on or before age 50 years was significantly greater in physicians with low compared with high childhood SES (P = .01). Incidence of CHD, fatal CHD, and total mortality by 50 and 70 years are given in Table 3.
|
|
|
|
Figure. Cumulative probability of coronary heart disease in 1131 white male medical school graduates according to childhood socioeconomic status (SES).
|
|
|
|
|
|
|
Table 3. Kaplan-Meier Analysis of All CHD, CHD Mortality, and Total Mortality by Ages 50 and 70 Years in The Johns Hopkins Precursors Study
|
|
|
In univariate proportional hazards analysis, the unadjusted relative risk of developing CHD on or before age 50 years associated with low childhood SES was 2.40 (95% confidence interval [CI], 1.21-4.74; Table 4). In bivariate Cox proportional hazards models, the risk of developing early CHD associated with low childhood SES was not reduced after adjusting for serum cholesterol level during medical school, amount of exercise during medical school, amount of cigarette smoking or coffee drinking during follow-up, BMI during follow-up, parental history of premature CHD, or development of diabetes mellitus, hypertension, or depression during follow-up (Table 4).
|
|
|
|
Table 4. Risk of CHD Associated With Low Childhood SES at Different Age Thresholds in 1131 White Male Medical School Graduates in The Johns Hopkins Precursors Study*
|
|
|
CHILDHOOD SES AND MORTALITY
During a median follow-up of 40 years, 52 deaths related to CHD and 224 total deaths occurred. When the entire follow-up was considered, participants with low childhood SES demonstrated a trend toward increased CHD mortality (hazard ratio [HR], 2.0; 95% CI, 0.99-3.90) compared with physicians with high childhood SES, but no such association was seen for all-cause mortality (HR, 1.08; 95% CI, 0.78-1.48). There were few events by age 50 years (6 deaths due to CHD and 42 total deaths). When only these events were considered, there was the suggestion of an association of low SES with CHD death (HR, 4.27; 95% CI, 0.86-21.17), but not with all-cause mortality (HR, 0.99; 95% CI, 0.46-2.14).
SENSITIVITY ANALYSIS
When information on the mother's occupation was used to reclassify 19 of the participants with low childhood SES as high-SES subjects, our results were unchanged. In addition, analyses using 3 levels of childhood SES also showed a higher risk of premature CHD in the lowest SES group (data not shown).
COMMENT
The present study found that low childhood SES is a risk factor for incident CHD before age 50 years in men with uniformly high adulthood SES. We noted a trend toward increased CHD mortality in physicians of low childhood SES, but no difference in all-cause mortality. This increased risk exists despite physicians' high level of SES as adults, their medical knowledge, and their access to high-quality health care. The higher risk of early CHD was not mediated by BMI, cholesterol level, exercise, depression, coffee drinking, smoking, hypertension, diabetes mellitus, or parental history of CHD.
Several conceptual models have been proposed to explain how lower childhood and adulthood SES may lead to increased risk for cardiovascular disease.7 The latent effects model proposes that adverse early life experiences permanently affect the individual in a way that is not influenced by adult experiences. The pathway model suggests that early life experiences affect adult health by influencing adult behavior and risk factors. The cumulative model hypothesizes that health is determined by the cumulative number of years that an individual spends in either a low- or high-SES category. Individuals with low childhood SES in our study did have higher BMI and were more likely to smoke cigarettes than were individuals with high childhood SES, supporting the pathway model. Low childhood SES was associated with higher CHD risk only before the age of 50 years. After that age, individuals with low SES in childhood in this cohort had spent proportionately more of their lifetime at a high SES than at a low SES.
Low childhood SES may confer an increased risk of CHD on or before age 50 years but not later in life for several reasons. First, other CHD risk factors are more prevalent later in life; thus, the proportionate effect of low childhood SES may be reduced. A similar relationship has been noted in The Johns Hopkins Precursors Study cohort with other risk factors.36 Second, the current study may have been underpowered to detect a small risk of CHD at older ages. For example, in the Nurses’ Health Study of 117 006 participants, the age-adjusted risk of total cardiovascular disease events was 1.13 (95% CI, 1.02-1.24) for nurses with low vs high childhood SES,17 similar to the risk seen in the present study for incident CHD over the lifespan, 1.29. Likewise, the lack of statistical significance for the 2-fold increase in the risk of CHD mortality associated with low childhood SES likely reflects lack of statistical power.
Three other studies have examined the risks of CHD in individuals who have moved from lower SES to higher SES. Two of them, a case-control study of former Harvard University students37 and the Nurses’ Health Study,17 found a higher risk in persons with low childhood SES. A study of Finnish men born in the late 1950s found that adulthood SES had a greater effect on mortality than did childhood SES, although childhood SES had a persistent effect on mortality from cardiovascular disease.38
Besides these studies, which specifically examined the move from low childhood SES to high adulthood SES, many other studies have investigated the relationship between childhood SES and cardiovascular events.12-29 However, most of these studies were conducted outside the United States,12-16,18-19,21-29 ascertained childhood SES in late adulthood,12-14,19, 21, 25-27,29 or, if a prospective design was used, started follow-up in midlife, assessing only for possible confounders occurring later than age 40 years.20, 28 Nevertheless, low childhood SES was associated with a higher risk of cardiovascular events in all of the studies, although the effects of adjustment for established CHD risk factors and adulthood SES varied.15-16,18 Thus, compared with all studies of childhood SES and CHD, the present study offers a unique perspective of early CHD in a well-defined cohort of medical school graduates.
The present study adds to the body of information on childhood SES and CHD in several ways. First, data on childhood SES were collected earlier in adulthood, before clinical events had occurred, minimizing possible recall bias. Second, all of the participants graduated from medical school and thus had uniformly high adulthood SES, thereby eliminating confounding by changes in adulthood SES. Finally, unlike the other studies, we examined the relationship between childhood SES and early CHD.
Although different life-course models help to conceptualize the relationship between childhood SES and the development of CHD in adulthood, the underlying biological factors are less clear. The association between lower SES in adulthood and CHD risk has been ascribed to a higher prevalence of CHD risk factors in adults with low SES, including hypertension,39 the metabolic syndrome,40 and unhealthy behaviors, including smoking, high-fat diets, and low levels of physical activity.41 Evidence also suggests that adults with low SES have differential activation of biological pathways that are implicated in the development of CHD. Compared with adults of high SES, those with lower SES have higher levels of cortisol,42 higher levels of C-reactive protein,43 greater platelet activation,44 and more atherogenic lipid profiles.45 More data are needed on the persistence of the relationships between low SES and these biological variables.
Some limitations of our study deserve mention. Our exposure definition, parental occupation, is based on self-report, which can be subject to error. If persons with low childhood SES systematically reported higher levels, as defined by parental occupation, then the true association between low SES and CHD would most likely be diluted. In addition, these findings should be generalized with caution to groups other than male physicians of European ancestry. Furthermore, our conclusions are based on a relatively small number of events before age 50 years. Another limitation is the use of paternal occupation as a measure of childhood SES. Socioeconomic status is a multidimensional construct, and other studies have used parents' level of education, occupation, and/or income as measures.46-47 Income may be the best marker of childhood SES,48-50 but occupation is used in about a quarter of studies and is a reasonable surrogate for childhood SES.6, 48-50
Nevertheless, The Johns Hopkins Precursors Study cohort offers study strengths. The strengths of the present study include a long follow-up period and an excellent response rate from participants. The cohort design also allows for accurate measurement of confounders that vary over time and for precise measurement of exposure status before disease onset without the risk of recall bias or reverse causality. In addition, self-reports of CHD risk factors and clinical outcomes have been validated in this cohort.51
In conclusion, these results indicate that, even for individuals with uniformly high SES in adulthood, the presence of low SES in childhood confers an increased risk of developing CHD before age 50 years. This increased risk is not mediated by established CHD risk factors. These findings highlight the importance of childhood events in the development of CHD in adulthood. More importantly, the data illustrate the difficulty in eliminating health status disparities between low-SES and high-SES populations: even an intervention that allowed low-SES individuals to assume the lifestyle of physicians did not totally eliminate disparities in early CHD outcomes.
AUTHOR INFORMATION
Correspondence: Michelle M. Kittleson, MD, PhD, The Johns Hopkins Precursors Study, 2024 E Monument St, Suite 2-200, Baltimore, MD 21205 (mkittleson{at}mednet.ucla.edu).
Accepted for Publication: August 29, 2006.
Author Contributions: All authors had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Kittleson, Wang, Ford, and Klag. Acquisition of data: Kittleson, Wang, Ford, and Klag. Analysis and interpretation of data: Kittleson, Meoni, Wang, Chu, Ford, and Klag. Drafting of the manuscript: Kittleson. Critical revision of the manuscript for important intellectual content: Kittleson, Meoni, Wang, Chu, Ford, and Klag. Statistical analysis: Kittleson, Meoni, Wang, Chu, Ford, and Klag. Obtained funding: Klag. Administrative, technical, and material support: Ford and Klag. Study supervision: Ford and Klag.
Financial Disclosure: None reported.
Funding/Support: This study was supported by grants K24 DK02856, R01 AG01760, and T32 HL007227-30 from the National Institutes of Health.
Author Affiliations: Divisions of Cardiology (Dr Kittleson) and General Internal Medicine (Ms Meoni and Drs Wang, Ford, and Klag), Department of Medicine, The Johns Hopkins School of Medicine, and Departments of Epidemiology (Ms Chu and Drs Ford and Klag), Biostatistics (Ms Meoni), and Health Policy and Management (Drs Ford and Klag), Johns Hopkins Bloomberg School of Public Health, The Johns Hopkins University, Baltimore, Md. Dr Kittleson is now with the Division of Cardiology, David Geffen School of Medicine at UCLA, Los Angles, Calif.
REFERENCES
1. Anderson RN, Smith BL. Deaths: leading causes for 2001. Natl Vital Stat Rep. 2003;52;(9):1-85.
PUBMED
2. Smith GD, Shipley MJ, Rose G. Magnitude and causes of socioeconomic differentials in mortality: further evidence from the Whitehall Study. J Epidemiol Community Health. 1990;44:265-270.
FREE FULL TEXT
3. Rose G, Marmot MG. Social class and coronary heart disease. Br Heart J. 1981;45:13-19.
FREE FULL TEXT
4. Rosengren A, Orth-Gomer K, Wilhelmsen L. Socioeconomic differences in health indices, social networks and mortality among Swedish men: a study of men born in 1933. Scand J Soc Med. 1998;26:272-280.
WEB OF SCIENCE
| PUBMED
5. Woodward M, Oliphant J, Lowe G, Tunstall-Pedoe H. Contribution of contemporaneous risk factors to social inequality in coronary heart disease and all causes mortality. Prev Med. 2003;36:561-568.
FULL TEXT
|
WEB OF SCIENCE
| PUBMED
6. Kaplan GA, Keil JE. Socioeconomic factors and cardiovascular disease: a review of the literature. Circulation. 1993;88:1973-1998.
FREE FULL TEXT
7. Pollitt RA, Rose KM, Kaufman JS. Evaluating the evidence for models of life course socioeconomic factors and cardiovascular outcomes: a systematic review. BMC Public Health. 2005;5:7.
FULL TEXT
| PUBMED
8. Ward E, Jemal A, Cokkinides V, et al. Cancer disparities by race/ethnicity and socioeconomic status. CA Cancer J Clin. 2004;54:78-93.
WEB OF SCIENCE
| PUBMED
9. Bagger JP, Zindrou D, Taylor PK. Postoperative infection with meticillin-resistant Staphylococcus aureus and socioeconomic background. Lancet. 2004;363:706-708.
FULL TEXT
|
WEB OF SCIENCE
| PUBMED
10. Stockwell EG, Goza FW, Luse VO. Infectious disease mortality among adults by race and socioeconomic status: metropolitan Ohio, 1989-1991. Soc Biol. 1997;44:148-152.
WEB OF SCIENCE
| PUBMED
11. Isaacs SL, Schroeder SA. Class—the ignored determinant of the nation's health. N Engl J Med. 2004;351:1137-1142.
FULL TEXT
|
WEB OF SCIENCE
| PUBMED
12. Burr ML, Sweetnam PM. Family size and paternal unemployment in relation to myocardial infarction. J Epidemiol Community Health. 1980;34:93-95.
FREE FULL TEXT
13. Notkola V, Punsar S, Karvonen MJ, Haapakoski J. Socio-economic conditions in childhood and mortality and morbidity caused by coronary heart disease in adulthood in rural Finland. Soc Sci Med. 1985;21:517-523.
FULL TEXT
|
WEB OF SCIENCE
| PUBMED
14. Coggon D, Margetts B, Barker DJ, et al. Childhood risk factors for ischaemic heart disease and stroke. Paediatr Perinat Epidemiol. 1990;4:464-469.
PUBMED
15. Hasle H. Association between living conditions in childhood and myocardial infarction. BMJ. 1990;300:512-513.
FREE FULL TEXT
16. Lundberg O. The impact of childhood living conditions on illness and mortality in adulthood. Soc Sci Med. 1993;36:1047-1052.
FULL TEXT
|
WEB OF SCIENCE
| PUBMED
17. Gliksman MD, Kawachi I, Hunter D, et al. Childhood socioeconomic status and risk of cardiovascular disease in middle aged US women: a prospective study. J Epidemiol Community Health. 1995;49:10-15.
FREE FULL TEXT
18. Marmot M, Shipley M, Brunner E, Hemingway H. Relative contribution of early life and adult socioeconomic factors to adult morbidity in the Whitehall II study. J Epidemiol Community Health. 2001;55:301-307.
FREE FULL TEXT
19. Wamala SP, Lynch J, Kaplan GA. Women's exposure to early and later life socioeconomic disadvantage and coronary heart disease risk: the Stockholm Female Coronary Risk Study. Int J Epidemiol. 2001;30:275-284.
FREE FULL TEXT
20. Lynch JW, Kaplan GA, Cohen RD, et al. Childhood and adult socioeconomic status as predictors of mortality in Finland. Lancet. 1994;343:524-527.
FULL TEXT
|
WEB OF SCIENCE
| PUBMED
21. Vagero D, Leon D. Effect of social class in childhood and adulthood on adult mortality. Lancet. 1994;343:1224-1225.
WEB OF SCIENCE
| PUBMED
22. Smith GD, Hart C, Blane D, Hole D. Adverse socioeconomic conditions in childhood and cause specific adult mortality: prospective observational study. BMJ. 1998;316:1631-1635.
FREE FULL TEXT
23. Smith GD, Hart C. Life-course socioeconomic and behavioral influences on cardiovascular disease mortality: the collaborative study. Am J Public Health. 2002;92:1295-1298.
WEB OF SCIENCE
| PUBMED
24. Hart CL, Smith GD, Blane D. Inequalities in mortality by social class measured at 3 stages of the lifecourse. Am J Public Health. 1998;88:471-474.
WEB OF SCIENCE
| PUBMED
25. Dedman DJ, Gunnell D, Davey SG, Frankel S. Childhood housing conditions and later mortality in the Boyd Orr cohort. J Epidemiol Community Health. 2001;55:10-15.
FREE FULL TEXT
26. Frankel S, Smith GD, Gunnell D. Childhood socioeconomic position and adult cardiovascular mortality: the Boyd Orr Cohort. Am J Epidemiol. 1999;150:1081-1084.
FREE FULL TEXT
27. Claussen B, Davey Smith G, Thelle D. Impact of childhood and adulthood socioeconomic position on cause specific mortality: the Oslo Mortality Study. J Epidemiol Community Health. 2003;57:40-45.
FREE FULL TEXT
28. Osler M, Andersen AM, Due P, Lund R, Damsgaard MT, Holstein BE. Socioeconomic position in early life, birth weight, childhood cognitive function, and adult mortality: a longitudinal study of Danish men born in 1953. J Epidemiol Community Health. 2003;57:681-686.
FREE FULL TEXT
29. Kaplan GA, Salonen JT. Socioeconomic conditions in childhood and ischaemic heart disease during middle age. BMJ. 1990;301:1121-1123.
FREE FULL TEXT
30. Alphabetical Index of Industries and Occupations: 1950 Census of Population. Rev ed. Washington, DC: US Bureau of the Census; 1951.31. Klag MJ, Ford DE, Mead LA, et al. Serum cholesterol in young men and subsequent cardiovascular disease. N Engl J Med. 1993;328:313-318.
FULL TEXT
|
WEB OF SCIENCE
| PUBMED
32. Summary of the second report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). JAMA. 1993;269:3015-3023.
FREE FULL TEXT
33. Golden SH, Wang NY, Klag MJ, Meoni LA, Brancati FL. Blood pressure in young adulthood and the risk of type 2 diabetes in middle age. Diabetes Care. 2003;26:1110-1115.
FREE FULL TEXT
34. Chang PP, Ford DE, Mead LA, Cooper-Patrick L, Klag MJ. Insomnia in young men and subsequent depression: The Johns Hopkins Precursors Study. Am J Epidemiol. 1997;146:105-114.
FREE FULL TEXT
35. Schoenfeld D. Partial residuals for the proportional hazard regression model. Biometrika. 1982;69:239-241.
FREE FULL TEXT
36. Chang PP, Ford DE, Meoni LA, Wang NY, Klag MJ. Anger in young men and subsequent premature cardiovascular disease: the Precursors Study. Arch Intern Med. 2002;162:901-906.
FREE FULL TEXT
37. Gillum RF, Paffenbarger RS Jr. Chronic disease in former college students, XVII: sociocultural mobility as a precursor of coronary heart disease and hypertension. Am J Epidemiol. 1978;108:289-298.
FREE FULL TEXT
38. Pensola TH, Martikainen P. Cumulative social class and mortality from various causes of adult men. J Epidemiol Community Health. 2003;57:745-751.
FREE FULL TEXT
39. Colhoun HM, Hemingway H, Poulter NR. Socio-economic status and blood pressure: an overview analysis. J Hum Hypertens. 1998;12:91-110.
FULL TEXT
|
WEB OF SCIENCE
| PUBMED
40. Brunner EJ, Marmot MG, Nanchahal K, et al. Social inequality in coronary risk: central obesity and the metabolic syndrome: evidence from the Whitehall II study. Diabetologia. 1997;40:1341-1349.
FULL TEXT
|
WEB OF SCIENCE
| PUBMED
41. Hellerstedt WL, Jeffery RW. The association of job strain and health behaviours in men and women. Int J Epidemiol. 1997;26:575-583.
FREE FULL TEXT
42. Steptoe A, Kunz-Ebrecht S, Owen N, et al. Socioeconomic status and stress-related biological responses over the working day. Psychosom Med. 2003;65:461-470.
FREE FULL TEXT
43. Owen N, Poulton T, Hay FC, Mohamed-Ali V, Steptoe A. Socioeconomic status, C-reactive protein, immune factors, and responses to acute mental stress. Brain Behav Immun. 2003;17:286-295.
FULL TEXT
|
WEB OF SCIENCE
| PUBMED
44. Steptoe A, Magid K, Edwards S, Brydon L, Hong Y, Erusalimsky J. The influence of psychological stress and socioeconomic status on platelet activation in men. Atherosclerosis. 2003;168:57-63.
FULL TEXT
|
WEB OF SCIENCE
| PUBMED
45. Brunner EJ, Marmot MG, White IR, et al. Gender and employment grade differences in blood cholesterol, apolipoproteins and haemostatic factors in the Whitehall II study. Atherosclerosis. 1993;102:195-207.
FULL TEXT
|
WEB OF SCIENCE
| PUBMED
46. Lynch JW, Kaplan GA, Salonen JT. Why do poor people behave poorly? variation in adult health behaviours and psychosocial characteristics by stages of the socioeconomic lifecourse. Soc Sci Med. 1997;44:809-819.
FULL TEXT
|
WEB OF SCIENCE
| PUBMED
47. Winkleby MA, Robinson TN, Sundquist J, Kraemer HC. Ethnic variation in cardiovascular disease risk factors among children and young adults: findings from the Third National Health and Nutrition Examination Survey, 1988-1994. JAMA. 1999;281:1006-1013.
FREE FULL TEXT
48. Daly MC, Duncan GJ, McDonough P, Williams DR. Optimal indicators of socioeconomic status for health research. Am J Public Health. 2002;92:1151-1157.
WEB OF SCIENCE
| PUBMED
49. Lantz PM, House JS, Lepkowski JM, Williams DR, Mero RP, Chen J. Socioeconomic factors, health behaviors, and mortality: results from a nationally representative prospective study of US adults. JAMA. 1998;279:1703-1708.
FREE FULL TEXT
50. 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;52:153-160.
ABSTRACT
51. Klag MJ, He J, Mead LA, Ford DE, Pearson TA, Levine DM. Validity of physicians' self-reports of cardiovascular disease risk factors. Ann Epidemiol. 1993;3:442-447.
PUBMED
 CiteULike  Connotea  Delicious  Digg  Facebook  Reddit  Technorati  Twitter
What's this?
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
|
Protective Factors for Adults From Low-Childhood Socioeconomic Circumstances: The Benefits of Shift-and-Persist for Allostatic Load
Chen et al.
Psychosom. Med. 2012;74:178-186.
ABSTRACT
| FULL TEXT
Influence of Life-Course Socioeconomic Position on Incident Heart Failure in Blacks and Whites: The Atherosclerosis Risk in Communities Study
Roberts et al.
Am J Epidemiol 2010;172:717-727.
ABSTRACT
| FULL TEXT
Associations Between Childhood Socioeconomic Position and Adulthood Obesity
Senese et al.
Epidemiol Rev 2009;31:21-51.
ABSTRACT
| FULL TEXT
Low early-life social class leaves a biological residue manifested by decreased glucocorticoid and increased proinflammatory signaling
Miller et al.
Proc. Natl. Acad. Sci. USA 2009;106:14716-14721.
ABSTRACT
| FULL TEXT
Trends in risk factors for cardiovascular disease in Canada: temporal, socio-demographic and geographic factors
Lee et al.
CMAJ 2009;181:E55-E66.
ABSTRACT
| FULL TEXT
Life-Course Socioeconomic Position and Incidence of Coronary Heart Disease: The Framingham Offspring Study
Loucks et al.
Am J Epidemiol 2009;169:829-836.
ABSTRACT
| FULL TEXT
A National Agenda for America's Children and Adolescents in 2008: Recommendations From the 15th Annual Public Policy Plenary Symposium, Annual Meeting of the Pediatric Academic Societies, May 3, 2008
Genel et al.
Pediatrics 2008;122:843-849.
FULL TEXT
Low Childhood SES for Physicians Predicts Poor Medical Outcomes in Adulthood
Robbins
AAP Grand Rounds 2007;17:28-29.
FULL TEXT
|
