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Debbie A Lawlor, PhD, MSc, MBChB, George Davey Smith, DSc, MD and Shah Ebrahim, DM, MSc

The authors are with the Department of Social Medicine, University of Bristol, Bristol, United Kingdom.

Correspondence: Requests for reprints should be sent to Debbie A. Lawlor, PhD, MSc, MBChB, Department of Social Medicine, University of Bristol, Canynge Hall, Whiteladies Road, Bristol BS7 8QA, United Kingdom (email: d.a.lawlor{at}bristol.ac.uk).

	ABSTRACT

TOP ABSTRACT INTRODUCTION METHODS Statistical Analysis RESULTS DISCUSSION References

 

Objectives. We assessed the association between life-course socioeconomic status or position (SEP) and hormone replacement therapy (HRT).

Methods. We conducted a cross-sectional analysis of 4286 women aged 60 to 79 years.

Results. Women experiencing adverse socioeconomic circumstances across the life course were less likely to have used HRT. The associations of childhood socioeconomic measures with HRT use were independent of adult SEP, behavioral risk factors, and physiological risk factors for heart disease.

Conclusions. SEP from across the life course is associated with HRT use. Because the association between early life SEP and HRT is not fully explained by adult risk factors, residual confounding (which is not captured by adjustment for adult variables only) may explain some of the disparity between observational studies and randomized controlled trials in this area.

	INTRODUCTION

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The disparity between findings from observational studies and randomized controlled trials of the effects of hormone replacement therapy (HRT) on coronary heart disease (CHD)^1–4 has created considerable debate among researchers, practitioners, and post-menopausal women.^5–10 Observational studies have consistently found that use of HRT is protective against CHD, with a meta-analysis of observational studies yielding a summary relative risk for ever use of HRT of 0.56 (95% confidence interval [CI] = 0.50, 0.61).⁴ By contrast, recent randomized trials among women with established CHD and healthy women have found HRT to be associated with slightly increased risk of CHD or null effects. For example, the large Women’s Health Initiative randomized trial found that the hazards ratio for CHD associated with being allocated to HRT was 1.29 (95% CI = 1.02, 1.63), after 5.2 years of follow-up.¹

A number of explanations have been suggested for these disparities. Although some researchers have suggested that the results of the trials were biased because of contamination, and in the case of the Women’s Health Initiative, early termination of the arm assessing the effect of combined HRT, the consistency across a number of trials of a null effect makes these explanations unlikely. More plausible explanations are that women who participated in the trials were importantly different from those who participated in the observational studies or that the observational study results were confounded.^5,8,9,11

Women in the Women’s Health Initiative trial were older than the average age at which women take HRT and were more obese than the women who have been included in the observational studies.¹ These women may be more likely to have established atherosclerosis than younger and leaner women and therefore may be more prone to the prothrombotic effects of HRT.⁵ However, there was no evidence of interactions of treatment assignment with age, prior hormone use, or body mass index for any cardiovascular outcomes in the Women’s Health Initiative.^1,12

Of particular interest is whether the results in the observational studies are explained by residual confounding. Despite the fact that use of HRT is strongly socially patterned¹³ and that socioeconomic status or position (SEP) is associated with CHD,¹⁴ in many observational studies, adjustment for adult SEP has failed to have a marked impact on the HRT–CHD association.¹⁵ However, residual confounding by SEP across the life course may be particularly important.^16,17 SEP in childhood is strongly associated with CHD risk, independent of adult SEP.^14,18 The association between adverse SEP in early life and CHD is in part mediated by adult behavioral and physiological risk factors.¹⁴ Therefore, early life SEP could be an important confounder only if it were associated with HRT use and this association were independent of adult SEP and proximal adult risk factors that in part explain the association between early life SEP and CHD risk.

Our hypothesis was that the protective effect of HRT against CHD found in observational studies is explained at least in part by residual confounding related to early life socioeconomic factors that are not completely captured by adult risk factors. To assess this possibility, the primary aim of this study was to determine whether SEP in early life is associated with HRT use. Furthermore, we aimed to determine whether any association between early life SEP and HRT is fully explained by adult socioeconomic, behavioral, and physiological risk factors. If this association exists, then adequate adjustment for these adult risk factors should be sufficient to capture any potential confounding effect of early life SEP.

	METHODS

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Data from the British Women’s Heart and Health Study were used. Full details of the selection of participants and measurements used in the study have been previously reported.^19,20 Women aged 60 to 79 years were randomly selected from general practitioner lists in 23 British towns. A total of 4286 women (60% of those invited) participated, and baseline data were collected between April 1999 and March 2001. Local ethics committee approvals were obtained.

Data on socioeconomic indicators across the life course included data on the longest held occupation of the participant’s father during her childhood, childhood household amenities (i.e., bathroom, hot water, bedroom sharing, and car access), age at completion of full-time education, the longest held occupation of the participant and her spouse, adult housing tenure, car access, and pension arrangements. Childhood social class of each woman was based on her father’s longest held occupation and adult social class was based on her husband’s longest held occupation or her own longest held occupation for single women.²¹ Adult and childhood social class were defined according to the registrar general’s classification of occupations (I, II, III nonmanual, III manual, IV, and V, with I indicating professional occupations and V indicating manual unskilled occupations). We repeated the analyses using each woman’s own occupation for married women who were not permanent housewives and declared an occupation (74%). The results from these analyses were essentially unaltered from those presented here although, because of reduced numbers, they were less precise. Most of the indicators of SEP were binary variables. For the main analyses, we dichotomized adult and childhood social class into nonmanual (I, II, III nonmanual) and manual (III manual, IV, V) groups to minimize any possible misclassification bias. Pension arrangements were dichotomized as state only or state plus other and adult housing tenure as local authority or other. Age at leaving full-time education was dichotomized around the median value (15 years).

Use of HRT, socioeconomic indicators, age at menopause, history of a hysterectomy or oophorectomy, smoking history, and physical activity were obtained from the self-completed questionnaire and/or the research nurse interview, to which women were requested to bring their current medications.^19,20 Blood samples were taken after a minimum 6-hour fast (except for patients using insulin treatment) using evacuated tubes and were used to determine insulin resistance and lipid levels.^19,20 Blood pressure, weight, height, and waist and hip circumference were measured using standard procedures.^19,20 Coronary heart disease was considered to be present in any woman with a medical record of myocardial infarction (verified with respect to World Health Organization criteria²²), angina, angioplasty or coronary artery bypass grafting, and/or any woman with a self-report of a physician diagnosis of these.¹⁹

Of the 4286 participants, 911 (21.0%) stated that they had ever (current and past) used HRT and 368 stated (8.6%) that they were currently using HRT. Of those who had ever used HRT, 43% did not know the name or type of preparation (or gave only vague details such as "tablets" or "patches"), 32% used a combined estrogen–progestogen preparation, 18% used unopposed estrogen, and 7% were not actually using HRT (e.g., tibolone, raloxifene). Of current users, only 9% did not know the name or type, 40% were taking a combined preparation, 39% were taking unopposed estrogen, and 12% were not actually using HRT. Those who had not or were not actually using HRT were categorized as not using HRT; those who did not know the type of HRT that they had used were all assumed to have used HRT. Thus, in the main analysis, 848 women (19.8%) were categorized as ever using HRT, and 323 (7.5%) were categorized as currently using HRT. In a sensitivity analysis, all women who defined themselves as ever (n = 911) or currently taking HRT (n = 368) were defined as exposed. The results of this sensitivity analysis did not differ substantively from those presented here. All of those who were currently using unopposed estrogen had had a hysterectomy.

	Statistical Analysis

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Age-adjusted prevalences and 95% confidence intervals for each indicator of SEP are presented for all women in the study and for current, past, and never users of HRT. Multiple logistic regression was used to assess the associations of each individual indicator of SEP with HRT use. For each indicator, 3 logistic regression models were undertaken. In the first, crude associations were assessed. In the second, childhood indicators were adjusted for age (entered as a continuous variable) and adult indicators of SEP (adult social class, car access, local authority housing, and pension arrangements entered as full categorical [indicator] variables, except car access, which is binary). In the third model, all other adult behavioral and physiological risk factors that might capture any association between childhood SEP and HRT use were added to the age- and adult SEP–adjusted model. In this model, systolic blood pressure, high-density lipoprotein cholesterol, triglyceride levels (logged), body mass index, waist-to-hip ratio, and age of menopause were all entered as continuous variables; smoking and physical activity were entered as indicator variables. Homeostasis model assessment scores (insulin resistance) were not estimated for individuals with diabetes, and an indicator variable representing insulin resistance–diabetes was calculated as fifths of homeostasis model assessment scores for nondiabetics together with a sixth category for patients with diabetes.¹⁸ Covariates were decided a priori, rather than being data driven, for example, by stepwise regression.²³ Uptake of HRT has increased over recent decades, and it is possible that as HRT use becomes more widespread, any associations with SEP will be weaker in younger birth cohorts. To assess this possibility, age was dichotomized as 60 to 69 years and 70 to 79 years, and likelihood ratio tests were used to determine statistical evidence for any interactions between age and socioeconomic indicators in their association with HRT use.

In addition to assessing the association of each individual life-course indicator of SEP, we assessed the cumulative effect of life-course SEP by generating a life-course SEP score from the 10 dichotomized indicators. Two scores were developed, one in which equal weight was given to each indicator and another in which the inverse of prevalence weights was used. The first score has the advantage of being easy to understand because the score gives the actual number of adverse indicators. The score ranged from 0 (most advantaged position across the life course) to 10 (most disadvantaged position across the life course). Because there were very small numbers in the 0 category (n = 77) and in the 10 category (n = 57), the 0 category was combined with the 1 category and the 10 category with the 9 category. The second score in which each indictor was weighted by the inverse of its prevalence gave the greatest weight to adverse indicators that were least prevalent. The resulting weighted score was highly positively skewed, with a range from 0 to 28.9. The 2 composite socioeconomic scores were strongly correlated (Spearman rank correlation coefficient = 0.95) and showed identical linear trends in their association with HRT use. Results for the un-weighted score only are therefore presented. Likelihood ratio tests were used to assess departure from linearity in the associations between the scores and HRT use.

	RESULTS

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Most women provided data on each of the socioeconomic indicators, with details of pension arrangements being the variable with the greatest amount of missing data (3828 [89%] women provided data for this indicator). There were no significant differences in SEP indicators or risk factor distributions between women with complete data on all indicators and those with some missing data (all P values >.25). Table 1 shows the prevalence of each indicator of SEP for all study participants and by HRT use.

	DISCUSSION

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Our response rate (60%) is moderate but consistent with other baseline data collected in large epidemiological surveys.²⁴ Responders were younger and less likely to have had a stroke than nonresponders, although CHD prevalence was similar among responders and nonresponders.¹⁹ The social class distribution of the British Women’s Heart and Health Study is similar to that found for the 1991 census for England and Wales (57% manual social class in British Women’s Heart and Health Study vs 55% of women aged 65 and older in the 1991 census), which provides some evidence to suggest that our sample is not affected by selection bias based on SEP.

Our study is cross-sectional and so may be affected by reverse causality and survivor bias. In the association of early life SEP with HRT use, reverse causality is not an issue, and for adult SEP it is difficult to imagine HRT use having an effect on socioeconomic circumstances. Our results for the association between HRT and CHD are consistent with those from prospective cohort studies.⁴ Survivor bias would be important for the association between childhood SEP and HRT use if the association between these 2 among women who died prematurely was either null or in the opposite direction to that presented here (i.e., women from poor SEP were more likely to use HRT). Although this cannot be ruled out, it seems unlikely.

We have no information on how women who were prescribed HRT were screened by their physicians, and it is likely that confounding by indication also will have biased previous observational studies.¹¹ That is, doctors may have been less likely to prescribe HRT to women who were at greater risk of CHD because of obesity, high blood pressure, or other CHD risk factors. To some extent, this may be controlled for by adjustment for these adult risk factors, but adjustment for life-course SEP may capture this effect to a greater extent by reflecting these exposures over the life course. However, our study is not suitable for fully examining the importance of confounding by indication in the HRT–CHD associations.

Our study cohort consisted of women who were born in Great Britain between 1919 and 1940, and the results may not be generalizable to women from other countries and those from different birth cohorts. For example, a study of women born in 1946 in Great Britain found no association between childhood SEP and HRT use.²⁵ Because observational studies of the protective effect of HRT were largely conducted on cohorts born before the 1940s,⁴ our results have relevance for the current debate about the disparities between observational and trial results but do not necessarily mean that for all populations childhood SEP will be associated with HRT use.

Data on HRT use were confirmed by review of medication among current users and by self-report for past users, which may have led to some misclassification for the ever use category. Over two fifths (43%) of women who stated that they had ever used HRT were unable to name the preparation, and 4% who named their preparation were using a related but nonhormonal preparation such as raloxifene. However, the results of this study were consistent for current use of HRT (where actual preparations were checked at the interview) and ever use (where some misclassification is likely). Furthermore, most other observational studies have relied on self-report of HRT use only and are likely to have included some women who were using nonhormonal preparations, as in this study. Finally, our results for the association between HRT use and CHD are consistent with previous prospective studies that have used either self-report or medical record data.⁴

We have not assessed all factors that may affect HRT use and CHD risk and may thus have confounded the associations presented in earlier observational studies. For example, ethnicity may determine HRT use and is associated with CHD risk. Over 99% of women in this study were White; we were therefore unable to determine the effect of ethnicity on HRT use in this study.

Childhood SEP may affect future use of HRT by means of a number of mechanisms, including the individual’s attitudes toward health, preventive treatment, and natural physiological processes such as menopause and aging, gained from their parent’s attitudes toward these; the ability to access health care; and discrimination based on patient characteristics. Although the actual mechanisms are not discernible from our data, it is plausible that adult attitudes toward the use of HRT and access to HRT are formed by SEP in earlier life.

The importance of our results is in the contribution that they make to the debate concerning disparities in observational and trial evidence. We believe that these results support the trial evidence of no protective effect. Our results also have general implications for observational epidemiological studies. Future observational studies, in this and other areas, should aim to collect (even retrospectively) information on socioeconomic circumstances from across the life course to be able to adjust as fully as possible for potential confounding factors. Sensitivity analyses to assess the possibility of residual confounding should also become routine practice in observational epidemiology.^26,27 In addition, specificity of association should be considered.^26,28 As long ago as 1986, Diana Petitti pointed out in observational studies that HRT was apparently equally protective against accidental and violent deaths as it was against death resulting from cardiovascular disease.²⁹ She pointed out that given the lack of any biologically plausible link between HRT and these external causes of death, both associations should be considered to be attributable to residual confounding.²⁹ We have discussed approaches to strengthening inferences from observational studies in detail elsewhere.^30,31

	Acknowledgments

 
The British Women’s Heart and Health Study is funded by the Department of Health and the British Heart Foundation. D. A. Lawlor is funded by a UK Department of Health Career Scientist Award.

The British Women’s Heart and Health Study is codirected by S. Ebrahim, Professor Peter Whincup, Dr Goya Wannamethee, and D. A. Lawlor. The authors thank Carol Bedford, Alison Emerton, Nicola Frecknall, Karen Jones, Rita Patel, Mark Taylor, and Katherine Wornell for collecting and entering data; all of the general practitioners and their staff who have supported data collection; and the women who have participated in the study.

Note. The views expressed in this publication are those of the authors and not necessarily those of any of the funding bodies.

Human Participant Protection
The British Women’s Heart and Health Study has ethics approval from UK local ethics committees in each town in which the study participants reside.

	Footnotes

 
Contributors
All authors developed the study aim. S. Ebrahim and D. A. Lawlor managed data collection, storage, and cleaning for the British Women’s Heart and Health Study. D. A. Lawlor undertook the analysis and coordinated writing of the article. All authors contributed to writing the article. D. A. Lawlor acted as guarantor.

Peer Reviewed

Accepted for publication January 17, 2004.

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This Article Abstract Full Text (PDF) Submit a response View Shopping Cart Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by Lawlor, D. A Articles by Ebrahim, S. Search for Related Content PubMed PubMed Citation Articles by Lawlor, D. A Articles by Ebrahim, S. Related Collections Socioeconomic Factors Other Statistics/Evaluation/Research Women's Health Cardiovascular Disease