American Journal of Epidemiology Advance Access originally published online on February 16, 2006
American Journal of Epidemiology 2006 163(7):615-621; doi:10.1093/aje/kwj081
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Original Contribution |
Association between Height and Coronary Heart Disease Mortality: A Prospective Study of 35,000 Twin Pairs
1 Department of Public Health, University of Helsinki, Helsinki, Finland
2 Division of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
3 Danish Twin Registry, University of Southern Denmark, Odense, Denmark
4 Department of Epidemiology and Public Health, Queen's University Belfast, Belfast, Northern Ireland, United Kingdom
5 Department of Mental Health and Alcohol Research, National Public Health Institute, Helsinki, Finland
Correspondence to Dr. Karri Silventoinen, Department of Public Health, University of Helsinki, P.O. Box 41, Mannerheimintie 172, Helsinki, Finland FIN-00014 (e-mail: karri.silventoinen{at}helsinki.fi).
Received for publication August 23, 2005. Accepted for publication October 26, 2005.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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An inverse association between height and risk of coronary heart disease (CHD) is well demonstrated, but it is not known whether this association is because of genetic factors, socioeconomic background, or other environmental factors. Four population-based twin cohorts with register-based follow-up data on CHD mortality from Denmark (1966–1996), Finland (1975–2001), and Sweden (1963–2001 and 1972–2001) were used to investigate this question; response rates varied between 65% and 86%. Together, the cohorts included 74,704 twin individuals (35,042 complete twin pairs) with 5,943 CHD deaths during 1.99 million person-years of follow-up. Cox and conditional logistic regression models were used. Per 1-standard deviation decrease in height, height was inversely associated with CHD mortality in men (hazard ratio = 1.08, 95% confidence interval (CI): 1.04, 1.12) and in women (hazard ratio = 1.06, 95% CI: 1.01, 1.10). A twin who had died from CHD was on average shorter than the co-twin within monozygotic pairs (odds ratio = 1.27, 95% CI: 1.12, 1.44, with no sex difference), whereas a weaker association was found within dizygotic pairs in men (odds ratio = 1.01, 95% CI: 0.91, 1.13) and in women (odds ratio = 1.14, 95% CI: 1.01, 1.28). The inverse association between height and CHD mortality found within monozygotic discordant twin pairs suggests that this association is because of environmental factors that directly affect height and CHD risk.
body height; coronary disease; environment; genome, human; risk factors; twins
Abbreviations: CHD, coronary heart disease; CI, confidence interval; DZ, dizygotic; HR, hazard ratio; ICD, International Classification of Diseases; MZ, monozygotic; OR, odds ratio
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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An inverse association between height and coronary heart disease (CHD) risk has been reported in many previous prospective epidemiologic studies (1
–7), although there are some exceptions (8–11). The mechanism of this association is poorly understood. Since both height (12) and CHD risk (13) are associated with social position, it is possible that the association is generated by socioeconomic factors. It is also possible that malnutrition in fetal life and childhood resulting in suboptimal growth (14) is also a risk factor for CHD in later life (15). The third possibility is that shared genetic factors are behind this association.
A twin study design offers a unique opportunity for studying the reasons for this association. First, if the association between height and CHD risk is because of family background, the association should be found only between, but not within, twin pairs reared together. Second, if the association is because of genetic factors, the association should be found within dizygotic (DZ) twin pairs, who share on average 50 percent of their segregating genes, but not within monozygotic (MZ) twin pairs, who share the same genes. Finally, if the association is because of nonfamilial environmental factors, it should be found within both MZ and DZ twin pairs (16).
We are aware of only two previous studies that have reported information on twin pairs discordant for height and CHD through a period of follow-up. In a Swedish study of CHD mortality (17), a statistically significant inverse association within discordant twin pairs was found when MZ and DZ twins were pooled together, but zygosity-specific results were not reported. In a Finnish study of incident CHD (18), no association was found within MZ twins, whereas there was some evidence for a moderate inverse association within DZ twins; the zygosity interaction was marginally statistically significant in men. Together, these two studies indicate that the association between height and CHD risk can be found within discordant twin pairs and, thus, is not due exclusively to family background. However, because of the relatively small number of discordant twin pairs, these studies had inadequate power to study the zygosity-specific associations needed to examine the role of genetic factors behind these associations.
Since any single twin cohort does not include sufficient numbers of twin pairs discordant for height and CHD to study this question with adequate power, we pooled the Nordic population-based twin cohorts that have follow-up information on CHD mortality. The aim of this study is to examine whether the previously reported inverse association between height and CHD risk is found in the following: 1) only between twin individuals but not within MZ or DZ pairs, indicating a role of family background; 2) within DZ but not MZ pairs, indicating a role of genetic liability; or 3) within MZ and DZ pairs, indicating a role of environmental factors.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Twin cohorts from Denmark (19
), Finland (20), and Sweden (21) with baseline data on height and follow-up data on CHD mortality were used. Only same-sex pairs reared together were included in the analyses. From each cohort, we selected all the twin individuals with known zygosity and data on height at baseline. The Finnish (18) and the Swedish older cohort (17) baseline data were used in previous papers on this topic, but follow-up data have been updated for the current analyses. The follow-up data were linked to the baseline data by the personal identification numbers assigned to every resident of Denmark, Finland, and Sweden. During the follow-up periods, four International Classification of Diseases (ICD) classifications were used to identify CHD deaths: ICD, Seventh Revision (codes 420.0–420.99 and 422.1); ICD, Eighth Revision and Ninth Revision (codes 410.00–414.99); and ICD, Tenth Revision (codes I20–I25). Data collection was approved in each country by a local ethics committee and followed the rules and principles of the Helsinki Declaration.
The Danish data were derived from the Danish Twin Register (19). In 1966, a questionnaire was mailed to same-sex twins who had been born between 1890 and 1920 and were living in Denmark. The response rate was 65 percent. Those with unknown zygosity (nine persons) or who did not report their height (258 persons) were excluded from the data set. The final Danish data included 3,421 twin individuals. Death status was obtained from the Central Person Register and the Danish Cause-of-Death Register. Follow-up data were available to the end of 1996.
The Finnish data were derived from the older cohort of the Finnish Twin Cohort Study (20). This cohort covers all Finnish same-sex twin pairs born before 1958 with both co-twins alive in 1974. The first questionnaire was mailed in 1975, and the response rate was 86 percent, yielding 26,225 individuals who reported their height. We supplemented these data for those who had not returned the first questionnaire in 1975 but returned a second questionnaire sent in 1981. This second survey yielded 2,106 new respondents who reported their height. There were 3,072 individuals with unknown zygosity, and they were removed from the data set. Thus, the final Finnish data set included 25,259 twin individuals. Follow-up based on the Finnish Cause-of-Death Register maintained by Statistics Finland was available to the end of 2001.
The Swedish data are taken from two birth cohorts (21). The Swedish older cohort covers all same-sex twin pairs born between 1886 and 1925, where both co-twins were living in Sweden in 1961. A questionnaire sent to these individuals in 1963 had a response rate of 85 percent. Those with unknown zygosity (694 persons) or who did not report their height (475 persons) were removed from the data set. The final data set for the Swedish older cohort included 17,606 twin individuals. The Swedish middle-aged cohort covers all the same-sex twin pairs born between 1926 and 1958 with both co-twins living in Sweden in 1970. A questionnaire was sent to these individuals in 1972, and the response rate was 82 percent. Again, those with unknown zygosity (3,210 persons) and those who did not report their height (363 persons) were removed from the data set. The final data set for the Swedish middle-aged cohort included 28,418 twin individuals. Both Swedish cohorts were followed up to the end of 2001 through the Swedish Cause-of-Death Registry.
Table 1 shows the characteristics of each of the four twin cohorts. Together in the pooled data, there were 74,704 twin individuals including 35,042 complete twin pairs. The follow-up periods varied from 25 years in Finland to 38 years in the Swedish older cohort. During the follow-up of 1.99 million person-years, 5,943 CHD deaths occurred. Height was correlated with year of birth in these data, and thus the mean height was lowest in the Danish cohort, representing the oldest birth cohorts, and greatest in the Swedish middle-aged cohort, representing the youngest birth cohorts. Zygosity and height were based on questionnaire information in each cohort. Determination of zygosity was based on questions of physical similarity at school age; the questionnaire-based diagnoses of zygosity have been shown in Denmark (19), Finland (22), and Sweden (21) to be valid and accurate. Self-reported height was validated in a subsample of individuals in the Finnish (23) study who were invited to a clinical examination after they had returned the questionnaire; measured height showed strong correlation with self-reported height (r = 0.97).
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Because the data sets were collected independently, the risk factors for CHD available in each data set were not the same. Information on current smoking status was available in all cohorts and was classified as current, former, and never smokers. In Finland and Denmark, we additionally had information on self-reported hypertension and diabetes at baseline, average alcohol consumption as grams of alcohol per day, and leisure time physical activity. In Denmark, leisure time physical activity was classified as no, or almost no, exercise, light exercise, a lot of exercise, and regular sport, and in Finland as no exercise, occasional exercise, and conditioning exercise.
Regarding statistical analyses, two sets of analyses were undertaken: 1) between individuals, in which all twin individuals were eligible for inclusion regardless of whether or not their co-twin was included in the data; and 2) within twin pairs discordant for height and CHD mortality.
In the analyses between individual twins, we used height as both a categorical variable (quartiles of height) to assess linearity of the association and a continuous variable. Because of the substantial differences in the mean heights between the cohorts, sex- and cohort-specific height quartiles were used. When used as a continuous variable, height was standardized by subtracting the mean from each height measure and dividing it by the standard deviation separately for each cohort and sex. Proportional hazard ratios were calculated using Cox regression modeling, with follow-up time in days and CHD death as the outcome variable. The results were adjusted for age and cohort by including the main and the interaction effects of age and cohort in the models, as the interaction effect between age and cohort was statistically significant. Follow-up time was calculated from the time of baseline measures to the date of CHD death, date of death from other causes, or the end of the follow-up period for the given cohort (whichever was earliest). The effect of the twin pair sample design on standard errors was taken into account by computing robust estimators of variance and using the cluster option of the STATA statistical package (24). The proportional hazards assumptions were tested by use of Schoenfeld residuals and found not to be violated (p values for height of 0.72 in men and of 0.93 in women).
In analyses of discordant twin pairs, we started by regarding a twin pair as discordant for CHD if a twin had died from CHD during the follow-up period and the co-twin had not died from CHD regardless of whether the co-twin was alive at the end of the follow-up or had died from another cause. Using this definition of discordance yielded 1,003 MZ and 2,387 DZ discordant twin pairs. We next tested the robustness of the results by using other definitions of discordance for CHD and height. Thus, to test whether the association was related to premature CHD mortality only, we included in the analyses only those individuals who were under 70 years of age at follow-up (n = 330 MZ and 891 DZ discordant twin pairs). Finally, since it is possible that these results might be biased because of an association between height and other causes of death of the co-twin, we repeated the analyses, on this occasion regarding a twin pair as discordant if a twin had died from CHD and the co-twin was still alive and did not die from CHD later (n = 639 MZ and 1,609 DZ discordant twin pairs). Height discordance was first analyzed as a dichotomized variable by classifying a twin as either taller than or shorter than the co-twin and then as a continuous variable by computing the height difference between co-twins. The data for discordant twin pairs were analyzed by use of conditional logistic regression models in STATA software (24), with CHD as the dependent variable and height discordance (dichotomized or continuous) as an independent variable in the model. In both the individual-level analyses and the analyses for discordant twin pairs, heterogeneity of the association due to cohort, zygosity, and sex was investigated by including interaction terms in the model.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Table 2 presents the hazard ratios for the association between CHD mortality per 1-standard deviation decrease in height and CHD mortality in height quartiles in the first series of analyses including all twin individuals. Statistically significant heterogeneity for center was found in MZ women (p = 0.005) but not in DZ women or in men. Detailed analyses of cohort-specific results revealed that the heterogeneity in MZ women was mainly because of the strong inverse association between height and CHD mortality in the Swedish middle-aged cohort (per 1-standard deviation decrease in height: hazard ratio (HR) = 1.79, 95 percent confidence interval (CI): 1.26, 2.55). Otherwise, the hazard ratios per 1-standard deviation decrease in height were broadly similar across the cohorts and varied from 0.93 in male MZ twins in the Danish cohort to 1.20 in female DZ twins in the Swedish middle-aged cohort (data not shown). The hazard ratios per 1-standard deviation decrease in height were very similar in all four sex-zygosity groups (MZ men: HR = 1.10, 95 percent CI: 1.03, 1.18; DZ men: HR = 1.07, 95 percent CI: 1.02, 1.12; MZ women: HR = 1.04, 95 percent CI: 0.97, 1.13; and DZ women: HR = 1.07, 95 percent CI: 1.02, 1.13), and no heterogeneity for zygosity or sex was found. However, linearity of the association differed somewhat between men and women. In men, the association between height and CHD mortality was fully linear, and increased risk was found in the second and the third height quartiles compared with the tallest quartile, with the highest risk observed in the shortest quartile. In women, increased risk for CHD mortality was found only in the shortest quartile, while the second and the third quartile associations did not differ from that for the tallest quartile.
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We continued the analyses by studying in each cohort how adjusting for the risk factors of CHD available in this particular cohort affected the association between height and CHD risk (data not shown). Adjusting for the risk factors had only a marginal effect on the association between height and CHD mortality. In Finnish men, adjustment for smoking, leisure time physical activity, alcohol consumption, baseline diabetes, and hypertension marginally decreased the hazard ratio from 1.16 to 1.13 (MZ and DZ twins together). In the other cohorts, the decrease in effect size was smaller or did not exist.
Table 3 presents the second series of analyses, that is, for twin pairs discordant for height and CHD mortality. The twin who died from CHD was, on average, shorter than the co-twin who died from other causes or who was alive at the end of follow-up. In both men and women, a higher risk was found within discordant MZ than DZ pairs (test for heterogeneity: p = 0.06 in men and 0.19 in women). Shorter stature was associated with an increased risk of having a CHD death in MZ men (odds ratio (OR) = 1.23, 95 percent CI: 1.04, 1.45) and in both MZ (OR = 1.32, 95 percent CI: 1.10, 1.59) and DZ (OR = 1.14, 95 percent CI: 1.01, 1.28) women. In DZ men, the association was weaker and statistically nonsignificant (OR = 1.01, 95 percent CI: 0.91, 1.13). No heterogeneity was found for country or sex. The results were very similar when we used other definitions for CHD discordance (data not shown). However, the number of discordant twin pairs in these analyses was smaller than in the above analyses, and thus the confidence intervals were wider. Nevertheless, in the pooled data including men and women and both zygosity groups, a clear association between height and CHD mortality was found when we restricted the age at follow-up to less than 70 years (OR = 1.13, 95 percent CI: 1.01, 1.27) and after exclusion of co-twins who had died from other causes before the death of the case from CHD (OR = 1.09, 95 percent CI: 1.00, 1.19).
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Finally, we repeated the analyses for CHD discordant twin pairs by using the height difference in centimeters as a measure of discordance for height (data not shown). These analyses yielded weaker associations than those using height discordance as a dichotomized variable. Among all pairs discordant for CHD (case died from CHD and control died from other causes or was alive at the end of follow-up), controls were slightly taller than cases, and the difference was somewhat larger in DZ (0.25 cm in men and 0.47 cm in women) than in MZ (0.19 cm in men and 0.37 cm in women) twins. This zygosity difference, however, was because of larger height discordance within all DZ pairs (mean discordance: 5.0 cm in men and 4.6 cm in women) compared with MZ pairs (2.2 cm in men and 2.1 cm in women), and no larger effect size was found in DZ than in MZ twins. Using this definition, we found little evidence for an association in either men (per 1-standard deviation decrease in within-pair height difference: OR = 1.08, 95 percent CI: 0.99, 1.19) or women (OR = 1.14, 95 percent CI: 1.04, 1.25) when data for MZ and DZ twins were pooled.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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This study shows that height is inversely associated with risk for CHD death not only between twin individuals but also within twin pairs discordant for height and CHD irrespective of the definition of pairwise CHD discordance. Since the association was also found within MZ pairs alone, our results strongly suggest that the association between height and CHD risk is due to environmental factors. In individual-level analyses, the association was similar among MZ and DZ twins and for men and women. In contrast to the individual-level analyses, the association between height and CHD mortality was stronger within discordant MZ than DZ pairs. This finding also supports the role of environmental factors, since height discordance in MZ twins is exclusively because of environmental factors and measurement error, while within DZ pairs, in view of the large heritability of height (25
), much of the intrapair differences is probably due to genetic factors. Thus, these genetic differences are likely to dilute the association within DZ pairs if within-pair disparities in height caused by genetic factors are not associated with differences in CHD risk.
Our results suggest that environmental factors not related to family environment affect height and CHD risk. This indicates that the association between height and CHD risk cannot be due to social background of the family only, but that there are likely to be individual specific environmental factors directly affecting both height and CHD risk. We could not identify these childhood exposures, and future studies incorporating direct measurements of likely candidates such as childhood diseases, diet, and passive smoking are needed to shed more light on this association. It is also possible that this association is at least partly because of health behavioral factors that originate in childhood and adolescence. Biologic programming during fetal life suggested by Barker (15) is a possibility as well and might explain a stronger association within MZ than DZ twin pairs. Environmental variation in utero is probably stronger in MZ twins, because a majority of MZ pairs are monochorionic (26). They are hence more susceptible to the effects of the twin-to-twin transfusion syndrome and other factors affecting differential prenatal growth patterns of the two twins. However, when we studied the association between height and CHD risk between twin individuals, the association was similar in MZ and DZ twins, suggesting that there is no environmental component specific to MZ twin individuals affecting height and CHD risk.
Our study has several important strengths. The size of our data set is very large, it includes both men and women, and the response rates at baseline were high. The follow-up time is long, and the mortality registers in Nordic countries, used in this study, cover the entire population. In our previous study based on Finnish data (18), we found that the association between height and CHD was similar in singletons and twins. This suggests that the results from our study including twins may be applicable to the general population, and that there are no additional sources of variation affecting this association in twins due to specific features of twin pregnancies. This is a plausible result, since previous studies have shown that the CHD risk in twins is similar to that of the general population (17, 18, 27).
The main limitation of our study is that our data represent genetically relatively homogeneous populations, and the results may not generalize to non-Caucasian populations. The previous studies that have reported the association between height and CHD risk have been carried out in largely Caucasian populations (1–7), and the only large epidemiologic study representing Asian populations that we are aware of showed only weak evidence of an inverse association between adult height and CHD mortality (11). Thus, it would be important to study this association in populations with different ethnicities and nutritional profiles to determine whether it is specific to Caucasian ethnicity or a Westernized diet. Another limitation of our data is that height was self-reported. Even when the validity of self-reported height is good, it is possible that misreporting has increased the number of pairs falsely discordant for height. This misclassification is likely to weaken the association between height and CHD, and thus it is possible that the real effect is somewhat underestimated in our study. Finally, we had relatively little information on other coronary risk factors that may mediate the association between height and CHD mortality: Adjusting for self-reported baseline diabetes, hypertension, smoking, and physical activity had virtually no effect on the association between CHD and height. However, if more detailed risk factor data had been available, for example, laboratory measures of metabolic factors, it is possible that we would have been able to better understand how the association between height and CHD mortality is generated.
In our data set, we had information on standing height but not, for example, on sitting height or leg length. There is some previous evidence that leg length is more strongly associated with CHD risk than is standing height (28, 29). This is in accordance with the hypothesis that leg growth is more sensitive to postnatal environmental factors than is truncal growth (30, 31). Hence, it is plausible that, if we had been able to investigate the relation between leg length and CHD mortality, the associations may have been stronger than the ones we observed. Nevertheless, these results support the conclusion that the association between height and CHD risk is because of the effect of environmental factors.
In conclusion, our results strongly suggest that there are environmental factors leading to both short stature and high CHD risk in adulthood. A challenge for future research is to identify these factors and to find means to affect them to promote optimal growth. This would have beneficial effects on CHD rates in the population.
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ACKNOWLEDGMENTS |
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As part of the GenomEUtwin Project, this study receives support from the European Commission through the Quality of Life and Management of Living Resources Programme implemented under the Fifth Framework Programme (grant QLG2-CT-2002-01254). Additional financial support for the Swedish Twin Registry is through grants from the Department of Higher Education, the Swedish Scientific Council, and AstraZeneca. K. S. is supported by the Academy of Finland (grant 108297). P. M. is supported by a career scientist award funded by the Research and Development Office for Health and Personal Social Services in Northern Ireland. A. M. H. and K. C. are supported by the National Institute of Aging (NIA-PO1-AG08761).
Conflict of interest: none declared.
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