IJE Advance Access originally published online on October 28, 2005
International Journal of Epidemiology 2006 35(1):159-166; doi:10.1093/ije/dyi223
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Article |
Weight history and risk of endometrial cancer among Chinese women
1 Department of Epidemiology, Shanghai Cancer Institute, Cancer Institute of Shanghai Jiaotong University, 2200/25 Xie Tu Road, Shanghai 200032, P. R. C
2 Department of Medicine, Center for Health Services Research, Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville TN 37232-8300, USA
* Corresponding author. Center for Health Services Research, 6009 Medical Center East, Vanderbilt University, 1215 21st Ave South, Nashville TN 37232-8300, USA. E-mail: Xiao-Ou.Shu{at}vanderbilt.edu
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Abstract |
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Background Adult obesity is a well-established risk factor for endometrial cancer. However, little is known about the association of endometrial cancer risk with body size early in life and weight change during adulthood. We investigated whether women with greater early-age body size or with greater weight change during adulthood have an increased risk of endometrial cancer.
Methods We analysed data from a population-based case–control study of endometrial cancer conducted between 1997 and 2001 in Shanghai, China. Included in this analysis were 832 endometrial cancer cases aged 30–69 years and 846 population controls. Information on weight and height history from adolescence through adulthood was obtained via structured in-person interviews. A logistic regression model was used to derive odds ratios (ORs) and 95% confidence intervals (CIs) for endometrial cancer in association with adolescent and adult adiposity, as well as adult body weight change. All ORs were adjusted for age, education, menstrual status, duration of menstruation, number of pregnancies, oral contraceptive use, and family history of cancer.
Results Perceived weights and heights during puberty that were greater than average were associated with a modestly increased risk of cancer. The association for perceived weight was substantially weakened after adjustment for current body mass index (BMI). High BMI at all adult ages significantly predicted endometrial cancer risk, with recent BMI being the strongest predictor. Further analyses disclosed that weight gain during adulthood, particularly during the peri-menopausal period (age 40–50 years), was associated with a significantly elevated risk of endometrial cancer, even among currently non-obese women. Gaining >5 kg between age 40 and 50 was related to ORs of 2.3 (95% CI 1.4–3.9) for women with a BMI < 25 kg/m2 and 2.0 (95% CI 1.3–3.0) for women with BMI 
25 kg/m2.
Conclusions Adult weight gain, particularly during the peri-menopausal period, plays a significant role in the development of endometrial cancer risk.
Keywords Endometrial cancer, weight gain, obesity
Accepted 29 September 2005
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Introduction |
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The association between adult obesity and increased endometrial cancer risk has been consistently demonstrated in a number of epidemiological studies.1–3 Few studies, however, have investigated the effect of body size during different life cycles and adult weight change in the development of endometrial cancer.4–9 Given that endometrial cancer is primarily an oestrogen driven cancer,10 and body fat accumulation, as indicated by higher body mass index (BMI) or body weight gain, has been suggested to be related to oestrogen levels in circulation,11 it is possible that rapid growth or weight gain during crucial time windows, such as puberty or peri-menopause, may be related to higher risk of endometrial cancer than weight changes that occur during other periods of life. In this report, we describe a detailed analysis of self-reported weight history in relation to endometrial cancer risk using data collected from a population-based case–control study in Shanghai.
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Materials and methods |
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All cases and controls for this study were permanent residents of urban Shanghai. From January 1997 to December 2001, we identified 982 newly diagnosed endometrial cancer cases aged 30–69 through the population-based Shanghai Cancer Registry. A total of 1165 eligible population controls were randomly selected through the Shanghai Resident Registry and frequency matched to cancer cases by age (5 year interval). Women who had had a hysterectomy were excluded (n = 36). Two cases but no controls in the study had a history of bilateral oophorectomy without hysterectomy. In-person interviews were completed for 832 (84.7%) cases and 846 controls (71.5%).
A structured, in-person interview was conducted by trained retired nurses to obtain information on demographic factors, menstrual and reproductive history, hormone use, usual dietary intake, prior disease history, tobacco and alcohol use, family history of cancer, and height and weight history during adolescence and adulthood. Perceived height and weight at ages 10, 15, and 20 years were obtained by asking women to compare their height and weight with that of their peers for those time periods. For example, for the relative weight at age 10, women were asked ‘When you were 10 years old, you were much heavier, a little heavier, about same, a little lighter or much lighter than your peers?’. The adult anthropometric history included height at age 20, weight at ages 20, 30, 40, 50, and 60 years and recently (1 year prior to the date of diagnosis for cases and date of interview for controls). BMI at ages 20, 30, 40, 50, 60 and recent were calculated as weight at the corresponding age in kilogrammes divided by height at age 20 in metres squared (kg/m2). Menopause was defined as the cessation of menstrual periods for at least 12 months before the reference date (date of diagnosis for cases, date of interview for controls), excluding those lapses caused by pregnancy or breastfeeding. Years of menstruation were calculated by taking age at the reference date and subtracting either age at menarche (pre-menopausal women) or age at menopause (post-menopausal women), excluding those lapses caused by pregnancy or oral and injected contraceptive use.
The risk of endometrial cancer associated with body size at different ages and changes in adult weight was estimated by odds ratios (ORs) and 95% confidence intervals (CIs) using unconditional logistic regression models. Categorical variables were treated as dummy variables in the model. Risk factors that could potentially alter the association of anthropometric status and endometrial cancer were entered into the model as potential confounding factors. Age, BMI at age 20, and initial body weight in each 10 year adulthood period were treated as continuous variables in the analyses. Potential confounders controlled for in the model included: educational level (no formal education or just elementary, middle school, college and above), menstrual status (pre-menopause/post-menopause), years of menstruation (<30, <35, <40, 40 years), oral contraceptive use (ever/never), number of pregnancies (never, 1, 2, 3, 4, 5), family history of cancer (yes/no), adolescent perceived weight (thinner, average, heavier) or height (shorter, average, taller) at ages 10, 15, and 20. Collinearity between variables was checked by variance inflation before they were included in the regression model. Tests for trend were performed by entering the ordinal variables as continuous parameters in the models. Eighteen women with induced menopause (nine caused by chemotherapy, two by bilateral oophorectomy, two by use of Chinese medicine, and five of unknown cause) were excluded from the analysis stratified by menopausal status.
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Results |
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Characteristics of cases and controls are described in Table 1. In brief, endometrial cancer cases and controls were similar with respect to age, with the mean age being 55.3 years for cases and 55.7 years for controls. No major case–control differences were found with respect to family income, exercise, total energy intake, and hormone replacement therapy (HRT) use. However, when compared with controls, cases were more likely to have higher education, earlier age at menarche, later age at menopause, more years of menstruation, fewer pregnancies, higher BMI and WHR, and a positive family history of any cancer and endometrial cancer. In addition, cases were less likely to drink alcohol or use oral contraceptives.
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Perceived weights during puberty that were greater than average were associated with a modestly increased risk of endometrial cancer, with the elevated risk being predominantly seen among pre-menopausal women. The corresponding ORs for higher perceived weight at age 10, 15, and 20 were 1.9 (95% CI 1.1–3.2), 1.9 (95% CI 1.1–3.3), and 1.7 (95% CI 1.0–2.7), respectively, in pre-menopausal women. However, the associations were substantially weakened and no longer significant after accounting for current BMI. Perceived height at age 10 was related to a moderately increased risk of endometrial cancer for all combined (OR = 1.3, 95% CI 1.1–2.1), and perceived height at age 20 was related to a marginally increased risk of post-menopausal endometrial cancer (OR = 1.5, 95% CI 1.0–2.3). Similarly, additional adjustment for BMI attenuated their positive associations with the disease (data not shown).
Table 2 presents the association of BMI during different decades of life and the risk of endometrial cancer. The median of BMI rose steadily over adult time, ranging from 19.14 at age 20 to 23.52 at age 60. The ORs for the highest vs lowest quartile of BMI at different decades of life also rose from 1.3, 1.5, 2.0, 2.5 to 2.9. Recent BMI was the strongest predictor of endometrial cancer, with the adjusted OR comparing the extreme quartiles of recent BMI reaching 3.3 (95% CI 2.4–4.5). Similar to perceived weight at early ages, BMI at adult ages was also, in general, a stronger predictor for pre-menopausal than post-menopausal endometrial cancer, although tests for multiplicative interaction were not statistically significant. A clear dose–response relation between BMI increment since age 20 and endometrial cancer risk was also noted, with ORs being 1.0, 1.4 (95% CI 1.0–1.9), 1.6 (95% CI 1.1–2.2), and 3.1 (95% CI 2.2–4.3) across quartiles of BMI increment (P for trend <0.0001).
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Table 3 presents the risk of endometrial cancer associated with weight change during adulthood. Consistent with the observation for BMI increment since age 20, weight gain or percentage of weight gain since age 20 was also associated with a significantly elevated risk of endometrial cancer. Compared with those who had a weight change of <2.5 kg since age 20, women who gained 2.5, 10, 15, or 20 kg and more had an OR of 1.1 (95% CI 0.7–1.7), 1.3 (95% CI 0.8–1.9), 1.8 (95% CI 1.2–2.8), and 2.9 (95% CI 1.9–4.5), respectively, after adjusting for potential confounding variables, including BMI at age 20. Weight gain during every decade since age 20 was also consistently found to be related to increased risk of endometrial cancer with the strongest association observed for weight gain during the peri-menopausal period.
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Further analysis stratifying by current BMI revealed that perceived weight at early ages was associated with cancer risk only among currently overweight women (Table 4), while weight gain, especially during a woman's 40s, was related to cancer risk for both normal weight and overweight women. For example, weight gain of 5 kg during a woman's 40s was associated with a 2.3-fold elevated risk (95% CI 1.4–3.9) and 2.0 (95% CI 1.3–3.0), respectively, for women whose current BMI was <25 kg/m2 and
25 kg/m2.
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Discussion |
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In this population-based case–control study, we found that adiposity at all ages and weight gain during adulthood, particularly during the peri-menopausal period, were associated with a significantly elevated risk of endometrial cancer. The increased risk associated with weight and height in early life was only seen among currently obese women, while weight gain during the peri-menopausal period was related to increased risk regardless of current BMI.
Childhood height is affected by the timing of puberty, genetic constitution, and energy balance during that period.12 Most pre-puberty growth, usually occurring at age 10 or younger in Chinese women,13 is due to increases in leg length. Pre-pubertal leg length has been shown to be associated with mortality from sex hormone dependent cancers, with one possible mechanism being that rapid growth leads to an earlier onset of puberty, resulting in a longer lifetime exposure to sex hormones.14 In the current study population, perceived height at age 10 (r = –0.16, P < 0.01) and 15 (r = –0.13, P < 0.01) were inversely associated with age at menarche. Approximately 18% of those who considered themselves taller at age 10 started menstruation before age 13, while only 8.9 and 7.4% of those in the average and shorter groups were younger than 13 at menarche. However, adult height was not related to age at menarche, possibly owing to faster closure of the epiphyseal growth discs during adolescence under the influence of oestrogens.15 These observations are consistent with the finding of a stronger association of endometrial cancer risk with relative height at age 10 than with adult height. These observations are also consistent with Gunnell's hypothesis,14 indicating that rapid pre-pubertal growth may increase endometrial cancer risk through an associated earlier onset of puberty and longer lifetime duration of oestrogen exposure. Childhood height has also been suggested to predict obesity among adults.16 In our study, a higher relative height at age 10 predicted a larger adult body size, both in height and in weight. This may explain the observation that an increased risk associated with height in early life was only seen among currently obese women. Nevertheless, these results should be interpreted with caution given that no anthropometric measurements from subjects' early life were available. Longitudinal studies with detailed records of body height through childhood are needed to address the hypothesis.
An independent effect of adolescent adiposity on endometrial cancer has been suggested in Olson and Blitzer's studies.8,9 Fat accumulation during adolescence is one of the major determinants of age at menarche, a well-established risk factor for endometrial cancer.13 Adiposity in adolescence has been linked to insulin resistance and polycystic ovary disease,17–19 both of which have been associated with endometrial cancer, particularly among young women.20–21 In agreement with these findings, we also found that the association between adolescent adiposity and risk of endometrial cancer was more pronounced in pre-menopausal women. However, the association was substantially attenuated after adjustment for current weight, consistent with the report of Le Marchand et al.,6 in which the association was based on detailed records.6 Further analyses showed that adolescent weight was related to endometrial cancer risk only among currently overweight women. These findings suggest that adolescent adiposity does not play a large role in the aetiology of endometrial cancer unless it is followed by weight gain later in life. It has been hypothesized that peri-pubertal adiposity and maintenance of excess weight during adulthood lead to ovarian hyperandrogenism, progesterone deficiency, and endometrial cancer among pre-menopausal women.22 However, we found that among pre-menopausal obese women (BMI 25), perceived weight at ages 10 and 15 was not associated with the average length or with the regularity of menstrual cycles, both of which are possible indices of anovulatory cycles (data not shown). Given the difficulty of obtaining accurate information on the length and regularity of menstrual cycles,23 a more objective index of anovulatory cycles is needed to test the above-mentioned hypothesis. Because adolescent obesity can track into adulthood and its relative contribution to the prevalence of adult obesity remains unclear,24–26 it is difficult to separate out the contribution of adolescent obesity to incidence of endometrial cancer from that of adult obesity.
Obesity in adulthood is a well-established risk factor for endometrial cancer. In the current study, we found that BMI increased with age, similar to our earlier findings from the Shanghai Women's Health Study.27 Adult weight gain is largely reflected in body fat accumulation. Excessive conversion of androstenedione to oestrone and decreased serum levels of SHBG related to obesity create an oestrogen-rich environment that stimulates the development of endometrial cancer cells.28,29 Several studies have shown a positive association between adult weight gain and endometrial cancer.6,8,30,31 However, most of these studies did not address the effect of the timing of weight gain,6,8,31 and some did not adjust for initial body weight.8,30 In our study, although weight gain throughout adulthood was related to increased risk, weight gain from age 40 to 50 was related to a higher risk than other life cycles. This result suggests that keeping body weight from increasing during the peri-menopausal period might be an effective disease-prevention strategy.
Recall of body size from different periods of time, particularly during earlier life is subject to recall bias. Instead of asking for exact anthropometric measurements, we estimated early body size by asking the subjects to categorize their weight and height as average, below or above average compared with their peers. This procedure may have minimized potential misclassification. Adult height at age 20 and weight at different adult ages were obtained by recall. The high correlations of body height at age 20 with measurements of current height (r = 0.94, P = 0.0001) and of recent weight with measurements of current weight (r = 0.97, P = 0.0001) indicate that recall of adult anthropometric measurements, particularly those from more recent years, was reasonably accurate. It has been reported that females, particularly obese females, tend to underestimate their body weight.32 This misclassification is likely to lead to an underestimation of the strength of the association in our study.
Our study has several strengths. The low rate of hysterectomy in this population minimizes the selection bias, while infrequent use of HRT removes concerns of its potential confounding effect. Detailed obesity history, covering the lifespan since age 10, plus current anthropometric measurements offer a unique opportunity to investigate the time effect of weight gain on endometrial cancer risk.
In summary, this study suggests that weight gain throughout adulthood, particularly during the peri-menopausal period, increases the risk of endometrial cancer. Preventing weight gain should be recommended to curtail this and other chronic diseases in women.
KEY MESSAGES
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Acknowledgments |
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We thank Dr Fan Jin for her contributions in implementing the study in Shanghai and Ms Bethanie Hull for her assistance in the preparation of this manuscript. This study would not have been possible without the support of all of the study participants and research staff of the Shanghai Endometrial Cancer Study. This work was supported by USPHS grant R01CA92585 from the National Cancer Institute.
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