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© 1999 American Society for Clinical Oncology Adjuvant Treatment and Onset of Menopause Predict Weight Gain After Breast Cancer DiagnosisFrom the Department of Medicine, Division of Clinical Epidemiology, Samuel Lunenfeld Research Institute; Mount Sinai Hospital; Division of Medical Oncology, Department of Surgery, Toronto-Sunnybrook Regional Cancer Centre; Princess Margaret Hospital; Women's College Hospital; St. Michael's Hospital; Clinical Epidemiology and Health Care Research Program; and University of Toronto, Toronto, Ontario, Canada. Address reprint requests to Pamela Goodwin, MD, Mount Sinai Hospital, 1284-600 University Ave, Toronto, Ontario M5G 1X5, Canada.
PURPOSE: Weight gain is common during the first year after breast cancer diagnosis. In this study, we examined clinical factors associated with body size at diagnosis and weight gain during the subsequent year. PATIENTS AND METHODS: An inception cohort of 535 women with newly diagnosed locoregional breast cancer underwent anthropometric measurements at baseline and 1 year. Information was collected on tumor- and treatment-related variables, as well as diet and physical activity.
RESULTS: Mean age was 50.3 years; 57% of women were premenopausal. Mean baseline body mass index (weight [kg] divided by height [m] squared) was 25.5 kg/m2. Overall, 84.1% of the patients gained weight. Mean weight gain was 1.6 kg (95% confidence interval, 1.2 to 1.9 kg), 2.5 kg (95% confidence interval, 1.8 to 3.2 kg) in those receiving chemotherapy, 1.3 kg (95% confidence interval, 0.7 to 1.8 kg) in those receiving tamoxifen only, and 0.6 kg (95% confidence interval, 0.01 to 1.3 kg) in those receiving no adjuvant treatment. Menopausal status at diagnosis (P = .02), change in menopausal status over the subsequent year (P = .002), axillary nodal status (P = .009), and adjuvant treatment (P = .0002) predicted weight gain in univariate analysis. In multivariate analysis, onset of menopause and administration of chemotherapy were independent predictors of weight gain (all P CONCLUSION: Weight gain is common after breast cancer diagnosis; use of adjuvant chemotherapy and onset of menopause are the strongest clinical predictors of this weight gain.
SEVERAL RECENT STUDIES HAVE examined change in weight during the first year after breast cancer diagnosis. Initially an unexpected finding,1 the common, although not universal, occurrence of weight gain during this period has been confirmed in several studies2-13 (others reviewed in14). A small minority of women (up to 20%) maintain stable weight or lose weight during this time. Although the pathophysiologic basis for weight gain remains unclear, biologic factors including chemotherapy, hormonal therapy, menopausal status, and metabolic rate have been suggested as potential contributors.2,6 A number of psychologic factors that influence eating behavior, as well as diet, may also play a role11,12; however, caloric intake per se has not been linked to weight gain in the few studies that have examined this factor.11,14-16 Weight gain of the magnitude that has been reported (1.2 to 8.3 kg during the first year) is of concern because of its impact on self-image and general health; there is also evidence to suggest that it may exert an adverse prognostic effect over and above that of other recognized prognostic factors. The strongest evidence for such an effect is provided by Camoriano et al,3 who reported a 1.5-fold increased risk of recurrence in premenopausal women who gained more than the median during the first year after diagnosis (5-year survival 55% v 70% in those gaining less than the median). This observation underscores the need to better understand the phenomenon of weight gain in this group of patients and to prospectively examine its impact on prognosis. Obesity at diagnosis may also influence prognosis. Studies examining this potential effect published before 1989 were critically reviewed by us17; other reports have appeared subsequently.18-36 Despite methodologic shortcomings, including failure to measure body size in a standard fashion and inability to control for important confounders, the majority of these studies have demonstrated an adverse prognostic effect of obesity of modest magnitude; however, several recent well-conducted studies have failed to identify an adverse effect.30-33,35 We have assembled an inception cohort of 535 women with newly diagnosed locoregional breast cancer to prospectively examine the prognostic effects of baseline body size and subsequent weight gain on outcome and to understand factors contributing to weight gain during the first year after diagnosis. In this report, we describe baseline body size and weight gain during the first year after diagnosis, and we analyze clinical variables that predict change in body size during the first year after diagnosis. We also examine, in a descriptive fashion, diet and physical activity in relation to the clinical predictors of weight gain.
Population Assembly The study population consists of an inception cohort of newly diagnosed pre- and postmenopausal women with locoregional breast cancer (T1-3N0-1M0) presenting to Mount Sinai Hospital, Women's College Hospital, and St. Michael's Hospital at the University of Toronto, between July 1989 and June 1996. Before June 12, 1992, only premenopausal women were recruited (118 in total); these women also participated in a study of breast cancer risk.37,38 Women were identified through surgical lists at each participating hospital, and a log book was maintained to record eligibility and refusals. All women undergoing surgery for invasive breast cancer were approached for eligibility assessment. Women were included if they met all of the following criteria: (1) age less than 75 years, (2) complete resection (lumpectomy with margins clear of invasive cancer, or mastectomy), and (3) axillary node dissection for invasive breast cancer (T1-3N0-1M0). Women were excluded if they met any of the following criteria: (1) preoperative systemic therapy, (2) prior history of malignancy (excluding nonmelanoma carcinoma of the skin and carcinoma-in-situ of the cervix), (3) primary surgical and/or medical treatment for breast cancer given elsewhere, (4) presence of a serious medical condition that could alter food absorption or prognosis, (5) use of medications that could influence lipids or insulin levels, (6) inability to speak English sufficiently well to complete study questionnaires, and (7) refusal to provide informed consent to participate in the study. This research was conducted in accordance with approval granted by the Human Subjects Committee of the University of Toronto and participating hospitals. All participants provided written informed consent for their participation in the study.
Measurement During a standardized interview, women provided information on demographics, breast cancer risk factors, use of hormone replacement therapy at diagnosis, and exercise during the preceding week. The latter was recorded as the number of weekday and weekend hours devoted to mild, moderate, and strong physical activity at work, at home, or during leisure activities.39 Standard descriptions of each type of activity were included (eg, performing housework was classified as mild, playing squash as strong). Weight was measured with a balance beam scale. Women fasted overnight before weight measurement and wore only a hospital gown. Height and skinfold thickness were measured at the same time. Women also completed the Block Food Frequency Questionnaire,40 which measures food intake during the previous year. At 1 year, women provided updated information on menopausal status and physical activity, they permitted weight and skinfold thickness to be measured, and they again completed the Block questionnaire. Of the 118 women enrolled before June 12, 1992, the 1-year weights were obtained on only 61 women. Thus, information on change in body size was available on 445 women. Information on pathologic characteristics of tumors was obtained from the pathology reports of participating institutions. These reports were reviewed prospectively to ensure eligibility; pathologic characteristics of the tumors were abstracted onto standard data forms.
Statistical Analysis
t tests were used to compare means when there were two categories. For more than two categories, one-way analysis of variance was used. If the overall result was significant at the 5% level, Tukey's studentized range test was used to identify which pairs differed. This approach minimized the number of secondary comparisons performed, and it allowed an exploration of the nature of overall differences between multiple groups. Proportions were compared by means of two-way tables and Change in variables measured at baseline and at 1 year was calculated as the difference between the two observed values (1 year minus baseline), and a one-sample t test or a signed rank test was used to determine whether the change over time was significantly different from zero. Univariate and multivariate analysis of change in weight. The relationship between change in weight and BMI during the first year after diagnosis and clinical variables was examined using univariate and multivariate linear regression. The candidate explanatory variables in the univariate analyses were age and BMI at diagnosis (continuous), use of hormone replacement therapy at diagnosis (yes, no), surgery (mastectomy, lumpectomy), tumor size (T1, T2, T3), nodal status (N0, N1), baseline menopausal status (premenopausal, perimenopausal, postmenopausal), change in menopausal status (premenopausal throughout, onset of menopause during the first year after diagnosis, postmenopausal throughout), and systemic adjuvant treatment administered (hormones only, any chemotherapy, none). After a number of variables univariately associated with weight gain were identified, a multivariate analysis was performed using multiple linear regression to understand the simultaneous contribution of these factors to weight gain. The purpose of this analysis was to study the simultaneous contribution of these factors, identifying those clinical factors that jointly provided the best prediction of weight gain. Variables that were significant or nearly significant predictors of weight gain in univariate tests (P < .10) were considered for use in the regression. The weight gain predicted by the multivariate model was then visually compared with the observed weight gain in groups defined by the clinical variables that had been shown to be most important. Of the 535 women enrolled, follow-up weight measurements were available for 445 women, and full information on all variables involved in the multivariate analysis was available for 394 (88.5%) of these women. This latter group was used in the multivariate analysis. The pattern of missing values was investigated. Eighty percent of the women without full follow-up measurements were the premenopausal women recruited before July 1992 for whom 1-year measurements were not planned. As expected, these women were found to be younger, more likely to be premenopausal, and, reflecting treatment practices in the late 1980s, more likely to have had a mastectomy and to have had no adjuvant radiation or hormone treatment. Variables were investigated for correlations and outliers. Age at diagnosis was highly correlated with menopausal status and treatment; nodal status, treatment, and menopausal status were all highly intercorrelated. Baseline menopausal status was clearly related to change in menopausal status. Because the latter was more strongly associated with weight gain univariately and because it incorporated baseline menopausal status, it was selected for inclusion. Four outliers (obese women with baseline BMI > 30 kg/m2 who lost an average of 10.4 kg) were identified visually from plots. Their presence enhanced an otherwise weak linear relationship between weight (or BMI) change and baseline weight (or BMI). No unusual attributes were found for these four women. They were included in the primary analysis. The analysis was then repeated without these women to explore their effect on the associations identified. Multivariate analysis proceeded with age and baseline BMI as continuous variables, and nodal status, change in menopausal status, and treatment were represented by one, two, and two dummy variables, respectively. In a stepwise fashion, the variable with the largest P value was removed from the model after determination that it was not significant in a two-way interaction with any one of the remaining variables, using "F-to-remove" tests. This process was repeated until no variable could be removed using the threshold P value of .1; the final model contained baseline BMI, treatment, and menopausal status. All possible interaction terms involving these variables were tested to see whether they improved the fit. Thus, all possible interactions of remaining and removed variables were tested, but none was significant. The residuals obtained from the final model were inspected, and a few large residuals were identified. Removal of these residuals did not cause substantive changes. Exploratory analysis of caloric intake and physical activity. After our primary objective of identifying clinical factors associated with weight change was satisfied, an exploratory analysis of two potential mechanisms for weight gain (caloric intake and physical activity) was performed. Means and standard deviations at baseline and at 1 year and change over 1 year were generated for each of these variables for all women and for groups defined by factors that were predictive of weight gain in the multivariate analysis. These included menopausal status (remained premenopausal, remained postmenopausal, became menopausal) and systemic adjuvant treatment (chemotherapy, hormones only, no therapy). Caloric intake and physical activity in these groups were compared using one-way analysis of variance, followed by Tukey's studentized range test when overall differences were significant (P < .05) to identify which pairs differed. The association of these factors with weight change overall and in these subgroups was examined using Pearson's correlation coefficients.
Description of the Study Population During the period of recruitment, 1,441 women underwent surgery for invasive breast cancer at the participating institutions and were potential candidates for the study. Two hundred forty-one (16.7%) of these women refused participation. Of the remaining women, 665 (46.1%) were ineligible and 535 were enrolled onto the study. Reasons for ineligibility included the following: previous breast cancer, 129 women (19.4%); previous other cancer, 38 women (5.7%); primary treatment given elsewhere (ie, not part of our inception cohort), 113 women (17.2%); axillary node dissection not performed, 50 women (7.5%); positive resection margins, 24 women (3.6%); T4 primary or metastatic disease at diagnosis, 38 women (5.7%); serious concurrent medical condition, 34 women (5.1%); concurrent medications, 88 women (13.3%); inability to speak English, 74 women (11.1%); and other, 58 women (8.7%). Baseline characteristics of the entire study population and of those who participated in measurement of change during the first year are listed in Table 1. As expected, women in the latter group were significantly older (51.1 ± 9.9 [SD] years v 50.3 ± 9.7 years; P < .0001) and more likely to be postmenopausal. Just over half (51%) of postmenopausal women had been taking hormone replacement therapy at diagnosis; all discontinued this medication.
Treatments are listed in Table 2. The majority of women with both node-negative and node-positive breast cancer underwent lumpectomy and axillary node dissection. This proportion was significantly higher in node-negative women (81.9% v 68.5%; P < .001 overall, and 82.2% v 67.6%; P = .001 in those who participated in change measurements). In keeping with the high frequency of lumpectomy, the majority of women received postoperative radiation. Node-positive women were significantly more likely to receive adjuvant chemotherapy than were node-negative women (76.4% v 21.4%; P = .001). There was a predominance of non–anthracycline-based chemotherapy in both groups. A little more than one third of women received adjuvant tamoxifen; no significant difference was seen according to nodal status. Women who participated in change measurements (primarily recruited after mid-1992) were more likely to receive tamoxifen (P = .006) than women in the overall group, likely reflecting changes in treatment practices over time.
Anthropometric Variables
Mean baseline BMI was 25.5 kg/m2, just above the upper limit for the ideal range of 20.0 to 25.0 kg/m2. Overall, 45.3% of women had a BMI above 25 kg/m2, and 8% had a BMI below 20 kg/m2. Premenopausal women had a lower baseline BMI (24.6 ± 4.8 kg/m2) than perimenopausal women (25.8 ± 6.0 kg/m2) or postmenopausal women (26.7 ± 4.8 kg/m2). Significant differences existed between these three means (F-test P = .0001), with postmenopausal women having a significantly larger BMI than premenopausal women (P Three hundred seventy-four women (84.1%) gained weight during the first year after diagnosis. The average weight gain was 1.6 kg (95% CI, 1.2 to 1.9 kg). This weight gain was significantly greater than zero (P < .05). Changes in BMI mirrored those in weight. There were corresponding increases in waist and hip circumference; however, changes in the waist-to-hip ratio did not occur. There were modest increases in most skinfold thicknesses.
Clinical Predictors of Weight Change: Univariate Analysis As can be seen in Table 4, baseline menopausal status (pre- or perimenopausal v postmenopausal) was significantly associated with weight change (P = .02), as was change in menopausal status over the first year. Women who remained premenopausal had a mean gain of 1.07 kg (95% CI, 0.4 to 1.8 kg), those who remained postmenopausal had a mean gain of 1.05 kg (95% CI, 0.5 to 1.6 kg), whereas those who became menopausal had a mean gain of 2.65 kg (95% CI, 1.7 to 3.6 kg) (overall F-test P = .002). Those whose menopausal status changed gained significantly more weight than those whose status did not change (P < .05). Weight gain in all three groups defined by menopausal status was significantly different from zero (all P < .05). Findings were similar when BMI was substituted for weight.
Weight gain was significantly greater in node-positive than in node-negative women (P = .007); however, important differences in administration of adjuvant treatment were seen between these two groups. Women receiving no adjuvant treatment gained the least amount of weight (0.63 kg; 95% CI, 0.01 to 1.3 kg), those receiving only tamoxifen gained an intermediate amount (1.26 kg; 95% CI, 0.7 to 1.8 kg), and those receiving any form of chemotherapy gained the greatest amount (2.50 kg; 95% CI, 1.8 to 3.2 kg). The difference between those receiving chemotherapy and all others was statistically significant (P = .0002). In this analysis, women who received chemotherapy alone or with tamoxifen were combined into a single group because no significant difference was seen between these two groups (weight gain 2.60 ± 4.77 kg v 2.03 ± 3.54 kg; P = .41). Results were similar when BMI was substituted for weight. Other clinical variables (use of hormone replacement therapy at diagnosis, type of surgery, or tumor size) were not associated with weight gain in univariate analyses (data not shown; all P > .50) and were not pursued further.
Clinical Predictors of Weight Gain: Multivariate Analysis All variables were initially included. Using stepwise regression, as described above, age at diagnosis and nodal status were removed (P = .68 and .55, respectively). The remaining model included BMI at diagnosis, adjuvant chemotherapy, and change in menopausal status, each of which made a significant contribution to the prediction of weight gain (Table 5). The significance of baseline BMI was lost when four outliers were excluded. The weight gain predicted by this model, as well as the observed mean weight gain, are shown in Fig 1. It can be seen that the observed values are similar to those predicted by the model for each of the groups defined by the two important clinical variables (change in menopausal status and adjuvant chemotherapy).
Caloric Intake and Physical Activity
During the first year after diagnosis, physical activity increased overall and in all subgroups except those receiving hormones only. The increase differed significantly from zero in all groups except those who were postmenopausal throughout. The changes did not differ significantly between subgroups defined by change in menopausal status (F-test P = .23), but they did differ significantly between subgroups defined by adjuvant treatment (F-test P = .01). Women receiving adjuvant chemotherapy increased their physical activity significantly more than those receiving hormones only (P < .05) despite having gained the most weight. Baseline activity was lower in the former group (P = .06), and final activity levels were higher (P = .03). Change in physical activity did not correlate with weight change overall or in any of the subgroups examined.
Just over 8% of our study population had a BMI below the ideal range of 20 to 25 kg/m2, and 45.3% had a BMI above this range at breast cancer diagnosis. There was a tendency for women diagnosed postmenopausally to be heavier than those diagnosed premenopausally. This is in keeping with reports that obesity is a risk factor for postmenopausal, but not premenopausal, breast cancer41 and with observations that older women are heavier than younger women in the general population.42,43 On average, women in our study gained 1.6 kg (3.5 pounds) over 1 year. Age and baseline BMI were weak predictors of weight gain in univariate analyses; baseline BMI remained a predictor of weight gain in multivariate analysis only when four outliers were included. These were women who were markedly obese at diagnosis (BMI > 30 kg/m2) and who lost considerable weight during the subsequent year. They did not seem to differ from the remaining study population in any other way. Because the significance of BMI in multivariate analysis was due entirely to these four women (representing only 1% of the study population), the apparent association of baseline BMI with weight gain in our multivariate model should not be overinterpreted; we have neither confirmed nor refuted that baseline BMI makes a significant independent contribution to weight gain. Further research is recommended. Menopausal status, nodal status, and adjuvant treatment were significant univariate predictors of weight gain. The onset of menopause during the first year after diagnosis of breast cancer was a strong predictor of weight gain in both univariate and multivariate analyses. The greater weight gain seen in women with involved axillary nodes seems to have been due to the administration of systemic adjuvant therapy. Women who received chemotherapy of any type (anthracycline or nonanthracycline) were more likely to gain weight than those who received tamoxifen only or those who received no adjuvant treatment. An association of adjuvant chemotherapy and weight gain has been noted previously.2-6,9-14 In our patient population, no difference in weight gain was observed between those receiving anthracycline or non–anthracycline-based chemotherapy. The most commonly used form of anthracycline-based chemotherapy was CEF,44 a regimen including 14 days of oral cyclophosphamide with intravenous epirubicin and fluorouracil on days 1 and 8. Thus, it is very similar to the Bonadonna CMF (cyclophosphamide, methotrexate, fluorouracil) that has been associated with weight gain.45 Although the use of adjuvant chemotherapy in premenopausal women was correlated with onset of menopause, both onset of menopause and use of adjuvant chemotherapy made significant independent contributions to weight gain. The weight gain that we have observed is comparable to that reported by others in women with newly diagnosed breast cancer. Mean weight gain has been reported to be as high as 18 pounds (8.2 kg) in women with involved axillary nodes receiving adjuvant chemotherapy with prednisone for a full year4 and as low as 1.2 to 1.8 kg2,3 in those receiving no systemic adjuvant treatment. In those receiving adjuvant chemotherapy without prednisone, a mean weight gain of between 1.7 kg6 and 6.0 kg12 during the first 1 to 2 years after diagnosis has been reported. A larger weight gain (4.3 to 4.5 kg)6,10 has been reported when adjuvant chemotherapy was administered for 1 year, as opposed to the 6-month period used in this study. The observed weight gain for women receiving 6 months of chemotherapy was 2.5 kg in our study. It is possible that the degree of weight gain may, to a certain extent, be dependent on the duration of adjuvant treatment. The weight gain we have observed is larger than that observed by others in healthy women or in women undergoing menopause. Williamson et al42 prospectively studied weight gain over a 10-year period in 6,135 women who participated in the First National Health and Nutrition Examination Survey Epidemiologic Follow-Up Study. Over 10 years, women aged 25 to 34 years gained 3.45 kg (0.35 kg/yr), those aged 45 to 55 years (closest in age to our study population) gained only 0.79 kg (0.08 kg/yr), whereas those aged 55 years and older lost weight. Poehlman et al46 and Wing et al47 prospectively investigated weight change as healthy women in the general population approached menopause. Poehlman et al46 observed a 0.5-kg weight gain over 6 years (0.08 kg/yr) in women who became menopausal, compared with a 1.0-kg weight loss (0.17 kg/yr) in an age-matched group who remained premenopausal. Wing et al47 observed a mean weight gain of 2.25 kg over 3 years (0.75 kg/yr) in women first studied at ages 42 to 50 years while premenopausal; weight gain was smaller in those who underwent a natural menopause (1.4 kg over 3 years, 0.47 kg/yr) than in those who remained premenopausal (2.1 kg over 3 years, 0.7 kg/yr). The largest weight gain (3.3 kg over 3 years, 1.1 kg/yr) was seen in hormone users. Our results cannot be compared directly with these published observations; however, women with breast cancer may experience a greater weight gain than women in the general population. We have reported two potential mechanisms for weight gain: caloric intake and physical activity. Although change in caloric intake was weakly correlated with change in weight overall, there was no correlation in those who entered menopause who were at greatest risk for weight gain. This suggests that the contribution of diet to the weight gain we have observed is not straightforward. It may play a minor role in those with stable menopausal status who experience small amounts of weight gain, but it is not an important mechanism in those who become menopausal and gain larger amounts of weight. Other mechanisms, such as change in energy expenditure (metabolic rate and/or physical activity), may be more important in this group. Our observations are in keeping with previous reports that have failed to find a relationship between caloric intake and weight gain in women with breast cancer11,15,16; however, further evaluation using weighed food records, rather than a food frequency questionnaire, is recommended to ensure that an effect has not been missed as a result of inaccuracy in dietary measurements obtained using a food frequency questionnaire. This is particularly important because of reports that interventions to reduce fat or caloric intake in women with breast cancer may prevent weight gain.48-50 Our data fail to show a correlation of physical activity with weight gain. This result must be interpreted cautiously, because we measured self-reported physical activity over a 1-week period at baseline and 1 year only; we did not examine physical activity throughout the year, and it is possible that an association of physical activity over the course of the year with change in weight was missed. For example, women receiving chemotherapy may have reduced their physical activity while receiving treatment, with a resultant weight gain, and subsequently increased their physical activity in an attempt to lose the weight they had gained. In previous studies,15,51 we have shown that physical activity (measured prospectively on a monthly basis) was the most important predictor of success in a weight management intervention developed for women with newly diagnosed breast cancer, the likelihood of success increasing 70% for each additional 30 minutes of exercise performed weekly. Because of this, and because of the measurement technique used in this study, the contribution of physical activity to weight gain in this population requires further evaluation. One recent study52 has examined a second category of energy expenditure, basal metabolic rate (BMR), and suggested that a transient reduction in BMR during chemotherapy may, to some extent, be associated with weight gain in women with breast cancer receiving adjuvant chemotherapy. This observation was not replicated by our group in a small study53; however, low power may have explained our negative findings. Because onset of menopause was found, in one study,46 to be associated with decreases in BMR, further research is recommended to examine metabolic rate in women with newly diagnosed breast cancer. This research should also include an evaluation of fat-free mass, which has been reported to decline with menopause46 and is associated with both BMR and physical activity. In conclusion, most women with newly diagnosed breast cancer gain weight during the first year after diagnosis. This weight gain is larger than that previously reported in studies of healthy women. It is greatest in women who became menopausal and in those receiving chemotherapy. Increases in caloric intake do not seem to explain weight gain in those women at greatest risk, and other mechanisms, such as alterations in energy expenditure (ie, physical activity and BMR), may be important. Future research should focus on these women at greatest risk (premenopausal, adjuvant chemotherapy planned), with careful evaluation of both physical activity and BMR throughout the first year after diagnosis.
Supported by the Medical Research Council of Canada and the Canadian Breast Cancer Research Initiative
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Copyright © 1999 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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ABSTRACT
INTRODUCTION
.05). Caloric intake decreased (P < .01) and physical activity increased (P < .05) during the year after diagnosis; these factors did not explain the observed weight gain. 
2 tests. Five percent significance levels were used throughout, and all P values reported are two-tailed. 
). Bars extend two standard errors, approximating 95% confidence intervals.
