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. Author manuscript; available in PMC: 2022 Jun 1.
Published in final edited form as: Obesity (Silver Spring). 2021 Jun;29(6):960–965. doi: 10.1002/oby.23163

Obesity And Cancer Death In White And Black Adults: A Prospective Cohort Study

Justin C Brown 1,2,3, Shengping Yang 1, Emily F Mire 1, Xiaocheng Wu 2,3,4, Lucio Miele 2,3, Augusto Ochoa 2,3, Jovanny Zabaleta 2,3, Peter T Katzmarzyk 1
PMCID: PMC8422242  NIHMSID: NIHMS1736204  PMID: 34029447

Abstract

Objective:

Determine if race modifies the association between obesity and cancer death.

Methods:

The Pennington Center Longitudinal Study included 18,296 adults; 35.0% male and 34.3% black. Body mass index (BMI) was calculated as weight indexed by the square of height (kg/m2). The primary endpoint was death from cancer.

Results:

During a follow-up of 14.3 years, 346 cancer deaths occurred. Among men, race modified the association of BMI and cancer death (Pinteraction=0.045); compared to a BMI of 22 kg/m2, a BMI of 35 kg/m2 in white men was associated with a hazard ratio of 1.74 (95% CI: 1.38–2.21), in black men the hazard ratio was 0.64 (95% CI: 0.45–0.90). Among women, race did not modify the association of BMI and cancer death (Pinteraction=0.43); however, compared to a BMI of 22 kg/m2, a BMI of 35 kg/m2 in white women was associated with a hazard ratio of 1.42 (95% CI: 1.18–1.70), in black women, the hazard ratio was 0.99 (95% CI: 0.82–1.20).

Conclusions:

In this diverse cohort of adults, having obesity was associated with an increased risk of cancer death in white men and women. In contrast, having obesity was associated with a reduced risk of cancer death in black men and did not influence risk in black women.

Keywords: Body Mass Index, Cohort Study, Disparities, Mortality, Waist Circumference

INTRODUCTION

In the United States, black men and women born in 1980 have a life expectancy that is 6.9 and 5.6 years shorter than white men and women born that same year (1). Black adults have a higher prevalence of obesity (2), but the extent to which differences in obesity explain disparities in life expectancy remains unclear (3). Among white adults, having obesity increases the risk of all-cause death (4, 5). However, among black adults, having obesity is inconsistently associated with all-cause death (6, 7) and may vary by sex (8–11).

Cancer causes one in five deaths in the United States (12). Obesity increases the risk of death from some cancers in men and women (13, 14), but it is currently unknown if obesity increases this risk at a similar magnitude in white and black adults. By the year 2030, 57% of black adults in the United States are predicted to have obesity (15). Describing the association of obesity with cancer death in black individuals and contrasting this association with that of white individuals is essential to inform evidence-based interventions and policies to improve outcomes and reduce racial disparities in cancer death (16, 17).

This study tested the hypothesis that participant race modifies the association of anthropometric measures of obesity and cancer death in a diverse cohort of adults.

METHODS

Study Population and Design

The Pennington Center Longitudinal Study (PCLS) is an ongoing prospective cohort study designed to investigate the effects of obesity, physical activity, and diet on developing chronic disease and death. The PCLS includes men and women aged ≥18 years who participated in clinical trials conducted at Pennington Biomedical Research Center in Baton Rouge, Louisiana, since 1992. This report uses data obtained from baseline examinations conducted before any study-specific interventions were received. Each participant provided written informed consent, and all PCLS procedures, including this analysis, were approved by the Pennington Biomedical Research Center institutional review board. This cohort was registered in 2009 on clinicaltrials.gov as NCT00959270. The investigators conducted statistical analyses from January to May 2021.

Anthropometric Measures of Obesity

Anthropometric measures were obtained on all participants using standardized procedures. Height was measured in duplicate with a wall-mounted stadiometer. Participants removed their shoes and held an inhaled breath while the technician maintained alignment with the Frankfort Horizontal Plane (18). The average of two heights was used for analysis; a third measurement was obtained if the difference of the first two measures exceeded 0.5 cm. Body weight was measured in duplicate using a calibrated scale after all outer clothing, pocket items, and shoes were removed. The average of two body weights was used for analysis; a third measurement was obtained if the difference of the first two measures exceeded 0.5 kg. BMI was calculated as weight indexed by the square of height (kg/m2). Waist circumference (WC) was measured in duplicate at the midpoint between the inferior border of the ribcage and the superior aspect of the iliac crest using a flexible spring-loaded measuring tape (19); a third measurement was obtained if the difference of the first two measures exceeded 1.0 cm. Construction of the anthropometric measures database was completed by staff who were blinded to study endpoint status.

BMI and WC are correlated at the population level [r = 0.93; (20)] but are not exchangeable at the individual level (21). To examine the joint effects of BMI and WC at the individual level, we used the residuals of WC regressed on BMI (22). The residual value represents the difference between the observed WC and the predicted WC estimated using BMI (e.g., larger residuals correspond to participants who have a bigger WC than would be expected, conditional on their BMI).

Covariates

Information on covariates was collected from participants at enrollment (baseline) for inclusion in regression models. Age was computed from birth and enrollment dates. Participant race was self-reported. Smoking status was self-reported in the categories of never, former, and current. The median year of enrollment was 2003 [IQR: 1998, 2007], and the median sample size of the included clinical trials was n=25 [IQR: 9, 60].

Study Outcomes

The primary endpoint of this analysis was the time from enrollment to death attributable to cancer. The secondary endpoint was death attributable to obesity-related cancer. Deaths were identified from the National Death Index using Social Security Administration data. Deaths were included if cancer was documented as an underlying or contributing cause of death on the death certificate. Obesity-related cancer deaths included the 13 malignancies identified by the International Agency for Research on Cancer (IARC) as being convincingly related to obesity, including: esophageal adenocarcinoma, gastric cardia, colon and rectum, liver, gallbladder, pancreas, postmenopausal breast, uterine, ovarian, renal cell kidney, meningioma, thyroid, and multiple myeloma (23). All participants were followed for death through December 31, 2017.

Statistical Analysis

This analysis was restricted to participants who 1) self-reported no history of cancer at enrollment (excluding nonmelanoma skin cancer); 2) were aged <90 years at the time of PCLS enrollment (due to data linkage confidentiality protections); and 3) had at least one year of follow-up since enrollment. Multivariable adjusted Cox proportional hazards models were used to quantify the cause-specific hazard ratio between baseline BMI, WC, and WC residuals with cancer death. The cause-specific hazard ratio quantifies the relative change in the instantaneous rate of cancer death in patients who have not yet died from a non-cancer cause (24). The conclusions from the cause-specific hazard model presented herein are consistent with the sub-distribution hazard model using a Fine and Gray competing risk model (25) (results not shown).

We modeled BMI and WC as continuous variables using B-splines (26). B-splines accommodate nonlinearity and provide statistically efficient and visually intuitive depictions of prognostic associations (27). All models were conducted separately for men and women because of established sex differences in obesity and the underlying risk of cancer death (28, 29). Models were adjusted for age (continuous), smoking status (never vs. former vs. current vs. unknown), year of examination (continuous), study size (sample size n ≤ 16 vs. n > 16). Year of examination was used to account for temporal trends in baseline measurements; study size was used to account for the small sample sizes of the included pilot and feasibility studies. Model parsimony was assessed with the Akaike Information Criterion.

Graphical depictions of the statistical associations are presented so that readers can quantify numerous contrasts of interest. To enhance interpretability, in the results section, we report the point estimates and 95% confidence intervals of BMI at 35 kg/m2 (class II obesity) relative to that of 22 kg/m2 (normal weight). We selected WC values of 80 cm and 110 cm, as these WC measures, on average, correspond to BMI of 22 kg/m2 and 35 kg/m2 in both white and black men and women in our study sample (30). Linearity and nonlinearity were inspected visually using spline plots and examined statistically with the likelihood ratio test. The assumption of proportional hazards was confirmed by visual inspection of graphical log-log plots and statistical testing in a generalized linear model of the scaled Schoenfeld residuals on time (31).

Effect modification by participant race was determined by including an interaction term in the regression model and tested using the likelihood ratio statistic. Baseline characteristics were examined using the χ2 test for categorical variables and t-test for continuous variables. All statistical tests were two-sided. Statistical analyses were conducted using SAS (version 9.4; Cary, NC) and R (version 4.0; R Core Team).

RESULTS

Characteristics of the Study Cohort

The analytic sample included 18,296 participants (Appendix Figure 1); 6,405 (35.0%) were male sex and 6,273 (34.3%) were black race (Table 1). During a median follow-up of 14.3 years (interquartile range: 10.1–19.2 years), cancer death occurred in 346 participants, and obesity-related cancer death occurred in 161 participants (Appendix Table 1). Compared to white men, the age-adjusted hazard ratio for cancer death in black men was 1.45 (95% CI: 0.99–2.13). Compared to white women, the age-adjusted hazard ratio for cancer death in black women was 1.16 (95% CI: 0.85–1.58).

Table 1.

Baseline characteristics of the study population

Characteristic Overall Cohort Men Women
White Black White Black
N 18,296 4,877 1,528 7,146 4,745
Age (y) 42.2 (14.8) 41.1 (16.1) 38.2 (13.7) 44.6 (14.9) 40.9 (12.7)
Body Mass Index (kg/m2) 31.3 (7.8) 29.8 (6.7) 30.2 (7.3) 30.9 (8.2) 33.7 (7.9)
Body Mass Index, n (%)
 Underweight (<18.5 kg/m2) 106 (0.6) 19 (0.4) 12 (0.8) 52 (0.7) 23 (0.5)
 Normal Weight (18.5–24.9 kg/m2) 3809 (20.8) 1,156 (23.7) 365 (23.9) 1,760 (24.6) 528 (11.1)
 Overweight (25.0–29.9 kg/m2) 5017 (27.4) 1,606 (32.9) 448 (29.3) 1,863 (26.1) 1,100 (23.2)
 Obese (≥30.0 kg/m2) 9364 (51.2) 2,096 (43.0) 703 (46.0) 3,471 (48.6) 3,094 (65.2)
Waist Circumference* (cm) 95.6 (18.5) 98.9 (17.4) 95.8 (17.4) 92.4 (19.4) 96.9 (17.7)
Waist Circumference*, n (%)
 Low (<88 cm women; <102 cm men) 6977 (49.0) 2,354 (61.1) 817 (67.6) 2,561 (46.5) 1,245 (33.9)
 High (≥ 88 cm women; ≥102 men) 7266 (51.0) 1,497 (38.9) 392 (32.4) 2,946 (53.5) 2,431 (66.1)
Smoking History, n (%)
 Never 11291 (61.7) 2,935 (60.2) 956 (62.6) 4,110 (57.5) 3,290 (69.3)
 Former 2807 (15.3) 1,044 (21.4) 265 (17.3) 1,072 (15.0) 426 (9.0)
 Current 1149 (6.3) 199 (4.1) 146 (9.6) 517 (7.2) 287 (6.0)
 Unknown 3049 (16.7) 699 (14.3) 161 (10.5) 1,447 (20.2) 742 (15.6)
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*

n=14,243.

Anthropometric Measures of Obesity

The mean (SD) BMI and WC among all participants were 31.3 kg/m2 (7.8) and 95.6 cm (18.5), respectively. Detailed descriptions of differences in anthropometric measures of obesity between participant race and sex have been reported previously (30).

Effect of Body Mass Index and Race on Cancer Death

Among men, participant race modified the prognostic association of BMI and cancer death (Pinteraction = 0.045). Compared to a BMI of 22 kg/m2, a BMI of 35 kg/m2 in white men was associated with a hazard ratio of 1.74 (95% CI: 1.38–2.21), whereas in black men, the hazard ratio was 0.64 [(95% CI: 0.45–0.90); Figure 1A]. Among women, participant race did not statistically significantly modify the association of BMI cancer death (Pinteraction = 0.43). However, compared to a BMI of 22 kg/m2, a BMI of 35 kg/m2 in white women was associated with a hazard ratio of 1.42 (95% CI: 1.18–1.70), whereas in black women, the hazard ratio was 0.99 [(95% CI: 0.82–1.20); Figure 1B].

Figure 1.

Figure 1.

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Risk of cancer death by anthropometric measure of obesity on the relative hazard scale. Shaded regions indicate 95% confidence bands for the risk of cancer death as a function of body mass index among men (Panel A) and body mass index among women (Panel B); waist circumference among men (Panel C) and waist circumference among women (Panel D); and waist circumference residuals among men (Panel E) and waist circumference residuals among women (Panel F). White participants are depicted in blue color and black participants are depicted in red color. Estimates are multivariable adjusted.

Effect of Waist Circumference and Race on Cancer Death

Among men, participant race did not statistically significantly modify the prognostic association of WC and cancer death (Pinteraction = 0.41). However, compared to a WC of 80 cm, a WC of 110 cm in white men was associated with a hazard ratio of 1.52 (95% CI: 1.12–2.03), whereas in black men, the hazard ratio was 0.82 [(95% CI: 0.54–1.25); Figure 1C]. Among women, participant race did not statistically significantly modify the association of WC and cancer death (Pinteraction = 0.66). Though a WC of 110 cm in white women was associated with a hazard ratio of 1.58 (95% CI: 1.22–2.05), whereas in black women, the hazard ratio was 1.19 [(95% CI: 0.88–1.59); Figure 1D] when compared to a WC of 80 cm.

Effect of Waist Circumference Residuals and Race on Cancer Risk

Among men, participant race did not statistically significantly modify the prognostic association of WC residual and cancer death (Pinteraction = 0.41). Compared to a WC residual of 0 cm, a WC residual of 10 cm in white men was associated with a hazard ratio of 1.09 (95% CI: 0.75–1.59), whereas in black men the hazard ratio was 1.80 [(95% CI: 0.96–3.35); Figure 1E]. Among women, participant race did not statistically significantly modify the association of WC residuals and cancer death (Pinteraction = 0.55). However, compared to a WC residual of 0 cm, a WC residual of 10 cm in white women was associated with a hazard ratio of 1.11 (95% CI: 0.86–1.44); in black women, the hazard ratio was 1.40 [(95% CI: 1.00–1.98); Figure 1F].

Secondary and Sensitivity Analyses

Conclusions based on the secondary endpoint of obesity-related cancer death did not substantively differ from the primary endpoint of all-cancer death (Appendix Figure 2).

DISCUSSION

In this prospective cohort study of 18,296 white and black adults, we found meaningful differences in the prognostic associations of obesity and cancer death by participant race and sex. Having obesity was associated with an increased risk of cancer death in white men and white women. In contrast, having obesity was associated with a reduced risk of cancer death in black men and did not influence the risk of cancer death in black women. Contrary to our expectations, cancer death increased with a larger BMI among white men and women, but risk decreased for black men and was null for black women. These results may therefore inform interventions and policies to ensure that appropriate, evidence-based, obesity prevention and treatment measures are implemented to improve outcomes and reduce racial disparities in cancer death.

We have previously reported in the PCLS cohort that obesity, defined using BMI, increased the risk of all-cause death in white men and women but did not increase the risk of death in black men and women (Pinteraction < 0.05); (32). For each 1 kg/m2 increase in BMI, the hazard ratio for all-cause death in white adults was 1.30 (95% CI: 1.15–1.47), whereas the hazard ratio in black adults was 1.03 (95% CI: 0.85–1.26); (32). We have also reported in the PCLS cohort that obesity increased the risk of cancer among white men and white and black women but did not increase the risk of cancer among black men (Pinteraction < 0.05); (30). The current analysis offers further insight regarding the differential effects of obesity on health status and prognosis in different population subgroups.

In the Multiethnic Cohort study, the association between having obesity and the risk of all-cause and breast cancer specific death did not differ by race in women (33). Several studies have explored racial differences in the association between obesity and death among those diagnosed with cancer (e.g., postdiagnosis survival) (34, 35). Although the risk estimates from our study have a distinct interpretation from studies restricted to cancer survivors (36), the findings offer complementary insight where data are generally limited. Regarding prostate cancer, having obesity is associated with a 78% increased the risk of prostate cancer-specific mortality, which did not differ between white and black men (34). Conversely, considering breast cancer, having obesity is associated with an increased the risk of all-cause and cancer-specific mortality among white women, but not among black women (35). The limited and inconsistent findings in the literature reveal a significant research gap regarding our understanding of the prognostic relationships of obesity in different population subgroups (37). Nevertheless, bodyweight management remains an important goal for overall health in all subgroups of the population (38).

The mechanisms through which obesity promotes cancer progression and subsequent death are not entirely understood, but a common hypothesis relates to excess visceral adiposity and resultant insulin resistance (39–41). Although BMI and WC are common anthropometric measures of obesity (38), they do not consistently quantify excess adiposity and metabolic abnormalities across white and black populations (42–44). At a specific BMI or WC, black individuals have less visceral adiposity and lower insulin resistance than white individuals (45–48). We hypothesize that anthropometric surrogates, such as BMI and WC, may obscure associations with health outcomes by race. The direct measurement of adiposity, such as intraabdominal visceral adipose tissue with dual-energy X-ray absorptiometry, may reveal more consistent prognostic associations across population subgroups (49, 50).

There are limitations to this analysis. All observational studies are susceptible to residual confounding. We obtained anthropometric measures of obesity at a solitary time point; it is unknown how changes in BMI or WC, such as purposeful weight loss, impact cancer death in this cohort. Race is a social and not a biological construct; however, race remains helpful in describing health patterns because data in the United States are often reported by race (2). Despite the large overall sample size, our analysis was unable to examine how participant race modifies the associations of anthropometric measures of obesity and site-specific cancer deaths due to the relative infrequency of these specific malignancies. The sample size and event rate of cancer death also constrained our ability to report statistically significant effect modification by race for select associations between anthropometric measures of obesity and cancer death; the point estimates and graphical patterns of these associations are consistent with the hypothesis of effect modification by race. Our cohort did not systematically measure potentially important confounding variables, such as a family history of cancer, dietary patterns, diagnosis of type 2 diabetes or prediabetes, or socioeconomic status. Information on cancer stage and post-diagnosis treatments were not available in our dataset. Participants in this cohort were concurrently enrolled in various lifestyle and metabolic studies conducted at Pennington Biomedical Research Center; therefore, our cohort may be generalizable to individuals who are sufficiently motivated to volunteer and participate in clinical research studies. We cannot exclude the possibility that our findings are explained by differential unmeasured health behaviors between racial subgroups.

There are strengths to this analysis. The population was sampled from the Baton Rouge metropolitan statistical area of Louisiana, which has some of the highest cancer death rates in the nation (51). Participants were diverse (65% women; 34.3% black) and similar to that of the area from which they were recruited; the Baton Rouge metropolitan statistical area is 56% White and 40% Black (52). The diverse sample size enabled us to conduct informative sex- and race-stratified analyses. Anthropometric measures of obesity were obtained objectively by study staff who adhered to a standardized protocol. The ascertainment of two complementary anthropometric measures of obesity—BMI and WC—enabled us to contrast how different overall and abdominal obesity measures prognosticate cancer death. The cohort had a broad range of age, BMI, and WC, which improves the generalizability of the cohort. This cohort was initiated in 1992, and ≥75% of cohort participants were observed for ≥10 years.

CONCLUSION

In a large and diverse cohort of adults, participant race and sex modified the prognostic associations of anthropometric measures of obesity and cancer death.

Supplementary Material

supinfo

Study Importance.

What is already known?

  • Cancer causes one in five deaths in the United States.

  • Obesity increases the risk of death from some cancers in men and women, but it is unknown if obesity increases cancer death to a similar magnitude in white and black individuals.

What does this study add?

  • In this prospective cohort of 18,296 white and black adults, participant race and sex modified the association between obesity and cancer death.

  • Obesity increased the risk of cancer death in white men but reduced the risk of cancer death in black men.

  • Obesity increased the risk of cancer death in white women but did not influence the risk of cancer death in black women.

How might these results change the focus of clinical practice?

  • If replicated, this study may inform interventions and policies that aim to reduce disparities in cancer death.

Funding:

This work was supported by the National Institute of General Medicine Sciences of the National Institutes of Health under Award Number U54-GM104940, the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health under Award Number P30-DK072476, and the National Cancer Institute of the National Institutes of Health under Award Numbers R00-CA218603; and R25-CA203650.

Disclosure:

Dr. Brown reports receiving grants paid to his institution from the National Cancer Institute, American Institute for Cancer Research, and the Susan G. Komen Foundation during the study. All other authors disclosed no relevant relationships.

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