Associations between early-life growth pattern and body size and follicular lymphoma risk and survival: a family-based case-control study
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- Title :Associations between early-life growth pattern and body size and follicular lymphoma risk and survival: a family-based case-control study
- Author: Michael K. Odutola a, Marina T. van Leeuwen a, Jennifer Turner b, Fiona Bruinsma c,John F. Seymour d, H. Miles Prince e, Samuel T. Milliken f, Mark Hertzberg g, Judith Trotman h,Stephen S. Opati, Robert Lindeman j, Fernando Roncolato k, Emma Verner h, Michael Harvey l,Campbell Tiley m, Craig R. Underhill n, Geza Benke o, Graham G. Giles c,p, Claire M. Vajdic a,q,*
- Publication: Cancer Epidemiology
- Publisher: Elsevier Inc
- Year: 2022
- Language: English
- Pages: 10
- Format: PDF
- File size: 595 KB
- DOI:10.1016/j.canep.2022.102241
- CBID: CBR185
Abstract
Background
The influence of early-life growth pattern and body size on follicular lymphoma (FL) risk and survival is unclear. In this study, we aimed to investigate the association between gestational age, growth during childhood, body size, changes in body shape over time, and FL risk and survival.
Methods
We conducted a population-based family case-control study and included 706 cases and 490 controls. We ascertained gestational age, growth during childhood, body size and body shape using questionnaires and followed-up cases (median=83 months) using record linkage with national death records. We used a group-based trajectory modeling approach to identify body shape trajectories from ages 5–70. We examined associations with FL risk using unconditional logistic regression and used Cox regression to assess the association between body mass index (BMI) and all-cause and FL-specific mortality among cases.
Results
We found no association between gestational age, childhood height and FL risk. We observed a modest increase in FL risk with being obese 5 years prior to enrolment (OR=1.43, 95 %CI=0.99–2.06; BMI ≥30 kg/m 2 ) and per 5-kg/m 2 increase in BMI 5 years prior to enrolment (OR=1.14, 95 %CI=0.99–1.31). The excess risk for obesity 5 years prior to enrolment was higher for ever-smokers (OR=2.00, 95 %CI=1.08–3.69) than never-smokers (OR=1.14, 95 %CI=0.71–1.84). We found no association between FL risk and BMI at enrolment, BMI for heaviest lifetime weight, the highest categories of adult weight or height, trouser size, body shape at different ages or body shape trajectory. We also observed no association between all-cause or FL-specific mortality and excess adiposity at or prior to enrolment.
Conclusion
We observed a weak association between elevated BMI and FL risk, and no association with all-cause or FL-specific mortality, consistent with previous studies. Future studies incorporating biomarkers are needed to elucidate possible mechanisms underlying the role of body composition in FL etiology.
Highlights
- • Obesity 5 years prior to enrolment and per 5-kg/m 2 increase in BMI 5 years prior to enrolment modestly increases follicular lymphoma (FL) risk.
- • There is no association between gestational age, growth during childhood, adult height or weight, trouser size, body shape at different ages or body shape trajectories and FL risk.
- • There is no evidence of an association between body mass index and all-cause or FL-specific mortality.
- • Future studies should examine adiposity using objective, longitudinal measures of body composition and biomarkers.
1Introduction
Follicular lymphoma (FL) is the second most common non-Hodgkin lymphoma (NHL) subtype in western countries accounting for 20–25 % of all new NHL cases . In Australia, FL incidence increased by 2.5 % per year between 1997 and 2006 and then stabilised at 3.0 per 100,000 persons , while in the US, FL incidence reached 3.4 per 100,000 persons in 2003 and declined by 0.5–2.0 % thereafter . Obesity prevalence is increasing worldwide with higher prevalence in western countries . Understanding the relationship between body fatness and FL risk may provide insight into FL etiology and inform risk prevention strategies.
The relationship between FL risk and early-life events is unknown. One cohort study found no association between NHL risk and gestational age or twinning . No prior studies have examined FL risk and gestational age or growth during childhood. The precursor molecular lesion of FL, the t(14;18) translocation, can be found decades prior to the clinical diagnosis of FL potentially implicating early-life environmental exposures in the initiation of FL .
The effects of changes in body size (body fatness) and body shape on FL risk are unclear. Meta-analyses of body size showed significant positive associations with NHL risk overall and weak positive associations with FL risk . A recent pooled analysis of US cohort studies found a 22 % increased FL risk per 10-cm increase in height , while a prior meta-analysis of observational studies found a similar 9 % increased FL risk per 5-cm increase in height and non-significant excess risk per 5-kg increase in weight . Height in adulthood is influenced by nutritional status during early life but the mechanism by which height might contribute to FL risk is unknown. A meta-analysis reported a modest positive association between FL risk and obesity as an adult but no association with being overweight or per 5-kg/m 2 increase in weight in early adulthood . The only study to examine FL risk and body shape in childhood and adolescence using pictograms found a positive relationship with the highest category of body shape in female adolescents, and no association in males or during childhood in both sexes . No prior studies have examined associations between FL risk and body shape trajectories or trouser size. Evidence suggests that trouser size can be used as a proxy measure of abdominal fatness based on its high correlation with waist circumference . Excess body fatness has been shown to be associated with increased
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