TY - JOUR
T1 - Plasma leptin levels and risk of incident cancer
T2 - Results from the dallas heart study
AU - Gupta, Arjun
AU - Herman, Yehuda
AU - Ayers, Colby
AU - Beg, Muhammad S.
AU - Lakoski, Susan G.
AU - Abdullah, Shuaib M.
AU - Johnson, David H.
AU - Neeland, Ian J.
N1 - Publisher Copyright:
© 2016 Gupta et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2016/9
Y1 - 2016/9
N2 - Purpose Leptin dysregulation has been postulated to affect cancer risk through its effects on obesity and inflammation. Epidemiological data evaluating this relationship are conflicting and studies in non-white cohorts is lacking. Therefore, we examined the association of leptin with the risk of incident cancer in the multiethnic Dallas Heart Study (DHS). Methods Participants enrolled in the DHS without prevalent cancer and with baseline leptin measurements were included. Incident cancer cases were identified through a systematic linkage of the DHS and the Texas Cancer Registry. Leptin was evaluated both as a continuous variable and in sex-specific quartiles. Multivariable Cox proportional hazards modeling was performed to examine the association between leptin levels with incident cancer after adjusting for age, sex, race, smoking status, alcohol use, family history of malignancy, body mass index (BMI), diabetes mellitus and C-reactive protein. Results Among 2,919 participants (median age 44 years; 54% women; 70% nonwhite; median BMI 29.4 kg/m2), 190 (6.5%) developed cancer after median follow-up of 12 years. Median leptin levels were 12.9 (interquartile range [IQR] 5.8-29.5) ng/ml in the incident cancer group vs. 12.3 (IQR 5.4-26.4) ng/ml those without an incident cancer (p = 0.34). Leptin was not associated with cancer incidence in multivariable analysis (unit standard deviation increase in log-Transformed leptin, hazard ratio 0.95; 95% confidence interval, 0.77-1.16; p = 0.60). No association was observed in analyses stratified by sex, race/ethnicity, diabetes, or obesity status. Conclusions In this study of a predominantly minority population, no association between premorbid leptin levels and cancer incidence was demonstrated. Despite preclinical rationale and positive findings in other studies, this association may not replicate across all racial/ethnic populations.
AB - Purpose Leptin dysregulation has been postulated to affect cancer risk through its effects on obesity and inflammation. Epidemiological data evaluating this relationship are conflicting and studies in non-white cohorts is lacking. Therefore, we examined the association of leptin with the risk of incident cancer in the multiethnic Dallas Heart Study (DHS). Methods Participants enrolled in the DHS without prevalent cancer and with baseline leptin measurements were included. Incident cancer cases were identified through a systematic linkage of the DHS and the Texas Cancer Registry. Leptin was evaluated both as a continuous variable and in sex-specific quartiles. Multivariable Cox proportional hazards modeling was performed to examine the association between leptin levels with incident cancer after adjusting for age, sex, race, smoking status, alcohol use, family history of malignancy, body mass index (BMI), diabetes mellitus and C-reactive protein. Results Among 2,919 participants (median age 44 years; 54% women; 70% nonwhite; median BMI 29.4 kg/m2), 190 (6.5%) developed cancer after median follow-up of 12 years. Median leptin levels were 12.9 (interquartile range [IQR] 5.8-29.5) ng/ml in the incident cancer group vs. 12.3 (IQR 5.4-26.4) ng/ml those without an incident cancer (p = 0.34). Leptin was not associated with cancer incidence in multivariable analysis (unit standard deviation increase in log-Transformed leptin, hazard ratio 0.95; 95% confidence interval, 0.77-1.16; p = 0.60). No association was observed in analyses stratified by sex, race/ethnicity, diabetes, or obesity status. Conclusions In this study of a predominantly minority population, no association between premorbid leptin levels and cancer incidence was demonstrated. Despite preclinical rationale and positive findings in other studies, this association may not replicate across all racial/ethnic populations.
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U2 - 10.1371/journal.pone.0162845
DO - 10.1371/journal.pone.0162845
M3 - Article
C2 - 27636369
AN - SCOPUS:84992366120
SN - 1932-6203
VL - 11
JO - PloS one
JF - PloS one
IS - 9
M1 - e0162845
ER -