Plasma leptin levels and risk of incident cancer: Results from the dallas heart study

Arjun Gupta, Yehuda Herman, Colby Ayers, Muhammad S. Beg, Susan G. Lakoski, Shuaib M. Abdullah, David H. Johnson, Ian J. Neeland

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Article numbere0162845
JournalPLoS One
Volume11
Issue number9
DOIs
StatePublished - Sep 1 2016

Fingerprint

Leptin
leptin
heart
Plasmas
neoplasms
Neoplasms
Medical problems
Hazards
body mass index
gender
obesity
Body Mass Index
Obesity
cultural heritage
incidence
C-Reactive Protein
C-reactive protein
diabetes mellitus
nationalities and ethnic groups
Incidence

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)

Cite this

Plasma leptin levels and risk of incident cancer : Results from the dallas heart study. / Gupta, Arjun; Herman, Yehuda; Ayers, Colby; Beg, Muhammad S.; Lakoski, Susan G.; Abdullah, Shuaib M.; Johnson, David H.; Neeland, Ian J.

In: PLoS One, Vol. 11, No. 9, e0162845, 01.09.2016.

Research output: Contribution to journalArticle

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abstract = "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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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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