Blood Lipid Metabolic Profiles and Causal Links to Site-Specific Cancer Risks: A Mendelian Randomization Study

Observational and Mendelian randomization (MR) studies have established links between dyslipidemia and select cancer susceptibilities. However, there is a lack of comprehensive exploration of causal relationships spanning diverse cancer types. Here, we conducted a two-sample MR analysis to elucidate...

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Bibliographic Details
Published in:Nutrition and cancer 2024, Vol.76 (2), p.175-186
Main Authors: Chen, Kai, Li, Jin, Ouyang, Yanfeng, Liu, Guichao, Xie, Yulong, Xu, Guiqiong, Peng, Weibin, Liu, Yonglin, He, Han, Huang, Rong
Format: Article
Language:English
Subjects:
Adiponectin
Apolipoprotein A-I
Apolipoprotein B
Apolipoproteins
Blood
Breast cancer
Breast Neoplasms
Causality
Cervical cancer
Cholesterol
Cholesterol, HDL
Cholesterol, LDL - genetics
Disease prevention
Dyslipidemia
Endometrial cancer
Endometrial Neoplasms - etiology
Endometrial Neoplasms - genetics
Endometrium
Health risks
High density lipoprotein
Humans
Leptin
Lipids
Lipoprotein(a)
Low density lipoprotein
Male
Melanoma
Mendelian Randomization Analysis
Metabolic disorders
Metabolism
Ovarian cancer
Polymorphism, Single Nucleotide
Prostate cancer
Prostatic Neoplasms - genetics
Randomization
Risk
Risk Factors
Skin cancer
Triglycerides
Uterine cancer
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Summary:Observational and Mendelian randomization (MR) studies have established links between dyslipidemia and select cancer susceptibilities. However, there is a lack of comprehensive exploration of causal relationships spanning diverse cancer types. Here, we conducted a two-sample MR analysis to elucidate the causative connections between 9 blood lipid metabolic profiles (namely, adiponectin, leptin, lipoprotein A, apolipoprotein A1, apolipoprotein B, cholesterol, triglycerides, LDL-cholesterol, and HDL-cholesterol) and 21 site-specific cancer risks. Our findings reveal genetically predicted adiponectin levels to be associated with a reduced ovarian cancer risk, while genetically determined leptin increases bladder cancer risk but decreases prostate cancer risk. Lipoprotein A elevates risk of prostate cancer while diminishing risk of endometrial cancer, while apolipoprotein A1 heightens risks of breast and cervical cancers. Furthermore, elevated levels of cholesterol are positively correlated with kidney cancer, and triglycerides demonstrate a positive association with non-melanoma skin cancer but a negative association with breast cancer. Protective effects of genetically predicted LDL-cholesterol on endometrial cancer and adverse effects of HDL-cholesterol on breast cancer are also observed. Our study conclusively establishes that blood lipid metabolic profiles exert causal effects on cancer susceptibility, providing more robust evidence for cancer prevention and prompting contemplation regarding the future health of the human populace.
ISSN:0163-5581
1532-7914
1532-7914
DOI:10.1080/01635581.2023.2294521