Association of 25-hydroxyvitamin D with liver cancer incidence and chronic liver disease mortality in Finnish male smokers of the ATBC study.
Cancer Epidemiol Biomarkers Prev. 2018 May 2. pii: cebp.0877.2017. doi: 10.1158/1055-9965.EPI-17-0877. [Epub ahead of print]
- Smoking reduces vitamin D
- Liver cancer nicely treated by high dose vitamin D for 16 weeks (early stage, in rats) – April 2018
- Liver, Liver Cancer, and Vitamin D – Feb 2018
- Liver cancer incidence probably reduced by Vitamin D and Vitamin K – July 2017
- Liver cancer half as likely if high level of vitamin D – Feb 2014
Lai GY1, Wang JB2, Weinstein SJ3, Parisi D4, Horst RL5, McGlynn KA3, Männistö S6, Albanes D3, Freedman ND7.
1 Environmental Epidemiology Branch, National Cancer Institute, NIH, DHHS laigy at mail.nih.gov.
2 Department of Epidemiology and Health Statistics, Zhejiang University.
3 Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH.
4 Information Management Services, Inc.
5 Heartland Assays, Inc.
6 Department of Health, National Institute for Health and Welfare.
7 Department of Cancer Epidemiology and Genetics, National Cancer Institute.
BACKGROUND:
Although circulating 25-hydroxyvitamin D [25(OH)D] concentrations were linked to liver cancer and chronic liver disease (CLD) in laboratory studies, few epidemiologic studies have addressed the associations.
METHODS:
Within the ATBC Study, we measured 25(OH)D in baseline serum of 202 incident liver cancer cases and 225 CLD deaths that occurred during nearly 25 years of follow-up, and 427 controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression. We examined pre-determined clinically defined cut-points, and season-specific and season-standardized quartiles.
RESULTS:
Low serum 25(OH)D concentrations were associated with higher risk of liver cancer (<25 nmol/L versus ≥50 nmol/L: 1.98, 95% CI: 1.22-3.20; p-trend across categories=0.003) and CLD mortality (1.93, 1.23-3.03; p-trend=0.006) in models adjusted for age and date of blood draw. After additional adjustment for BMI, diabetes, smoking, and other potential confounders, the association remained statistically significant for liver cancer (1.91, 1.16-3.15, p-trend=0.008), but was somewhat attenuated for CLD mortality (1.67, 1.02-2.75; p-trend=0.05). Associations were similar for analyses using season-specific and season-standardized quartiles, and after excluding participants with diabetes, or hepatitis B or C.
CONCLUSIONS:
Our results suggest a possible preventive role for vitamin D against liver cancer and CLD, although the importance of the liver for vitamin D metabolism and the lack of information about underlying liver disease makes reverse causality a concern.
IMPACT:
Future studies are needed to evaluate associations of vitamin D with liver cancer and disease in other populations, particularly those with a different constellation of risk factors.
PMID: 29720370 DOI: 10.1158/1055-9965.EPI-17-0877