ABSTRACT
AIM: This study aimed to test the dose-response relationship between fasting blood glucose (FBG) levels and risk of prostate cancer. METHODS: A systematic search was done of PubMed and Scopus from their inception up to January 2017. Prospective and retrospective studies reporting risk estimates of prostate cancer for two or more categories of blood glucose levels were identified, and two independent authors extracted the information. Relative risk (RR) was calculated using random-effects models and pooled. RESULTS: Ten prospective cohort studies, one nested case-control study, one case-cohort study and three case-control studies (total n=1,214,947) involving 12,494 cases of prostate cancer were reviewed. The pooled RR of prostate cancer for the highest vs. lowest category of FBG was 0.88 (95% CI: 0.78-0.98, I2=25.5%, n=15 studies). A 10mg/dL increment in FBG level was not associated with risk of prostate cancer (0.98, 95% CI: 0.96-1.00, I2=45.4%, n=11 studies). Subgroup analyses yielded a significant inverse association only in the subgroup of cohort studies. Non-linear dose-response meta-analysis showed a very slight decrement in risk with increasing FBG levels. Sensitivity analyses using cohort studies showed a steep decrease in risk along with an increase in FBG from baseline levels of ≈70mg/dL across prediabetes and diabetes ranges. CONCLUSION: Higher FBG levels are associated with lower risk of prostate cancer in cohort studies, but not in case-control studies, findings that limit interpretation of our present results.
Subject(s)
Blood Glucose , Fasting , Prostatic Neoplasms , Adult , Aged , Aged, 80 and over , Blood Glucose/analysis , Blood Glucose/physiology , Diabetes Mellitus, Type 2/blood , Diabetes Mellitus, Type 2/epidemiology , Fasting/blood , Fasting/physiology , Humans , Male , Middle Aged , Prostatic Neoplasms/blood , Prostatic Neoplasms/epidemiologyABSTRACT
We aimed to investigate the potential association between vitamin D and serum leptin levels by pooling together the results from observational studies and clinical trials. A systematic literature search of PubMed, Scopus and Google Scholar was conducted up to March 2015. The analysis of observational studies was conducted on six papers that reported nine correlation coefficients using Fisher's Z and its standard error. Then, effect sizes of eligible trials were pooled using random-effects models (the DerSimonian-Laird estimator). Results of observational studies showed an inverse association between leptin and 25-hydroxyvitamin D (25(OH)D) (Fisher's Z=-0.93, 95% CI: -0.95, -0.91). After combining trials, pooled mean difference (PMD) for 25(OH)D was 24.06 ng/ml (95% CI, 17.27-30.85; P<0.001) with significant heterogeneity among studies (P<0.001; I2=89.1%). Raising 25(OH)D was associated with significant increase in leptin level (PMD=4.60 ng/ml, 95% CI, 0.55-8.66, P=0.026) with significant heterogeneity (P<0.001; I2=96.4%). Population with diabetes (PMD: 13.63 ng/ml), age younger than 50 years (PMD: 1.884 ng/ml), doses less than 1000 IU/day (PMD: 1.53 ng/ml), duration less than 24 weeks (PMD: 14.668 ng/ml) and baseline 25(OH)D <50 nmol/l (PMD: 13.483 ng/ml) were sources of heterogeneity. Current evidence indicates that inverse association between leptin level and 25(OH)D concentration was observed in observational studies, which was not demonstrated in intervention studies with high heterogeneity. Clearly, there is a need for properly designed and large prospective dose-response trials with long-term follow-up to assess the sources of heterogeneity.
