METHODS: A systematic literature search was performed in Scopus, Embase, Web of Science, and PubMed databases up to February 2020 for RCTs that investigated the effect of DHEA supplementation on testosterone levels. The estimated effect of the data was calculated using the weighted mean difference (WMD). Subgroup analysis was performed to identify the source of heterogeneity among studies.
RESULTS: Overall results from 42 publications (comprising 55 arms) demonstrated that testosterone level was significantly increased after DHEA administration (WMD: 28.02 ng/dl, 95% CI: 21.44-34.60, p = 0.00). Subgroup analyses revealed that DHEA increased testosterone level in all subgroups, but the magnitude of increment was higher in females compared to men (WMD: 30.98 ng/dl vs. 21.36 ng/dl); DHEA dosage of ˃50 mg/d compared to ≤50 mg/d (WMD: 57.96 ng/dl vs. 19.43 ng/dl); intervention duration of ≤12 weeks compared to ˃12 weeks (WMD: 44.64 ng/dl vs. 19 ng/dl); healthy participants compared to postmenopausal women, pregnant women, non-healthy participants and androgen-deficient patients (WMD: 52.17 ng/dl vs. 25.04 ng/dl, 16.44 ng/dl and 16.47 ng/dl); and participants below 60 years old compared to above 60 years old (WMD: 31.42 ng/dl vs. 23.93 ng/dl).
CONCLUSION: DHEA supplementation is effective for increasing testosterone levels, although the magnitude varies among different subgroups. More study needed on pregnant women and miscarriage.
METHODS: In this work, we performed a systematic review and meta-analysis to precisely examine the association between circulating levels of leptin and adiponectin and CRC risk. A systematic literature search was performed in PubMed/MEDLINE, Scopus, Web of Science, and EMBASE databases from inception until October 2020. The pooled effect size was then estimated by calculating the odds ratio (OR).
RESULTS: A total of 23 records (comprising 26 studies) were included in the meta-analysis. The overall analysis found that circulating levels of leptin and adiponectin were not significantly associated with CRC risk (P > 0.05). Interestingly, subgroup analysis revealed that a higher level of adiponectin was significantly associated with an increased CRC risk among overweight individuals (OR = 1.16; 95 % CI: 1.02, 1.32), and a decreased CRC risk among normal weight individuals (OR = 0.76; 95 % CI: 0.62, 0.92). Besides, a higher level of adiponectin was also significantly associated with a decreased risk of CRC in men (OR = 0.76; 95 % CI: 0.59, 0.98).
CONCLUSIONS: In conclusion, circulating leptin level was not associated with CRC risk, but that of adiponectin was associated with CRC risk only in specific subgroups.
METHODS: The Web of Science, Scopus, PubMed/Medline, Embase, and Google Scholar databases were searched for all available observational studies that reported the risk of venous thromboembolism (VTE) based on serum vitamin D levels categories. The search was performed up to March 2020.
RESULTS: Seven studies were included. The overall analysis showed a significantly increased risk of VTE in subjects with low levels of serum vitamin D compared with those with normal vitamin D levels (RR = 1.34; 95% CI: 1.07-1.69; P = 0.011). In a sensitivity analysis, we did not observe a significant effect of any individual study on the combined effect sizes. Nevertheless, significant heterogeneity was present among the studies (Cochrane Q test, p = 0.018, I2 = 61%). In the stratified analysis, low vitamin D levels were positively associated with an increased risk of VTE in prospective population-based studies (RR = 1.31; 95% CI: 1.06-1.61; P = 0.010) and in subjects below 60 years old (RR = 1.28; 95% CI: 1.07-1.54; P = 0.060).
CONCLUSION: our systematic review and meta-analysis showed that a low serum vitamin D level was indeed associated with an increased risk of VTE.
METHODS: Online literature search databases including Scopus, Web of Science, PubMed/Medline, Embase and Google Scholar were searched to discover relevant articles available up to 17 March 2020. We used mean changes and SD of the outcomes to assess treatment response from baseline and mean difference, and 95 % CI were calculated to combined data and assessment effect sizes in astaxanthin and control groups.
RESULTS: 14 eligible articles were included in the final quantitative analysis. Current study revealed that astaxanthin consumption was not associated with FBS, HbA1c, TC, LDL-C, TG, BMI, BW, DBP, and SBP. We did observe an overall increase in HDL-C (WMD: 1.473 mg/dl, 95 % CI: 0.319-2.627, p = 0.012). As for the levels of CRP, only when astaxanthin was administered (i) for relatively long periods (≥ 12 weeks) (WMD: -0.528 mg/l, 95 % CI: -0.990 to -0.066), and (ii) at high dose (> 12 mg/day) (WMD: -0.389 mg/dl, 95 % CI: -0.596 to -0.183), the levels of CRP would decrease.
CONCLUSION: In summary, our systematic review and meta-analysis revealed that astaxanthin consumption was associated with increase in HDL-C and decrease in CRP. Significant associations were not observed for other outcomes.
METHODS: A comprehensive systematic search was carried out in PubMed/MEDLINE, SCOPUS, Web of Science, and EMBASE databases for (nested) case-control studies that reported the levels of IGF-1 and IGFBP in GC cases and healthy controls, from inception until October 2020. Weighted mean difference (WMD) was calculated for estimating combined effect size. Subgroup analysis was performed to identify the source of heterogeneity among studies.
RESULTS: We found eight and five eligible studies (with 1541 participants) which provided data for IGF-1 and IGFBP, respectively. All studies on IGFBP reported the IGFBP-3 isoform. The pooled results indicate that GC patients had significantly lower serum IGF-1 [WMD = -26.21 ng/mL (95% CI, -45.58 to -6.85; P = .008)] and IGFBP-3 [WMD = -0.41 ng/mL (95% CI, -0.80 to -0.01; P = .04; I2 = 89.9%; P
METHODS: A comprehensive systematic search was performed in Scopus, EMBASE, Web of Science, and PubMed/MEDLINE, by investigators, from database inception until November 2019, without using any restrictions. Weighted mean difference (WMD) with the 95 % CI was used for assessing the effects of maternal vitamin D supplementation on 25(OH) D levels in infants.
RESULTS: Overall results from 14 studies revealed a non-significant effect of maternal vitamin D administration on the level of 25(OH) D in breastfeeding infants (WMD: -0.464 ng/mL, 95 % CI: -6.68 to 5.75, p = 0.884, I2 = 98 %). Subgroup analyses demonstrated that vitamin D supplementation dosage ≥2000 IU/day (WMD: 9 ng/mL, 95 % CI: 8.19, 9.82, I2 = 99 %) and intervention duration ≥20 weeks (WMD: 16.20 ng/mL, 95 % CI: 14.89, 17.50, I2 = 99 %) significantly increased 25(OH) D.
CONCLUSIONS: The main results indicate a non-significant increase in infant vitamin D following maternal vitamin D supplementation. Additionally, vitamin D supplementation dosage ≥2000 IU/day and intervention duration ≥20 weeks significantly increased infant 25(OH) D.
METHODS: This meta-analysis was performed based on the PRISMA recommendations. PubMed, Web of Science, Scopus, Embase, and Google Scholar databases were searched for all published observational studies that reported the risk of UTI based on BMI categories up to March 2020.
RESULTS: Fourteen (n = 14) articles comprising 19 studies in different populations met our inclusion criteria. The overall analysis showed a significant increased risk of UTI in subjects affected by obesity vs. individuals without obesity (RR = 1.45; 95% CI: 1.28 - 1.63; I2 = 94%), and a non-significant increased risk of UTI in subjects who were overweight (RR = 1.03; 95% CI: 0.98 - 1.10; I2 = 49.6%) and underweight (RR = 0.99; 95% CI: 0.81 - 21; I2 = 0.0%) when compared to subjects who had normal weight. In the stratified analysis, we showed that obesity increased the risk of UTI in females (RR = 1.63; 95% CI: 1.38 - 1.93) and in subjects below 60 years old (RR = 1.53; 95% CI: 1.33 - 1.75).
CONCLUSION: This systematic review and meta-analysis recognized a significant relationship between BMI and incidence of UTI in obese vs. non-obese subjects, as well as in females and in individuals below 60 years old.
METHODS: PubMed, Scopus, Web of Science, and Embase databases were systematically searched from their inceptions until 10 December 2019 for randomized controlled trials (RCTs) comparing individuals who underwent resistance training and control participants. We applied a random-effects model to calculate the weighted mean difference (WMD).
RESULTS: 33 trials reported IGF-1 level as an outcome measure. The pooled estimate demonstrated a significant increase in IGF-1 (WMD: 10.34 ng/ml, 95 % CI: 4.93, 15.74, p = 0.000, I2 = 90.3 %) after resistance training compared with the control group. Subgroup analysis demonstrated that the increase in IGF-1 levels following resistance training was only statistically significant in treatment duration ≤16 weeks (WMD: 8.04 ng/ml), participants aged more than 60 years old (WMD: 9.84 ng/ml); and in women (WMD: 17.27 ng/ml). Subsequent analysis of the relationship between participants' age with plasma IGF-1 alterations revealed a U shape correlation in non-liner dose response, in which resistance training resulted in a declined IGF-1 level up to 40 years of age. Beyond 40 years old, the IGF-1 level was increased following resistance training.
CONCLUSION: We have successfully demonstrated that resistance training was associated with an increased IGF-1 level among those who received the training for ≤16 weeks, among participants older than 60 years old, and among women. Further studies are warranted to clarify the mechanisms underlying the influence of resistance training on IGF-1.