To date, several systematic reviews and meta-analyses (SRMA) have investigated the effects of probiotics, but the certainty of the evidence for an effect on chemotherapy and radiotherapy-related diarrhoea has not been assessed. We conducted an overview of SRMA, searching MEDLINE, Scopus, and ISI Web of Science from inception up to February 2022. We summarised the findings of eligible SRMA. Subsequently, we included randomised clinical trials (RCT) from the SRMA in meta-analyses, using a quality effects model to calculate the OR and 95 % CI for each outcome. We used ‘A Measurement Tool to Assess Systematic Reviews’ and the Cochrane risk of bias tool to assess the methodological quality of the SRMA and their RCT, respectively. We used the ‘Grading of Recommendations Assessment, Development, and Evaluation’.We included thirteen SRMA, which reported pooled effect sizes for chemotherapy and radiotherapy-related diarrhoea based on a total of eighteen RCT. Our meta-analyses demonstrated statistically significant beneficial effects from probiotics on all outcomes, except stool consistency; diarrhoea (any grade) OR 0·35 (95 % CI 0·22, 0·54), grade ≥ 2 diarrhoea 0·43 (0·25, 0·74), grade ≥ 3 diarrhoea 0·30 (0·15, 0·59), use of medication 0·49 (0·27, 0·88), soft stool 1·10 (0·44, 2·76) and watery stool 0·52 (0·29, 1·29). Probiotics use can reduce the incidence of diarrhoea in cancer patients in chemotherapy and radiotherapy, but the certainty of evidence for significant outcomes was very low and low.

The current systematic review and meta-analysis were conducted to evaluate the effects of oral Mg supplementation on glycaemic control in type 2 diabetes mellitus (T2DM) patients. Related articles were found by searching the PubMed, SCOPUS, Embase and Web of Science databases (from inception to 30 February 2020). A one-stage robust error meta-regression model based on inverse variance weighted least squares regression and cluster robust error variances was used for the dose–response analysis between Mg supplementation and duration of intervention and glycaemic control factors. Eighteen eligible randomised clinical trials were included in our final analysis. The dose–response testing indicated that the estimated mean difference in HbA1c at 500 mg/d was −0·73 % (95 % CI: −1·25, −0·22) suggesting modest improvement in HbA1c with strong evidence (P value: 0·004). And in fasting blood sugar (FBS) at 360 mg/d was −7·11 mg/dl (95 % CI: −14·03, −0·19) suggesting minimal amelioration in FBS with weak evidence (P value: 0·092) against the model hypothesis at this sample size. The estimated mean difference in FBS and HbA1c at 24 weeks was −15·58 mg/dl (95 % CI: −24·67, −6·49) and −0·48 (95 % CI: −0·77, −0·19), respectively, suggesting modest improvement in FBS (P value: 0·034) and HbA1c (P value: 0·001) with strong evidence against the model hypothesis at this sample size. Oral Mg supplementation could have an effect on glycaemic control in T2DM patients. However, the clinical trials so far are not sufficient to make guidelines for clinical practice.

This randomised clinical trial aimed to evaluate the effect of a pro-breast-feeding (BF) and healthy complementary feeding intervention performed during infants’ first months of life on ultraprocessed food (UPF) consumption at 4–7 years. We enrolled 323 teenage mothers and their infants from South Brazil, 163 allocated to the intervention group and 160 to the control group. Intervention consisted of sessions on BF and healthy complementary feeding promotion and was carried out in the maternity ward and at home after delivery. Food consumption was assessed using three 24-h food recalls at child’s age of 4–7 years. Foods were classified according to NOVA classification. Dietary contribution of UPF was adjusted for intra-individual variability by the SPADE method and categorised into tertiles. We used Poisson regression models with robust variance, adjusted for confounders, to estimate the effect of the intervention and duration of BF on the risk of high consumption of UPF. Our final analysis included 194 children, with mean age of 6·1 (sd 0·5) years. Mean dietary contribution of UPF was 38 % in the intervention group and 42·7 % in the control group, from total daily intakes. Results adjusted for BF duration, propensity score, income and total energy content demonstrated that the intervention reduced the risk of high consumption of UPF by 35 % (relative risk 0·65, 95 % CI 0·43, 0·98). BF duration was not associated with UPF consumption. The intervention was effective in reducing the risk of high UPF consumption at the age of 4–7 years.

We investigated the effects of high-Ca fat-free milk phase (MD) (prescription of approximately 1500 mg of Ca/d) v. low-Ca phase (CD) (prescription of approximately 800 mg of Ca/d) in an energy-restricted diet on the metabolic syndrome (MetS) and cardiometabolic measures in individuals with type 2 diabetes mellitus (T2DM) and low habitual Ca consumption (<600 mg/d). In this randomised cross-over design, fourteen adults with T2DM (49·5 (sd 8·6) years, BMI 29·4 (sd 4·5) kg/m2) consumed either MD or CD for 12 weeks, with a washout of 18 weeks between phases. A breakfast shake containing 700 mg (MD) or 6·4 mg (CD) of Ca was consumed in the laboratory. In addition, energy-restricted diets were prescribed (800 mg of dietary Ca/d). Waist circumference (WC), fasting glucose, fasting TAG, systolic (SBP) and diastolic blood pressure (DBP), fasting total cholesterol, fasting LDL-cholesterol, fasting HDL-cholesterol, HDL:LDL ratio, HDL:TAG ratio and lipid accumulation product (LAP) index were assessed at baseline and after each phase. Ca consumption during the study was equivalent to 1200 mg/d during MD and 525 mg/d during CD. There was a greater reduction in WC, SBP, DBP and LAP index after MD compared with CD. HDL:LDL ratio increased and total cholesterol, LDL-cholesterol, SBP, DBP and LAP index decreased only in MD. The consumption of approximately 1200 mg of Ca/d (700 mg from fat-free milk+500mg from other dietary sources) associated with an energy-restricted diet decreased some of the MetS components and cardiometabolic measures in adults with T2DM.

The effects of ruminant (R) trans-fatty acids (TFA) on the risk of CVD are still under debate. It could be argued that the lack of the effect of R-TFA may be the result of the small amount of their intake. Taking into consideration the growing available data from intervention studies, we carried out a systematic review and meta-regression to assess the impact of R-TFA intake levels on changes in the total cholesterol: HDL-cholesterol (TC:HDL-C) ratio. A systematic review of the literature was conducted and thirteen randomised clinical trials were included, yielding a total of twenty-three independent experimental groups of subjects. A univariate random-effects meta-regression approach was used to quantify the relationship between the dose of R-TFA and changes in the TC:HDL-C ratio. To consider several potential modifiers such as subject and dietary characteristics, a multivariate regression analysis was performed. We found no relationship between R-TFA intake levels of up to 4·19 % of daily energy intake (EI) and changes in cardiovascular risk factors such as TC:HDL-C and LDL-cholesterol (LDL-C):HDL-C ratios. In addition, a multivariate regression analysis that included other dietary variables, as well as subject baseline characteristics, confirmed that doses of R-TFA did not significantly influence the changes in the lipid ratio. Our findings showed that doses of R-TFA did not influence the changes in the ratios of plasma TC:HDL-C and LDL-C:HDL-C. These data suggest that TFA from natural sources, at least at the current levels of intake and up to 4·19 % EI, have no adverse effects on these key CVD risk markers in healthy people.

The primary aim of the trial was to investigate the influence of menopause on the incorporation of marine n-3 PUFA into platelets and adipose tissue. A secondary aim was to evaluate whether marine n-3 PUFA may change levels of circulating oestrogens in women. Ninety-two pre- and postmenopausal women were randomly assigned to consume 2·2 g of marine n-3 PUFA or control oil daily for 12 weeks. Adipose tissue biopsies and blood samples were collected at baseline and after intervention. Eighty-nine women completed the study. Baseline contents of total marine n-3 PUFA and each of the major long-chained n-3 PUFA, EPA, docosapentaenoic acid and DHA were all significantly lower (P < 0·05) in the premenopausal group both in platelets and adipose tissue, except for EPA in platelets (P = 0·05). After supplementation with fish oil, the content of all marine n-3 PUFA increased significantly in platelets and adipose tissue in both pre- and postmenopausal women. The increase in platelets and adipose tissue was, however, the same in both groups. There was no effect of fish oil on oestrogen levels in postmenopausal women. We found a significant difference in premenopausal women, in whom oestradiol (P < 0·04) and oestrone (P < 0·02) serum concentrations increased after the fish oil supplement. This trial did not reveal any difference in the ability of pre- and postmenopausal women to incorporate marine n-3 PUFA into platelets or adipose tissue. However, supplementation with fish oil increased oestrogen levels in premenopausal women.

In vitro and in vivo studies have shown that punicic acid, a type of conjugated fatty acid and the main constituent of pomegranate seed oil (PSO), has anti-atherogenic effects. The present study aimed at determining the effect of PSO treatment on serum lipid profiles. This double-blind placebo-controlled randomised clinical trial included fifty-one hyperlipidaemic subjects, diagnosed according to National Cholesterol Education Program definition, and randomly assigned to the PSO and the control groups. The PSO and placebo groups received 400 mg PSO and placebo twice daily, respectively and were followed up for 4 weeks. Serum concentrations of lipids and lipoproteins were measured before and 4 weeks after intervention. Mean concentration of TAG and the TAG:HDL cholesterol (HDL-C) ratio were significantly decreased after 4 weeks in the PSO group as compared with baseline values (2·75 (sd 1·40) v. 3·45 (sd 1·56) mmol/l, P = 0·009 and 5·7 (sd 4·6) v. 7·5 (sd 5·0), P = 0·031, respectively). The treatment effect was statistically significant in the PSO group as compared with controls in diminution of cholesterol:HDL-C ratio (5·4 (sd 1·5) v. 5·9 (sd 1·4), P < 0·05) adjusted for baseline values. We found a mean difference for PSO v. placebo in HDL-C concentration (0·13 v. − 0·02 mmol/l) and cholesterol:HDL-C ratio ( − 0·42 v. 0·01, P < 0·05). Serum cholesterol, LDL cholesterol and glucose concentrations and body composition variables remained unchanged. It is concluded that administration of PSO for 4 weeks in hyperlipidaemic subjects had favourable effects on lipid profiles including TAG and TAG:HDL-C ratio.