Vitamins A and D capsules BPC 1973

IntroductionFish consumption contributes to overall nutrient intake and health, but its effects on micronutrient status remain uncertain. We conducted a systematic review and meta-analysis to assess the impact of fish consumption on the micronutrient status of children.MethodsThree databases were searched (April 2025) for studies comparing biomarker-based micronutrient status among children (2-14 years) with fish versus low or no fish intake. Risk of bias was assessed using RoB2, and findings were synthesized through meta- and narrative analyses with GRADE evaluation.ResultsSeven studies (six randomized controlled trials) met inclusion criteria, covering nine biomarkers, including 25(OH)D, urinary iodine concentration, ferritin, hemoglobin, retinol, beta-carotene, calcium, cobalamin, and folate. Three studies had low risk of bias, two moderate, and one high. Meta-analysis was possible only for vitamin D (25(OH)D, 1,074 participants), showing a pooled mean difference of 4.08 nmol/L (95% CI: 1.73-6.43) favoring fish consumption; sensitivity analysis (850 participants) yielded 3.46 nmol/L (95% CI: 1.03-5.65), with no heterogeneity. Results for other biomarkers were largely nonsignificant.ConclusionFish consumption modestly improves vitamin D status in children, though effects may lack clinical relevance. Evidence for other micronutrients is inconsistent, highlighting the need for more rigorous studies.

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BackgroundBronchopulmonary dysplasia (BPD) is a prevalent and severe chronic respiratory condition in preterm infants, with vitamin deficiency recognized as a contributing factor. Although vitamins A and D are known to play protective roles in lung development, the optimal supplementation doses for BPD prevention remain unclear.MethodsSearch PubMed, Ovid, the Cochrane Library, Web of Science, CNKI, and Wanfang from database inception to November 30, 2024, identifying randomized controlled trials that investigated the role of vitamins A and D in the prevention of BPD in preterm infants. Data were extracted for network meta-analysis. Patient demographic data, the incidence of BPD, mortality, and mechanical ventilation duration were analyzed.ResultsIn our analysis, encompassing 20 studies with 4357 patients, we observed that high-dose vitamin D (HDVD, ≥800 IU/d) demonstrated the most notable reduction in the incidence of BPD; low-dose vitamin A (LDVA, ConclusionCurrent scholarly literature suggests that HDVD (≥800 IU/d) supplementation may be the most effective regimen for preventing BPD in preterm infants, followed by LDVA (<3330 IU/d). No statistically significant differences in mortality were observed among any of the supplementation strategies or placebo. High-dose vitamin A (≥3330 IU/d) was associated with a shorter duration of mechanical ventilation. Consequently, to prevent BPD in preterm infants, supplementation with HDVD (≥800 IU/d) and LDVA (<3330 IU/d) may be considered.

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BackgroundFat-soluble vitamins A, D, E, and K are critical during the postpartum period for maternal recovery and infant development.ObjectivesTo determine the concentrations of vitamins A, D, E, and K in maternal serum and breastmilk during the early postpartum period in breastfeeding women.MethodsThis was a secondary analysis of the WellFed 4-wk randomized controlled trial. Dietary recalls, serum, and breastmilk samples were collected from breastfeeding women at 4 and 8 wk postpartum (n = 48). Vitamin status and metabolic biomarkers were quantified using liquid chromatography-tandem mass spectrometry and a clinical analyzer, respectively. Associations were analyzed using correlation, regression, and mediation analysis (PROCESS macro for SPSS; IBM Corp).ResultsMean daily intakes for vitamins A, D, and E were 1230 ± 633 μg, 6.5 ± 4.6 μg and 13.3 ± 8.1 mg, respectively. All women were sufficient in serum retinol (2.1 ± 0.4, 2.1 ± 0.3 μmol/L), α-tocopherol (45.5 ± 9.5, 39.3 ± 8.7 μmol/L), and phylloquinone (1.0 ± 0.5, 1.1 ± 0.7 nmol/L) at weeks 4 and 8, respectively. Sixty-five percent of the cohort were vitamin D sufficient (61.7 ± 22.2 nmol/L, 56.7 ± 19.2 nmol/L). Vitamin A intake was positively associated with serum retinol concentrations (r = 0.386, P = 0.012, adjusted P = 0.048). Breastmilk retinol (3.7 ± 1.2, 3.2 ± 1.1 μmol/L) and α-tocopherol (15.3 ± 7.4, 12.4 ± 5.1 μmol/L) concentrations were adequate at both timepoints, 25(OH)D2 and 25(OH)D3 were below the analytical detection limit. Serum and breastmilk α-tocopherol were correlated (r = 0.363, P = 0.013, adjusted P = 0.026). Total cholesterol, triglycerides, and CRP predicted up to 56% of serum α-tocopherol variance.ConclusionsMaternal serum concentrations of vitamins A, E, and K are adequate, whereas approximately two-thirds of women are vitamin D sufficient. Breastmilk vitamins A and E are adequate and higher than previously reported, whereas vitamin D metabolites are undetectable. Dietary intake is positively associated with serum vitamins A and D, whereas serum vitamin E is associated with lipid-related biomarkers and correlated with breastmilk α-tocopherol, highlighting a potential link between maternal metabolic health and vitamin E in breastmilk. This trial is registered at clinicaltrials.gov as NCT05924633 (https://clinicaltrials.gov/study/NCT05924633).

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IntroductionWhether retinoids and carotenoids impact on graft-versus-host disease (GVHD) following allogeneic stem cell transplantation (ASCT) is unknown.MethodsWe conducted a 1:1 randomized controlled trial with extracorporeal photopheresis for GVHD-prophylaxis as the intervention. The plasma levels of retinoids and carotenoids were determined at randomization and 3 months after ASCT.ResultsWe found no significant difference in GVHD occurrence and levels of retinoids between the intervention and control groups at either of the two time points.ConclusionWhether routine vitamin A supplementation is warranted for GVHD prevention, needs further study. Our exploratory study highlights the complex role of retinoid homeostasis in immune function during ASCT.Trial registrationClinicalTrials.gov identifier: NCT03204721.

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Purpose of reviewInherited retinal diseases (IRDs) are genetically and phenotypically heterogeneous disorders that cause progressive vision loss and lack broadly effective disease-modifying therapies. Increasing evidence implicates metabolic stress, oxidative injury, and photoreceptor-retinal pigment epithelium (RPE) dysfunction in IRD pathophysiology. This review evaluates the evidence and limitations surrounding nutritional and metabolic interventions for retinitis pigmentosa and Stargardt disease.A narrative review of preclinical studies, randomized controlled trials, and contemporary genetic re-analyses was performed. Nutritional interventions reviewed include vitamin A, vitamin E, N-acetylcysteine (NAC), omega-3 fatty acids (docosahexaenoic acid), carotenoids and apocarotenoids, and the deuterated vitamin A analog C20-D3-retinyl acetate (ALK-001).Recent findingsInitial studies suggesting a protective effect of vitamin A in retinitis pigmentosa were not confirmed in subsequent trials or genetic re-analyses, which identified baseline differences between groups as a possible contributor to the original findings. In contrast, supplemental vitamin E may accelerate disease progression. NAC demonstrated acceptable tolerability and modest short-term improvements in visual function in early-phase trials, with a phase 3 study ongoing. Omega-3 fatty acids, carotenoids, and apocarotenoids have not shown consistent clinically meaningful benefit in retinitis pigmentosa or Stargardt disease despite strong mechanistic rationale. In Stargardt disease, ALK-001 reduces lipofuscin accumulation in animal models and clinical trials are ongoing to assess efficacy in patients.SummaryMost nutritional supplements studied to date have not demonstrated durable or clinically meaningful benefit in IRDs. Vitamin A supplementation in retinitis pigmentosa is no longer supported by current evidence, while NAC remains a promising metabolic therapy under investigation. High-quality, genotype-informed clinical trials with clinically relevant endpoints are needed before nutritional interventions can be incorporated into IRD management guidelines.

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