scholarly journals Impact of Maternal Nutritional Supplementation during Pregnancy and Lactation on the Infant Gut or Breastmilk Microbiota: A Systematic Review

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1137
Author(s):  
Aneesa Z. Zaidi ◽  
Sophie E. Moore ◽  
Sandra G. Okala

Recent evidence indicates that maternal dietary intake, including dietary supplements, during pregnancy and lactation may alter the infant gut or breastmilk microbiota, with implications for health outcomes in both the mother and infant. To review the effects of maternal nutritional supplementation during pregnancy and lactation on the infant gut or breastmilk microbiota a systematic literature search was conducted. A total of 967 studies published until February 2020 were found, 31 were eligible and 29 randomized control trials were included in the qualitative synthesis. There were 23 studies that investigated the effects of probiotic supplementation, with the remaining studies investigating vitamin D, prebiotics or lipid-based nutrient supplements (LNS). The effects of maternal nutritional supplementation on the infant gut microbiota or breastmilk microbiota were examined in 21 and 12 studies, respectively. Maternal probiotic supplementation during pregnancy and lactation generally resulted in the probiotic colonization of the infant gut microbiota, and although most studies also reported alterations in the infant gut bacterial loads, there was limited evidence of effects on bacterial diversity. The data available show that maternal probiotic supplementation during pregnancy or lactation results in probiotic colonization of the breastmilk microbiota. There were no observed effects between probiotic supplementation and breastmilk bacterial counts of healthy women, however, administration of Lactobacillus probiotic to nursing women affected by mastitis was associated with significant reductions in breastmilk Staphylococcal loads. Maternal LNS supplementation during pregnancy and lactation increased bacterial diversity in the infant gut, whilst vitamin D and prebiotic supplementation did not alter either infant gut bacterial diversity or counts. Heterogeneity in study design precludes any firm conclusions on the effects of maternal nutritional supplementation during pregnancy and lactation on the infant gut or breastmilk microbiota, warranting further research.

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1675 ◽  
Author(s):  
Catharina Missailidis ◽  
Nikolaj Sørensen ◽  
Senait Ashenafi ◽  
Wondwossen Amogne ◽  
Endale Kassa ◽  
...  

Dysbiosis and a dysregulated gut immune barrier function contributes to chronic immune activation in HIV-1 infection. We investigated if nutritional supplementation with vitamin D and phenylbutyrate could improve gut-derived inflammation, selected microbial metabolites, and composition of the gut microbiota. Treatment-naïve HIV-1-infected individuals (n = 167) were included from a double-blind, randomized, and placebo-controlled trial of daily 5000 IU vitamin D and 500 mg phenylbutyrate for 16 weeks (Clinicaltrials.gov NCT01702974). Baseline and per-protocol plasma samples at week 16 were analysed for soluble CD14, the antimicrobial peptide LL-37, kynurenine/tryptophan-ratio, TMAO, choline, and betaine. Assessment of the gut microbiota involved 16S rRNA gene sequencing of colonic biopsies. Vitamin D + phenylbutyrate treatment significantly increased 25-hydroxyvitamin D levels (p < 0.001) but had no effects on sCD14, the kynurenine/tryptophan-ratio, TMAO, or choline levels. Subgroup-analyses of vitamin D insufficient subjects demonstrated a significant increase of LL-37 in the treatment group (p = 0.02), whereas treatment failed to significantly impact LL-37-levels in multiple regression analysis. Further, no effects on the microbiota was found in number of operational taxonomic units (p = 0.71), Shannon microbial diversity index (p = 0.82), or in principal component analyses (p = 0.83). Nutritional supplementation with vitamin D + phenylbutyrate did not modulate gut-derived inflammatory markers or microbial composition in treatment-naïve HIV-1 individuals with active viral replication.


2021 ◽  
Vol 22 (5) ◽  
pp. 2674
Author(s):  
Chien-Ning Hsu ◽  
Julie Y. H. Chan ◽  
Kay L. H. Wu ◽  
Hong-Ren Yu ◽  
Wei-Chia Lee ◽  
...  

Gut microbiota-derived metabolites, in particular short chain fatty acids (SCFAs) and their receptors, are linked to hypertension. Fructose and antibiotics are commonly used worldwide, and they have a negative impact on the gut microbiota. Our previous study revealed that maternal high-fructose (HF) diet-induced hypertension in adult offspring is relevant to altered gut microbiome and its metabolites. We, therefore, intended to examine whether minocycline administration during pregnancy and lactation may further affect blood pressure (BP) programmed by maternal HF intake via mediating gut microbiota and SCFAs. Pregnant Sprague-Dawley rats received a normal diet or diet containing 60% fructose throughout pregnancy and lactation periods. Additionally, pregnant dams received minocycline (50 mg/kg/day) via oral gavage or a vehicle during pregnancy and lactation periods. Four groups of male offspring were studied (n = 8 per group): normal diet (ND), high-fructose diet (HF), normal diet + minocycline (NDM), and HF + minocycline (HFM). Male offspring were killed at 12 weeks of age. We observed that the HF diet and minocycline administration, both individually and together, causes the elevation of BP in adult male offspring, while there is no synergistic effect between them. Four groups displayed distinct enterotypes. Minocycline treatment leads to an increase in the F/B ratio, but decreased abundance of genera Lactobacillus, Ruminococcus, and Odoribacter. Additionally, minocycline treatment decreases plasma acetic acid and butyric acid levels. Hypertension programmed by maternal HF diet plus minocycline exposure is related to the increased expression of several SCFA receptors. Moreover, minocycline- and HF-induced hypertension, individually or together, is associated with the aberrant activation of the renin–angiotensin system (RAS). Conclusively, our results provide a new insight into the support of gut microbiota and its metabolite SCAFs in the developmental programming of hypertension and cast new light on the role of RAS in this process, which will help prevent hypertension programmed by maternal high-fructose and antibiotic exposure.


2015 ◽  
Vol 21 (2) ◽  
pp. 283-290 ◽  
Author(s):  
Yin Bun Cheung ◽  
Ying Xu ◽  
Charles Mangani ◽  
Yue-Mei Fan ◽  
Kathryn G. Dewey ◽  
...  

2016 ◽  
Vol 3 (1) ◽  
pp. 5-13 ◽  
Author(s):  
A Dhungel ◽  
MS Alam

Background and Objectives: Pneumonia is the inflammation of parenchyma of lungs. It strictly represents any inflammatory condition that involves the lungs along with the visceral pleura, airways, alveoli, connective tissues and vascular structures. The objective of the study was to see the efficacy of vitamin D in children with pneumonia.Material and Methods: A randomized control study was conducted in Department of Pediatric Medicine, Mayo Hospital, Lahore, Pakistan. One hundred patients with pneumonia received vitamin D along with appropriate antibiotics and one hundred were treated with antibiotics but without vitamin D. The patients were discharged after the fast breathing and chest in drawing settled. The duration of hospital stay was noted. They were followed up for next 90 days after discharge from hospital and any new episode of pneumonia was noted and recorded.Results: The mean number of days to recovery were similar between the group receiving vitamin D (5.7 ± 2.7 days) and the group not receiving vitamin D (6.1 ± 2.8days), (p=0.28). While comparing repeat episode of pneumonia within next three months, the repeat episode of pneumonia was significantly lower in the intervention group (2%) than the group without supplementation (9%; p = 0.002) within 30 days of supplementation of vitamin D.Conclusion: Vitamin D supplementation in a single dose to the children diagnosed as pneumonia significantly reduces the occurrence of new episodes of pneumonia within one month of discharge.Janaki Medical College Journal of Medical Sciences (2015) Vol. 3 (1):5-13


2017 ◽  
Vol 28 (2) ◽  
pp. 135-143 ◽  
Author(s):  
Carina Venter ◽  
Kari R. Brown ◽  
Kate Maslin ◽  
Debra J. Palmer

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