Should Pregnant Women Consume Probiotics to Combat Endocrine-Disrupting Chemical-Induced Health Risks to Their Unborn Offspring?

Abstract

Endocrine-disrupting chemicals (EDCs) have become so pervasive in our environment and daily lives that it is impossible to avoid contact with such compounds, including pregnant women seeking to minimize exposures to themselves and their unborn children. Developmental exposure of humans and rodent models to bisphenol A (BPA) and other EDCs is linked to increased anxiogenic behaviors, learning and memory deficits, and decreased socio-sexual behaviors. Prenatal exposure to BPA and other EDCs leads to longstanding and harmful effects on gut microbiota with reductions in beneficial bacteria, i.e., gut dysbiosis, and such microbial changes are linked to host changes in fecal metabolites, including those involved in carbohydrate metabolism and synthesis, and neurobehavioral alterations in adulthood, in particular, social and cognitive deficits. Gut dysbiosis is increasingly being recognized as a key driver of a myriad of diseases, ranging from metabolic, cardiovascular, reproductive, and neurobehavioral disorders via the gut-microbiome-brain axis. Thus, EDCs might induce indirect effects on physical and mental health by acting as microbiome-disrupting chemicals. Findings raise the important question as to whether pregnant women should consume a probiotic supplement to mitigate pernicious effects of EDCs, especially BPA, on themselves and their unborn offspring. Current studies investigating the effects of maternal probiotic supplementation on pregnant women's health and that of their unborn offspring will be reviewed. Data will inform on the potential application of probiotic supplementation to reverse harmful effects of EDCs, especially BPA, in pregnant women unwittingly exposed to these compounds and striving to give their offspring the best start in life.

Keywords: DOHaD; bisphenol A; genistein; gestation; gut microbiota; in utero; microbiome; neurobehavioral disorders; xenoestrogens.

Figure 1

Hormonal and behavioral changes observed in germ-free (GF) mice that established the existence of a gut-microbiome–brain axis. GF mice must be raised in aseptic conditions to prevent exposure to microorganisms that might otherwise colonize the gut and other organ systems. The absence of gut bacteria results in profound changes in stress-hormone signaling pathways, morphological and gene-expression changes in the brain, altered responses to pathogenic organisms due to changes in microglial cells and increased blood–brain-barrier (BBB) permeability, and altered behavioral responses. This figure is from [94] and reproduced from permissions from Oxford University Press and Copyright Clearance Center, Inc.

Figure 2

Select mechanisms by which the gut microbiome may influence the brain and other organs, reproduced from [19]. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution, or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.

Figure 3

A mixOmics analysis approach to integrate, in this case, developmental exposure to genistein (GEN) vs. AIN (phytoestrogen-free diet) on gut microbiota changes with fecal metabolite and neurobehavioral changes in vocalizations and social behaviors. This integrative approach is one of the few that permits correlations between multiple omics approaches and phenotypic changes. Positive correlations are shown by the red lines linking specific categories together, whereas inverse or negative correlations between two categories are represented in blue. The correlation strength was set to 0.9, which is quite stringent [17]. This figure was reproduced with permissions from Copyright Clearance Center, Inc.

Figure 4

The triad relationship between developmental exposure to EDCs, such as BPA, gut-microbiome changes, and host genetic/epigenetic/phenotypic status. If individuals cannot eliminate exposure to EDCs and it is unrealistic to reverse direct effects of EDCs on our genetic, epigenetic, and disease status, then EDCs acting as microbiome-disrupting chemicals might provide an avenue to intervene and abate the harmful effects of EDCs.

Figure 5

Intervention mechanisms to modify gut microbiota and/or their products. In so doing, such approaches might be used to prevent/treat human diseases, including those originating due to early exposure to EDCs, such as BPA. This figure is from [100]. This publication is an open-access article distributed under the terms of the Creative Commons (CC BY) license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.