Periconceptional influences on offspring sex ratio and placental responses

Rosenfeld, Cheryl S.

doi:10.1071/rd11906

Cited by 30 publications

(23 citation statements)

References 117 publications

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“…It is also thought of as the primary organ to buffer the fetus against environmental insults (Rosenfeld, 2011). While initial doubts were cast on whether the microbiome identified truly originated from the fetal placenta (Kliman, 2014), subsequent work by the original and other groups supports this pioneering finding.…”

Section: Other Microbiomesmentioning

confidence: 50%

Microbiome Disturbances and Autism Spectrum Disorders

2015

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Autism spectrum disorders (ASDs) are considered a heterogenous set of neurobehavioral diseases, with the rates of diagnosis dramatically increasing in the past few decades. As genetics alone does not explain the underlying cause in many cases, attention has turned to environmental factors as potential etiological agents. Gastrointestinal disorders are a common comorbidity in ASD patients. It was thus hypothesized that a gut-brain link may account for some autistic cases. With the characterization of the human microbiome, this concept has been expanded to include the microbiota-gut-brain axis. There are mounting reports in animal models and human epidemiologic studies linking disruptive alterations in the gut microbiota or dysbiosis and ASD symptomology. In this review, we will explore the current evidence that gut dysbiosis in animal models and ASD patients correlates with disease risk and severity. The studies to date have surveyed how gut microbiome changes may affect these neurobehavioral disorders. However, we harbor other microbiomes in the body that might impact brain function. We will consider microbial colonies residing in the oral cavity, vagina, and the most recently discovered one in the placenta. Based on the premise that gut microbiota alterations may be causative agents in ASD, several therapeutic options have been tested, such as diet modulations, prebiotics, probiotics, synbiotics, postbiotics, antibiotics, fecal transplantation, and activated charcoal. The potential benefits of these therapies will be considered. Finally, the possible mechanisms by which changes in the gut bacterial communities may result in ASD and related neurobehavioral disorders will be examined.

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Section: Other Microbiomesmentioning

confidence: 50%

Microbiome Disturbances and Autism Spectrum Disorders

2015

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“…In animal studies maternal nutrition at the time of conception is observed to influence gender specific survival of fetuses, with a relative excess of male offspring born at times of nutritional plenty [38]. In humans however this phenomenon is debated [39,40].…”

Section: Discussionmentioning

confidence: 99%

Chorionic plate arterial function is altered in maternal obesity

et al. 2013

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ObjectivesTo characterise Chorionic Plate Artery (CPA) function in maternal obesity, and investigate whether leptin exposure reproduces the obese CPA phenotype in normal-BMI women.Study designCPA responses to the thromboxane-A2 mimetic U46619 (pre/post leptin incubation), to the nitric oxide donor sodium nitroprusside (SNP) and the occurrence of tone oscillations (pre/post leptin incubation) were assessed in 46 term placentas from women of normal (18.5–24.9) or obese (>30) Body Mass Index (BMI).Outcome measuresArea Under the dose response Curve (AUC), maximum response (Vmax), sensitivity (EC50) to U46619 (pre/post leptin) and SNP; average vessel tone, oscillation amplitude and frequency (pre/post leptin).ResultsU46619 vasoconstriction was similar between BMI categories (p > 0.05), however vasodilatation to SNP was reduced in obesity (AUC p = 0.02, Vmaxp = 0.04) compared to normal-BMI women. Leptin incubation altered responses to U46619 in both normal-BMI (EC50 at 100 ng/ml leptin; p < 0.05) and obese women (AUC at 50 ng/ml; p < 0.05) but vasomotion was unaffected (p > 0.05).ConclusionsMaternal obesity is associated with altered placental vascular function which may adversely affect placental oxygen and nutrient transport, placing the fetus at risk. Leptin incubation altered CPA vascular function but did not reproduce the obese phenotype.

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“…Biological mechanisms underlying offspring sex is not settled 32 . High caloric intake is known to skew offspring sex ratio towards males in mice, cows and horses 33–35 .…”

Section: Discussionmentioning

confidence: 99%

Offspring sex and parental health and mortality

Næss

Mortensen

Vikanes

et al. 2017

Sci Rep

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Increased mortality has been observed in mothers and fathers with male offspring but little is known regarding specific diseases. In a register linkage we linked women born 1925–1954 having survived to age 50 (n = 661,031) to offspring and fathers (n = 691,124). Three approaches were used: 1) number of total boy and girl offspring, 2) sex of the first and second offspring and 3) proportion of boys to total number of offspring. A sub-cohort (n = 50,736 mothers, n = 44,794 fathers) from survey data was analysed for risk factors. Mothers had increased risk of total and cardiovascular mortality that was consistent across approaches: cardiovascular mortality of 1.07 (95% CI: 1.03–1.11) per boy (approach 2), 1.04 (1.01–1.07) if the first offspring was a boy, and 1.06 (1.01–1.10) if the first two offspring were boys (approach 3). We found that sex of offspring was not associated with total or cardiovascular mortality in fathers. For other diseases or risk factors no robust associations were seen in mothers or fathers. Increased cardiovascular risk in mothers having male offspring suggests a maternal disease specific mechanism. The lack of consistent associations on measured risk factors could suggest other biological pathways than those studied play a role in generating this additional cardiovascular risk.

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Periconceptional influences on offspring sex ratio and placental responses

Cited by 30 publications

References 117 publications

Microbiome Disturbances and Autism Spectrum Disorders

Microbiome Disturbances and Autism Spectrum Disorders

Chorionic plate arterial function is altered in maternal obesity

Offspring sex and parental health and mortality

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