Publisher Health

When high blood pressure was induced in young mice, they had bone loss and osteoporosis-related bone damage comparable to older mice, according to new research presented today at the American Heart Association’s Hypertension Scientific Sessions 2022 conference, held Sept. 7-10, 2022, in San Diego. The meeting is a scientific exchange focused on recent advances in basic and clinical research on high blood pressure and its relationship to cardiac and kidney disease, stroke, obesity and genetics.
High blood pressure and osteoporosis are prevalent diseases, and people may have both at the same time. In this study, researchers examined inflammation associated with high blood pressure in mice and found it may be connected to osteoporosis.
“Bone marrow is where both new bone and new immune cells are produced. We suspect that more pro-inflammatory immune cells in the bone marrow may be leading to damage of the bone and making it weaker,” said lead study author Elizabeth Maria Hennen, a Ph.D.-candidate in biomedical engineering at Vanderbilt University in Nashville, Tennessee. “By understanding how hypertension contributes to osteoporosis, we may be able to reduce the risk of osteoporosis and better protect people later in life from having fragility fractures and a lower quality of life.”
In the study, researchers compared young mice with induced hypertension to older mice without hypertension to assess the potential relationship of hypertension to bone aging. The human age equivalent was about 20-30 years old for the young mice and about 47-56 years old for the older mice, Hennen said. A group of 12 young mice (4 months old) were given angiotensin II, a hormone that leads to high blood pressure. The young mice received 490 nanograms/kilogram of angiotensin II for six weeks. A group of 11 older mice (16 months old) also received 490 nanograms/kilogram of angiotensin II for six weeks. Two control groups of 13 young mice and 9 old mice received a buffer solution that did not include angiotensin II, and these mice did not develop high blood pressure.
After six weeks, researchers analyzed the bones of mice from all four groups using micro-computed tomography, an advanced imaging technique. Bone health was determined by strength and density of the bone. Mathematical algorithms were used to estimate the potential effects of hypertension and aging on the microstructure and strength of the bone in the mice.
When compared to the young mice without hypertension, the young mice with induced hypertension had a significant 24% reduction in bone volume fraction, an 18% reduction in the thickness of the sponge-like trabecular bone located at the end of long bones, such as femurs and the spinal column, and a 34% reduction in estimated failure force, which is the ability of bones to withstand different types of force.

If you spend 30 minutes less on social media every day and engage in physical activity instead, you do a lot to improve your mental health. This is shown in a study conducted by a team from the Mental Health Research and Treatment Center at Ruhr-Universität Bochum headed by assistant professor Dr. Julia Brailovskaia. Participants who followed this advice for two weeks felt happier, more satisfied, less stressed by the Covid-19 pandemic and less depressed than a control group. These effects lasted even six months after the study had ended. The researchers published their findings in the Journal of Public Health on Sept. 2, 2022.
The downside of social media
In times of lockdowns and contact restrictions due to the Covid-19 pandemic, social media channels like Instagram, TikTok, Facebook, Twitter and WhatsApp ensured that we still felt connected to other people. They distracted us from the stress brought about by the pandemic, which caused many people to experience anxiety, insecurities, and hopelessness. But social media consumption has also its drawbacks. Heavy use can lead to addictive behaviour that manifests itself in, for example, a close emotional bond to the social media. In addition, fake news and conspiracy theories can spread uncontrollably on social channels and trigger even more anxiety.
“Given that we don’t know for certain how long the coronavirus crisis will last, we wanted to know how to protect people’s mental health with services that are as free and low-threshold as possible,” explains Julia Brailovskaia. To find out whether the type and duration of social media use can contribute to this, she conducted an experimental study as part of her fellowship at the Center for Advanced Internet Studies (CAIS).
A two-week experiment
She and her team recruited a total of 642 volunteers, assigning them randomly to one of four groups of roughly equal size. The first group reduced the daily social media consumption by 30 minutes during an intervention period of two weeks. Since previous studies had shown that physical activity can increase well-being and reduce depressive symptoms, the second group increased the duration of physical activity by 30 minutes daily during this period, while continuing to use social media as usual. The third group combined both, reducing social media use and increasing physical activity. A control group didn’t change the behaviour during the intervention phase.
Before, during and up to six months after the two-week intervention phase, the participants responded to online surveys on the duration, intensity and emotional significance of their social media use, physical activity, their satisfaction with life, their subjective feeling of happiness, depressive symptoms, the psychological burden of the Covid-19 pandemic and their cigarette consumption.
Healthy and happy in the age of digitalisation
The findings clearly showed that both reducing the amount of time spent on social media each day and increasing physical activity have a positive impact on people’s well-being. And particularly the combination of the two interventions increases one’s satisfaction with life and subjective feeling of happiness and reduces depressive symptoms. The effects last for a long time: even six months after the two-week intervention phase had ended, participants in all three intervention groups spent less time on social media than before: namely about a half hour in the groups that had either reduced social media time or increased their daily exercise, and about three-quarters of an hour in the group that had combined both measures. Six months after the intervention, the combination group engaged one hour and 39 minutes more each week in physical activity than before the experiment. The positive influence on mental health continued throughout the entire follow-up period.
“This shows us how vital it is to reduce our availability online from time to time and to go back to our human roots,” concludes Julia Brailovskaia. “These measures can be easily implemented into one’s everyday life and they’re completely free — and, at the same time, they help us to stay happy and healthy in the digital age.”
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Materials provided by Ruhr-University Bochum. Original written by Meike Drießen; translated by Donata Zuber. Note: Content may be edited for style and length.

Detailed characterization of human pancreatic islets is key to elucidate the pathophysiology of all forms of diabetes mellitus, including its most common form known as type 2 diabetes (T2D). However, access to pancreatic islets is limited and pancreatic tissue for islet retrieval can be either obtained from cadaveric or brain-dead organ donors or from patients undergoing pancreatectomy, henceforth defined as living donors. Moreover, different protocols for procurement of islets substantially impact their molecular profiles and function. These factors coupled with heterogeneity among individuals result in analytical challenges to separate genuine disease pathology or differences between human donors from experimental noise. These and other topics are addressed in a new review article that a team of renowned experts, including Prof. Michele Solimena of the Paul Langerhans Institute Dresden, published in the journal Nature Metabolism.
Affecting >500 millions of people worldwide diabetes mellitus is a growing burden to the patients’ longevity and quality of life, as well as an increasing challenge to healthcare systems. The disease ultimately results from the inability of pancreatic islet beta cells to produce enough insulin to meet metabolic needs. Thus, the study of pancreatic islets is critical to find means to prevent the disease or treat the causes of beta cell failure. To this aim, multiple academic and commercial entities around the world provide human pancreatic islets for research, with increasing data characterizing this important mini organ for diabetes becoming available. However, critical questions remain about the significance and accuracy of the metabolic phenotyping of these donors and the modalities for islet collection and downstream analysis. “We wrote the article with the intention, to overview the status of the field, highlight the challenges and propose actions which could accelerate progress in the understanding of T2D and thus slow its pandemic spreading.,” says Prof. Michele Solimena, speaker of the Paul Langerhans Institute Dresden (PLID) of the German Center for Diabetes Research (DZD) and co-corresponding author together with Prof. Anna Gloyn of this perspective article.
Islets sources, their procurement and related limitations
“Human pancreatic islets can be obtained from various sources and both its source as well as the applied procurement technique have an impact on the information that can be obtained. While for example tissue samples from autopsy are useful for the histological study of islet cell morphology or morphometry, they lack functional data and provide only limited molecular information,” continues Prof. Michele Solimena. In recent years, most information on human islets and the insulin-producing beta cells within the islet has come either from islets isolated from brain-dead organ donors or, more recently, from surgical specimens of pancreatectomized patients. These living donors, most of whom have undergone a pancreatectomy due to pancreatic ductal adenocarcinoma, can be metabolically phenotyped prior to surgery, whilst their detailed family, clinical and pharmacological history, is available. Islets within the surgical specimens can then be retrieved by laser capture microdissection for multi-omics profiling and characterized regarding their physiology and morphological features in fresh tissue slices or fixed sections. Although data on clinical and family history of brain-dead donors is more limited, islets isolated from these donors remain of great importance for research. This approach involves the resection of the whole pancreatic gland, thereby enabling the enzymatic digestion and isolation of many islets, which could be then widely distributed to many laboratories for extensive imaging, functional, and -omics studies, also involving genetic and pharmacological perturbations.
Data Analysis, Integration and Federation — What about FAIRness?
Research on the physiology and pathophysiology of human islets continues to be of paramount importance. To increase the possibilities of uncovering causal mechanisms for T2D, and the potential to address them prior to disease onset, changes to current operational models are required. These include the availability of additional islet sources, more powerful and reliable technological platforms for the standardized generation of quantitative islet data as well as the implementation of more transparent and coordinated interaction models for the sharing of samples and the integration of datasets. “We believe that the FAIR principles, meaning Findability, Accessibility, Interoperability and Reusability are of tremendous importance for future studies,” explains Michele Solimena. Currently only few international teams have established independent biorepositories of multi-omic data on human islets and many other existing cohorts still fall short on these basic principles. “This is, in our opinion, an enormous loss to the field as individually these collections are underpowered for most analyses but collectively, they have the potential to make significant headway in understanding disease heterogeneity and diabetes pathogenesis,” so Solimena.
“With our perspective article, we aimed to shed light on the current scientific situation regarding the opportunities associated with the use of pancreatic islets for the understanding of T2D, but at the same time to keep in mind their limitations. The availability of additional islet sources, more powerful and reliable technological platforms for the standardized generation of quantitative islet data as well as the implementation of more transparent and coordinated interaction models for the sharing of samples and the integration of datasets offer new opportunities to uncover such causal mechanisms and tackle them even prior to disease onset. This is especially timely in view of the recent identification of different prediabetes and T2D clusters, which argue for a more precise molecular taxonomy, including that of the islets,” concludes Michele Solimena.

Monitoring of viruses in wastewater enables the course of a pandemic and its burdens on various parts of the health-care sector to be predicted, independently from official public testing capacity and scope for infection tracking. This has been established in a study from the University of Gothenburg.
The measurements and analyses of coronavirus levels in the wastewater of Gothenburg attracted a great deal of attention during the pandemic. The weekly reports have shown both how widespread SARS-CoV-2 infection is in the community and its distribution among variants of the virus.
Beginning in February 2020, the virus measurements taken in the monitoring rapidly became a useful indicator for forecasting load peaks in health care. High concentrations of SARS-CoV-2 in the wastewater were followed by rising numbers of people with COVID-19 needing hospitalization.
The association emerges with striking precision in the study now published in the scientific journal iScience. Each of the four pandemic waves in 2020-2022 exhibits a pattern in which, within a couple of weeks after SARS-CoV-2 peaked in the wastewater, a rise in the number of newly admitted hospital patients with COVID-19 ensued.
Increased pressure on 1177 Vårdguiden
The virus peaks in the wastewater were followed not only by heavier burdens on inpatient care, but also by predictable increases in pressure on the 1177 Vårdguiden e-service. One to two weeks after a wastewater virus peak, more calls were coming in about acute breathlessness in adults.

Researchers from the University of Missouri School of Medicine and MU Health Care have discovered how obstructive sleep apnea affects the gut microbiome in mice and how transplanting gut bacteria from sleep apnea affected mice can cause cardiovascular changes in the recipient mice.
Obstructive sleep apnea (OSA) is a chronic sleep condition affecting more than 1 billion people worldwide. Evidence suggests OSA can alter the gut microbiome and may promote OSA-associated comorbidities, including diabetes, hypertension, ischemic heart disease, and cognitive problems.
This study examined a group of mice given gut bacteria from mice exposed to conditions that mimic sleep apnea. The researchers compared cardiovascular outcomes in those mice to a separate group that was given bacteria from mice that weren’t exposed to apnea conditions. Over six weeks, the researchers monitored arterial blood pressure, coronary artery and aorta function along with blood analysis measuring a gut-derived metabolite known to promote hardening of the arteries.
“We discovered that the mice with transplanted gut bacteria from donors exposed to sleep apnea conditions experienced a blood pressure increase, higher harmful metabolite levels and impairments in aortic and coronary function,” said study co-author Mohammad Badran, PhD, assistant professor at MU’s Child Health Research Institute. “In other words, the changes in gut microbiome alone were sufficient to induce some of the changes in cardiovascular function that are characteristically seen in patient with OSA.”
The researchers also gave each group of mice a probiotic to see if beneficial gut bacteria would mitigate the damage caused to the cardiovascular system.
“Our results showed targeted probiotic supplementation exerts protective effects against cardiovascular disease for the mice that received transplanted gut bacteria, but we were surprised to learn that the benefit did not extend to the mice being directly exposed to apnea conditions,” said senior author David Gozal, MD, the Marie M. and Harry L. Smith Endowed Chair of Child Health at the MU School of Medicine. “These findings indicate probiotics alone are insufficient to protect against the many adverse effects induced by chronic sleep apnea, including inflammation, metabolic dysregulation and antioxidant imbalance, and that probiotics may need to be given in conjunction with the standard treatment of OSA which is CPAP to enhance the probiotic benefit.”
Gozal said this data shows that altered gut bacteria is one factor — but not the only one — responsible for modulating sleep apnea-induced cardiovascular disease. However, he said this study reveals that probiotics may be a promising therapy to mitigate the impact of sleep apnea on the cardiovascular system.
In addition to Gozal and Badran, the study authors include fellow MU School of Medicine collaborators Clementine Puech, PhD, postdoctoral fellow; Zachary McAdams, graduate student; and Abdelnaby Khalyfa, PhD, associate professor. Also contributing to the report was Aaron Ericsson, DVM, assistant professor of the MU College of Veterinary Medicine; and Shawn Bender, PhD, associate professor, Department of Biomedical Sciences.
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Materials provided by University of Missouri-Columbia. Note: Content may be edited for style and length.

Results of a small, but unique research study, led by researchers from the Seaver Autism Center for Research and Treatment at Mount Sinai and published online in Human Genetics and Genomic Advances, suggest that low-dose ketamine is generally safe, well-tolerated and effective to treat clinical symptoms in children diagnosed with ADNP syndrome (also known as Helsmoortel-VanDerAa syndrome), a rare neurodevelopmental disorder caused by mutations in the activity dependent neuroprotective protein (ADNP) gene.
The ADNP gene affects brain formation, development, and function, and the protein produced from it helps control the expression of other genes. ADNP mutations are one of the most common single-gene causes of autism. Ketamine was approved in the United States in 1970 and is used for anesthesia and pain management, and more recently as a treatment for depression. Studies in animal models suggest that low-dose ketamine may be neuroprotective and increase expression of the ADNP gene.
“We were intrigued by the preclinical evidence suggesting that low-dose ketamine may increase levels of the ADNP protein and compensate for its loss in ADNP syndrome, so we designed this study to evaluate the safety, tolerability, and behavioral outcomes of low-dose ketamine in children with the syndrome,” says Alexander Kolevzon, MD, Clinical Director of the Seaver Autism Center. “We also sought to explore the feasibility of using electrophysiological biomarkers and computerized eye-tracking to assess sensitivity to treatment.”
In order to evaluate the effect of ketamine, the Mount Sinai research team used a single-dose (0.5mg/kg), open-label design, with ketamine infused intravenously over 40 minutes. Ten children with ADNP syndrome, ages six to 12 years, were enrolled. They found ketamine was generally well-tolerated, and there were no serious adverse events. The most common adverse events were elation/silliness (50 percent), fatigue (40 percent), and increased aggression (40 percent). Using parent-report instruments to assess treatment effects, ketamine was associated with improvements in a wide array of domains, including social behavior, attention deficit and hyperactivity, restricted and repetitive behaviors, and sensory sensitivities, a week after administration.
Results from the clinician-rated assessments indicated improvement based on the Clinical Global Impression-Improvement scale, a seven-point scale commonly used by clinicians to assess how much a patient’s illness has improved or worsened relative to a baseline state at the beginning of an intervention. Importantly, results across clinician-rated and caregiver-rated assessments were largely consistent. The results also highlight the potential of assessing early changes in social attention with computerized eye-tracking and the electrophysiological measurement of a listening task known as auditory steady-state response.
“We are encouraged by these findings, which provide preliminary support for ketamine to help reduce negative effects of this devastating syndrome,” Dr. Kolevzon says. “Future studies using a placebo-controlled design and studying the effects of repeated dosing over a longer duration of time and in a larger cohort of participants are needed before ketamine is used clinically, but our study is a promising first step in that process.”
Ongoing studies are using RNA sequencing to measure change in ADNP expression and other genes, as well as DNA methylation analysis, which has been previously described as relevant in ADNP syndrome. DNA methylation regulates and silences the expression of genes and is vital for embryonic development. Increased occurrence of rare and extreme DNA methylation levels have been linked with neurodevelopmental disorders and congenital anomalies.

Seasonal changes in light — longer days in summer, shorter in winter — have long been associated with human behaviors, affecting everything from sleep and eating patterns to brain and hormonal activity. Seasonal affective disorder (SAD) is a prime example: A type of depression related to diminished exposure to natural sunlight, typically occurring during winter months and more often at higher latitudes when daylight hours are shortest.
Bright light therapy has proven an effective remedy for treating SAD, plus maladies such as non-seasonal major depression, postpartum depression and bipolar disorder, but how seasonal changes in day length and light exposure affect and alter the brain at the cellular and circuit levels has kept scientists largely in the dark.
In a new study, publishing September 2, 2022 in Science Advances, researchers at University of California San Diego School of Medicine used a mouse model to illuminate a process in which affected neurons switch expression of neurotransmitters in response to day length stimuli, triggering related behavioral changes.
The work was led by senior study author Davide Dulcis, PhD, associate professor in the Department of Psychiatry at UC San Diego School of Medicine and a member of the Center for Circadian Biology at UC San Diego.
Tucked within the hypothalamus of the human brain is a small structure called the suprachiasmatic nucleus (SCN), each consisting of approximately 20,000 neurons. (The average human brain contains roughly 86 billion neurons and another 85 billion non-neuronal cells.)
The SCN is the body’s timekeeper, regulating most circadian rhythms — physical, mental and behavioral changes that follow a 24-hour cycle and affect everything from metabolism and body temperature to when hormones are released. The SCN operates based on input from specialized photosensitive cells in retina, which communicate changes in light and day length to our body.
In the new study, Dulcis and colleagues describe how SCN neurons coordinate with each other to adapt to different lengths of daylight, changing at cellular and network levels. Specifically, they found that in mice, whose brains function similarly to humans, the neurons changed in mix and in expression of key neurotransmitters that, in turn, altered brain activity and subsequent daily behaviors.
Seasonal changes in light exposure have also been shown to alter the number of neurotransmitter-expressing neurons in the paraventricular nucleus (PVN), a region of the brain that plays essential roles in controlling stress, metabolism, growth, reproduction, immune and other autonomic functions.
“The most impressive new finding in this study is that we discovered how to artificially manipulate the activity of specific SCN neurons and successfully induce dopamine expression within the hypothalamic PVN network,” said Dulcis.
“We revealed novel molecular adaptations of the SCN-PVN network in response to day length in adjusting hypothalamic function and daily behavior,” added first author Alexandra Porcu, PhD, a member of Dulcis’ lab. “The multi-synaptic neurotransmitter switching we showed in this study might provide the anatomical/functional link mediating the seasonal changes in mood and the effects of light therapy.”
The authors suggest their findings provide a novel mechanism explaining how the brain adapts to seasonal changes in light exposure. And because the adaptation occurs within neurons exclusively located in the SCN, the latter represents a promising target for new treatments for disorders associated with seasonal changes in light exposure.
Co-authors include: Anna Nilsson, Sathwik Booreddy, Samuel A. Barnes and David K. Welsh, all at UC San Diego.
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Materials provided by University of California – San Diego. Original written by Scott LaFee. Note: Content may be edited for style and length.

Research led by Sanford Burnham Prebys professor Francesca Marassi, Ph.D., is helping to reveal the molecular secrets of macular degeneration, which causes almost 90% of all age-related vision loss. The study, published recently in the Biophysical Journal, describes the flexible structure of a key blood protein involved in macular degeneration and other age-related diseases, such as Alzheimer’s and atherosclerosis.
“Proteins in the blood are under constant and changing pressure because of the different ways blood flows throughout the body,” says Marassi. “For example, blood flows more slowly through small blood vessels in the eyes compared to larger arteries around the heart. Blood proteins need to be able to respond to these changes, and this study gives us fundamental truths about how they adapt to their environment, which is critical to targeting those proteins for future treatments.”
There are hundreds of proteins in our blood, but the researchers focused on vitronectin, one of the most abundant. In addition to circulating in high concentrations in the blood, vitronectin is found in the scaffolding between cells and is also an important component of cholesterol.
Vitronectin is a key player in many age-related diseases, but for Marassi’s team, the most promising target is macular degeneration, which affects as many as 11 million people in the United States. This number is expected to double by 2050.
“This protein is an important target for macular degeneration because it accumulates in the back of the eye, causing vision loss. Similar deposits appear in the brain in Alzheimer’s disease and in the arteries in atherosclerosis,” says Marassi. “We want to understand why this happens and leverage this knowledge to develop new treatments.”
To approach this question, the researchers were interested in learning how the protein changes its structure at different temperatures and under different levels of pressure, approximating what happens in the human body.
“Determining the structure of a protein is the most important part of determining its function,” adds Marassi. Through detailed biochemical analysis, the researchers found that the protein can subtly change its shape under pressure. These changes cause it to bond more easily to calcium ions in the blood, which the researchers suggest leads to the buildup of calcified plaque deposits characteristic of macular degeneration and other age-related diseases.
“It’s a very subtle rearrangement of the molecular structure, but it has a big impact on how the protein functions,” says Marassi. “The more we learn about the protein on a structural and mechanistic level, the better chance we have of successfully targeting it with treatments.”
These structural insights will streamline the development of treatments for macular degeneration because it will allow researchers and their partners in the biotech industry to custom-design antibodies that selectively block the protein’s calcium binding without disrupting its other important functions in the body.
“It will take some time to convert it into a clinical treatment, but we hope to have a working antibody as a potential treatment in a few years’ time,” says Marassi. “And since this protein is so abundant in the blood, there may be other exciting applications for this new knowledge that we don’t even know about yet.”
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Materials provided by Sanford Burnham Prebys. Note: Content may be edited for style and length.

Key studies in the last decade have shown that the gut microbiome, the collection of hundreds of bacterial species that live in the human digestive system, influences neural development, response to cancer immunotherapies, and other aspects of health. But these communities are complex and without systematic ways to study the constituents, the exact cells and molecules linked with certain diseases remain a mystery.
Stanford University researchers have built the most complex and well-defined synthetic microbiome, creating a community of over 100 bacterial species that was successfully transplanted into mice. The ability to add, remove, and edit individual species will allow scientists to better understand the links between the microbiome and health, and eventually develop first-in-class microbiome therapies.
Many key microbiome studies have been done using fecal transplants, which introduce the entire, natural microbiome from one organism to another. While scientists routinely silence a gene or remove a protein from a specific cell or even an entire mouse, there is no such set of tools to remove or modify one species among the hundreds in a given fecal sample.
“So much of what we know about biology, we wouldn’t know if it weren’t for the ability to manipulate complex biological systems piecewise,” said Michael Fischbach, Institute Scholar at Sarafan ChEM-H and corresponding author on the study, published in Cell on Sept. 6.
Fischbach, who is an associate professor of bioengineering and of microbiology and immunology, and others saw one solution: Build a microbiome from scratch by growing individually and then mixing its constituent bacteria.
Building the ark
Each cell in the microbiome occupies a specific functional niche, performing reactions that break down and build up molecules. To build a microbiome, the team had to ensure that the final mixture was not only stable, maintaining a balance without any single species overpowering the rest, but also functional, performing all the actions of a complete, natural microbiome. Selecting species to include in their synthetic community was also difficult given the natural variation across individuals; two people selected at random share less than half of their microbial genes.

Pregnant people who had bigger fluctuations in stress from one moment to the next — also called lability — had infants with more fear, sadness and distress at three months old than mothers with less stress variability, reports a new Northwestern University study that examined how a child’s developmental trajectory begins even before birth.
Prior research has found that mothers’ distress during pregnancy has been related to infant temperament and behavior, but this is one of the first studies to measure mothers’ experience of stress in real time on many occasions, which enables a closer look at whether changes in mothers’ stress across pregnancy matter for infant development.
The study will be published Sept. 7 in the journal Infancy.
“Research often examines stress as a static, unchanging construct — one that is either high or low, present or absent — but most of us have a lot of ebbs and flows in our stress depending on what is going on around us,” said lead study author Leigha MacNeill, research assistant professor of medical social sciences at Northwestern University Feinberg School of Medicine and a member of the Northwestern Institute for Innovations in Developmental Sciences (DevSci).
“That variability is inherent in our daily lives, so this lability is capturing an important aspect of stress and offers insight into how to measure stress going forward. This is of particular importance as we work to closely capture the maternal-fetal environment as it relates to how babies develop over time.”
For instance, one mother who has consistent levels of stress over pregnancy and another mother who moves between very low and very high levels of stress over pregnancy may in the end have a similar average level of stress across that time, but that average may not best capture meaningful differences in what the fetus is exposed to, MacNeill explained.