Publisher Health

Obesity afflicts approximately 42 percent of the U.S. adult population and contributes to the onset of chronic diseases, including diabetes, cancer, and other conditions. While popular healthy diet mantras advise against midnight snacking, few studies have comprehensively investigated the simultaneous effects of late eating on the three main players in body weight regulation and thus obesity risk: regulation of calorie intake, the number of calories you burn, and molecular changes in fat tissue. A new study by investigators from Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system, found that when we eat significantly impacts our energy expenditure, appetite, and molecular pathways in adipose tissue. Their results are published in Cell Metabolism.
“We wanted to test the mechanisms that may explain why late eating increases obesity risk,” explained senior author Frank A. J. L. Scheer, PhD, Director of the Medical Chronobiology Program in the Brigham’s Division of Sleep and Circadian Disorders. “Previous research by us and others had shown that late eating is associated with increased obesity risk, increased body fat, and impaired weight loss success. We wanted to understand why.”
“In this study, we asked, ‘Does the time that we eat matter when everything else is kept consistent?'” said first author Nina Vujovic, PhD, a researcher in the Medical Chronobiology Program in the Brigham’s Division of Sleep and Circadian Disorders. “And we found that eating four hours later makes a significant difference for our hunger levels, the way we burn calories after we eat, and the way we store fat.”
Vujovic, Scheer and their team studied 16 patients with a body mass index (BMI) in the overweight or obese range. Each participant completed two laboratory protocols: one with a strictly scheduled early meal schedule, and the other with the exact same meals, each scheduled about four hours later in the day. In the last two to three weeks before starting each of the in-laboratory protocols, participants maintained fixed sleep and wake schedules, and in the final three days before entering the laboratory, they strictly followed identical diets and meal schedules at home. In the lab, participants regularly documented their hunger and appetite, provided frequent small blood samples throughout the day, and had their body temperature and energy expenditure measured. To measure how eating time affected molecular pathways involved in adipogenesis, or how the body stores fat, investigators collected biopsies of adipose tissue from a subset of participants during laboratory testing in both the early and late eating protocols, to enable comparison of gene expression patterns/levels between these two eating conditions.
Results revealed that eating later had profound effects on hunger and appetite-regulating hormones leptin and ghrelin, which influence our drive to eat. Specifically, levels of the hormone leptin, which signals satiety, were decreased across the 24 hours in the late eating condition compared to the early eating conditions. When participants ate later, they also burned calories at a slower rate and exhibited adipose tissue gene expression towards increased adipogenesis and decreased lipolysis, which promote fat growth. Notably, these findings convey converging physiological and molecular mechanisms underlying the correlation between late eating and increased obesity risk.
Vujovic explains that these findings are not only consistent with a large body of research suggesting that eating later may increase one’s likelihood of developing obesity, but they shed new light on how this might occur. By using a randomized crossover study, and tightly controlling for behavioral and environmental factors such as physical activity, posture, sleep, and light exposure, investigators were able to detect changes the different control systems involved in energy balance, a marker of how our bodies use the food we consume.
In future studies, Scheer’s team aims to recruit more women to increase the generalizability of their findings to a broader population. While this study cohort included only five female participants, the study was set up to control for menstrual phase, reducing confounding but making recruiting women more difficult. Going forward, Scheer and Vujovic are also interested in better understanding the effects of the relationship between meal time and bedtime on energy balance.
“This study shows the impact of late versus early eating. Here, we isolated these effects by controlling for confounding variables like caloric intake, physical activity, sleep, and light exposure, but in real life, many of these factors may themselves be influenced by meal timing,” said Scheer. “In larger scale studies, where tight control of all these factors is not feasible, we must at least consider how other behavioral and environmental variables alter these biological pathways underlying obesity risk. ”
Disclosures:
During the execution of this project, Scheer received lecture fees from Bayer HealthCare, Sentara HealthCare, Philips, Vanda Pharmaceuticals, and Pfizer Pharmaceuticals; received consulting fees from the University of Alabama at Birmingham; and served on the Board of Directors for the Sleep Research Society. Scheer’s interests were reviewed and managed by Brigham and Women’s Hospital and Partners HealthCare in accordance with their conflict of interest policies. None of these are related to the current work. Vujovic has been compensated for consulting services provided to the Novartis Institutes of Biomedical Research, also unrelated to the current work.

The hepatitis B virus (HBV) is responsible for one of the most serious and common infectious diseases. Transmitted through biological fluids, it attacks the liver cells. The chronic form of the disease can lead to serious complications, including cirrhosis and liver cancer. There is no effective treatment for the chronic form of the disease, which can only be prevented by vaccination. After identifying a key protein complex that is active when our body is infected by the virus, a team from the University of Geneva (UNIGE) has deciphered the precise functioning of this protective mechanism, opening the way to new therapeutic targets. These results can be read in the journal Nature Structural and Molecular Biology.
Hepatitis B is the most common form of hepatitis. It is a viral disease caused by the hepatitis B virus. It is mainly blood or sexually transmitted. It is up to 100 times more contagious than HIV. By infecting the liver cells, this virus causes a transitory inflammation of this organ that can also evolve towards a chronic infection. This can then lead to serious pathologies, such as cirrhosis or liver cancer. It is estimated that nearly one million people die each year from this disease worldwide. There is no definitive treatment for chronic hepatitis B. The only way to prevent it is to be vaccinated before the disease appears.
In 2016, a UNIGE team led by Michel Strubin, an associate professor in the Department of Microbiology and Molecular Medicine and in the Geneva Centre for Inflammation Research at the UNIGE Faculty of Medicine, revealed a mechanism that is crucial for understanding this disease: when our immune system defends itself against it, a complex — i.e. an interdependent set — of six proteins called SMC5/6, present in our cells, detects the viral DNA and blocks it. The virus then strikes back and produces a specific protein, the X protein. This protein enters the cell and degrades SMC5/6, which is no longer able to play its sentinel role.
A three-step mechanism
Before this discovery, the antiviral function of SMC5/6 was unknown. It was only identified as a key complex for the structural maintenance of our chromosomes. Today, Michel Strubin’s team has made a new breakthrough. In a recent study, conducted in collaboration with the American pharmaceutical company Gilead Sciences, the UNIGE researchers identified the three steps and the specific proteins required for SMC5/6 to play its antiviral role.
”In the first step, a protein of the SMC5/6 complex detects the virus’ DNA and traps it”, explains Fabien Abdul, a senior research and teaching assistant in the Department of Microbiology and Molecular Medicine at the UNIGE Faculty of Medicine and first author of the study. ”Then, a second protein of the complex — SLF2 — takes the trapped DNA of the virus into a sub-compartment of the nucleus of the attacked cell, called the PML body. A third protein — Nse2 — then comes into play and inhibits the virus’ chromosome.”
As SMC is a large family of protein complexes, the researchers also wanted to know whether other ‘members’ of this family were able to bind to hepatitis B viral DNA. ”We discovered that this competence was unique to SMC5/6”, says Fabien Abdul.
Towards new therapeutic targets
To achieve these results, the research team worked on in vitro cell cultures. ”We used molecular biology techniques and more specifically genetic scissors called CRISPR-Cas9. This tool allowed us to cut the DNA strands within the cells and thus delete or modify the gene coding for each protein constituting the SMC5/6 complex. Thanks to this technique, we were able to make one or other of the proteins disappear and thus understand their respective functions within the complex”, explains Michel Strubin, the study’s last author. Based on these observations, the three steps of the antiviral mechanism could be established.
This discovery provides a better understanding of how the complex functions during its antiviral action. It could thus pave the way for the identification of new therapeutic targets to combat the hepatitis B virus. ”The next stage of research will consist of better deciphering the mechanism of inhibition of the virus in the sub-compartment of the cell nucleus”, indicates Aurélie Diman, a postdoctoral researcher in Michel Strubin’s laboratory. Work will also have to be carried out on the X protein, whose role was identified by the UNIGE researchers in 2016, in order to better understand the counter-attack mechanism of hepatitis B against the antiviral activity of the cellular SMC5/6.
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Approximately 90% of cancer-related deaths are due to metastasis when cancer spreads and forms new tumors. The liver is considered the most vulnerable organ to metastatic cancer: the 5-year survival rate after surgery to remove liver metastases is as low as 30-50%, so developing treatments to prevent liver metastasis is urgently needed.
A group of researchers including graduate student Truong Huu Hoang and Professor Norifumi Kadawa from the Osaka Metropolitan University Graduate School of Medicine, and Associate Professor Misako Matsubara from the Graduate School of Veterinary Science, has identified an alternative pathway for liver metastasis, showing that cancer cells invade via intracellular gap formation in endothelial cells, and clarified the molecular mechanism involved. The results of their research are expected to lead to the development of drugs to prevent and treat metastatic liver cancer.
Metastasizing cancer cells are known to change the microenvironment of liver cells in ways that promote metastasis, but the extent of these interactions has not been fully investigated. Cancer cells carried in the bloodstream come into contact with liver sinusoidal endothelial cells (LSECs), which line the blood vessels of the liver to form a protective barrier. LSECs are responsible for the detoxification functions of the liver and have numerous small pores, through which the liquid components of blood and small particles — but not cancer cells — can enter the liver. LSECs are constantly exposed to toxic substances carried by the blood that can disrupt these small pores under stressful conditions; this causes larger intracellular gaps to form in the LSECs, weakening the protective barrier. This led the research group to consider that the LSECs’ intracellular gaps may be involved in liver metastasis.
The research group created a mouse model of liver metastasis — by injecting cancer cells into the spleen — and performed omics analysis to observe changes in the LSECs. They found that when cancer cells moved from the spleen to the liver, they induced the LSECs to produce multiple proteins. The expression of one of these proteins — matrix metalloproteinase 9 (MMP9) — in LSECs caused the intracellular gaps to form.
Furthermore, using electron microscopy and 3D tomography reconstruction, the researchers showed that cancer cells extended their projections directly into the intracellular gaps of LSECs, allowing them to infiltrate the liver tissue. They found a positive correlation between the number of intracellular gaps in the LSECs and the number of new metastatic liver tumors that formed in the mice. However, new tumors could be prevented from forming by treating the mice with a MMP9 inhibitor, suggesting that MMP9 is a promising therapeutic target to prevent liver metastasis.
Professor Matsubara concluded, “In this study, we discovered a new phenomenon related to metastasis: cancer cells induce LSEC intracellular gap formation and infiltrate the liver through those gaps. With these results we are continuing our research to develop new treatments for liver metastasis, targeting intracellular gap formation in LSECs.”
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Children and young adults* with Down Syndrome are four times more likely to be diagnosed with diabetes, according to new research led by Queen Mary University of London and King’s College London.
The study, published in Diabetes Care, examined just under 10,000 people with Down Syndrome and nearly 40,000 without. The population-based study was created using data across three decades (from 1990 to 2020) from the UK Clinical Practice Research Datalink — one of the most populated databases.
It is the first time that the researchers have looked at the incidence of diabetes and obesity in Down Syndrome across the life span in one of the biggest Down Syndrome cohorts in the world.
Researchers found that children aged five-14 with Down Syndrome have a 10 times greater chance of having type 2 diabetes than children without the condition. It suggests that annual health checks for children with Down Syndrome need to more closely monitor for excess weight, obesity and early signs of diabetes to help catch diabetes as early as possible, given how susceptible this group is and the complications it can bring in later life.
While the study found that people with Down Syndrome are typically diagnosed with diabetes much earlier — the average age of diagnosis for someone with Down Syndrome was 38 years old, compared to 53 in those without Down Syndrome — the heightened risk for those far younger than this underlines the importance of vigilant, early-stage monitoring.
Genetics and excess bodyweight are thought to be the primary reasons behind this. People with Down Syndrome were found to have a higher Body Mass Index and reach its peak at an earlier age, which means a greater risk of type 2 diabetes at a younger age. There is also an increased risk of type 1 diabetes due to extra chromosomes and issues with the immune system in those with Down Syndrome.
Dr Li Chan, senior author, Reader in Molecular Endocrinology and Metabolism and Consultant Paediatric Endocrinologist at Queen Mary University of London said: “This study highlights the importance of early screening for diabetes and weight issues in people with Down Syndrome, especially children and young adults.”
“Currently there is a sizeable gap in research into the condition, which affects around 40,000 people in the UK. To help plug this gap in knowledge, we are conducting further research into how genetics affects a person with Down Syndrome’s predisposition to diabetes and obesity, and hope to shed further light on this important medical issue.”
Professor Andre Strydom, corresponding author, Professor in Intellectual Disabilities at King’s College London said: “This is the largest study ever conducted in Down Syndrome patients to show that they have unique needs with regards to diabetes and obesity, and that screening and intervention- including a healthy diet and physical activity — at younger ages is required compared to the general population.
“The results will help to inform the work of NHSE’s LeDeR programme to reduce inequalities and premature mortality in people with Down Syndrome and learning disabilities.”
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The Finnish Retirement and Aging study FIREA of the University of Turku used accelerometers to study how the 24-hour movement behaviours, i.e. sleep, sedentary behaviour, light physical activity and moderate-to-vigorous physical activity change in relation to each other when a person retires. The results show an increase in the amount of sleep, which contributed to decreased amount of physical activity.
The 24-hour activity behaviours can be divided into different sections, such as sleeping, sedentary time, light physical activity and moderate-to-vigorous physical activity. Increasing the time spent on one section will inevitably lead to a decrease in at least one other section, as there is a limited number of hours in a day. The study conducted at the University of Turku, Finland, used sensitive accelerometers and Compositional Data Analysis as the statistical method to study the simultaneous changes in these daily behaviours.
When studying people who retired from manual work or the service industry, the amount of sleep and sedentary behaviour increased in relation to physical activity. This change was stronger in women than in men. As for people who had retired from non-manual work, the proportion of sleep increased in relation to physical activity and sedentary time. Moderate-to-vigorous physical activity decreased more than light physical activity.
“The decrease in the amount of physical activity is probably explained by the absence of activity related to work duties and commute to and from work when a person retires. These are replaced to some extent by sleep and, in the case manual workers, also sedentary time,” says primary author of the research article, Postdoctoral Researcher Kristin Suorsa.
More moderate-to-vigorous activity to retirement days
Previous research shows that replacing moderate-to-vigorous physical activity with any other movement behaviour predisposes people to cardiovascular diseases and type 2 diabetes.
“Based on our research, people who are retiring should aim to increase the amount of physical activity, particularly moderate-to-vigorous activity. At the same time, long periods of sedentary time should be avoided and sitting should be divided into shorter periods with frequent walking breaks,” says Suorsa.
The FIREA study has compiled tips for more active retirements days on a video: https://youtu.be/ymaMMwre5ek.
The Finnish Retirement and Aging study (FIREA) was commenced at the University of Turku in 2013, and its main goal is to investigate the changes in living habits, health and functional capacity as well as the factors affecting them in the age of retirement. The study is led by Professor of Public Health and Epidemiology Sari Stenholm.
The results are based on a population of 551 people working in the municipal sector who used a wrist-worn accelerometer around the clock for a week at the same time of the year before and after they retired. The accelerometer measures acceleration and allows the researchers to measure daily sleep, sedentary time, and physical activity. The FIREA study is funded by the Academy of Finland, the Ministry of Education and Culture, and the Juho Vainio Foundation.
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The kidneys are often the unsung heroes in maintaining healthy blood pressure, filtering 180 liters of fluid and a pound of salt every day to keep levels in check. But new research by University of Pittsburgh geneticists and nephrologists shows that, surprisingly, a cellular channel outside the kidneys is doing some of the heavy lifting when it comes to keeping blood pressure under control.
The finding, reported today in the American Heart Association journal Hypertension, points to a promising new target for clinical trials to test existing medications for their potential to lower blood pressure.
“Our findings were entirely unexpected,” said Brandon Michael Blobner, Ph.D., who did the research as part of his doctoral dissertation at Pitt and is now a bioinformatics scientist at BlueSphere Bio in Pittsburgh. “Previously there had been some hints that mutations to salt-processing channels outside the kidneys affected blood pressure, but it would have been impossible to confirm the mechanism without the massive genetics databases that we had access to through cross-disciplinary partnerships.”
Nearly half of U.S. adults have high blood pressure, or hypertension, which is associated with chronic kidney disease and stroke, and it disproportionately affects Black individuals. Only 1 in 4 people have their high blood pressure under control, making it one of the nation’s biggest public health problems, according to the U.S. Centers for Disease Control and Prevention.
High blood pressure is caused, in part, by the levels of fluid and salt getting out of whack, putting stress on artery walls and damaging blood vessels and organs.
The Pitt study focused on the passages — or channels — that the membranes of certain cells use to regulate fluid volume, based on how much sodium the cells contain. Blobner was curious if mutations in the genes that encode subunits of that channel might affect blood pressure.

A new discovery about how cells make antibodies has revealed the surprisingly random way the body’s immune system defends against infection and disease.
The study, led by researchers at WEHI in Melbourne, Australia, showed cells responsible for making antibody proteins use a randomisation process to determine which type of antibody to make, behaviour that scientists have dubbed ‘molecular roulette’.
Researchers have leveraged the critical insights to create a formula for predicting this allocation process, in a major step towards understanding why some people are biologically prone to developing diseases like asthma, autoimmune conditions and infections.
At a glance First study to show B cells use a randomisation process when determining which type of antibody to create. Antibodies protect the body against pathogens and viruses. WEHI-led finding unravels first mathematical model that could predict the type and amount of antibody that will be produced. Landmark discovery could lead to future research that can prevent this process from being disrupted to cause disease, while bringing the field significantly closer to using quantifiable data to map how the immune system behaves.Antibodies are produced by immune cells to protect our body against disease by alerting the immune system to foreign invaders, like pathogens and viruses.
B cells are a type of immune cell (also known as B lymphocytes) that produce five different classes of antibodies, each tailored to defend the body against a specific bug — including bacteria and parasites.

Children with food allergies, along with their parents, often experience heightened anxiety over risks of casual contact with food allergens. They also wonder whether they should avoid social situations involving food and whether medical interventions such as oral food challenges and oral immunotherapy are safe. A new study in Annals of Allergy, Asthma and Immunology, the scientific journal of the American College of Allergy, Asthma and Immunology (ACAAI), shows that targeted cognitive behavioral therapy (CBT) can significantly lessen food allergy-related anxiety (FAA) for both children and parents.
“To our knowledge, this is the first study of an outpatient use of CBT in a sample of children diagnosed with an anxiety disorder related to their food allergy,” said allergist Jonathan Spergel, MD, PhD, ACAAI member and co-author of the study. “We found that, although it was a small sample of 10 children, 100% of the children and their parents showed symptom improvement as reported by multiple sources (child, parent, therapist) and across multiple domains (food allergy-specific anxiety, general anxiety and health-related quality of life.)” The study included a follow up assessment 2-4 months past the active treatment with results suggesting the gains were maintained.
The study participants were 10 children aged 8-12 years (80% female) referred by their allergists specifically for evaluation and treatment of FAA. The children had to have confirmed IgE mediated food allergy/allergies that were well-controlled, as well as excessive anxiety and medically unnecessary and impairing anxious avoidance related specifically to their food allergy. The CBT included 5-8 “proximity exposure sessions” with the patient, with each session typically lasting between 30 and 90 minutes depending on whether it was a group or individual session. An allergist or mental health provider led the sessions.
“A variety of graded exposures such as sniffing their allergen, touching their allergen, or eating a needlessly feared and avoided food were performed in each session by the whole group, and assigned for homework,” said Katherine Dahlsgaard, PhD, CBT therapist who worked with the families, and lead author of the study. “One or both parents of 100% of the children completed a treatment satisfaction questionnaire posttreatment. Parents rated the treatment as highly satisfactory and helpful, and all 10 children were rated as much improved or very much improved.”
Although the sample size was small and randomized trials still need to be performed, allergists and others who work with children with FAA, including mental health professionals, may be assisted by CBT in their treatment efforts. “This manualized treatment was brief — just 6 sessions — and can be given in allergists’ offices by nurse practitioners or other providers,” said Megan Lewis, CRNP and co-author of the study.
Allergists are specially trained to test for, diagnose and manage food allergies. To find an allergist near you who can help create a personal plan to deal with your child’s food allergies, and help them live their best life, use the ACAAI allergist locator.
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In one of the largest single-center COVID-19 cohort studies to date, researchers at the Icahn School of Medicine at Mount Sinai, using samples collected during the peak of the pandemic in New York City, have identified a key driver of COVID-19 disease severity.
The findings, published in the September 14 edition of Science Translational Medicine, suggest that lung damage is linked to the loss of immune cells called macrophages that normally reside in the lung and organize tissue repair, followed by an influx of new macrophages from the blood into the lung that cause inflammation. Blocking the entry of inflammatory macrophages and preventing the loss of reparative lung resident macrophages may be a therapeutic strategy for treating SARS-CoV-2 and other viral lung diseases.
Nearly three years since the start of the COVID-19 pandemic in late 2019, the virus continues to fuel a worldwide health crisis.
“Despite the development of vaccines that prevent disease, and therapies to treat COVID-19 and other infections, these critical viral diseases remain a major unmet need in medicine,” said lead author Steven Chen, a recent MD/PhD graduate in the laboratory of Miriam Merad,MD, PhD, a senior author of the study and Director of the Marc and Jennifer Lipschultz Precision Immunology Institute (PrIISM) at the Icahn School of Medicine at Mount Sinai. “Our study sought to identify drivers of disease severity and mortality in order to identify therapeutic strategies that could halt the progression of severe lung viral infections.”
In the study, blood and lung fluid samples of healthy controls and 583 COVID-19 patients admitted to Mount Sinai were collected as part of the Health System’s COVID-19 Biobank. The cohorts were longitudinally followed from March through December 2020.
The investigators used serum proteomics and immune cell phenotyping to compare the two groups’ systemic immune responses and identify potential disease severity drivers that could predict which patients were most at risk and guide new treatment protocols. They found that COVID-19 severity was linked to a shift in the specialized functions of different macrophage populations in the lung. This may partly explain why older adults, who have fewer reparative lung resident macrophages to start with and can produce more inflammatory blood-derived macrophages, may be predisposed to severe disease, say the researchers.
The researchers emphasize that the study highlights the need to improve measurements of the immune system in patients. “Clinically available immune tests are very limited, which is unfortunate because understanding the composition of immune cells circulating in the blood, and the inflammatory molecules they produce, can be extremely informative and help identify new treatments for many different diseases,” says Dr. Merad.
“Our study demonstrates that immune profiling could help stratify patients according to their disease drivers and identify therapeutic strategies tailored to these drivers,” said Dr. Merad. “In our investigation, a subset of patients could have significantly benefited from restoring reparative lung resident macrophages. The use of immune profiling studies in the clinic would have helped make this call quite early during the disease process.”
“Together with co-senior authors Alex Charney, MD, PhD, and Sacha Gnjatic, PhD, we are now following our COVID-19 cohort described in this study and will compare extensive immune profiling of the patients who develop long COVID with those who fully recover, in order to identify drivers and treatment strategies for long COVID.”
The paper is titled, “A shift in lung macrophage composition is associated with COVID-19 severity and recovery.”
This work was funded by National Institutes of Health grants F30CA243210, U24CA224319, U01DK124165, P30CA196521, NCI 75N91020R00055, R33CA263705, U24AI118644-05S1, and P30CA196521-05S2

Newly discovered biological changes in mothers who suffer postpartum depression may help explain the condition, yield long-sought treatments and let doctors identify those at risk even before their babies are born.
Postpartum depression strikes up to 20% of new moms and can have terrible consequences for both mother and child. Roughly 20% of maternal deaths after childbirth are from suicide. Postpartum depression can cause new moms to feel anxious and irritable, suffer self-doubt and have difficulty bonding with their baby, in addition to interfering with their ability to think, sleep and eat. For the child, maternal postpartum depression can translate into problems with cognitive, emotional and social development.
Risk factors for postpartum depression are thought to include the mother’s age at childbirth, diabetes and prior history of mental health issues. But the new discovery, from a UVA Health researcher and her collaborators at John Hopkins Medicine and Weill Cornell Medicine, suggests a previously unknown biological contributor: an impairment of the body’s ability to clean up old genetic material and other cellular debris.
“The finding that cells aren’t cleaning out old proteins and cellular debris, called autophagy, occurs before women develop depression symptoms, indicating that it could be part of the disease process,” said Jennifer L. Payne, MD, director of the Reproductive Psychiatry Research Program at the University of Virginia School of Medicine. “There are several medications that promote autophagy in cells, so this finding might open the door to new treatments and to identification of women at risk of postpartum depression before they become ill.”
Understanding Postpartum Depression
Payne and her colleagues wanted to determine if a recently discovered form of communication among cells, called “extracellular RNA communication,” might contribute to postpartum depression. This form of cellular communication is heightened during pregnancy and is critical in the implantation of the fertilized embryo and in the body’s inflammatory response afterward, among other roles.
The researchers analyzed blood plasma samples collected from 14 research participants during and after their pregnancies. This included both women who suffered postpartum depression and those who did not. The researchers found that extracellular RNA communication in immune cells was altered extensively in women who suffered postpartum depression. Further, they determined that this “large and consistent” change significantly limited the women’s bodies’ ability to perform important cellular cleanup — suggesting a potential biological cause for their depression.
“Deficits in autophagy are thought to cause toxicity that may lead to the changes in the brain and body associated with depression,” Payne said. “We have never fully understood the biological basis for postpartum depression, and this finding gets us closer to an understanding.”
Now that this biological issue has been identified, researchers may be able to target it to develop treatments for postpartum depression. They also may be able to use the finding to develop a blood test that can identify those at risk, even before their babies are born. That could help doctors intervene earlier and make life easier and better for new moms.
“I hope very much this finding leads to better treatments for postpartum depression,” Payne said. “Our goal is to one day prevent PPD in women at risk.”
The work was supported by the National Institutes of Health’s National Institute of Mental Health, grants R01 MH112704 and 1K23 MH110607, and the NIH’s National Institute of Allergy and Infectious Diseases, grant T32 AI007417.
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