The agency faulted the device maker for delayed notice of mounting complications, citing increasing reports of how use of the device perforated the walls of the heart.A troubled heart pump that has now been linked to 49 deaths and dozens of injuries worldwide will be allowed to remain in use, despite the Food and Drug Administration’s decision to issue an alert about the risk that it could puncture a wall of the heart.The tiny Impella pumps, about the width of a candy cane, are threaded through blood vessels to take over the work of the heart in patients who are undergoing complex procedures or have life-threatening conditions.The F.D.A. said the manufacturer of the device, Abiomed, should have notified the agency more than two years ago, when the company first posted an update on its website about the perforation risk. Such a notice, the F.D.A. added, would have led to a much broader official agency warning to hospitals and doctors.The alert is the latest of concerns raised in recent years about the deadly side effects of cardiac devices, especially those that take over the heart’s role in circulating blood. It is the third major F.D.A. action for an Impella device in a year.A series of studies suggested that the Impella heart devices heighten the risk of death in patients with unstable medical conditions. Meanwhile, the device maker has spent millions of dollars promoting the device and awarding consulting payments to cardiologists and grants to hospitals.Since Abiomed’s first notice about the Impella’s complications in October 2021, the F.D.A. received 21 additional reports of heart-wall tears linked to patient deaths, according to Audra Harrison, a spokeswoman for the agency.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

A device called LightSound is being distributed to help the blind and visually impaired experience this year’s event.On Aug. 21, 2017, Kiki Smith’s teenage sons giddily prepared to watch the partial solar eclipse in Rochester, N.Y. As Ms. Smith listened to their chatter, she felt excluded.“I felt very alone,” she said. Ms. Smith was diagnosed with a degenerative condition as a child and lost the last of her vision in 2011. The local buzz around the eclipse, and the national media attention, unexpectedly touched a nerve.The eclipse “was about experiencing a historic moment in community, and I wasn’t part of that,” she said.Ms. Smith, 52, who works for a community development organization in Rochester, determined to do things differently for the April 8 total eclipse that is passing through her city. She is helping to organize a public gathering that prioritizes accessibility for people with vision loss. Her event will include specially designed devices named LightSound that translate changing light intensity into musical tones, allowing blind and visually impaired people to listen as the sky grows dark and then brightens again.During this eclipse, Ms. Smith said, “I will be with community. And I will have at my fingertips all of these fabulous resources to experience what I felt I missed last time.”People across the United States with limited vision or blindness will experience the eclipse with the aid of about 900 LightSound devices distributed by a team led by Allyson Bieryla, a Harvard University astronomer.The Path of the EclipseOn April 8, a total solar eclipse will cross North America from Mazatlán, Mexico, to the Newfoundland coast near Gander, Canada. Viewers outside the path of the total eclipse will see a partial eclipse, if the sky is clear.

The guidelines for weight gain during pregnancy in obese women have long been questioned. New research from Karolinska Institutet supports the idea of lowering or removing the current recommendation of a weight gain of at least 5 kg. The results are published in The Lancet.
International guidelines from the US Institute of Medicine (IOM) state that women with obesity should gain a total of 5 to 9 kg during pregnancy, compared to 11.5 to 16 kg for normal-weight women. The guidelines have long been questioned, but there has been no evidence to warrant a re-examination.
A new study from Karolinska Institutet in Sweden now shows that there are no increased health risks for either the mother or the child with weight gain below current guidelines for women with obesity class 1 and 2 (BMI of 30-34.9 and 35-39.9 respectively). On the contrary, for women with obesity class 3 (BMI over 40), weight gain below current guidelines might even be beneficial for those with class 3 obesity.
The study supports previous calls to either lower or remove the current recommended lower limit of a weight gain of at least 5 kg, according to Kari Johansson, docent at the Department of Medicine, Solna.
“We hope that our research can inform a re-examination of national and international guidelines on weight gain during pregnancy,” she says.
The study is based on electronic medical records and registry data for 15,760 women with obesity in Stockholm and Gotland (the so-called Stockholm Gotland Perinatal Cohort). 11,667 of the women in the study had obesity class 1, 3,160 had obesity class 2 and 933 had obesity class 3. The study included singleton pregnancies that delivered between 2008 and 2015. The women were followed for a median of eight years after delivery.
Ten known adverse outcomes associated with weight gain during pregnancy were studied: pre-eclampsia, gestational diabetes, excess postpartum weight retention, maternal cardiometabolic disease, unplanned caesarean delivery, preterm birth, large for gestational age and small for gestational age at birth, stillbirth and infant death. These adverse outcomes were assigned weights according to their severity and combined into an adverse composite outcome.

Overall, the study shows no increased risks of the adverse composite outcome with weight gain below current IOM guidelines in women with obesity classes 1 and 2. For women with obesity class 3, on the contrary, weight gain values below the guidelines or weight loss were associated with reduced risk of the adverse composite outcome. For example, an absence of weight gain (i.e. 0kg) was associated with a risk reduction of about 20 per cent.
“Based on this, we have concluded that weight gain below current recommendations is likely safe in pregnancies with obesity, and might even be beneficial for those with class 3 obesity,” says Kari Johansson.
The results also indicate that there is a need for specific recommendations for women with class 3 obesity.
“Unlike today, this group could receive separate recommendations,” says Kari Johansson.
The researchers will now proceed with similar studies on overweight, normal weight and underweight women.
The study was conducted in collaboration with the University of British Columbia, Canada, the University of Pittsburgh, USA, and the University of California, USA. Funders were Karolinska Institutet Research Grants and the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD).
Kari Johansson and co-authors Lisa Bodnar and Jennifer Hutcheon are part of a WHO initiative for global standards for weight gain during pregnancy. However, the views expressed in the study do not reflect the views of the WHO. Olof Stephansson is co-founder and co-owner of a Swedish pregnancy app, One Million Babies. No other conflicts of interest are reported.

Replacing sugar with artificial and natural sweeteners in foods does not make people hungrier — and also helps to reduce blood sugar levels, a significant new study has found.
The double blind randomised controlled trial found that consuming food containing sweeteners produced a similar reduction in appetite sensations and appetite-related hormone responses as sugary foods — and provides some benefits such as lowering blood sugar, which may be particularly important in people at risk of developing type 2 diabetes.
The use of sweeteners in place of sugar in foods can be controversial due to conflicting reports about their potential to increase appetite. Previous studies have been carried out but did not provide robust evidence.
However, the researchers say their study, which meets the gold standard level of proof in scientific investigation, provides very strong evidence that sweeteners and sweetness enhancers do not negatively impact appetite and are beneficial for reducing sugar intake.
The trial was led by the University of Leeds in collaboration with the The Rhône-Alpes Research Center for Human Nutrition. It is the latest study to be published by the SWEET consortium of 29 European research, consumer and industry partners which is working to develop and review evidence on long term benefits and potential risks involved in switching over to sweeteners and sweetness enhancers in the context of public health and safety, obesity, and sustainability. It was funded by Horizon Europe.
Lead author Catherine Gibbons, Associate Professor in the University of Leeds’ School of Psychology, said: “Reducing sugar consumption has become a key public health target in the fight to reduce the rising burden of obesity-related metabolic diseases such as type 2 diabetes.
“Simply restricting sugar from foods without substitution may negatively impact its taste or increase sweet cravings, resulting in difficulties sticking to a low-sugar diet. Replacing sugars with sweeteners and sweetness enhancers in food products is one of the most widely used dietary and food manufacturing strategies to reduce sugar intake and improve the nutritional profile of commercial foods and beverages.”
Principal investigator Graham Finlayson, Professor of Psychobiology in the University of Leeds’ School of Psychology, said: “The use of sweeteners and sweetness enhancers has received a lot of negative attention, including high profile publications linking their consumption with impaired glycaemic response, toxicological damage to DNA and increased risk of heart attack and stroke. These reports contribute to the current befuddlement concerning the safety of sweeteners and sweetness enhancers among the general public and especially people at risk of metabolic diseases.

“Our study provides crucial evidence supporting the day-to-day use of sweeteners and sweetness enhancers for body weight and blood sugar control.”
The study, which is the first of its kind, looked at the effects of consuming biscuits containing either sugar or two types of food sweetener: natural sugar substitute Stevia, or artificial sweetener Neotame on 53 adult men and women with overweight or obesity.
Until now, virtually all studies of the effects of sweeteners and sweetness enhancers on appetite and glycaemia have been conducted using beverages as the vehicle. Few studies include volunteers with overweight or obesity and few have included volunteers of both sexes.
Most studies have only compared a single sweetener, mostly aspartame, with a control, and very few studies have examined the effect of repeated daily intake of a known sweetener or sweetness enhancer in the normal diet.
The new trial took place at the University of Leeds and the Rhône-Alpes Research Center for Human Nutrition (CRNH-RA), France between 2021 and 2022. Participants were all aged 18 to 60, with overweight or obesity.
The trial consisted of three two-week consumption periods, where participants consumed biscuits with either fruit filling containing sugar; natural sugar substitute Stevia, or artificial sweetener Neotame, each separated by a break of 14-21 days. Day 1 and day 14 of the consumption periods took place in the lab.

Participants were instructed to arrive in the lab after an overnight fast, a blood sample was taken to establish baseline levels of glucose, insulin and appetite-related hormones. They were also asked to rate their appetite and food preferences.
After consuming the biscuits, they were asked to rate how full they felt over several hours. Glucose and insulin levels were measured, as were ghrelin, glucagon-like peptide 1 and pancreatic polypeptide — hormones associated with the consumption of food.
The results from the two sweetener types showed no differences in appetite or endocrine responses compared to sugar, but insulin levels measured over two hours after eating were reduced, as were blood sugar levels.
SWEET project joint co-ordinator Professor Anne Raben, from the University of Copenhagen, Denmark, said: “The findings show that sweeteners are a helpful tool to reduce intake of added sugar without leading to a compensatory increase in appetite or energy intake, thereby supporting the usefulness of sweeteners for appetite, energy and weight management.”

Researchers at Karolinska Institutet, in collaboration with JLP Health and others, have identified how the tick-borne Crimean-Congo haemorrhagic fever virus enters our cells. The results are published in Nature Microbiology and are an important step in the development of drugs against the deadly disease.
Crimean-Congo haemorrhagic fever virus (CCHF virus) is spread through tick bites and can cause haemorrhagic fever. The disease is serious and has a mortality rate of up to 40 per cent depending on the health status of the person infected. Common symptoms include fever, muscle pain, abdominal pain, joint pain, vomiting and haemorrhaging that can cause organ failure.
The disease has spread to Europe
The virus is present in around 40 countries, including Central Asia, the Middle East and parts of Africa. In recent years, the disease has spread to new geographical areas as a result of climate change, including Spain and France. The tick species that can spread the disease has also been observed in Germany and Sweden. There are currently no effective treatments for the disease.
In a new study, researchers at Karolinska Institutet in Sweden and others have found that the virus enters our cells via a protein on the cell surface, the so-called LDL receptors that regulate blood cholesterol levels.
To identify the protein, the researchers used human mini-organs grown in test tubes and an advanced stem cell library from JLP Health. The same platform has previously been used to identify how the Ebola virus enters cells.
The results were also confirmed in tests on mice, which showed that mice lacking the LDL receptor did not get as sick as others.

Researchers want to trick the virus
The discovery is an important step towards developing drugs for Crimean-Congo haemorrhagic fever, according to Ali Mirazimi, adjunct professor at the Department of Laboratory Medicine, Karolinska Institutet, and one of the researchers behind the study.
“Once we know which receptor the virus uses, we can produce the receptor in test tubes and administer it as a drug,” he says. “Then we can trick the virus into binding to those receptors instead of to the cells and thus stop the virus from spreading in our bodies.”
This knowledge is essential if the disease were to become more common and spread to new areas. Normally it takes many years to develop a drug, but the COVID-19 pandemic and the development of the SARS-CoV-2 vaccine showed that it can be done much faster if everyone decides it is a priority.
Ticks are spread by migratory birds
“This is an important step in our preparedness for the disease,” says Ali Mirazimi. “Crimean-Congo haemorrhagic fever is a disease we would rather not have. The ticks are spread by migratory birds and have already been found in Sweden. If the disease starts appearing in more places, we may already have a drug that we can take into clinical trials.”
The research was conducted in collaboration with the Medical University of Vienna, Austria, Helmholtz Centre for Infection Research, Germany, the National Institutes of Health, USA, and the company JLP Health. It was financed mainly by the Swedish Research Council and the EU. No conflicts of interest have been reported.

Over the past 30 years, Australia’s Tasmanian devil population has been afflicted with an infectious cancer that has pushed the species to near extinction. The marsupials are highly susceptible to devil facial tumor disease, which is almost always fatal to their species. The genomic interactions between the disease and its host correlate with how quickly a susceptible animal becomes infected after exposure to the pathogen.
Through DNA sequencing of the animals and their tumors, University of South Florida Assistant Professor of Integrative Biology Mark Margres and doctoral student Dylan Gallinson have tracked the genomic interactions between the devils and the cancer. Their findings are published in a coauthored paper, “Intergenomic signatures of coevolution between Tasmanian devils and an infectious cancer,” in the Proceedings of the National Academy of Sciences.
“A big question in biology is the genetic basis for disease. The classic way to determine this is through genome studies and regression analysis that matches genes with disease risk,” Margres said. “Previously there hadn’t been a technique to study the interactions between both genomes.”
Using a recently developed joint genome-wide association study, Margres and Gallinson assessed 960 genomes and 15 years of data on captured devils to track the co-evolution of the devils and the cancer.
“Our collaborators in Tasmania have been monitoring the spread of the disease and collecting tissue samples,” Gallinson said. “We sequenced the DNA of both the tumors and the devils to find the mutation that contributes to the manifestation of the disease.”
Their findings can inform both epidemiological models that track infectious diseases and devil management strategies that focus on saving the endangered species.

A single genetic test could potentially replace the current two-step approach to diagnosing rare developmental disorders in children. This shift could enable earlier diagnoses for families and save the NHS vital resources.
Researchers from the Wellcome Sanger Institute, and their collaborators at the University of Exeter and the University of Cambridge, were able to reassess genetic data from nearly 10,000 families from the Deciphering Developmental Disorders study.
In a new study, recently published in Genetics in Medicine, they show for the first time that using exome sequencing — which reads only protein-coding DNA — is as accurate, if not better, than standard microarrays at identifying disease-causing structural genetic variations.
Its adoption offers hope for faster and more accurate diagnoses of rare genetic diseases. It could also deliver substantial cost savings for the NHS, though more training is needed for specialists to generate and analyse the data, say researchers.
Changes in our genetic code can range from single letter changes to the deletion or duplication of larger stretches of DNA. These bigger changes — called copy number variations (CNVs) — can be harder for clinical teams to detect in sequencing data and understand, which is why microarrays are used. While usually harmless, making up one of the major sources of genetic diversity in humans, these large-scale variations can sometimes cause various neurodevelopmental disorders, including Angelman syndrome, DiGeorge syndrome, and Williams-Beuren syndrome.
Currently, children suspected to have genetic diseases arising from these large deletions or duplications of DNA go through a lengthy process of testing and waiting for results from multiple diagnostic approaches, starting with a microarray test before progressing to a broader genome-wide sequencing test (such as exome or genome sequencing). In this new study, scientists set out to develop a single approach to detect these structural changes, using data available from genome-wide exome sequencing assays.
Using data from the Deciphering Developmental Disorders study, the team developed a single-assay approach that combined four algorithms using machine learning methods to analyse exome sequencing data.

Comparison of the new single-assay approach with current standard clinical methods revealed it could reliably detect 305 large-scale pathogenic mutations, including 91 not previously detectable using standard clinical microarrays. The findings suggest it could replace the current methods.
Caroline Wright, Professor of Genomic Medicine at the University of Exeter, and author of the study, said: “Using exome sequencing data to detect clinically important large-scale changes, at the same time as small genetic variants, marks a significant step forward in making genetic testing simpler, cheaper and more accessible.”
Helen Firth, Professor of Clinical Genomics at the University of Cambridge, lead clinician and author of the study, said: “Under the current system, children often endure a lengthy, step-wise process of different genetic tests before reaching a diagnosis. This research brings hope that, in the near future, families might only need one test.”
Professor Matthew Hurles, Director of the Wellcome Sanger Institute and senior author of the study, said: “We are still learning how large-scale genetic variations impact human health. This study proves that with the right computational methods, a single test can accurately detect them. Our findings support its widespread adoption in NHS clinical practice, and the adequate bioinformatics training to support this.”

Researchers from Rutgers believe they are among the leaders in a race to find an oral COVID-19 treatment to supplement or replace Paxlovid — an antiviral medication that helps keep high-risk patients out of the hospital.
Their report, which will appear in Science, shows that an alternative medication, a viral papain-like protease inhibitor, inhibits disease progression in animals, a necessary step before human drug trials.
“COVID-19 remains the nation’s third leading cause of death, so there’s already a massive need for additional treatment options,” said Jun Wang, senior author of the study and an associate professor who runs a research lab at Rutgers’ Ernest Mario School of Pharmacy. “That need will grow more urgent when, inevitably, COVID-19 mutates in ways that prevent Paxlovid from working.”
The Rutgers team hoped to make a drug that interfered with viral papain-like protease (PLpro), a protein that performs important functions in all known strains of COVID-19.
Creating such a drug required detailed information about PLpro’s structure, which Wang’s team got from the Arnold Lab at Rutgers’ Center for Advanced Biotechnology and Medicine (CABM).
Precise knowledge of PLpro’s structure enabled Wang’s team to design and synthesize 85 drug candidates that would bond to – and interfere with — this vital protein.
“The PLpro crystal structures showed an unexpected arrangement of how the drug candidate molecules bind to its protein target, leading to innovative design ideas implemented by professor Wang’s medicinal chemistry team,” said Eddy Arnold, who is a professor at CABM and the Rutgers Department of Chemistry and Chemical Biology.

Laboratory testing established that the most effective of those drug candidates, a compound dubbed Jun12682, inhibited several strains of the SARS-CoV-2 virus, including strains that resist treatment with Paxlovid.
Subsequent testing on SARS-CoV-2-infected mice by the Deng lab at Oklahoma State University showed that oral treatment with Jun12682 reduced viral lung loads and lesions while improving survival rates.
“Our treatment was about as effective in mice as Paxlovid was in its initial animal tests,” said Wang, who added the experimental drug appears to have at least one major advantage over the older drug.
“Paxlovid interferes with many prescription medications, and most people who face the highest risk of severe COVID-19 take other prescription medicines, so it’s a real problem,” Wang said. “We tested our candidate Jun12682 against major drug-metabolizing enzymes and saw no evidence that it would interfere with other medications.”
Disclosure: Rutgers has submitted patent applications for Jun12682, along with the other 84 drug candidates, and is looking for partners to help move the drug candidate forward through further stages of testing and development.

The human brain consumes vast amounts of energy, which is almost exclusively generated from a form of metabolism that requires oxygen. While the efficient and timely delivery of oxygen is known to be critical to healthy brain function, the precise mechanics of this process have largely remained hidden from scientists.
A new bioluminescence imaging technique, described today in the journal Science, has created highly detailed, and visually striking, images of the movement of oxygen in the brains of mice. The method, which can be easily replicated by other labs, will enable researchers to more precisely study forms of hypoxia in the brain, such as the denial of oxygen to the brain that occurs during a stroke or heart attack. The new research tool is already providing insight into why a sedentary lifestyle may increase risk for diseases like Alzheimer’s.
“This research demonstrates that we can monitor changes in oxygen concentration continuously and in a wide area of the brain,” said Maiken Nedergaard, co-director of the Center for Translational Neuromedicine (CTN), which is based at both the University of Rochester and the University of Copenhagen. “This provides us a with a more detailed picture of what is occurring in the brain in real time, allowing us to identify previously undetected areas of temporary hypoxia, which reflect changes in blood flow that can trigger neurological deficits.”
Fireflies and serendipitous science
The new method employs luminescent proteins, chemical cousins of the bioluminescent proteins found in fireflies. These proteins, which have been used in cancer research, employs a virus that delivers instructions to cells to produce a luminescent protein in the form of an enzyme. When the enzyme encounters a second chemical compound, a substrate called furimazine, the chemical reaction generates light.
Like many important scientific discoveries, employing this process to image oxygen in the brain was stumbled upon by accident. Felix Beinlich, PhD, an assistant professor in the CTN at the University of Copenhagen, had originally intended to use the luminescent protein to measure calcium activity in the brain. It became apparent that there was an error in the production of the proteins, causing a months-long delay in the research.
While Beinlich waited for a new batch from the manufacturer, he decided move forward with the experiments to test and optimize the monitoring systems. The virus was used to deliver enzyme-producing instructions to astrocytes, ubiquitous support cells in the brain that maintain the health and signaling functions of neurons, and the substrate was injected into the brain via a craniotomy. The recordings revealed activity, identified by a fluctuating intensity of bioluminescence, something that the researchers suspected, and would later confirm, reflected the presence and concentration of oxygen. “The chemical reaction in this instance was oxygen dependent, so when there is the enzyme, the substrate, and oxygen, the system starts to glow,” said Beinlich.

While existing oxygen monitoring techniques provide information about a very small area of the brain, the researchers were able to observe, in real time, a large section of the cortex of the mice. The intensity of the bioluminescence corresponded with the concentration of oxygen, which the researchers demonstrated by changing the amount of oxygen in the air the animals were breathing. Changes in light intensity also corresponded with sensory processing. For example, when the mice’s whiskers were stimulated with a puff of air, the researchers could see the corresponding region of the brain light up.
“Hypoxic pockets” could point to Alzheimer’s risk
The brain cannot survive long without oxygen, a concept demonstrated by the neurological damage that quickly follows a stroke or heart attack. But what happens when very small parts of the brain are denied oxygen for brief periods? This question was not even being asked by researchers until the team in the Nedergaard lab began to look closely at the new recordings. While monitoring the mice, the researchers observed that specific tiny areas of the brain would go dark, sometimes for minutes, meaning that the oxygen supply was being cut off.
Oxygen is circulated throughout the brain via a vast network of arteries and smaller capillaries-or microvessels-which permeate brain tissue. Through a series of experiments, the researchers were able to determine that oxygen was being denied due to capillary stalling, which occurs when white blood cells temporarily block microvessels and prevent the passage of oxygen carrying red blood cells. These areas, which the researchers named “hypoxic pockets,” were more prevalent in the brains of mice during a resting state, compared to when the animals were active. Capillary stalling is believed to increase with age and has been observed in models of Alzheimer’s disease.
“The door is now open to study a range of diseases associated with hypoxia in the brain, including Alzheimer’s, vascular dementia, and long COVID, and how a sedentary lifestyle, aging, hypertension, and other factors contribute to these diseases,” said Nedergaard. “It also provides a tool to test different drugs and types of exercise that improve vascular health and slow down the road to dementia.”
Additional authors include Hajime Hirase with the University of Rochester, Antonios Asiminas, Verena Untiet, Zuzanna Bojarowska, Virginia Plá, and Björn Sigurdsson with the University of Copenhagen, and Vincenzo Timmel, Lukas Gehrig, and Michael H. Graber with the University of Applied Sciences and Arts Northwestern Switzerland. The study was supported with funding from the National Institute of Neurological Disorders and Stroke, the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation, the Novo Nordisk Foundation, the Lundbeck Foundation, Independent Research Fund Denmark, and the US Army Research Office.

Women affected by premenstrual disorders have a higher risk of perinatal depression compared with those who do not, according to research published March 28 in the open access journal PLOS Medicine. The relationship works both ways: those with perinatal depression are also more likely to develop premenstrual disorders after pregnancy and childbirth. This study suggests that a common mechanism might contribute to the two conditions.
Menstruating women experience cyclical hormone fluctuations through puberty, menstrual cycle, pregnancy and menopause. Some women have difficult to manage symptoms of low mood and depression during these fluctuations. Between a fifth and a third of women are reportedly affected by premenstrual disorders and 11% of mothers suffer perinatal depression — depressive symptoms during pregnancy and up to 12 months after delivery.
Qian Yang and colleagues at the Karolinska Institutet, Sweden and University of Iceland used the Swedish nationwide registers from 2001 to 2018 and identified 84,949 women with perinatal depression and 849,482 unaffected women. The researchers matched the women on age and calendar year, and further controlled for demographic factors, smoking, BMI, parity and history of psychiatric disorders. Among women with perinatal depression, almost 3% had premenstrual disorders before pregnancy compared with 0.6% of matched unaffected women. Women with perinatal depression were also twice as likely to report premenstrual disorders when the menstruation resumed after childbirth, compared to those unaffected by perinatal depression.
The research sheds light on the association between the two conditions and supports a theory that they may share underlying biological mechanisms and/or risk factors. Understanding this association could help healthcare providers to better target support to women most likely to be affected.
The authors add, “This study reveals a strong bidirectional relationship between perinatal depression and premenstrual disorders, using data from over 900,000 pregnancies. The findings suggest that both disorders may exist on a continuum, and emphasize the importance of recognizing these susceptibilities in clinical practice.”