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Thursday, August 13, 2026

 

Women with endometriosis may lose a month’s salary each year



Semmelweis University
Women with endometriosis may lose a month’s salary each year 

image: 

Dr. Dóra Balogh, Assistant Professor in the Department of Obstetrics and Gynecology at Semmelweis University and senior author of the study. 

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Credit: Photo: Bálint Barta - Semmelweis University, Budapest, Hungary





Menstrual leave and flexible work arrangements are the forms of support women with endometriosis say would help them most, according to a new study by researchers at Semmelweis University published in Preventive Medicine Reports. Pain and fatigue lead to more frequent absences from work and reduced job performance. The first large-scale study of its kind from Central and Eastern Europe found that women with endometriosis lose an average of €1,757 in income each year - roughly equivalent to one month’s average salary in Hungary. This estimate reflects income lost because of work absences and does not include the costs of reduced productivity at work or health care expenses.

Researchers at Semmelweis University analyzed data from 566 women with endometriosis and 447 women without the condition. Using internationally validated questionnaires, they assessed work productivity, absenteeism, and work ability. Women with endometriosis lost an average of 12.7 work hours over a four-week period because of health-related problems, compared with 5.7 hours among women in the control group. Based on the hours missed, the researchers estimated an average annual income loss of €1,757 per affected woman.

“The impact of endometriosis is not only a health issue but also a major social and economic one. The condition affects women during one of the most active stages of their lives, meaning it can influence employment, career development, and long-term financial security,” said Dr. Dóra Balogh, Assistant Professor in the Department of Obstetrics and Gynecology at Semmelweis University and senior author of the study.

Endometriosis affects about 10% of women of reproductive age worldwide. In this chronic gynecological condition, tissue similar to the lining of the uterus grows outside the uterus, causing chronic pelvic pain, painful periods, fatigue, and, in some cases, infertility. Symptoms often persist for many years before the condition is diagnosed.

The study found that 42% of women with endometriosis had poor work ability, compared with 17.9% of women in the control group. Poor work ability means that a person's health makes it harder to perform their job and increases the risk of prolonged work disability or leaving the workforce.

“The most surprising finding was that nearly half of the women with endometriosis fell into this category. Without appropriate support, the condition may not only make day-to-day work more difficult but also threaten women's ability to remain in the workforce over the long term,” said Dr. Dominika Miklós, a resident physician in the Department of Obstetrics and Gynecology at Semmelweis University and first author of the study.

The researchers also found that many workplaces are not adequately prepared to support employees with endometriosis. Fifty-four percent of respondents said their employer had little or no knowledge of the condition, while only 17% believed their workplace was sufficiently informed about it. Participants said they would most value menstrual leave, flexible work hours, remote or hybrid work options, and greater understanding and support from employers. Some European countries, including Spain and Portugal, already allow menstrual leave under certain circumstances. 

Part of a larger research program
The study was conducted as part of the international FEMaLe (Finding Endometriosis with Machine Learning) research program, launched in 2020. At Semmelweis University, the project is led by Dr. Attila Bokor, Associate Professor in the Department of Obstetrics and Gynecology. Its aim is to improve understanding of endometriosis, promote earlier diagnosis, and investigate the health, social, and economic impact of the disease.

This is the first comprehensive study in Central and Eastern Europe to examine the effects of endometriosis on work productivity, work ability, and workplace support simultaneously. Its findings are consistent with studies from Western Europe and Australia, suggesting that the impact of endometriosis on working life is similar across regions. The researchers conclude that flexible work arrangements and better-informed employers could help women with endometriosis remain in the workforce.

 

First 3D map of ovary throughout reproductive lifespan reveals mouse reproductive organ counts its own eggs



Despite same rearing conditions and identical DNA, mice have very different egg reserves, yet keep the same constant fraction of them ready for activation throughout their entire lives




Center for Genomic Regulation

Transparent whole mouse ovary 

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A whole mouse ovary, made transparent and imaged in three dimensions. Each bright sphere is one of the roughly 5,000 egg cells a mouse is born with and will ever have. Larger ones are already growing while the smaller specks lie dormant, awaiting their turn across the reproductive lifespan.

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Credit: Arturo D'Angelo/Centro de Regulación Genómica






As mice age, their total egg reserve collapses around tenfold. Yet, according to a new study in Nature Ageing, the proportion of eggs in the brief window where a follicle is shifting from dormant to growing stays constant throughout life, at approximately 14%.

"The same percentage of oocytes are being activated regardless of old the mouse is. That means the ovary has a sensing mechanism which knows how many oocytes are in there and only awakens a fixed proportion. No one has ever known that before. It is completely new biology,” says Dr. Elvan Böke, group leader at the Centre for Genomic Regulation (CRG) in Barcelona and senior author of the study.

The finding challenges the perception that ovaries are a passive reservoir of eggs. The authors of the study reframe the female reproductive organ as an actively monitored system and suggest the ovary could be counting its own egg supply because of a yet-to-be-identified hormone or neuronal signalling.

The discovery was possible thanks to the first complete three-dimensional map of how a mammalian ovary changes across its reproductive lifespan. The CRG researchers combined high-resolution microscopy with artificial intelligence to count and classify every single egg cell, or oocyte, in more than 100 intact ovaries spanning the full reproductive lifespan of a mouse.

Earlier studies have imaged both human and mouse ovaries in three dimensions but couldn’t track oocyte growth with as much precision as the CRG researchers, who are the first to follow a mouse throughout its reproductive life, oocyte by oocyte, in three-dimensional space. In total, they tracked over 85,000 cells, producing a dataset of unprecedented scale and resolution.

The study also made a second surprising finding. By the time they reach puberty, a mouse can end up with three times as many egg cells compared to another mouse, despite both animals being genetically identical and raised in the exact same conditions.

“These mice are essentially identical twins of the same age with the same living conditions yet have completely different ovaries. We found huge variability and it's not genetic. It means there's something else going on that we don't understand yet,” says Dr. Böke.

The variability was already present in mice before they reached puberty, suggesting it originates very early in life, possibly during embryonic development. Mice with smaller ovarian reserves also had smaller ovaries and fewer growing eggs, suggesting that these early events shape ovarian function for life.

A third important finding overturns an old assumption about egg activation. At any given moment, only a handful of oocytes activate, despite the ovary having hundreds of thousands of dormant eggs stored. One long-standing hypothesis suggested that densely packed dormant eggs suppress one another.

The CRG’s research found the opposite to be true. Regions of the ovary with the highest density of dormant eggs were also where the most eggs emerged from dormancy. "This idea has always floated around, but this is the first time there's actual data," says Arturo D'Angelo, first author of the study.

In another finding, the researchers also found a previously unrecognised developmental bottleneck at a particular stage of egg growth, around 60 micrometres in diameter, where many follicles appear to pause before becoming hormonally responsive.

The discovery is important because female mammals, including humans, are born with all the eggs they will have in their lifetime. Understanding what controls this checkpoint could matter for any future intervention aimed at extending reproductive lifespan or delaying menopause.

"We have thousands and thousands of oocytes in our bodies that we don't need," said Dr. Böke. "If we figure out why they're being lost without ever being ovulated, then we could tune the system. It could help keep the hormonal cycle going and help delay menopause, which half the world's population must go through. The health and economic implications are enormous."

The study is also careful about linking mouse biology to humans. Humans are born with roughly a million oocytes which decrease to 400,000 by puberty, and 1,000 by menopause. Only about 400 oocytes last for a lifetime. Mice have similar depletion rates but start with around 5,000.

However, mice ovulate from both ovaries every four to five days, while women typically release a single egg roughly every 28 days. Those differences in scale and tempo likely shape how the reserve is spent. Even so, the authors argue that the discovery that the ovary keeps a fixed fraction of eggs primed for activation regardless of age may be a universal feature of mammalian reproduction.

The authors of the study also believe the variation in ovarian reserve in women, with all their genetic and environmental diversity, is likely to be far larger compared to mice. They warn human studies will need larger cohorts to draw firm conclusions.

"In my mind, this data should have been out there 20 years ago, so we could have started building on it. It really changes how experiments should be planned," she says.

As a proof-of-concept, Böke and D’Angelo also show the method works on human ovarian cortex tissue, opening the door to similar studies in humans, although Dr. Böke cautions that the practical challenges are substantial. "The method is ready, but a lifespan study in humans is much harder," she says.

The new insights into mammalian reproductive biology were possible thanks to technical achievements. Mapping the entire ovarian reserve in three dimensions across an animal's lifespan required tissue clearing, whole-organ imaging on a microscope at EMBL Barcelona's Mesoscopic Imaging Facility and AI-driven image segmentation developed with collaborators at the Donostia International Physics Center (DIPC), the University of the Basque Country (UPV/EHU) and the Biofisika Institute.

"We wanted this tool to be useful to other scientists, not just for our own study. The complete workflow is freely available through BiaPy, our open-source platform for AI-based image analysis, and we've also released the microscopy images and the trained AI model itself. That means other labs can check our work, or point the same method at their own images without having to build it from scratch," says Ignacio Arganda-Carreras, leader of the CVPD group at the University of the Basque Country (UPV/EHU) and co-developer of BiaPy.


A region of a mouse ovary, made transparent so its depths can be seen at once. Each bright sphere is one of the roughly 5,000 egg cells a mouse is born with and will ever have

Credit

Montserrat Coll Lladó, Arturo D'Angelo/Centro de Regulación Genómica and EMBL Barcelona

A whole mouse ovary, imaged in 3D. [VIDEO] 

A complete ovary from a five-week-old mouse, made transparent and scanned in hundreds of slices from top to bottom to build a 3D view. The eggs are coloured in green and the nuclei of every other cell in the organ glow magenta.

Credit

Angelo et al. (2026) Nature Aging



Counting eggs in human ovarian tissue [VIDEO] 

Monday, August 10, 2026

 

Why a doctor saying 'it's normal' can backfire




University of California - San Diego






Doctors may think they're saying “Don't panic." But many patients hear "Don't bother" instead.

A new study from the University of California San Diego Rady School of Management suggests that when physicians try to reassure patients by saying their symptoms are “normal,” patients may actually infer that treatment isn't necessary – and become less inclined to seek it.

Published in Nature Human Behaviour, the findings held across 14 experiments involving 9,371 participants and a wide range of health conditions, from menopause and migraines to dental pain, seasonal allergies and elevated blood glucose levels. 

Why ‘normal’ can send the wrong message

The idea for the research grew from first author Seyi Lawal's interest in communication around menopause, where patients sometimes report feeling dismissed after being told disruptive symptoms are simply a normal part of aging. Could it be, she wondered, that doctors and patients were interpreting the same conversations differently?

To find out, the researchers conducted 14 studies involving members of the public and healthcare providers. Participants read realistic medical scenarios in which healthcare providers either described symptoms as "normal" or did not. The researchers then measured the participants' willingness to pursue treatment and compared it with what providers expected patients would do.

"Providers expected that normalizing a patient's symptoms would increase their treatment likelihood, or at worst have no impact, but patients actually reacted in the opposite way," said Lawal, a doctoral student at the UC San Diego Rady School of Management.

Doctors use "normal," it seems, to mean common and well understood. Patients often interpret it as meaning acceptable – or not worth treating.

Fixing the communication gap, making reassurance work

The findings come amid broader conversations about patients feeling dismissed in healthcare settings, sometimes described as “medical gaslighting.” The study identifies a communication gap that may contribute to those experiences, even when doctors are trying to help.

The good news is that miscommunication isn’t inevitable. The researchers also tested two simple ways to reduce it: pairing normalizing language with an explicit recommendation for treatment, and explaining that "normal" was meant in a statistical, not normative or prescriptive, sense. 

Both approaches helped close the communication gap.

"Doctors usually have a noble goal. They mean to ease anxiety, but somehow it backfires," said senior author On Amir, professor of marketing and holder of  the Wolfe Family Presidential Endowed Chair in Life Sciences Innovation and Entrepreneurship at the UC San Diego Rady School of Management. "Doctors shouldn’t stop reassuring patients. But they should make their meaning unmistakable.”

Co-author Brianna Chew, a doctoral student at the Rady School, said the same lesson applies to patients. Hearing that symptoms are “normal,” she said, shouldn't be taken to mean they are any less serious.

The key takeaway for patients: If you're unsure what your doctor means when they say a symptom is "normal," don't assume it means treatment isn't recommended and you should just live with it. Ask. 

Common symptoms can still deserve attention – and treatment.

Full study: “Reassurance through normalization inadvertently suppresses treatment.” 

The study was funded in part by the T. Denny Sanford Institute for Empathy and Compassion.

Friday, August 07, 2026

 

Why women need to be prioritized in longevity research


Buck scientists propose the Reproductive Resilience



Buck Institute for Research on Aging

The ovary impacts many biological systems; aging matters 

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This illustration presents the ovary as a central biological hub that helps coordinate health across the female body. Developing follicles populate one side of the clock face, while the impacted tissues are on the other side. Their placement symbolizes how reproductive signals may influence multiple organs throughout life. As ovarian resilience declines with age, this coordinated rhythm may become disrupted, contributing to broader changes in metabolism, immunity, cognition, cardiovascular function, and tissue maintenance. Rather than functioning only as a reproductive organ, the ovary is depicted as an important regulator of systemic biological timing and resilience.

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Credit: Parminder Singh, PhD




Why do women, on average, live longer than men, yet often face a greater burden of chronic disease later in life? Why do some of the most fertile animals in nature, including queen bees and naked mole-rat queens, also live exceptionally long lives?

A perspective, to be published on August 6th in Cell, introduces the Reproductive Resilience Hypothesis (RRH), a new way to think about these questions. The hypothesis, developed by Buck professor Pankaj Kapahi, PhD and senior postdoc Parminder Singh, PhD, proposes that reproduction and longevity, often seen as opposing biological forces, may be tightly linked in the context of life history. The authors posit that women could be the key players in efforts to discover ways to extend human healthspan.

“If we wish to understand why organisms age, nature points us toward studying women, the sex in which reproduction most profoundly shapes the course of aging,” says Buck professor Pankaj Kapahi, PhD, senior author of the paper.

“The Reproductive Resilience Hypothesis is a new evolutionary framework for understanding why reproduction accelerates aging in some biological settings but is associated with exceptional longevity in others,” says Singh. “The central question is not simply how much an organism reproduces. It is whether continued survival remains important for future reproductive success, offspring survival, caregiving, or inclusive fitness.”

Reframing the relationship between reproductive investment and aging

 

Classical evolutionary theories of aging often describe reproduction and longevity as a trade-off. Because organisms have limited energy, investing heavily in reproduction should leave fewer resources for maintaining the body over time. The authors say that while this explanation is useful, it does not fully account for a recurring pattern across nature: in many species, the sex that invests most heavily in pregnancy, lactation, offspring care, or colony reproduction is also the longer-lived sex.

RRH proposes that when reproductive success depends on surviving long enough to reproduce repeatedly, care for offspring, or support kin and social groups, evolution may favor biological programs that strengthen the body’s ability to withstand stress. In these settings, reproduction and long-term maintenance may become linked rather than opposed.

“Our perspective helps explain why female mammals often outlive males, why queen insects can combine extraordinary fertility with longevity, and why male lifespan can equal or exceed female lifespan in species where fathers provide substantial infant care,” says Singh, who leads the research in the Kapahi lab.

A new lens on menopause and female healthspan

The framework also provides a new way to interpret human menopause and the female health-survival paradox. Women generally live longer than men, yet they often spend a greater proportion of later life with chronic disease, disability, or frailty.

The authors propose that menopause should not be viewed only as the end of fertility. Instead, it may represent an important inflection point in the progressive loss of reproductive resilience.

During reproductive life, ovarian signals are integrated with systems controlling metabolism, bone maintenance, immune regulation, brain function, stress responses, tissue repair, and communication among organs. As ovarian function declines, this reproductive-somatic communication network may become destabilized, exposing vulnerabilities that were previously buffered.

In this framework, menopause is not simply the loss of estrogen. It represents a broader disruption of the signals and physiological networks that connect reproductive function with whole-body maintenance.

“The ovary should not be viewed only as an organ that produces eggs and sex hormones,” Singh says. “It may also function as a communication hub whose endocrine, metabolic, immune, and paracrine signals help coordinate the physiological state of distant organs. When this communication declines, the consequences may extend far beyond fertility.”

The authors emphasize that RRH is not an estrogen-only explanation of female aging. Estrogen has complex, tissue-specific effects that depend on receptor type, timing, genetic background, inflammatory state, and disease stage. Aging also proceeds through processes such as DNA damage, protein aggregation, mitochondrial dysfunction, stem-cell exhaustion, and tissue-specific degeneration that may occur independently of reproductive state.

“We are not proposing that ovarian aging is the sole cause of systemic aging,” Kapahi said. “Rather, ovarian decline may remove an important layer of physiological coordination. That loss can interact with chronological aging, genetics, inflammation, metabolism, environmental exposures, and tissue-specific damage.”

Loss of reproductive resilience as a sex-specific hallmark of aging

The authors propose that loss of reproductive resilience should be considered a sex-specific hallmark-level process in aging. Like other hallmarks, it appears during normal aging, and its acceleration can worsen age-related decline. Interestingly, restoring aspects of ovarian function or signaling in experimental models has been shown to improve health-related outcomes.

Calling loss of reproductive resilience a sex-specific hallmark changes how we interpret reproductive aging, Singh said. It is not merely a marker that fertility has ended. It may be an upstream and temporally defined transition that changes the trajectory of several tissues and aging mechanisms at the same time.

Kapahi says RRH challenges a longstanding limitation in biomedical research. “For decades, many preclinical studies relied largely on male animals or young female animals that had never been pregnant. Yet pregnancy, lactation, menopause, ovarian surgery, and reproductive history can produce lasting changes in metabolism, immunity, the brain, and other organs. Treating these features only as sources of experimental variability may cause researchers to miss fundamental mechanisms of resilience and disease vulnerability.”

From evolutionary hypothesis to experimental discovery

Building on this framework, Singh and Kapahi are investigating how the ovary communicates with distant organs, including the brain, bone, immune system, and metabolic tissues. Their work aims to understand how reproductive aging disrupts this communication and whether beneficial ovarian signals can be restored without relying exclusively on conventional hormone replacement.

The broader goal is to determine whether the mechanisms that evolved to preserve females through reproduction, caregiving, and physiological stress can be identified and used to protect health later in life.

“Studying females is not a specialized branch of aging research,” Kapahi said. “It is an opportunity to discover biological mechanisms that evolution has already developed to preserve survival under the demanding conditions of reproduction and caregiving.”

“Female biology should be prioritized not only to correct a longstanding gap in biomedical research,” Singh added, “but because it may reveal resilience mechanisms that help us understand how to extend healthspan in both women and men.”

Rethinking the future of research on aging

The authors outline 11 ramifications of RRH that could reshape how research on aging is designed and translated into medicine. They call for human studies to routinely document reproductive history, including puberty, pregnancy, lactation, menopause, hormone therapy, and ovarian surgery. Animal studies, they say, should also move beyond comparisons between males and virgin females by including reproductively experienced, post-reproductive, and ovarian-signal-loss models.

“Reproductive history should not be treated simply as experimental variability,” said Singh. “It may reveal important mechanisms of resilience, disease vulnerability, and treatment response that conventional studies have overlooked.”

The authors also propose developing sex- and reproductive-state-specific biomarkers, mapping how reproductive transitions affect aging across organs, and identifying ovary-derived signals beyond classical sex hormones. These discoveries could guide interventions aimed at preserving systemic health without necessarily extending fertility. Comparative studies of queen insects, naked mole-rats, and other unusually resilient species may also reveal naturally evolved mechanisms that connect reproduction with long-term somatic maintenance.

“These ramifications provide a roadmap for converting the hypothesis into testable experiments and more precise interventions,” said Kapahi. “To fully understand aging, we need to consider not only biological sex, but also reproductive state and life history.”

Citation: Why Studying Females Reveals More About Aging: The Reproductive Resilience Hypothesis as an Evolutionary Framework for Studying Sex-Specific Aging

DOI: 10.1016/j.cell.2026.07.013

Other collaborators include:
Vineeta Tanwar, Yifan Xiang, Lizabeth Enriquez Najera, Buck Institute, and Steven N. Austad, Department of Biology, The University of Alabama at Birmingham, Alabama.
 

Acknowledgements:

The work was supported by grants from the National Institute of Health (R01AG068288, R01AG061165) as well as the Larry L. Hillblom Foundation and the Hevolution Foundation.

About the Buck Institute for Research on Aging

At the Buck, we aim to end the threat of age-related diseases for this and future generations. We bring together the most capable and passionate scientists from a broad range of disciplines to study mechanisms of aging and to identify therapeutics that slow down aging. Our goal is to increase human health span, or the healthy years of life. Located just north of San Francisco, we are globally recognized as the pioneer and leader in efforts to target aging, the number one risk factor for serious diseases including Alzheimer’s, Parkinson’s, cancer, macular degeneration, heart disease, and diabetes. The Buck wants to help people live better longer. Our success will ultimately change healthcare. Learn more at: https://buckinstitute.org