Medical Bulletin 20/December/2025

Iron plays a critical role in energy, concentration, and oxygen transport. Yet, many teenagers fail to recognize the link between menstrual health, diet, and fatigue. To explore this, researchers studied 394 girls aged 15 and older from two upper secondary schools. Each participant completed questions about their menstrual experiences and dietary habits, followed by blood tests measuring hemoglobin (Hb) and ferritin, a marker of iron stores.

The results were striking. Girls with heavy menstrual bleeding were three times more likely to have low iron levels than those with normal cycles. When combined with a meat restricted or vegetarian diet, the risk increased dramatically—up to thirteen fold higher than their peers. Among those reporting heavy bleeding, 52% had iron deficiency compared with 26% among girls with normal bleeding. Similarly, 62% of participants who avoided red meat had low iron stores, and in the group with both risk factors—heavy bleeding and no red meat intake—iron deficiency soared to 71%.

To address early detection, the team tested a Spanish screening tool called the SAMANTA questionnaire, designed to assess the severity of menstrual bleeding. For the first time, it was used among teenagers, and it successfully identified girls most likely to have low iron. Researchers say this tool could be easily integrated into school health programs or youth clinics to guide early interventions such as dietary counseling or iron supplementation.

Lead researcher Dr. Moa Wolff stressed that many young people underestimate their symptoms or rely solely on personal comparisons. “We see many girls who are tired and distracted, but linking that to menstruation isn't obvious,” she said. By recognizing heavy bleeding as more than an inconvenience, the study urges schools, families, and clinicians to take menstrual health seriously—because treating iron deficiency early can improve wellbeing now and protect women’s health later in life.

REFERENCE: Söderman, L., et al. (2025). Exploring the effect of menstrual loss and dietary habits on iron deficiency in teenagers: A cross-sectional study. PLOS One. DOI: 10.1371/journal.pone.0336688.https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0336688

Estrogen found to trigger gut pain, explaining higher IBS rates in women

For years, scientists have known that women are far more likely than men to suffer from irritable bowel syndrome (IBS)—a chronic disorder marked by abdominal pain, bloating, and digestive distress. But why has remained a mystery. Now, researchers from UC San Francisco may have found the answer. In a study published in Science, the team discovered that estrogen directly activates pain pathways in the colon, making the female gut more sensitive to certain foods and inflammation.

Working with mouse models, the team led by Dr. Holly Ingraham and Nobel laureate Dr. David Julius began by tracing where estrogen acts in the gut. They expected to find receptors in enterochromaffin (EC) cells—the usual suspects in transmitting pain signals from the gut to the nervous system. Instead, they found that estrogen receptors cluster in a different cell type called L cells, particularly in the lower colon. This discovery led to a deeper exploration of how L cells might contribute to gut sensitivity.

Through a series of molecular and behavioral experiments, the researchers uncovered a chain reaction triggered by estrogen. When the hormone binds to L cells, they release peptide YY (PYY)—a hormone once thought to primarily suppress appetite. PYY, in turn, stimulates neighboring EC cells to release serotonin, which then activates pain sensing nerve fibers in the colon. When researchers removed the ovaries or blocked estrogen, serotonin, or PYY in female mice, their gut pain responses dropped to male like levels. Injecting estrogen into male mice, however, amplified gut sensitivity—matching that seen in females.

The study also identified another molecule, Olfr78, that becomes more active in response to estrogen. This receptor detects short chain fatty acids produced when gut bacteria digest certain carbohydrates. More Olfr78 means L cells become hypersensitive to these metabolites, producing even more PYY—and therefore more pain signaling.

This “double hit” of estrogen and microbial metabolites explains why low FODMAP diets, which reduce fermentable carbohydrates, often relieve IBS symptoms—especially in women. It also sheds light on why menstrual cycles, pregnancy, or hormone therapies can influence gut sensitivity.

“These findings move us beyond speculation to mechanism,” said Ingraham. “We can now see exactly how hormones tune gut pain pathways, opening new doors for gender specific IBS treatments.” The team is now exploring how targeting PYY or Olfr78 could lead to safer, easier to follow alternatives to restrictive diets for gut pain disorders.

REFERENCE: Venkataraman, A., et al. (2025). A cellular basis for heightened gut sensitivity in females. Science. doi: 10.1126/science.adz1398. https://www.science.org/doi/10.1126/science.adz1398

Study finds gestational diabetes causes molecular changes in the placenta

Gestational diabetes doesn’t just affect mothers during pregnancy—it can leave a lasting imprint on their babies. A new study published in Diabetes reveals why: the condition appears to disrupt how the placenta reads and processes genetic instructions, throwing off key molecular steps in protein production. The research, led by scientists at the Hebrew University of Jerusalem and Tel Aviv University, may finally explain how gestational diabetes mellitus (GDM) leads to complications such as preterm delivery, abnormal birth weights, and increased risks of obesity and diabetes in childhood.

GDM, which develops during pregnancy due to altered glucose metabolism, creates a nutrient rich environment that can stress both mother and fetus. To uncover how this affects the placenta—a vital organ that regulates oxygen, nutrient, and hormone exchange—the research team analyzed RNA from placental tissue of women with and without gestational diabetes. Using advanced RNA sequencing techniques on two large cohorts from Europe and China, they examined how RNA molecules were “spliced”—the process that determines which versions of a gene are used to build proteins.

Their findings were striking. In GDM pregnancies, hundreds of RNA messages were assembled incorrectly, particularly those related to metabolism and insulin signaling. This mis splicing can alter how the placenta functions, impairing its ability to support healthy fetal growth. The researchers traced these disruptions to one key regulator: SRSF10, a protein that helps orchestrate RNA splicing. When they suppressed SRSF10 in placental cells grown in the lab, the same genetic errors seen in GDM appeared, confirming its central role.

This discovery points to a previously unknown link between maternal metabolism and placental gene expression. “By identifying molecular players like SRSF10, we’re opening a path to interventions that could help protect both mother and child,” said lead author Prof. Maayan Salton of Hebrew University. Co author Dr. Tal Schiller added that the next goal is to explore whether modulating SRSF10 activity could restore normal placental function.

While GDM is often managed through diet, exercise, or insulin, this study shows that its biology runs much deeper—affecting the very software that helps cells interpret genetic code. The findings may ultimately guide new molecular therapies to safeguard pregnancy and long term health for the next generation of children.

REFERENCE: Engal, E., et al. (2025). Gestational Diabetes Mellitus Alters Placental Precursor mRNA Splicing. Diabetes. doi: 10.2337/db25-0333. https://diabetesjournals.org/diabetes/article-abstract/doi/10.2337/db25-0333/163844/Gestational-Diabetes-Mellitus-Alters-Placental?redirectedFrom=fulltext