Medical Bulletin 18/May/2026 - Video

Here are the top medical news for today:

Researchers Find No Strong Evidence Connecting Pregnancy Antidepressants to Autism Risk

For years, many pregnant women taking antidepressants have faced a frightening question: could the medication harm their child’s brain development? A major new study now offers some of the strongest reassurance yet that, for most antidepressants, the answer appears to be no.

Published in The Lancet Psychiatry, the large systematic review and meta-analysis examined 37 studies involving more than 600,000 pregnancies exposed to antidepressants and nearly 25 million unexposed pregnancies. Researchers found no convincing causal link between antidepressant use during pregnancy and neurodevelopmental disorders such as autism or ADHD after accounting for parental mental health and other confounding factors.

Earlier studies had suggested antidepressant exposure might increase autism and ADHD risk. However, researchers found those associations weakened dramatically once factors such as maternal psychiatric conditions, genetics, and family environment were considered.

Interestingly, fathers who used antidepressants also showed a similar increase in the likelihood of having children with ADHD or autism. That finding strongly suggests the elevated risk may stem from shared genetic or mental health factors rather than the medications themselves.

The researchers emphasized that untreated depression during pregnancy also carries serious risks, including relapse, stress, and negative effects on both mother and baby. For women with moderate to severe depression, stopping medication may sometimes be more harmful than continuing treatment.

The study found that commonly prescribed selective serotonin reuptake inhibitors (SSRIs) were not linked to increased autism or ADHD risk when maternal mental health conditions were properly accounted for. Only older antidepressants remained associated with higher risks, though researchers believe this may reflect more severe underlying psychiatric illness among women prescribed those medications.

Researchers note that more studies are still needed to examine factors such as dosage, trimester-specific exposure, and socioeconomic influences. Still, the new analysis provides the clearest evidence so far that antidepressants themselves are unlikely to be driving autism or ADHD risk in children.

REFERENCE: Dr. Wing-Chung Chang, et al.; Maternal and paternal antidepressant use before and during pregnancy and offspring risk of neurodevelopmental disorders: a systematic review and meta-analysis; The Lancet Psychiatry; DOI: 10.1016/S2215-0366(26)00089-1

New Review Examines Whether Supplements Can Help Slow Parkinson’s Disease Progression

The search for a treatment that can slow Parkinson’s disease may be expanding beyond prescription drugs and into the kitchen cabinet. A new scientific review suggests certain dietary supplements could help target biological processes linked to the disease, though researchers caution that evidence remains limited and no supplement has yet been proven to stop progression.

Published in the Journal of Parkinson’s Disease, the review examined human clinical trials investigating whether supplements can modify pathways involved in Parkinson’s disease, including inflammation, oxidative stress, mitochondrial dysfunction, and gut microbiome imbalance.

Parkinson’s disease is the world’s fastest-growing neurological disorder and is expected to affect far more people by 2050. Current medications help control symptoms, but they cannot stop the ongoing loss of dopamine-producing brain cells.

Researchers found that omega-3 fatty acids, particularly when combined with vitamin E, showed some of the most promising early results. Several studies reported reduced inflammation, improved antioxidant defenses, and modest improvements in Parkinson’s symptom scores.

Another supplement attracting attention is nicotinamide riboside, a form of vitamin B3 linked to mitochondrial health. Since mitochondrial dysfunction is believed to contribute to Parkinson’s progression, scientists have explored whether boosting cellular energy production could help protect brain cells. Some trials using higher doses showed improved motor scores, though results have been inconsistent.

The review also examined probiotics and other “biotics” that target the gut microbiome. Digestive problems often appear years before Parkinson’s motor symptoms, leading scientists to suspect the gut may play an important role in disease development. Several studies found that probiotics reduced inflammation and improved some symptoms, especially multi-strain formulations.

Researchers stress that dietary supplements should not replace standard Parkinson’s treatment. Instead, they may eventually become part of broader strategies that combine medication, nutrition, exercise, and gut health support.

REFERENCE: Prasad, A., Shuler, M. S., Flanagan, R., Dayal, V., & Lithander, F. E. (2026). Dietary supplements for Parkinson's disease: State of the science. Journal of Parkinson’s Disease. DOI: 10.1177/1877718X261446386, https://journals.sagepub.com/doi/epub/10.1177/1877718X261446386

Scientists Discover Potential Liver Disease Treatment Through Removal of “Zombie” Cells

A hidden army of “zombie” immune cells may be quietly accelerating aging and fatty liver disease inside the body, according to striking new research from UCLA. Scientists found that removing these dysfunctional cells in mice dramatically reversed liver damage — even while the animals continued eating an unhealthy, high-fat diet.

The study, published in Nature Aging, focused on senescent cells, often nicknamed “zombie cells.” These are damaged cells that stop dividing but refuse to die. Instead, they remain trapped in tissues, releasing inflammatory chemicals that harm nearby cells and fuel chronic disease.

Researchers discovered that a specific type of immune cell called macrophages can become senescent with age and metabolic stress. Macrophages normally help clean up waste and defend tissues, but once they enter this dysfunctional state, they appear to drive persistent inflammation.

The UCLA team identified two proteins, p21 and TREM2, that together act as a clear signature for these harmful macrophages. In young mice, only about 5% of liver macrophages showed this senescent pattern. In older mice, however, the number jumped to as high as 80%, matching the rise in age-related liver inflammation.

Scientists also found that excess LDL cholesterol can trigger the process. When healthy macrophages were exposed to high cholesterol levels in the lab, they stopped functioning normally and began producing inflammatory signals linked to tissue damage.

To test whether removing these cells could reverse disease, researchers treated mice with a drug called ABT-263, which selectively destroys senescent cells. The results were dramatic. Fatty, enlarged livers shrank back toward healthy size, inflammation dropped sharply, and body weight fell significantly — all without changing the animals’ unhealthy diet.

Researchers then examined human liver biopsy data and found the same senescent macrophage signature strongly elevated in people with fatty liver disease, suggesting the mechanism may also occur in humans.

Although the drug used in the study is currently too toxic for routine human use, researchers are now searching for safer therapies that can specifically target and remove these harmful “zombie” cells before they trigger widespread tissue damage.

REFERENCE: Ivan A. Salladay-Perez; p21 TREM2 senescent macrophages fuel inflammaging and metabolic dysfunction-associated steatotic liver disease. Nature Aging, 2026; DOI: 10.1038/s43587-026-01101-6