Sleep shortage during pregnancy may hurt baby’s brain
(Reuters) – Pregnant women who do not get enough sleep may be at higher risk of having children with neurodevelopmental delays, a new study suggests.
Among mothers who averaged less than seven hours of sleep per night while pregnant, the effect on neurodevelopment of the baby was particularly evident in boys, according to a report published on Thursday in the Journal of Clinical Endocrinology and Metabolism.
In the study, the risk of neurodevelopmental delays – for example, in emotional, behavioral, motor, cognitive, or speech skills – in participants’ babies was associated with umbilical cord blood levels of serum C-peptide, a byproduct of insulin production by the pancreas.
Short sleep duration during pregnancy has previously been linked with higher risks for impaired glucose tolerance, insulin resistance and gestational diabetes, which on their own can impact babies’ neurodevelopment, the researchers noted.
The study cannot prove that skimping on sleep caused neurodevelopmental delays.
But it adds to evidence that a mother’s glucose metabolism during pregnancy may impact insulin secretion in the fetus, which is known to impact neurodevelopment.
“By shedding light on the connection between maternal sleep during pregnancy and children’s neurodevelopment, our study empowers families with knowledge that can shape healthier pregnancy habits and contribute to the well being of the next generation,” study leader Dr. Peng Zhu of Anhui Medical University in Hefei, China said in a statement.
Read also: Detailed Analysis of Conditions Affecting Fetal Health During Pregnancy
Merck drug promising for ulcerative colitis
An experimental monoclonal antibody developed by Merck & Co for ulcerative colitis was superior to placebo in a mid-stage study, and a genetic test showed promise for predicting who will benefit from it, researchers reported in The New England Journal of Medicine.
The randomized trial tested tulisokibart in 135 patients with moderate to severe ulcerative colitis that was not responding to commercially available drugs.
Twelve weeks after adding tulisokibart to their current drug regimen, 26% of patients had achieved clinical remission, meaning their symptoms had completely resolved. That rate was 1% in the placebo group.
In addition, 66% of those who received tulisokibart showed at least some improvement, versus 22% for the placebo group, and 37% on the Merck drug experienced healing in their intestines as documented during endoscopy, compared with 6% for placebo.
Tulisokibart works by blocking the effects of an inflammatory protein called tumor necrosis factor–like cytokine 1A (TL1A), which can contribute to inflammation and fibrosis, or scarring, in ulcerative colitis.
Researchers are also developing a genetic-based diagnostic test to identify patients most likely to respond to the drug. Among the 75 patients in this study with a positive “likely to respond” test result, clinical remission rates were 32% with tulisokibart versus 11% for placebo.
Being able to identify biomarkers that predict which patients will respond best to TL1A inhibition would pave the way for more personalized and targeted treatment strategies, the researchers said.
The “findings from this study are poised to have a remarkable impact on treatment for ulcerative colitis and IBD (inflammatory bowel disease) overall,” study co-author Dr. Stephan Targan of Cedars-Sinai Medical Center in Los Angeles said in a statement.
Larger confirmatory trials of tulisokibart are already underway.
Merck announced on Thursday that patients in the mid-stage trial who had responded to the treatment at 12 weeks were still responding to it nearly a year later.
Tulisokibart “shows promise as being both anti-inflammatory and anti-fibrotic. It represents a potential turning point in drug development and discovery, and it could change how this complex disease is treated in the future,” Targan said.
Reporting by Nancy Lapid; editing by Bill Berkrot
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