BEER-SHEVA, Israel, November 10, 2026 -- A new study from Ben-Gurion University of the Negev (BGU) and Soroka University Medical Center has uncovered the biological mechanism behind why many adults and children gain weight following successful treatment for obstructive sleep apnea. The research, published in Scientific Reports (10.1038/s41598-026-68370-4), reveals that the body retains a persistent "metabolic memory" that continues to drive increased appetite even after normal breathing is restored.
The study was co-led by Prof. Ariel Tarasiuk from BGU's Department of Physiology and Cell Biology and director of the Sleep-Wake Disorders Unit at Soroka University Medical Center, and Prof. Yael Segev from BGU's Shraga Segal Department of Microbiology, Immunology, and Genetics. The research team also included PhD student Haiat Nujedat, laboratory manager Dr. Eden Arazi, and Dr. Mohammad H. Assadi.
The Post-Treatment Weight Gain Paradox
Obstructive sleep apnea is a widespread breathing disorder affecting children and adults alike. While treatments such as surgical removal of the tonsils and adenoids or Continuous Positive Airway Pressure (CPAP) therapy successfully clear upper airway obstruction, a significant percentage of patients experience post-treatment weight gain. Until now, the underlying biological trigger for this unintended side effect remained largely unknown.
To investigate the puzzle, the researchers developed a unique animal model to monitor metabolic shifts during chronic upper airway obstruction and following its surgical relief.
A Two-Stage Metabolic Loop
The team discovered that the body undergoes a distinct, two-phase metabolic response to sleep apnea and its recovery:
- Stage 1 (Active Obstruction): The continuous physical strain of struggling to breathe against chronic obstructive airways activates the sympathetic nervous system ("fight-or-flight" response). This sustained physical stress dramatically increases baseline energy expenditure, leading to initial weight loss.
- Stage 2 (Post-Treatment Recovery): Once the airway obstruction is cleared and normal breathing resumes, the sympathetic nervous system fails to shut down. This lingering hyperactivity drives increased food intake, causing an average 15% increase in total body weight.
- Long-Lasting Cellular Memory: Pharmacologically dampening sympathetic activity only partially blunted weight gain, indicating that fat tissue and the autonomic nervous system maintain a long-lasting cellular "memory" of physical stress.
A Cellular Defense That Won't Turn Off
"In patients with sleep apnea, the body develops powerful compensatory mechanisms to cope with continuous respiratory efforts and sleep disruption," explains Prof. Tarasiuk. "When the obstruction is removed, these mechanisms do not immediately turn off. The autonomic system continues operating as if the physical threat were still present, driving post-treatment weight gain".
PhD student Haiat Nujedat notes that testing confirmed the condition was more than a passing phase: "When reducing sympathetic activity failed to return body weight to baseline levels, we realized this was a deeper cellular process rather than a temporary hormonal shift".
Prof. Yael Segev emphasizes the clinical takeaway: "Our findings show that fat tissue undergoes metabolic reprogramming at a cellular level that isn't automatically erased when breathing normalizes. This highlights the potential need for targeted metabolic interventions alongside standard respiratory treatments".
Rethinking Post-Treatment Care
The findings highlight the need for a multidisciplinary care model following sleep apnea therapy, integrating sleep specialists, pulmonologists, and endocrinologists. Combining nutritional and endocrine monitoring with standard airway treatments could help mitigate long-term risks of obesity and cardiovascular disease.
Future research will focus on developing targeted therapies capable of "resetting" this metabolic memory to prevent post-treatment weight gain entirely.
This work was supported by the Israel Science Foundation (ISF) (Grant No. 164/2018).
