Mahima Samraik, MS

America's looming physician shortage is accelerating. A decade-long study reveals that the percent of physicians leaving clinical practice jumped from 3.5% to 4.9% between 2013 and 2019—a troubling trend that threatens to compound the nation's projected shortage of up to 86,000 doctors by 2036.

 tracked more than 712,000 physicians caring for Medicare patients and found attrition rates climbing across every speciality, geographic region, and demographic group.

“Rates of attrition among physicians across specialties are increasing over the years studied,” says senior author 

, assistant professor of emergency medicine at Yale School of Medicine. “This includes male and female doctors, those practicing in rural and urban areas, across all specialties and age groups.”

Female physicians showed a 44% higher likelihood of attrition compared to male colleagues, whereas rural physicians faced a 19% increased risk compared to those in urban settings.

By specialty, psychiatrists and gynecologists showed particularly high attrition rates; psychiatry rates ranged from 7.4% in 2013 to 10.1% in 2019, whereas the attrition for physicians in obstetrics and gynecology soared from 6.1% in 2013 to 10.7% in 2019.

However, when accounting for patient complexity, hospital-based physicians emerged as the highest-risk group. Those with patients enrolled in both Medicare and Medicaid programs showed a 57% increased likelihood of leaving practice.

Rates of attrition among physicians across specialties are increasing over the years studied. This includes male and female doctors, those practicing in rural and urban areas, across all specialties and age groups.

Cameron Gettel, MD, MHSAssistant Professor of Emergency Medicine; Clinical Investigator, Center for Outcomes Research and Evaluation (CORE); Co-Director of Yale Emergency Scholars Fellowship, Emergency Medicine

Behind these statistics are physicians stretched thin, trying to do right by patients with far too little time, Gettel says. Doctors want to give complex patients the attention they deserve, but in today’s system—where appointments often last just minutes—that’s nearly impossible.

“You know the right thing to do, but the system may not allow you to do the right thing. That’s moral injury and it can increase the risk of the physician leaving the workforce,” he says.

The study emphasizes that with current projections estimating shortages of up to 86,000 physicians by 2036—including 40,000 primary care physicians—the accelerating attrition trend poses serious implications for access to care.

"Since attrition is increasing compared to prior years and certain populations are at increased risk, that projected shortage could balloon even higher," Gettel says. "This requires systematic solutions."

The study authors identified several underlying systemic pressures that may drive physicians from practice, such as electronic health record burden, inadequate staffing, prior authorization requirements, and workflow constraints.

"The more an organization addresses those pain points and proactively prevents them, the more likely physicians are to remain in the workforce and continue providing needed care," Gettel says.

The researchers suggest targeted interventions, including enhanced caregiving supports, access to virtual resources, particularly for rural practitioners, and greater physician control over work environments, including shift schedules and patient loads.

"It all comes back to the patient," Gettel says. "These types of workforce studies are so needed because they're a big component of access to care, which is integrally linked to the workforce and availability."

Additional Yale School of Medicine co-authors are Zili He, MS; James Dziura, MPH, PhD; Arjun Venkatesh, MD, MBA; and Edward Melnick, MD, MHS.

Articles

The physician shortage in the U.S. is worsening, with attrition rates rising from 3.5% to 4.9% between 2013 and 2019, potentially exacerbating the projected shortage of up to 86,000 doctors by 2036. The study highlights increased attrition across all specialties, demographics, and regions, with female and rural physicians at higher risk. Psychiatry and obstetrics/gynecology show particularly high attrition rates. Systemic pressures like electronic health record burdens and inadequate staffing contribute to this trend. Targeted interventions are needed to address these issues and improve physician retention.

Increases in Physician Attrition Rates Could Worsen Shortages

Noonan syndrome with multiple lentigines (NSML) is a rare genetic disorder that causes short stature, distinctive facial features, and clusters of dark skin spots called lentigines. But its most serious impact is a dangerous thickening of the heart muscle, the onset of which is not well understood.

Now, researchers at Yale School of Medicine (YSM) have discovered how certain genetic mutations can lead to this severe heart condition, additionally identifying a leukemia drug that shows promise as a therapeutic.

Their findings were published recently in 

Proceedings of the National Academy of Sciences

“Newborns with Noonan syndrome that have severe heart failure often die within the first six months of life. No treatment exists, which is why finding one is so important,” says 

 associate research scientist in the Department of Pharmacology at YSM and lead author of the study. “It is very difficult and time-consuming to develop a new drug, so we thought it's best if we could repurpose a drug that already exists.”

The molecules underlying heart thickening

NSML is caused by mutations in a gene that codes for an enzyme called SHP2, which plays a critical role in cell signalling. Previous research has found that in NSML, SHP2 variants are less active than typical forms of the enzyme. But Yale researchers discovered this wasn’t what was behind the heart-thickening condition known as hypertrophic cardiomyopathy.

“We revealed that the key lies not in SHP2's enzymatic action, but in its ability to act as a scaffolding platform due to these specific mutations,” says senior author 

 Dorys McConnell Duberg Professor of Pharmacology, professor of comparative medicine, and director of the Yale Center for Molecular and Systems Metabolism at YSM.

The researchers found that when mutated in NSML, SHP2 binds to another protein and recruits another enzyme called c-Src, a tyrosine kinase. Together, this molecular trio sets off a chain reaction that abnormally boosts two transcription factors—proteins that turn a gene on or off—that are critical for normal heart development.

These transcription factors were elevated in NSML mouse models, the research team found. And when they rose too high, they dramatically reduced levels of BMP10, a growth-regulating protein essential for healthy heart muscle structure.

With these findings in hand, the team used a drug known to inhibit c-Src activity, which they had found in earlier studies could reverse hypertrophic cardiomyopathy. They tested whether the drug—a leukemia treatment called dasatinib—could restore the balance of BMP10 molecules driving hypertrophic cardiomyopathy in Noonan syndrome.

The researchers found that very low doses of dasatinib returned BMP10 levels in NSML mice to normal levels. By inhibiting c-Src, dasatinib prevented the transcription factors from becoming overly active, essentially counteracting the effect of the mutated gene implicated in NSML.

The drug, therefore, offers a potential path for treating heart thickening in patients with NSML, the researchers say.

“We were able to connect the dots from gene expression all the way to protein structure and cardiac function,” says Perla. “That gives us confidence that targeting this pathway could actually work in patients.”

In future clinical trials, the work could lead the way towards the development of a lifesaving therapy for NSML patients.

Researchers at Yale School of Medicine have identified how genetic mutations in Noonan syndrome with multiple lentigines (NSML) lead to hypertrophic cardiomyopathy, a severe heart condition. They discovered that mutations in the SHP2 enzyme cause it to act as a scaffolding platform, recruiting c-Src, which triggers a chain reaction affecting heart development. The leukemia drug dasatinib, which inhibits c-Src, was found to restore normal levels of BMP10, a crucial growth-regulating protein, in NSML mouse models. This discovery offers a promising therapeutic avenue for NSML patients.