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UVA Defends Medical School Dean, Hospital CEO After Docs Call for Their Removal
The University of Virginia (UVA) is defending the CEO of its health system and its medical school dean in the wake of a very public call for their removal.
At least 128 members of the University of Virginia faculty who are employed by both the medical school and the UVA Physicians Group wrote to the UVA Board of Visitors and its peer-elected faculty leaders, expressing no confidence in K. Craig Kent, MD, CEO of UVA Health and executive vice president for health affairs, and Melina Kibbe, MD, dean of the medical school and chief health affairs officer.
Dr. Kibbe, a vascular surgeon and researcher, is also the editor in chief of JAMA Surgery.
“We call for the immediate removal of Craig Kent and Melina Kibbe,” wrote the physicians.
The letter alleged that patient safety was compromised because doctors, nurses, and other staff were pressured to abstain from reporting safety concerns and that physicians had been hired “despite concerns regarding integrity and quality.” Those who raised safety concerns faced “explicit and implicit threats and retaliation,” including delays and denials of promotion and tenure, said the letter.
The September 5 letter did not include signatures. The authors said that names were being protected, but that they would share the names with a limited audience.
UVA President Jim Ryan took issue with the notion that the signees were anonymous. He said in his own letter to medical school faculty that some of the accusations were about matters that had already been addressed or that were being worked on. As far as allegations that he was not previously aware of, “we will do our best to investigate,” he said.
The faculty who signed the letter “have besmirched the reputations of not just Melina and Craig,” wrote Mr. Ryan. “They have unfairly — and I trust unwittingly — cast a shadow over the great work of the entire health system and medical school.”
The authors claimed that reports about bullying and harassment of trainees had been “suppressed, minimized, and subsequently altered.”
And they said that spending on leadership was prioritized over addressing clinical and technical staff shortages. Whistleblowers who reported fraud were not protected, and clinicians were pressured to modify patient records to “obfuscate adverse outcomes and boost productivity metrics,” they wrote.
The 128 members of the UVA Physicians Group who signed the letter represent about 10% of the 1400 medical school faculty members.
It is not the first time that Dr. Kent has been given a vote of no confidence. In 2017, when he was the dean of the College of Medicine at the Ohio State University, Dr. Kent was accused in a “no confidence” letter from 25 physicians and faculty of helping to undermine the school’s mission and taking actions that led to resignations and early retirements of many staff, the Columbus Dispatch reported.
William G. Crutchfield Jr., a member of the UVA Health System Board, defended Dr. Kent and Dr. Kibbe in a lengthy statement shared with this news organization. He said that UVA Health’s four hospitals had received “A” ratings for safety, and that the system has a 5.1% turnover rate compared with a national average of 8.3%.
Dr. Kent and Dr. Kibbe have recruited faculty from top academic medical centers, Mr. Crutchfield wrote.
“If our work environment were so toxic, these people would not have joined our faculty,” he wrote.
Mr. Crutchfield credited Dr. Kent and Dr. Kibbe with crafting a new 10-year strategic plan and for hiring a chief strategy officer to lead the plan — a move that replaced “expensive outside consultants.”
Mr. Ryan said in his letter that his inbox “is overflowing with testimonials from some of the 1200-plus faculty who did not sign the letter, who attest that the health system today — under Melina and Craig’s leadership — is in the best shape it has ever been in, and that they have addressed changes that have needed to be made for more than two decades.”
A request to see some of these positive testimonials was not answered by press time.
Mr. Crutchfield, like Mr. Ryan, said that the letter writers were doing more harm than good.
“If a small cabal of people hiding behind anonymity can force outstanding leaders out of UVA, it will make it extremely difficult to recruit outstanding new physicians, nurses, technicians, and administrators,” he wrote.
A version of this article first appeared on Medscape.com.
The University of Virginia (UVA) is defending the CEO of its health system and its medical school dean in the wake of a very public call for their removal.
At least 128 members of the University of Virginia faculty who are employed by both the medical school and the UVA Physicians Group wrote to the UVA Board of Visitors and its peer-elected faculty leaders, expressing no confidence in K. Craig Kent, MD, CEO of UVA Health and executive vice president for health affairs, and Melina Kibbe, MD, dean of the medical school and chief health affairs officer.
Dr. Kibbe, a vascular surgeon and researcher, is also the editor in chief of JAMA Surgery.
“We call for the immediate removal of Craig Kent and Melina Kibbe,” wrote the physicians.
The letter alleged that patient safety was compromised because doctors, nurses, and other staff were pressured to abstain from reporting safety concerns and that physicians had been hired “despite concerns regarding integrity and quality.” Those who raised safety concerns faced “explicit and implicit threats and retaliation,” including delays and denials of promotion and tenure, said the letter.
The September 5 letter did not include signatures. The authors said that names were being protected, but that they would share the names with a limited audience.
UVA President Jim Ryan took issue with the notion that the signees were anonymous. He said in his own letter to medical school faculty that some of the accusations were about matters that had already been addressed or that were being worked on. As far as allegations that he was not previously aware of, “we will do our best to investigate,” he said.
The faculty who signed the letter “have besmirched the reputations of not just Melina and Craig,” wrote Mr. Ryan. “They have unfairly — and I trust unwittingly — cast a shadow over the great work of the entire health system and medical school.”
The authors claimed that reports about bullying and harassment of trainees had been “suppressed, minimized, and subsequently altered.”
And they said that spending on leadership was prioritized over addressing clinical and technical staff shortages. Whistleblowers who reported fraud were not protected, and clinicians were pressured to modify patient records to “obfuscate adverse outcomes and boost productivity metrics,” they wrote.
The 128 members of the UVA Physicians Group who signed the letter represent about 10% of the 1400 medical school faculty members.
It is not the first time that Dr. Kent has been given a vote of no confidence. In 2017, when he was the dean of the College of Medicine at the Ohio State University, Dr. Kent was accused in a “no confidence” letter from 25 physicians and faculty of helping to undermine the school’s mission and taking actions that led to resignations and early retirements of many staff, the Columbus Dispatch reported.
William G. Crutchfield Jr., a member of the UVA Health System Board, defended Dr. Kent and Dr. Kibbe in a lengthy statement shared with this news organization. He said that UVA Health’s four hospitals had received “A” ratings for safety, and that the system has a 5.1% turnover rate compared with a national average of 8.3%.
Dr. Kent and Dr. Kibbe have recruited faculty from top academic medical centers, Mr. Crutchfield wrote.
“If our work environment were so toxic, these people would not have joined our faculty,” he wrote.
Mr. Crutchfield credited Dr. Kent and Dr. Kibbe with crafting a new 10-year strategic plan and for hiring a chief strategy officer to lead the plan — a move that replaced “expensive outside consultants.”
Mr. Ryan said in his letter that his inbox “is overflowing with testimonials from some of the 1200-plus faculty who did not sign the letter, who attest that the health system today — under Melina and Craig’s leadership — is in the best shape it has ever been in, and that they have addressed changes that have needed to be made for more than two decades.”
A request to see some of these positive testimonials was not answered by press time.
Mr. Crutchfield, like Mr. Ryan, said that the letter writers were doing more harm than good.
“If a small cabal of people hiding behind anonymity can force outstanding leaders out of UVA, it will make it extremely difficult to recruit outstanding new physicians, nurses, technicians, and administrators,” he wrote.
A version of this article first appeared on Medscape.com.
The University of Virginia (UVA) is defending the CEO of its health system and its medical school dean in the wake of a very public call for their removal.
At least 128 members of the University of Virginia faculty who are employed by both the medical school and the UVA Physicians Group wrote to the UVA Board of Visitors and its peer-elected faculty leaders, expressing no confidence in K. Craig Kent, MD, CEO of UVA Health and executive vice president for health affairs, and Melina Kibbe, MD, dean of the medical school and chief health affairs officer.
Dr. Kibbe, a vascular surgeon and researcher, is also the editor in chief of JAMA Surgery.
“We call for the immediate removal of Craig Kent and Melina Kibbe,” wrote the physicians.
The letter alleged that patient safety was compromised because doctors, nurses, and other staff were pressured to abstain from reporting safety concerns and that physicians had been hired “despite concerns regarding integrity and quality.” Those who raised safety concerns faced “explicit and implicit threats and retaliation,” including delays and denials of promotion and tenure, said the letter.
The September 5 letter did not include signatures. The authors said that names were being protected, but that they would share the names with a limited audience.
UVA President Jim Ryan took issue with the notion that the signees were anonymous. He said in his own letter to medical school faculty that some of the accusations were about matters that had already been addressed or that were being worked on. As far as allegations that he was not previously aware of, “we will do our best to investigate,” he said.
The faculty who signed the letter “have besmirched the reputations of not just Melina and Craig,” wrote Mr. Ryan. “They have unfairly — and I trust unwittingly — cast a shadow over the great work of the entire health system and medical school.”
The authors claimed that reports about bullying and harassment of trainees had been “suppressed, minimized, and subsequently altered.”
And they said that spending on leadership was prioritized over addressing clinical and technical staff shortages. Whistleblowers who reported fraud were not protected, and clinicians were pressured to modify patient records to “obfuscate adverse outcomes and boost productivity metrics,” they wrote.
The 128 members of the UVA Physicians Group who signed the letter represent about 10% of the 1400 medical school faculty members.
It is not the first time that Dr. Kent has been given a vote of no confidence. In 2017, when he was the dean of the College of Medicine at the Ohio State University, Dr. Kent was accused in a “no confidence” letter from 25 physicians and faculty of helping to undermine the school’s mission and taking actions that led to resignations and early retirements of many staff, the Columbus Dispatch reported.
William G. Crutchfield Jr., a member of the UVA Health System Board, defended Dr. Kent and Dr. Kibbe in a lengthy statement shared with this news organization. He said that UVA Health’s four hospitals had received “A” ratings for safety, and that the system has a 5.1% turnover rate compared with a national average of 8.3%.
Dr. Kent and Dr. Kibbe have recruited faculty from top academic medical centers, Mr. Crutchfield wrote.
“If our work environment were so toxic, these people would not have joined our faculty,” he wrote.
Mr. Crutchfield credited Dr. Kent and Dr. Kibbe with crafting a new 10-year strategic plan and for hiring a chief strategy officer to lead the plan — a move that replaced “expensive outside consultants.”
Mr. Ryan said in his letter that his inbox “is overflowing with testimonials from some of the 1200-plus faculty who did not sign the letter, who attest that the health system today — under Melina and Craig’s leadership — is in the best shape it has ever been in, and that they have addressed changes that have needed to be made for more than two decades.”
A request to see some of these positive testimonials was not answered by press time.
Mr. Crutchfield, like Mr. Ryan, said that the letter writers were doing more harm than good.
“If a small cabal of people hiding behind anonymity can force outstanding leaders out of UVA, it will make it extremely difficult to recruit outstanding new physicians, nurses, technicians, and administrators,” he wrote.
A version of this article first appeared on Medscape.com.
What Do We Know About Postoperative Cognitive Dysfunction?
Postoperative cognitive dysfunction (POCD) is a form of cognitive decline that involves a functional deterioration of activities of the nervous system, such as selective attention, vigilance, perception, learning, memory, executive function, verbal and language abilities, emotion, visuospatial and visuomotor skills. It occurs in the absence of cranial trauma or other brain injuries, and prevalence rates range from 36.6% in young adults to 42.4% in older adults, as a consequence of significant invasive procedures such as cardiac, noncardiac, and carotid surgeries that are lengthy and intensive.
Alzheimer’s disease (AD), the most common form of dementia, accounts for about two thirds of all cases of dementia globally. It is estimated that 41 million patients with dementia remain undiagnosed worldwide, and 25% of patients are diagnosed only when they are fully symptomatic. AD is a neurodegenerative disorder defined by neuropathologic changes, including beta-amyloid (Abeta) plaques composed of aggregated Abeta and neurofibrillary tangles containing aggregated tau proteins.
Patients with AD are unaware of their condition. Dementia, especially in its early stages, is often a hidden disease. Even when suspected, patients and families may believe that the symptoms are part of normal aging and may not report them to the doctor. In these patients, surgery may unmask subclinical dementia.
The complex correlation between POCD and AD has sparked debate following numerous anecdotal reports of how older adults undergoing surgical procedures may experience long-term cognitive decline with clinical characteristics such as those of patients with dementia. Despite advances in knowledge, it is still difficult to establish a priori how much surgery and anesthesia can increase the risk or accelerate the progression of a prodromal and asymptomatic AD condition (stages I-II) to clinically evident stage III AD. The current trend of an aging population poses a challenge for anesthesiology surgery because as the age of patients undergoing surgery increases, so does the likelihood of developing POCD.
Recent research in these fields has improved knowledge of the characteristics, epidemiology, risk factors, pathogenesis, and potential prevention strategies associated with POCD. It has improved the perspectives of future prevention and treatment.
Definition and Diagnostic Criteria
POCD, according to the cognitive impairment classification in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, is characterized by mild neurologic disturbance resulting from routine surgical procedures, excluding conditions such as deafness, dementia, or amnesia. The definition of POCD involves prolonged cognitive decline that can last for weeks, months, or even years. POCD may be confused with postoperative delirium, an acute and fluctuating disorder of consciousness that typically occurs within 3 days of surgery.
The diagnosis of POCD is based primarily on neurocognitive function scales. Widely used assessments include the Montreal Cognitive Assessment, the Wechsler Memory Scale, and the Mini-Mental State Examination.
Epidemiology
POCD is prevalent among patients undergoing cardiac or orthopedic surgery. In patients undergoing aortic-coronary bypass and cardiopulmonary bypass, 50%-70% develop POCD 1 week after surgery. In addition, 10%-30% experience long-term effects on cognitive function at 6 months after the procedure. In patients undergoing hip arthroplasty, 20%-50% exhibit POCD within 1 week of surgery, with 10%-14% still presenting it after 3 months.
Risk Factors
Age
POCD is typically observed in patients older than 65 years. However, after surgery, around 30% of younger patients and about 40% of older patients develop POCD at the time of hospital discharge. Specifically, 12.7% of older patients continue to have POCD 3 months after surgery, compared with 5% of younger patients.
Type of Surgery
Hip and knee arthroplasty procedures entail a higher risk for POCD than general surgery. The same is true of cardiac surgery, especially aortic-coronary bypass and cardiopulmonary bypass.
Types of Anesthesia
Initial assessments of postoperative cognitive function in cardiac surgery did not provide significant correlations between observed changes and the type of anesthesia because of the high number of confounding factors involved. A more recent meta-analysis of 28 randomized clinical trials concluded that the incidence of POCD is lower in surgeries using intravenous anesthesia with propofol than in those using inhalation anesthesia with isoflurane or sevoflurane.
Pain
Postoperative pain is a common issue, mainly resulting from substantial surgical trauma or potential wound infection. Patient-controlled postoperative analgesia independently increases the risk for POCD, compared with oral postoperative analgesia. Meta-analyses indicate that persistent pain can lead to a decline in patients’ cognitive abilities, attention, memory, and information processing.
Evolving Scenarios
Current research on POCD has deepened our understanding of its pathogenesis, implicating factors such as central nervous system inflammation, neuronal apoptosis, synaptic plasticity damage, abnormal tau protein modification, chronic pain, and mitochondrial metabolic disorders. Several neuroprotective drugs are currently under study, but none have shown consistent benefits for the prevention and treatment of POCD. The available evidence on the subject does not unambiguously guide the practicing physician. But neither does it exclude the importance of a careful assessment of POCD risk factors and the cognitive status of an older patient before surgery to provide useful information to the patient, family, and doctors when deciding on appropriate and shared procedures.
This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Postoperative cognitive dysfunction (POCD) is a form of cognitive decline that involves a functional deterioration of activities of the nervous system, such as selective attention, vigilance, perception, learning, memory, executive function, verbal and language abilities, emotion, visuospatial and visuomotor skills. It occurs in the absence of cranial trauma or other brain injuries, and prevalence rates range from 36.6% in young adults to 42.4% in older adults, as a consequence of significant invasive procedures such as cardiac, noncardiac, and carotid surgeries that are lengthy and intensive.
Alzheimer’s disease (AD), the most common form of dementia, accounts for about two thirds of all cases of dementia globally. It is estimated that 41 million patients with dementia remain undiagnosed worldwide, and 25% of patients are diagnosed only when they are fully symptomatic. AD is a neurodegenerative disorder defined by neuropathologic changes, including beta-amyloid (Abeta) plaques composed of aggregated Abeta and neurofibrillary tangles containing aggregated tau proteins.
Patients with AD are unaware of their condition. Dementia, especially in its early stages, is often a hidden disease. Even when suspected, patients and families may believe that the symptoms are part of normal aging and may not report them to the doctor. In these patients, surgery may unmask subclinical dementia.
The complex correlation between POCD and AD has sparked debate following numerous anecdotal reports of how older adults undergoing surgical procedures may experience long-term cognitive decline with clinical characteristics such as those of patients with dementia. Despite advances in knowledge, it is still difficult to establish a priori how much surgery and anesthesia can increase the risk or accelerate the progression of a prodromal and asymptomatic AD condition (stages I-II) to clinically evident stage III AD. The current trend of an aging population poses a challenge for anesthesiology surgery because as the age of patients undergoing surgery increases, so does the likelihood of developing POCD.
Recent research in these fields has improved knowledge of the characteristics, epidemiology, risk factors, pathogenesis, and potential prevention strategies associated with POCD. It has improved the perspectives of future prevention and treatment.
Definition and Diagnostic Criteria
POCD, according to the cognitive impairment classification in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, is characterized by mild neurologic disturbance resulting from routine surgical procedures, excluding conditions such as deafness, dementia, or amnesia. The definition of POCD involves prolonged cognitive decline that can last for weeks, months, or even years. POCD may be confused with postoperative delirium, an acute and fluctuating disorder of consciousness that typically occurs within 3 days of surgery.
The diagnosis of POCD is based primarily on neurocognitive function scales. Widely used assessments include the Montreal Cognitive Assessment, the Wechsler Memory Scale, and the Mini-Mental State Examination.
Epidemiology
POCD is prevalent among patients undergoing cardiac or orthopedic surgery. In patients undergoing aortic-coronary bypass and cardiopulmonary bypass, 50%-70% develop POCD 1 week after surgery. In addition, 10%-30% experience long-term effects on cognitive function at 6 months after the procedure. In patients undergoing hip arthroplasty, 20%-50% exhibit POCD within 1 week of surgery, with 10%-14% still presenting it after 3 months.
Risk Factors
Age
POCD is typically observed in patients older than 65 years. However, after surgery, around 30% of younger patients and about 40% of older patients develop POCD at the time of hospital discharge. Specifically, 12.7% of older patients continue to have POCD 3 months after surgery, compared with 5% of younger patients.
Type of Surgery
Hip and knee arthroplasty procedures entail a higher risk for POCD than general surgery. The same is true of cardiac surgery, especially aortic-coronary bypass and cardiopulmonary bypass.
Types of Anesthesia
Initial assessments of postoperative cognitive function in cardiac surgery did not provide significant correlations between observed changes and the type of anesthesia because of the high number of confounding factors involved. A more recent meta-analysis of 28 randomized clinical trials concluded that the incidence of POCD is lower in surgeries using intravenous anesthesia with propofol than in those using inhalation anesthesia with isoflurane or sevoflurane.
Pain
Postoperative pain is a common issue, mainly resulting from substantial surgical trauma or potential wound infection. Patient-controlled postoperative analgesia independently increases the risk for POCD, compared with oral postoperative analgesia. Meta-analyses indicate that persistent pain can lead to a decline in patients’ cognitive abilities, attention, memory, and information processing.
Evolving Scenarios
Current research on POCD has deepened our understanding of its pathogenesis, implicating factors such as central nervous system inflammation, neuronal apoptosis, synaptic plasticity damage, abnormal tau protein modification, chronic pain, and mitochondrial metabolic disorders. Several neuroprotective drugs are currently under study, but none have shown consistent benefits for the prevention and treatment of POCD. The available evidence on the subject does not unambiguously guide the practicing physician. But neither does it exclude the importance of a careful assessment of POCD risk factors and the cognitive status of an older patient before surgery to provide useful information to the patient, family, and doctors when deciding on appropriate and shared procedures.
This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Postoperative cognitive dysfunction (POCD) is a form of cognitive decline that involves a functional deterioration of activities of the nervous system, such as selective attention, vigilance, perception, learning, memory, executive function, verbal and language abilities, emotion, visuospatial and visuomotor skills. It occurs in the absence of cranial trauma or other brain injuries, and prevalence rates range from 36.6% in young adults to 42.4% in older adults, as a consequence of significant invasive procedures such as cardiac, noncardiac, and carotid surgeries that are lengthy and intensive.
Alzheimer’s disease (AD), the most common form of dementia, accounts for about two thirds of all cases of dementia globally. It is estimated that 41 million patients with dementia remain undiagnosed worldwide, and 25% of patients are diagnosed only when they are fully symptomatic. AD is a neurodegenerative disorder defined by neuropathologic changes, including beta-amyloid (Abeta) plaques composed of aggregated Abeta and neurofibrillary tangles containing aggregated tau proteins.
Patients with AD are unaware of their condition. Dementia, especially in its early stages, is often a hidden disease. Even when suspected, patients and families may believe that the symptoms are part of normal aging and may not report them to the doctor. In these patients, surgery may unmask subclinical dementia.
The complex correlation between POCD and AD has sparked debate following numerous anecdotal reports of how older adults undergoing surgical procedures may experience long-term cognitive decline with clinical characteristics such as those of patients with dementia. Despite advances in knowledge, it is still difficult to establish a priori how much surgery and anesthesia can increase the risk or accelerate the progression of a prodromal and asymptomatic AD condition (stages I-II) to clinically evident stage III AD. The current trend of an aging population poses a challenge for anesthesiology surgery because as the age of patients undergoing surgery increases, so does the likelihood of developing POCD.
Recent research in these fields has improved knowledge of the characteristics, epidemiology, risk factors, pathogenesis, and potential prevention strategies associated with POCD. It has improved the perspectives of future prevention and treatment.
Definition and Diagnostic Criteria
POCD, according to the cognitive impairment classification in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, is characterized by mild neurologic disturbance resulting from routine surgical procedures, excluding conditions such as deafness, dementia, or amnesia. The definition of POCD involves prolonged cognitive decline that can last for weeks, months, or even years. POCD may be confused with postoperative delirium, an acute and fluctuating disorder of consciousness that typically occurs within 3 days of surgery.
The diagnosis of POCD is based primarily on neurocognitive function scales. Widely used assessments include the Montreal Cognitive Assessment, the Wechsler Memory Scale, and the Mini-Mental State Examination.
Epidemiology
POCD is prevalent among patients undergoing cardiac or orthopedic surgery. In patients undergoing aortic-coronary bypass and cardiopulmonary bypass, 50%-70% develop POCD 1 week after surgery. In addition, 10%-30% experience long-term effects on cognitive function at 6 months after the procedure. In patients undergoing hip arthroplasty, 20%-50% exhibit POCD within 1 week of surgery, with 10%-14% still presenting it after 3 months.
Risk Factors
Age
POCD is typically observed in patients older than 65 years. However, after surgery, around 30% of younger patients and about 40% of older patients develop POCD at the time of hospital discharge. Specifically, 12.7% of older patients continue to have POCD 3 months after surgery, compared with 5% of younger patients.
Type of Surgery
Hip and knee arthroplasty procedures entail a higher risk for POCD than general surgery. The same is true of cardiac surgery, especially aortic-coronary bypass and cardiopulmonary bypass.
Types of Anesthesia
Initial assessments of postoperative cognitive function in cardiac surgery did not provide significant correlations between observed changes and the type of anesthesia because of the high number of confounding factors involved. A more recent meta-analysis of 28 randomized clinical trials concluded that the incidence of POCD is lower in surgeries using intravenous anesthesia with propofol than in those using inhalation anesthesia with isoflurane or sevoflurane.
Pain
Postoperative pain is a common issue, mainly resulting from substantial surgical trauma or potential wound infection. Patient-controlled postoperative analgesia independently increases the risk for POCD, compared with oral postoperative analgesia. Meta-analyses indicate that persistent pain can lead to a decline in patients’ cognitive abilities, attention, memory, and information processing.
Evolving Scenarios
Current research on POCD has deepened our understanding of its pathogenesis, implicating factors such as central nervous system inflammation, neuronal apoptosis, synaptic plasticity damage, abnormal tau protein modification, chronic pain, and mitochondrial metabolic disorders. Several neuroprotective drugs are currently under study, but none have shown consistent benefits for the prevention and treatment of POCD. The available evidence on the subject does not unambiguously guide the practicing physician. But neither does it exclude the importance of a careful assessment of POCD risk factors and the cognitive status of an older patient before surgery to provide useful information to the patient, family, and doctors when deciding on appropriate and shared procedures.
This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
The Silent Exodus: Are Nurse Practitioners and Physician Assistants Quiet Quitting?
While she cared deeply about her work, Melissa Adams*, a family nurse practitioner (NP) in Madison, Alabama, was being frequently triple-booked, didn’t feel respected by her office manager, and started to worry about becoming burned out. When she sought help, “the administration was tone-deaf,” she said. “When I asked about what I could do to prevent burnout, they sent me an article about it. It was clear to me that asking for respite from triple-booking and asking to be respected by my office manager wasn’t being heard ... so I thought, ‘how do I fly under the radar and get by with what I can?’ ” That meant focusing on patient care and refusing to take on additional responsibilities, like training new hires or working with students.
“You’re overworked and underpaid, and you start giving less and less of yourself,” Ms. Adams said in an interview.
Quiet quitting, defined as performing only the assigned tasks of the job without making any extra effort or going the proverbial extra mile, has gained attention in the press in recent years. A Gallup poll found that about 50% of the workforce were “quiet quitters” or disengaged.
It may be even more prevalent in healthcare, where a recent survey found that 57% of frontline medical staff, including NPs and physician assistants (PAs), report being disengaged at work.
The Causes of Quiet Quitting
Potential causes of quiet quitting among PAs and NPs include:
- Unrealistic care expectations. Ms. Adams said.
- Lack of trust or respect. Physicians don’t always respect the role that PAs and NPs play in a practice.
- Dissatisfaction with leadership or administration. There’s often a feeling that the PA or NP isn’t “heard” or appreciated.
- Dissatisfaction with pay or working conditions.
- Moral injury. “There’s no way to escape being morally injured when you work with an at-risk population,” said Ms. Adams. “You may see someone who has 20-24 determinants of health, and you’re expected to schlep them through in 8 minutes — you know you’re not able to do what they need.”
What Quiet Quitting Looks Like
Terri Smith*, an NP at an academic medical center outpatient clinic in rural Vermont, said that, while she feels appreciated by her patients and her team, there’s poor communication from the administration, which has caused her to quietly quit.
“I stopped saying ‘yes’ to all the normal committee work and the extra stuff that used to add a lot to my professional enjoyment,” she said. “The last couple of years, my whole motto is to nod and smile when administration says to do something — to put your head down and take care of your patients.”
While the term “quiet quitting” may be new, the issue is not, said Bridget Roberts, PhD, a healthcare executive who ran a large physician’s group of 100 healthcare providers in Jacksonville, Florida, for a decade. “Quiet quitting is a fancy title for employees who are completely disengaged,” said Dr. Roberts. “When they’re on the way out, they ‘check the box’. That’s not a new thing.”
“Typically, the first thing you see is a lot of frustration in that they aren’t able to complete the tasks they have at hand,” said Rebecca Day, PMNHP, a doctoral-educated NP and director of nursing practice at a Federally Qualified Health Center in Corbin, Kentucky. “Staff may be overworked and not have enough time to do what’s required of them with patient care as well as the paperwork required behind the scenes. It [quiet quitting] is doing just enough to get by, but shortcutting as much as they can to try to save some time.”
Addressing Quiet Quitting
Those kinds of shortcuts may affect patients, admits Ms. Smith. “I do think it starts to seep into patient care,” she said. “And that really doesn’t feel good ... at our institution, I’m not just an NP — I’m the nurse, the doctor, the secretary — I’m everybody, and for the last year, almost every single day in clinic, I’m apologizing [to a patient] because we can’t do something.”
Watching for this frustration can help alert administrators to NPs and PAs who may be “checking out” at work. Open lines of communication can help you address the issue. “Ask questions like ‘What could we do differently to make your day easier?’” said Dr. Roberts. Understanding the day-to-day issues NPs and PAs face at work can help in developing a plan to address disengagement.
When Dr. Day sees quiet quitting at her practice, she talks with the advance practice provider about what’s causing the issue. “’Are you overworked? Are you understaffed? Are there problems at home? Do you feel you’re receiving inadequate pay?’ ” she said. “The first thing to do is address that and find mutual ground on the issues…deal with the person as a person and then go back and deal with the person as an employee. If your staff isn’t happy, your clinic isn’t going to be productive.”
Finally, while reasons for quiet quitting may vary, cultivating a collaborative atmosphere where NPs and PAs feel appreciated and valued can help reduce the risk for quiet quitting. “Get to know your advanced practice providers,” said Ms. Adams. “Understand their strengths and what they’re about. It’s not an ‘us vs them’ ... there is a lot more commonality when we approach it that way.” Respect for the integral role that NPs and PAs play in your practice can help reduce the risk for quiet quitting — and help provide better patient care.
*Names have been changed.
A version of this article first appeared on Medscape.com.
While she cared deeply about her work, Melissa Adams*, a family nurse practitioner (NP) in Madison, Alabama, was being frequently triple-booked, didn’t feel respected by her office manager, and started to worry about becoming burned out. When she sought help, “the administration was tone-deaf,” she said. “When I asked about what I could do to prevent burnout, they sent me an article about it. It was clear to me that asking for respite from triple-booking and asking to be respected by my office manager wasn’t being heard ... so I thought, ‘how do I fly under the radar and get by with what I can?’ ” That meant focusing on patient care and refusing to take on additional responsibilities, like training new hires or working with students.
“You’re overworked and underpaid, and you start giving less and less of yourself,” Ms. Adams said in an interview.
Quiet quitting, defined as performing only the assigned tasks of the job without making any extra effort or going the proverbial extra mile, has gained attention in the press in recent years. A Gallup poll found that about 50% of the workforce were “quiet quitters” or disengaged.
It may be even more prevalent in healthcare, where a recent survey found that 57% of frontline medical staff, including NPs and physician assistants (PAs), report being disengaged at work.
The Causes of Quiet Quitting
Potential causes of quiet quitting among PAs and NPs include:
- Unrealistic care expectations. Ms. Adams said.
- Lack of trust or respect. Physicians don’t always respect the role that PAs and NPs play in a practice.
- Dissatisfaction with leadership or administration. There’s often a feeling that the PA or NP isn’t “heard” or appreciated.
- Dissatisfaction with pay or working conditions.
- Moral injury. “There’s no way to escape being morally injured when you work with an at-risk population,” said Ms. Adams. “You may see someone who has 20-24 determinants of health, and you’re expected to schlep them through in 8 minutes — you know you’re not able to do what they need.”
What Quiet Quitting Looks Like
Terri Smith*, an NP at an academic medical center outpatient clinic in rural Vermont, said that, while she feels appreciated by her patients and her team, there’s poor communication from the administration, which has caused her to quietly quit.
“I stopped saying ‘yes’ to all the normal committee work and the extra stuff that used to add a lot to my professional enjoyment,” she said. “The last couple of years, my whole motto is to nod and smile when administration says to do something — to put your head down and take care of your patients.”
While the term “quiet quitting” may be new, the issue is not, said Bridget Roberts, PhD, a healthcare executive who ran a large physician’s group of 100 healthcare providers in Jacksonville, Florida, for a decade. “Quiet quitting is a fancy title for employees who are completely disengaged,” said Dr. Roberts. “When they’re on the way out, they ‘check the box’. That’s not a new thing.”
“Typically, the first thing you see is a lot of frustration in that they aren’t able to complete the tasks they have at hand,” said Rebecca Day, PMNHP, a doctoral-educated NP and director of nursing practice at a Federally Qualified Health Center in Corbin, Kentucky. “Staff may be overworked and not have enough time to do what’s required of them with patient care as well as the paperwork required behind the scenes. It [quiet quitting] is doing just enough to get by, but shortcutting as much as they can to try to save some time.”
Addressing Quiet Quitting
Those kinds of shortcuts may affect patients, admits Ms. Smith. “I do think it starts to seep into patient care,” she said. “And that really doesn’t feel good ... at our institution, I’m not just an NP — I’m the nurse, the doctor, the secretary — I’m everybody, and for the last year, almost every single day in clinic, I’m apologizing [to a patient] because we can’t do something.”
Watching for this frustration can help alert administrators to NPs and PAs who may be “checking out” at work. Open lines of communication can help you address the issue. “Ask questions like ‘What could we do differently to make your day easier?’” said Dr. Roberts. Understanding the day-to-day issues NPs and PAs face at work can help in developing a plan to address disengagement.
When Dr. Day sees quiet quitting at her practice, she talks with the advance practice provider about what’s causing the issue. “’Are you overworked? Are you understaffed? Are there problems at home? Do you feel you’re receiving inadequate pay?’ ” she said. “The first thing to do is address that and find mutual ground on the issues…deal with the person as a person and then go back and deal with the person as an employee. If your staff isn’t happy, your clinic isn’t going to be productive.”
Finally, while reasons for quiet quitting may vary, cultivating a collaborative atmosphere where NPs and PAs feel appreciated and valued can help reduce the risk for quiet quitting. “Get to know your advanced practice providers,” said Ms. Adams. “Understand their strengths and what they’re about. It’s not an ‘us vs them’ ... there is a lot more commonality when we approach it that way.” Respect for the integral role that NPs and PAs play in your practice can help reduce the risk for quiet quitting — and help provide better patient care.
*Names have been changed.
A version of this article first appeared on Medscape.com.
While she cared deeply about her work, Melissa Adams*, a family nurse practitioner (NP) in Madison, Alabama, was being frequently triple-booked, didn’t feel respected by her office manager, and started to worry about becoming burned out. When she sought help, “the administration was tone-deaf,” she said. “When I asked about what I could do to prevent burnout, they sent me an article about it. It was clear to me that asking for respite from triple-booking and asking to be respected by my office manager wasn’t being heard ... so I thought, ‘how do I fly under the radar and get by with what I can?’ ” That meant focusing on patient care and refusing to take on additional responsibilities, like training new hires or working with students.
“You’re overworked and underpaid, and you start giving less and less of yourself,” Ms. Adams said in an interview.
Quiet quitting, defined as performing only the assigned tasks of the job without making any extra effort or going the proverbial extra mile, has gained attention in the press in recent years. A Gallup poll found that about 50% of the workforce were “quiet quitters” or disengaged.
It may be even more prevalent in healthcare, where a recent survey found that 57% of frontline medical staff, including NPs and physician assistants (PAs), report being disengaged at work.
The Causes of Quiet Quitting
Potential causes of quiet quitting among PAs and NPs include:
- Unrealistic care expectations. Ms. Adams said.
- Lack of trust or respect. Physicians don’t always respect the role that PAs and NPs play in a practice.
- Dissatisfaction with leadership or administration. There’s often a feeling that the PA or NP isn’t “heard” or appreciated.
- Dissatisfaction with pay or working conditions.
- Moral injury. “There’s no way to escape being morally injured when you work with an at-risk population,” said Ms. Adams. “You may see someone who has 20-24 determinants of health, and you’re expected to schlep them through in 8 minutes — you know you’re not able to do what they need.”
What Quiet Quitting Looks Like
Terri Smith*, an NP at an academic medical center outpatient clinic in rural Vermont, said that, while she feels appreciated by her patients and her team, there’s poor communication from the administration, which has caused her to quietly quit.
“I stopped saying ‘yes’ to all the normal committee work and the extra stuff that used to add a lot to my professional enjoyment,” she said. “The last couple of years, my whole motto is to nod and smile when administration says to do something — to put your head down and take care of your patients.”
While the term “quiet quitting” may be new, the issue is not, said Bridget Roberts, PhD, a healthcare executive who ran a large physician’s group of 100 healthcare providers in Jacksonville, Florida, for a decade. “Quiet quitting is a fancy title for employees who are completely disengaged,” said Dr. Roberts. “When they’re on the way out, they ‘check the box’. That’s not a new thing.”
“Typically, the first thing you see is a lot of frustration in that they aren’t able to complete the tasks they have at hand,” said Rebecca Day, PMNHP, a doctoral-educated NP and director of nursing practice at a Federally Qualified Health Center in Corbin, Kentucky. “Staff may be overworked and not have enough time to do what’s required of them with patient care as well as the paperwork required behind the scenes. It [quiet quitting] is doing just enough to get by, but shortcutting as much as they can to try to save some time.”
Addressing Quiet Quitting
Those kinds of shortcuts may affect patients, admits Ms. Smith. “I do think it starts to seep into patient care,” she said. “And that really doesn’t feel good ... at our institution, I’m not just an NP — I’m the nurse, the doctor, the secretary — I’m everybody, and for the last year, almost every single day in clinic, I’m apologizing [to a patient] because we can’t do something.”
Watching for this frustration can help alert administrators to NPs and PAs who may be “checking out” at work. Open lines of communication can help you address the issue. “Ask questions like ‘What could we do differently to make your day easier?’” said Dr. Roberts. Understanding the day-to-day issues NPs and PAs face at work can help in developing a plan to address disengagement.
When Dr. Day sees quiet quitting at her practice, she talks with the advance practice provider about what’s causing the issue. “’Are you overworked? Are you understaffed? Are there problems at home? Do you feel you’re receiving inadequate pay?’ ” she said. “The first thing to do is address that and find mutual ground on the issues…deal with the person as a person and then go back and deal with the person as an employee. If your staff isn’t happy, your clinic isn’t going to be productive.”
Finally, while reasons for quiet quitting may vary, cultivating a collaborative atmosphere where NPs and PAs feel appreciated and valued can help reduce the risk for quiet quitting. “Get to know your advanced practice providers,” said Ms. Adams. “Understand their strengths and what they’re about. It’s not an ‘us vs them’ ... there is a lot more commonality when we approach it that way.” Respect for the integral role that NPs and PAs play in your practice can help reduce the risk for quiet quitting — and help provide better patient care.
*Names have been changed.
A version of this article first appeared on Medscape.com.
GLP-1 RA Therapy for Alcohol Use Disorder?
This transcript has been edited for clarity.
Akshay B. Jain, MD: Today we are very excited to have Dr. Leggio join us all the way from the National Institutes of Health (NIH). He is an addiction physician scientist in the intramural research program at NIH. Welcome, Dr. Leggio. Thanks for joining us.
Lorenzo Leggio, MD, PhD: Thank you so much.
Dr. Jain: We’ll get right into this. Your session was, in my mind, extremely informative. The session looked at glucagon-like peptide 1 receptor agonist (GLP-1 RA) therapy and its potential effects on mitigating alcohol misuse syndrome, so, reduction of alcohol addiction potentially.
We’ve seen in some previous clinical trials, including many from your group, that alcohol use is known to be reduced — the overall risk of incidence, as well as recurrence of alcohol use — in individuals who are on GLP-1 RA therapy.
Can you share more insights about the data already out there?
Dr. Leggio: At the preclinical level, we have a very robust line of studies, experiments, and publications looking at the effect of GLP-1 RAs, starting from exenatide up to, more recently, semaglutide. They show that these GLP-1 RAs do reduce alcohol drinking. They used different animal models of excessive alcohol drinking, using different species — for example, mice, rats, nonhuman primates — models that reflect the excessive alcohol drinking behavior that we see in patients, like physical alcohol dependence or binge-like alcohol drinking, and other behaviors in animal models that reflect the human condition.
In addition to that, we recently have seen an increase in human evidence that GLP-1 RAs may reduce alcohol drinking. For example, there is some anecdotal evidence and some analyses using social media showing that people on GLP-1 RAs report drinking less alcohol.
There are also some pharmacoepidemiology studies which are very intriguing and quite promising. In this case, people have been looking at electronic medical records; they have used the pharmacoepidemiology approaches to match patients on GLP-1 RAs because of diabetes or obesity, and have compared and matched to patients on different drugs as the controls.
A study was recently published Nature Communications by a group in Cleveland in collaboration with Dr. Nora Volkow from the National Institute on Drug Abuse. This study shows the association between being on a GLP-1 RA and the lower incidence of alcohol use disorder and lower drinking.
There is also some promise from prospective randomized clinical trials. In particular, there was one clinical trial from Denmark, a well-known and -conducted clinical trial where they looked at exenatide, and they didn’t see an effect of exenatide compared with placebo in the main analysis. But in a subanalysis, they did see that exenatide reduced alcohol drinking, but only in patients with alcohol use disorder and obesity.
This suggests that these medications may work for some patients and not for other patients. That’s fine, because just like in any other field in medicine, including diabetes, obesity, hypertension, Parkinson’s, and depression, not all medications work for everybody. If these medications will work for alcohol addiction, we do not expect that they will work for everybody.
One ongoing question in the field is to try to identify the phenotypes or the subgroup of people who may be more responsive to these medications.
Dr. Jain: This is such a fascinating field, and all these studies are coming out. In your review of all the literature so far, do you think this is dose dependent? Also, we see that, for instance, with certain individuals, when they take GLP-1 RA therapy, they might have a lot of gastrointestinal (GI) side effects. Recent studies have shown that the rate of these GI side effects does not necessarily correlate with the amount of weight loss. In the alcohol addiction field, do you think that the GI side effects, things like nausea, could also have a potential role in mitigating the alcohol addiction?
Dr. Leggio: This is a great question. They may play a role; they may contribute, too, but we don’t think that they are the driving mechanism of why people drink less, for at least a couple of reasons.
One is that, similar to the obesity field, the data we have so far don’t necessarily show a relationship between the GI side effects and the reduction in drinking. Plus, the reduction in drinking is likely to happen later when many GI side effects are gone or attenuated.
The second reason is from the neuroscience field. We are starting to better understand the mechanism at the brain level as to how these medications work. We don’t see that the nausea or, more generally, not feeling well — malaise, etc. — are driving mechanisms for how these medications work.
Again, it’s not to discount completely that the GI side effects may play a role, but I would say that, if anything, they may be more contributing to. And if they do, that will not be unique to this class of medication. For example, we have three medications approved by the US Food and Drug Administration (FDA) for alcohol use disorder.
One challenge we have in the addiction field is that many people don’t know that these medications exist — many primary care providers don’t know — and they are completely underutilized. Everybody here who is listening to us knows that roughly 85% of people with diabetes receive a medication for diabetes. For alcohol use disorder, the number is 2%. These are medications approved by the FDA.
One of them is naltrexone, which does give GI symptoms — in particular, nausea and vomiting. The other medication is acamprosate, which does give diarrhea.
You have medications approved for alcohol disorder where you do have some GI symptoms, but they are not the mechanism either for how these medications help people to curb craving and reduce alcohol drinking.
Dr. Jain: What about the dose-dependent action? Do you think that GLP-1 RAs, at a lower dose, may not have an effect on alcohol use disorder vs at a higher dose, or is everyone a little different?
Dr. Leggio: That’s a wonderful question. The short answer is, we don’t know, to be honest. Now, in some of the animal studies — my team has been in collaboration with other scientists in the NIH intramural research program, and also with scientists in academia, for example, at Scripps, UCLA — we see a dose response where the higher the dose, the higher the effect of the drug. In this case, semaglutide reduced binge drinking in a rat model of a physical alcohol dependence.
That said, I would be very cautious about claiming, based on the rodent data, that humans will have a dose response. It’s an open question. We really don’t know. Some of the pharmacoepidemiology data suggested that even lower doses — for example, using semaglutide for diabetes without going up to the obesity dose — may be just as effective as a higher dose in reducing the incidence of alcohol use disorder.
It’s important also to keep in mind that the pharmacoepidemiology data are always an association. Reduction in alcohol disorder is associated with the prescription GLP-1 RA, but they don’t really replace the more gold-standard, double-blind, placebo-controlled randomized clinical trial. Nonetheless, with the pharmacoepidemiology data, I think there is an argument to at least hypothesize that people may respond well, even to lower doses.
This also may be important from a safety standpoint.
Basically, we need to wait for results in the next years to come from randomized clinical trials to better unfold the question about doses. For example, just anecdotally, I will tell you that in the clinical trial we are conducting right now at the NIH Intramural Research Program, for which I’m the principal investigator (PI), we are going up to 2.4 mg — the highest dose of semaglutide.
We are collaborating with Kyle Simmons, PhD, from Oklahoma State University. Our two studies are not like a two-site clinical trial, but they are harmonized. In Dr. Simmons’ clinical trial, they’re going up to 1.0 mg. We are excited about this team approach because the trials are slightly different, but they’re harmonized to the point that, once the studies are done, we’ll be able to combine and compare data to better answer the question about dosing, and many other questions.
Dr. Jain: From a clinical perspective, we see that many people who are battling alcohol use disorder may not have obesity. They might actually be on the leaner side, and hence, we may not want to use a high dose of GLP-1 RA therapy. It’ll be very exciting to see when these results come out.
This brings me to the next question. I think everyone would love to know why this happens. Why is GLP-1 RA having this effect on alcohol use disorder? I know that your group has done many animal studies, as you pointed out, and one of the postulated theories was the effect on the GABA neurotransmission pathway.
Can you tell us more about what you feel is the underlying mechanism of action here?
Dr. Leggio: I will start by saying that we don’t fully know. There are many open questions. If I can sidetrack for one second: We come up with the idea that, first of all, alcohol use disorder and substance use disorder are addictive behaviors, addictive disorders. We define addiction as a brain disease.
Granted that addiction is a brain disease, it doesn’t mean that addiction works just in the brain in isolation. As we all know, the brain works in concert with the rest of the body. One specific approach my team has been taking is working on the analogy and the similarities between obesity and addiction to try to understand how the body-brain connection, such as the gut-brain-neuroendocrine pathway, may play a role in patients with addiction.
With that in mind, a large amount of work in my lab in the past 20 years — since I’ve been a PI — has been focused on studying this neuroendocrine pathways related to the gut-brain axis. For example, we have done work on insulin and leptin, primarily; we had done work on ghrelin, and since 2015 on the GLP-1 RAs.
With that in mind, the framework we are working on, which is also substantiated by many studies done by our team and other teams in the neuroscience field, kind of supports the idea that, similar to what we see in obesity, these medications may work by affecting what we call reward processing, or the seeking for addictive drugs, such as alcohol, and also the drugs such as the stimulants, opioids, nicotine, and so on.
The idea is that the mechanism is driven by the ability of the medication — semaglutide and all the GLP-1 RAs — to reduce the rewarding properties of alcohol and drugs. To maybe make the example more pragmatic, what does that mean? It means, for example, that a patient who typically has 10 drinks per day in the afternoon and night, while they are on the medication they may feel the lack of need to drink up to 10 to feel the same reward.
They may be able to stop after two or three drinks, which means a significant harm reduction and a beneficial outcome. This also brings us to another mechanism, which may be related to society. We don’t fully understand how much the society mechanism, including society mechanism related to GI motility, may also play a role.
With that said, we don’t think that the effect of the GLP-1 RAs is merely due to alcohol being a calorie-based nutrient because, in fact, we see alcohol as an addictive drug, not as a nutrient. Also, the GLP-1 RAs, at least in animal models, seem to work on other addictive drugs that don’t have calories, such as nicotine, and possibly with cannabis, opioids, and stimulants.
Then on the molecular level, our team recently showed, in collaboration with Dr. Marisa Roberto from Scripps in La Jolla, California, that semaglutide may in fact change the GABA transmission at the level of some brain regions, such as the amygdala and the prefrontal cortex. These are brain regions that are well-established hubs that play a role in the mechanism underlying addiction.
There are also some very exciting recent data showing how these medications may work not just on GABA or just on dopamine, which is the canonical way we conceive of reward processing, but by working on both by modulating GABA transmission — for example, at the ventral tegmental area and dopamine transmission at the nucleus accumbens.
Bottom line, if I summarize all of this, is that the mechanism is not fully understood, but there is definitely a contribution of this medication to effect and reward processing, possibly by altering the balance between GABA and dopamine. There are still some unknown questions, such as, are these mechanisms all brain driven or are they signaling from the periphery to the brain, or maybe both?
Also, as we all know, there are many differences across all these GLP-1 analogs in brain penetrance. Whether the drug needs to go to the brain to have an effect on alcohol drinking, cocaine seeking, or smoking is really an open question.
Dr. Jain: This is so thought-provoking. I guess the more we uncover, the more mesmerized we get with all the potential crosstalk. There is a large amount of overlap in the brain with each of these different things and how it all interplays with each other.
Speaking of interplay, I’m thinking about how many people prone to having alcohol use disorder can potentially develop complications, one of these being chronic pancreatitis. This is a well-known complication that can occur in people having alcohol addiction. Along that same line, we know that previous history of pancreatitis is considered a use-with-caution, or we don’t want to use GLP-1 RA therapy in people who have had pancreatitis.
Now it becomes this quagmire where people may have chronic pancreatitis, but we may want to consider GLP-1 RA therapy for management of alcohol use disorder. What are your thoughts about this, and the safety, potentially, in using it in these patients?
Dr. Leggio: This is another wonderful question. That’s definitely a top priority in our mind, to address these kinds of questions. For example, our RCT does have, as core primary outcomes, not only the efficacy defined as a reduction in alcohol drinking, but also safety.
The reason is exactly what you just explained. There are many unanswered questions, including whether giving a GLP-1 RA and alcohol together may have synergistic effects and increase the likelihood of having pancreatitis.
The good news is that, so far, based on the published literature, including the RCT done with exenatide in Denmark and published in 2022 and also the ongoing clinical trials — including my own clinical trial, but of course we are blind — pancreatitis has not been coming out as an adverse event.
However, it’s also true that it often happens in clinical medication development. Of course, we screen and select our population well. For example, we do exclude people who have a history of pancreatitis. We exclude people with high lipase or with any of the clinical symptomatology that makes us concerned about these people having pancreatitis.
As often happens when you move a medication from clinical trials to clinical practice, we still need to understand whether this medication works in patients. I’m just speculating, but even if the clinical trials do not raise red flags in terms of increased risk for some side effects such as pancreatitis, I think it will be very important for practitioners to keep a close eye on the death risk regardless.
It’s very interesting that it’s similar to alcohol liver disease. With pancreatitis, not every single patient with alcohol addiction has pancreatitis. We don’t really fully understand why some people develop pancreatitis and some people do not. The point being that there are many patients with alcohol addiction who don’t have pancreatitis and may benefit from these medications if they work. Again, we have to prove that in patients.
On the other side, as we all know, pancreatitis is a potentially life-threatening condition for those people who either have it or are at risk for it. I think we have to be very careful before we consider giving them a GLP-1 RA.
One could argue that alcohol is the leading cause of mortality and morbidity in the world. For example, right now, alcohol is the leading cause of liver disease. It’s the main reason for liver transplantation in our country. Alcohol is affecting thousands of people in terms of death and emergency room visits.
You could argue that the downside is not treating these people and they die because of alcohol addiction. A GLP-1 RA is not going to be for everybody. I will remind everybody that (1) we do have FDA-approved medications for alcohol addiction; and (2) there are also other medications not approved by the FDA, but with a proven efficacy in some clinical trials — for example, topiramate and gabapentin — and they’ve been endorsed by the American Psychiatric Association.
There is also some evidence for another medication, baclofen, which has been endorsed by the American College of Gastroenterology for patients with alcohol addiction and liver disease.
The point I’m making is that it’s not that either we use the GLP-1 RAs or we have no other tools. We have other tools. I think we have to personalize the treatment based on the patient’s profile from a safety standpoint and from a phenotypic standpoint.
Dr. Jain: I love that thought. I think individualization is the key here.
We know that people with diabetes have a higher risk for pancreatitis by virtue of having diabetes. People with obesity also have a higher risk for pancreatitis by virtue of having obesity. These are the two conditions where we are using a large amount of GLP-1 RA therapy. Again, the idea is looking at the person in front of us and then deciding, based on their past medical history and their current risk, whether or not a medication is a right fit for them.
I think more individualization here will come as we start using these medications that might be having potential effects on different organ systems. You mentioned a little bit about the liver, so a thought came in my mind. We know that people with diabetes who have alcohol use disorder are at a higher risk for potential hypoglycemia. If they have events when they have increased consumption of alcohol, there can be more hypoglycemia.
We now could potentially be using semaglutide or other GLP-1 RA therapy for management of alcohol use disorder. In your own experience in the studies that you’ve done or the literature that’s out there, has that been associated with an even higher risk for hypoglycemia?
Dr. Leggio: It’s a wonderful question. I’m not aware of any formal and published report of that association. That said, your thinking from a physiopathologist standpoint makes total sense. I could not agree more. The fact that nothing has been published, at least to my knowledge, doesn’t mean that the death risk doesn’t exist. In fact, I agree with you that it does exist.
Alcohol use disorder is interesting and tricky clinically because chronically, alcohol addiction or alcohol use disorder is associated with an increased risk for diabetes. Acutely, as you point out; and this could be with or without alcohol use disorder. An episode of a high volume of binge drinking may lead to hypoglycemia.
This is one of the reasons why people may show up to the emergency room with intoxication, and one of the symptoms detected at the emergency room is that they also have hypoglycemia in addition to vomiting, nausea, and everything else that we see in patients with acute intoxication.
Similar to the discussion about pancreatitis, as we work on understanding the possible role of GLP-1 RA in patients with alcohol use disorder, we do have to keep a close eye on the risk for hypoglycemia. The short answer is that this is not well established, but based on the simple concept of “first, do no harm,” I think we need to track that very carefully.
In the ongoing clinical trial we’re doing in Maryland in my program at the NIH, we do just that. We are tracking glucose levels. Of course, patients come to clinic weekly, so unless they have symptoms, typically we don’t see anything at the time.
More important, we educate our patients when they go through the consent process. We tell them that this medication per se does not give hypoglycemia. In fact, we’re including people with diabetes, so for people on other medications like metformin, we explain to them that technically such a risk should not exist, but because you’re drinking alcohol in excessive amounts, you do have a potential higher risk. We just don’t know how significant that risk could be.
We do a large amount of education at baseline when they enroll in our study. We also educate our patients on how to recognize early on the potential risk for hypoglycemia, exactly for the reasons you said. We explain to them the unknown potential that the GLP-1 RAs and alcohol together may synergize and give hypoglycemia.
Dr. Jain: I don’t know if you got this feeling at the ADA conference, but I felt, when attending all these sessions, that it seems like GLP-1 RA is the gift that keeps giving. We see the effect on diabetes, obesity, metabolic-associated steatotic liver disease, possibly with Alzheimer’s, chronic obstructive pulmonary disease, and so many things.
Now, of course, there’s potential use in alcohol use disorder. Do you think that using GLP-1 RA therapy is ready for prime time? Do you think we are now ready to prescribe this in people with alcohol use disorder?
Dr. Leggio: I would say we’re not there yet. As I mentioned at the beginning, the evidence keeps on growing. It’s getting stronger and stronger because the positive data keep on coming up. We have data from animal models, including the different species, ranging from rodents to nonhuman primates. We have anecdotal evidence and machine-learning approaches using, for example, big data and social media data. Now we have pharmacoepidemiology data and some small, initial, but still good randomized clinical trials.
What we are missing is the final step of having a substantial number of prospective, double-blind, placebo-controlled clinical trials to really prove or disprove whether these medications work, and to also better understand which patients may respond to these medications.
The good news is that there are many ongoing clinical trials. We are conducting a clinical trial in Maryland at the NIH. Dr. Simmons is doing a clinical trial at Oklahoma State University. Dr. Christian Hendershot at UNC is conducting a study at Chapel Hill. Dr. Josh Gowin is doing a study in Colorado. Dr. Anders Fink-Jensen is doing a study in Denmark. The momentum is very high.
I’m only mentioning those people who are doing alcohol-semaglutide clinical trials. There are also people doing clinical trials on smoking, stimulants, and opioids. There are actually some very fresh, still unpublished data from Penn State that were presented publicly at conferences, showing how these drugs may reduce opioid craving, which is, of course, critically important, given that we’re in the middle of a fentanyl pandemic that is killing one person every 7 minutes, for example, in Baltimore. It’s very alarming and we need more treatments.
The bottom line is that it’s very promising, but we need to wait for these clinical trials to have a definitive answer. I would say that if you have a patient with diabetes, obesity, and also alcohol addiction, and they are on semaglutide or any other GLP-1 RA, and in addition to using the medication for diabetes and obesity, they also have a beneficial effect on their alcohol drinking, then that’s fantastic. At the end of the day, that’s the mission we all share: helping people.
If it’s someone without obesity and diabetes, personally, at this stage, I will go with other medications that either have FDA approval or at least very solid evidence of efficacy from RCTs rather than going with the GLP-1 RA, at least until I see more definitive data from randomized clinical trials.
There is a large amount of hope. We are hoping that these clinical trials will be positive. We are very enthusiastic and we’re also very thrilled to see that Novo Nordisk recently launched a gigantic multisite clinical trial with — I forgot how many sites, but it’s very large across Europe, America, and maybe other continents as well.
Their primary outcome is improvement in alcohol-related liver disease, but they’re also looking at alcohol drinking as a secondary outcome. That’s very important because, unlike in the diabetes field, in the addiction field, we do struggle to build partnership with the private sector because sometimes the addiction field is not seen as an appetitive field from pharma.
We all know that the best success in any medication development story is when you put academia, the government, and pharma together. Think about the COVID-19 vaccine development. That’s unfortunately the exception rather than rule in the addiction field.
With the company doing a large clinical trial in the alcohol field, although they focus more on the liver but they also looked at drinking, I really hope we’ll see more and more companies in the private sector take more and more interest in addiction. Also, I hope to see more and more partnership between the private sector, the government, and academia.
Dr. Jain: Such exciting times, indeed. We can’t wait enough for the results of these and many other trials to come out. Dr. Leggio, it was an absolute delight chatting with you today. Thank you so much for joining us from ADA 2024.
Akshay B. Jain, MD, Clinical Instructor, Department of Endocrinology, University of British Columbia; Endocrinologist, TLC Diabetes and Endocrinology, Vancouver, British Columbia, Canada, has disclosed the following relevant financial relationships: Serve(d) as a speaker or a member of a speakers bureau for: Abbott; Acerus; AstraZeneca; Amgen; Bausch Healthcare; Bayer; Boehringer Ingelheim; Care to Know; CCRN; Connected in Motion; CPD Network; Dexcom; Diabetes Canada; Eli Lilly; GSK; HLS Therapeutics; Janssen; Master Clinician Alliance; MDBriefcase; Merck; Medtronic; Moderna; Novartis; Novo Nordisk; Partners in Progressive Medical Education; Pfizer; Sanofi Aventis; Timed Right; WebMD. Received research grants/research support from: Abbott; Amgen; Novo Nordisk. Received consulting fees from: Abbott; Acerus; AstraZeneca; Amgen; Bausch Healthcare; Bayer; Boehringer Ingelheim; Dexcom; Eli Lilly; Gilead Sciences; GSK; HLS Therapeutics; Insulet; Janssen; Medtronic; Novo Nordisk; Partners in Progressive Medical Education; PocketPills; Roche; Sanofi Aventis; Takeda. Lorenzo Leggio, MD, PhD, Clinical Director, Deputy Scientific Director, National Institute on Drug Abuse Intramural Research Program, National Institutes of Health, Baltimore, Maryland, has disclosed the following relevant financial relationships: Serve(d) as a US federal employee for: National Institutes of Health. He had received income in an amount equal to or greater than $250 from: UK Medical Council on Alcohol for his service as editor-in-chief for Alcohol and Alcoholism and received royalties from Rutledge as an editor for a textbook.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Akshay B. Jain, MD: Today we are very excited to have Dr. Leggio join us all the way from the National Institutes of Health (NIH). He is an addiction physician scientist in the intramural research program at NIH. Welcome, Dr. Leggio. Thanks for joining us.
Lorenzo Leggio, MD, PhD: Thank you so much.
Dr. Jain: We’ll get right into this. Your session was, in my mind, extremely informative. The session looked at glucagon-like peptide 1 receptor agonist (GLP-1 RA) therapy and its potential effects on mitigating alcohol misuse syndrome, so, reduction of alcohol addiction potentially.
We’ve seen in some previous clinical trials, including many from your group, that alcohol use is known to be reduced — the overall risk of incidence, as well as recurrence of alcohol use — in individuals who are on GLP-1 RA therapy.
Can you share more insights about the data already out there?
Dr. Leggio: At the preclinical level, we have a very robust line of studies, experiments, and publications looking at the effect of GLP-1 RAs, starting from exenatide up to, more recently, semaglutide. They show that these GLP-1 RAs do reduce alcohol drinking. They used different animal models of excessive alcohol drinking, using different species — for example, mice, rats, nonhuman primates — models that reflect the excessive alcohol drinking behavior that we see in patients, like physical alcohol dependence or binge-like alcohol drinking, and other behaviors in animal models that reflect the human condition.
In addition to that, we recently have seen an increase in human evidence that GLP-1 RAs may reduce alcohol drinking. For example, there is some anecdotal evidence and some analyses using social media showing that people on GLP-1 RAs report drinking less alcohol.
There are also some pharmacoepidemiology studies which are very intriguing and quite promising. In this case, people have been looking at electronic medical records; they have used the pharmacoepidemiology approaches to match patients on GLP-1 RAs because of diabetes or obesity, and have compared and matched to patients on different drugs as the controls.
A study was recently published Nature Communications by a group in Cleveland in collaboration with Dr. Nora Volkow from the National Institute on Drug Abuse. This study shows the association between being on a GLP-1 RA and the lower incidence of alcohol use disorder and lower drinking.
There is also some promise from prospective randomized clinical trials. In particular, there was one clinical trial from Denmark, a well-known and -conducted clinical trial where they looked at exenatide, and they didn’t see an effect of exenatide compared with placebo in the main analysis. But in a subanalysis, they did see that exenatide reduced alcohol drinking, but only in patients with alcohol use disorder and obesity.
This suggests that these medications may work for some patients and not for other patients. That’s fine, because just like in any other field in medicine, including diabetes, obesity, hypertension, Parkinson’s, and depression, not all medications work for everybody. If these medications will work for alcohol addiction, we do not expect that they will work for everybody.
One ongoing question in the field is to try to identify the phenotypes or the subgroup of people who may be more responsive to these medications.
Dr. Jain: This is such a fascinating field, and all these studies are coming out. In your review of all the literature so far, do you think this is dose dependent? Also, we see that, for instance, with certain individuals, when they take GLP-1 RA therapy, they might have a lot of gastrointestinal (GI) side effects. Recent studies have shown that the rate of these GI side effects does not necessarily correlate with the amount of weight loss. In the alcohol addiction field, do you think that the GI side effects, things like nausea, could also have a potential role in mitigating the alcohol addiction?
Dr. Leggio: This is a great question. They may play a role; they may contribute, too, but we don’t think that they are the driving mechanism of why people drink less, for at least a couple of reasons.
One is that, similar to the obesity field, the data we have so far don’t necessarily show a relationship between the GI side effects and the reduction in drinking. Plus, the reduction in drinking is likely to happen later when many GI side effects are gone or attenuated.
The second reason is from the neuroscience field. We are starting to better understand the mechanism at the brain level as to how these medications work. We don’t see that the nausea or, more generally, not feeling well — malaise, etc. — are driving mechanisms for how these medications work.
Again, it’s not to discount completely that the GI side effects may play a role, but I would say that, if anything, they may be more contributing to. And if they do, that will not be unique to this class of medication. For example, we have three medications approved by the US Food and Drug Administration (FDA) for alcohol use disorder.
One challenge we have in the addiction field is that many people don’t know that these medications exist — many primary care providers don’t know — and they are completely underutilized. Everybody here who is listening to us knows that roughly 85% of people with diabetes receive a medication for diabetes. For alcohol use disorder, the number is 2%. These are medications approved by the FDA.
One of them is naltrexone, which does give GI symptoms — in particular, nausea and vomiting. The other medication is acamprosate, which does give diarrhea.
You have medications approved for alcohol disorder where you do have some GI symptoms, but they are not the mechanism either for how these medications help people to curb craving and reduce alcohol drinking.
Dr. Jain: What about the dose-dependent action? Do you think that GLP-1 RAs, at a lower dose, may not have an effect on alcohol use disorder vs at a higher dose, or is everyone a little different?
Dr. Leggio: That’s a wonderful question. The short answer is, we don’t know, to be honest. Now, in some of the animal studies — my team has been in collaboration with other scientists in the NIH intramural research program, and also with scientists in academia, for example, at Scripps, UCLA — we see a dose response where the higher the dose, the higher the effect of the drug. In this case, semaglutide reduced binge drinking in a rat model of a physical alcohol dependence.
That said, I would be very cautious about claiming, based on the rodent data, that humans will have a dose response. It’s an open question. We really don’t know. Some of the pharmacoepidemiology data suggested that even lower doses — for example, using semaglutide for diabetes without going up to the obesity dose — may be just as effective as a higher dose in reducing the incidence of alcohol use disorder.
It’s important also to keep in mind that the pharmacoepidemiology data are always an association. Reduction in alcohol disorder is associated with the prescription GLP-1 RA, but they don’t really replace the more gold-standard, double-blind, placebo-controlled randomized clinical trial. Nonetheless, with the pharmacoepidemiology data, I think there is an argument to at least hypothesize that people may respond well, even to lower doses.
This also may be important from a safety standpoint.
Basically, we need to wait for results in the next years to come from randomized clinical trials to better unfold the question about doses. For example, just anecdotally, I will tell you that in the clinical trial we are conducting right now at the NIH Intramural Research Program, for which I’m the principal investigator (PI), we are going up to 2.4 mg — the highest dose of semaglutide.
We are collaborating with Kyle Simmons, PhD, from Oklahoma State University. Our two studies are not like a two-site clinical trial, but they are harmonized. In Dr. Simmons’ clinical trial, they’re going up to 1.0 mg. We are excited about this team approach because the trials are slightly different, but they’re harmonized to the point that, once the studies are done, we’ll be able to combine and compare data to better answer the question about dosing, and many other questions.
Dr. Jain: From a clinical perspective, we see that many people who are battling alcohol use disorder may not have obesity. They might actually be on the leaner side, and hence, we may not want to use a high dose of GLP-1 RA therapy. It’ll be very exciting to see when these results come out.
This brings me to the next question. I think everyone would love to know why this happens. Why is GLP-1 RA having this effect on alcohol use disorder? I know that your group has done many animal studies, as you pointed out, and one of the postulated theories was the effect on the GABA neurotransmission pathway.
Can you tell us more about what you feel is the underlying mechanism of action here?
Dr. Leggio: I will start by saying that we don’t fully know. There are many open questions. If I can sidetrack for one second: We come up with the idea that, first of all, alcohol use disorder and substance use disorder are addictive behaviors, addictive disorders. We define addiction as a brain disease.
Granted that addiction is a brain disease, it doesn’t mean that addiction works just in the brain in isolation. As we all know, the brain works in concert with the rest of the body. One specific approach my team has been taking is working on the analogy and the similarities between obesity and addiction to try to understand how the body-brain connection, such as the gut-brain-neuroendocrine pathway, may play a role in patients with addiction.
With that in mind, a large amount of work in my lab in the past 20 years — since I’ve been a PI — has been focused on studying this neuroendocrine pathways related to the gut-brain axis. For example, we have done work on insulin and leptin, primarily; we had done work on ghrelin, and since 2015 on the GLP-1 RAs.
With that in mind, the framework we are working on, which is also substantiated by many studies done by our team and other teams in the neuroscience field, kind of supports the idea that, similar to what we see in obesity, these medications may work by affecting what we call reward processing, or the seeking for addictive drugs, such as alcohol, and also the drugs such as the stimulants, opioids, nicotine, and so on.
The idea is that the mechanism is driven by the ability of the medication — semaglutide and all the GLP-1 RAs — to reduce the rewarding properties of alcohol and drugs. To maybe make the example more pragmatic, what does that mean? It means, for example, that a patient who typically has 10 drinks per day in the afternoon and night, while they are on the medication they may feel the lack of need to drink up to 10 to feel the same reward.
They may be able to stop after two or three drinks, which means a significant harm reduction and a beneficial outcome. This also brings us to another mechanism, which may be related to society. We don’t fully understand how much the society mechanism, including society mechanism related to GI motility, may also play a role.
With that said, we don’t think that the effect of the GLP-1 RAs is merely due to alcohol being a calorie-based nutrient because, in fact, we see alcohol as an addictive drug, not as a nutrient. Also, the GLP-1 RAs, at least in animal models, seem to work on other addictive drugs that don’t have calories, such as nicotine, and possibly with cannabis, opioids, and stimulants.
Then on the molecular level, our team recently showed, in collaboration with Dr. Marisa Roberto from Scripps in La Jolla, California, that semaglutide may in fact change the GABA transmission at the level of some brain regions, such as the amygdala and the prefrontal cortex. These are brain regions that are well-established hubs that play a role in the mechanism underlying addiction.
There are also some very exciting recent data showing how these medications may work not just on GABA or just on dopamine, which is the canonical way we conceive of reward processing, but by working on both by modulating GABA transmission — for example, at the ventral tegmental area and dopamine transmission at the nucleus accumbens.
Bottom line, if I summarize all of this, is that the mechanism is not fully understood, but there is definitely a contribution of this medication to effect and reward processing, possibly by altering the balance between GABA and dopamine. There are still some unknown questions, such as, are these mechanisms all brain driven or are they signaling from the periphery to the brain, or maybe both?
Also, as we all know, there are many differences across all these GLP-1 analogs in brain penetrance. Whether the drug needs to go to the brain to have an effect on alcohol drinking, cocaine seeking, or smoking is really an open question.
Dr. Jain: This is so thought-provoking. I guess the more we uncover, the more mesmerized we get with all the potential crosstalk. There is a large amount of overlap in the brain with each of these different things and how it all interplays with each other.
Speaking of interplay, I’m thinking about how many people prone to having alcohol use disorder can potentially develop complications, one of these being chronic pancreatitis. This is a well-known complication that can occur in people having alcohol addiction. Along that same line, we know that previous history of pancreatitis is considered a use-with-caution, or we don’t want to use GLP-1 RA therapy in people who have had pancreatitis.
Now it becomes this quagmire where people may have chronic pancreatitis, but we may want to consider GLP-1 RA therapy for management of alcohol use disorder. What are your thoughts about this, and the safety, potentially, in using it in these patients?
Dr. Leggio: This is another wonderful question. That’s definitely a top priority in our mind, to address these kinds of questions. For example, our RCT does have, as core primary outcomes, not only the efficacy defined as a reduction in alcohol drinking, but also safety.
The reason is exactly what you just explained. There are many unanswered questions, including whether giving a GLP-1 RA and alcohol together may have synergistic effects and increase the likelihood of having pancreatitis.
The good news is that, so far, based on the published literature, including the RCT done with exenatide in Denmark and published in 2022 and also the ongoing clinical trials — including my own clinical trial, but of course we are blind — pancreatitis has not been coming out as an adverse event.
However, it’s also true that it often happens in clinical medication development. Of course, we screen and select our population well. For example, we do exclude people who have a history of pancreatitis. We exclude people with high lipase or with any of the clinical symptomatology that makes us concerned about these people having pancreatitis.
As often happens when you move a medication from clinical trials to clinical practice, we still need to understand whether this medication works in patients. I’m just speculating, but even if the clinical trials do not raise red flags in terms of increased risk for some side effects such as pancreatitis, I think it will be very important for practitioners to keep a close eye on the death risk regardless.
It’s very interesting that it’s similar to alcohol liver disease. With pancreatitis, not every single patient with alcohol addiction has pancreatitis. We don’t really fully understand why some people develop pancreatitis and some people do not. The point being that there are many patients with alcohol addiction who don’t have pancreatitis and may benefit from these medications if they work. Again, we have to prove that in patients.
On the other side, as we all know, pancreatitis is a potentially life-threatening condition for those people who either have it or are at risk for it. I think we have to be very careful before we consider giving them a GLP-1 RA.
One could argue that alcohol is the leading cause of mortality and morbidity in the world. For example, right now, alcohol is the leading cause of liver disease. It’s the main reason for liver transplantation in our country. Alcohol is affecting thousands of people in terms of death and emergency room visits.
You could argue that the downside is not treating these people and they die because of alcohol addiction. A GLP-1 RA is not going to be for everybody. I will remind everybody that (1) we do have FDA-approved medications for alcohol addiction; and (2) there are also other medications not approved by the FDA, but with a proven efficacy in some clinical trials — for example, topiramate and gabapentin — and they’ve been endorsed by the American Psychiatric Association.
There is also some evidence for another medication, baclofen, which has been endorsed by the American College of Gastroenterology for patients with alcohol addiction and liver disease.
The point I’m making is that it’s not that either we use the GLP-1 RAs or we have no other tools. We have other tools. I think we have to personalize the treatment based on the patient’s profile from a safety standpoint and from a phenotypic standpoint.
Dr. Jain: I love that thought. I think individualization is the key here.
We know that people with diabetes have a higher risk for pancreatitis by virtue of having diabetes. People with obesity also have a higher risk for pancreatitis by virtue of having obesity. These are the two conditions where we are using a large amount of GLP-1 RA therapy. Again, the idea is looking at the person in front of us and then deciding, based on their past medical history and their current risk, whether or not a medication is a right fit for them.
I think more individualization here will come as we start using these medications that might be having potential effects on different organ systems. You mentioned a little bit about the liver, so a thought came in my mind. We know that people with diabetes who have alcohol use disorder are at a higher risk for potential hypoglycemia. If they have events when they have increased consumption of alcohol, there can be more hypoglycemia.
We now could potentially be using semaglutide or other GLP-1 RA therapy for management of alcohol use disorder. In your own experience in the studies that you’ve done or the literature that’s out there, has that been associated with an even higher risk for hypoglycemia?
Dr. Leggio: It’s a wonderful question. I’m not aware of any formal and published report of that association. That said, your thinking from a physiopathologist standpoint makes total sense. I could not agree more. The fact that nothing has been published, at least to my knowledge, doesn’t mean that the death risk doesn’t exist. In fact, I agree with you that it does exist.
Alcohol use disorder is interesting and tricky clinically because chronically, alcohol addiction or alcohol use disorder is associated with an increased risk for diabetes. Acutely, as you point out; and this could be with or without alcohol use disorder. An episode of a high volume of binge drinking may lead to hypoglycemia.
This is one of the reasons why people may show up to the emergency room with intoxication, and one of the symptoms detected at the emergency room is that they also have hypoglycemia in addition to vomiting, nausea, and everything else that we see in patients with acute intoxication.
Similar to the discussion about pancreatitis, as we work on understanding the possible role of GLP-1 RA in patients with alcohol use disorder, we do have to keep a close eye on the risk for hypoglycemia. The short answer is that this is not well established, but based on the simple concept of “first, do no harm,” I think we need to track that very carefully.
In the ongoing clinical trial we’re doing in Maryland in my program at the NIH, we do just that. We are tracking glucose levels. Of course, patients come to clinic weekly, so unless they have symptoms, typically we don’t see anything at the time.
More important, we educate our patients when they go through the consent process. We tell them that this medication per se does not give hypoglycemia. In fact, we’re including people with diabetes, so for people on other medications like metformin, we explain to them that technically such a risk should not exist, but because you’re drinking alcohol in excessive amounts, you do have a potential higher risk. We just don’t know how significant that risk could be.
We do a large amount of education at baseline when they enroll in our study. We also educate our patients on how to recognize early on the potential risk for hypoglycemia, exactly for the reasons you said. We explain to them the unknown potential that the GLP-1 RAs and alcohol together may synergize and give hypoglycemia.
Dr. Jain: I don’t know if you got this feeling at the ADA conference, but I felt, when attending all these sessions, that it seems like GLP-1 RA is the gift that keeps giving. We see the effect on diabetes, obesity, metabolic-associated steatotic liver disease, possibly with Alzheimer’s, chronic obstructive pulmonary disease, and so many things.
Now, of course, there’s potential use in alcohol use disorder. Do you think that using GLP-1 RA therapy is ready for prime time? Do you think we are now ready to prescribe this in people with alcohol use disorder?
Dr. Leggio: I would say we’re not there yet. As I mentioned at the beginning, the evidence keeps on growing. It’s getting stronger and stronger because the positive data keep on coming up. We have data from animal models, including the different species, ranging from rodents to nonhuman primates. We have anecdotal evidence and machine-learning approaches using, for example, big data and social media data. Now we have pharmacoepidemiology data and some small, initial, but still good randomized clinical trials.
What we are missing is the final step of having a substantial number of prospective, double-blind, placebo-controlled clinical trials to really prove or disprove whether these medications work, and to also better understand which patients may respond to these medications.
The good news is that there are many ongoing clinical trials. We are conducting a clinical trial in Maryland at the NIH. Dr. Simmons is doing a clinical trial at Oklahoma State University. Dr. Christian Hendershot at UNC is conducting a study at Chapel Hill. Dr. Josh Gowin is doing a study in Colorado. Dr. Anders Fink-Jensen is doing a study in Denmark. The momentum is very high.
I’m only mentioning those people who are doing alcohol-semaglutide clinical trials. There are also people doing clinical trials on smoking, stimulants, and opioids. There are actually some very fresh, still unpublished data from Penn State that were presented publicly at conferences, showing how these drugs may reduce opioid craving, which is, of course, critically important, given that we’re in the middle of a fentanyl pandemic that is killing one person every 7 minutes, for example, in Baltimore. It’s very alarming and we need more treatments.
The bottom line is that it’s very promising, but we need to wait for these clinical trials to have a definitive answer. I would say that if you have a patient with diabetes, obesity, and also alcohol addiction, and they are on semaglutide or any other GLP-1 RA, and in addition to using the medication for diabetes and obesity, they also have a beneficial effect on their alcohol drinking, then that’s fantastic. At the end of the day, that’s the mission we all share: helping people.
If it’s someone without obesity and diabetes, personally, at this stage, I will go with other medications that either have FDA approval or at least very solid evidence of efficacy from RCTs rather than going with the GLP-1 RA, at least until I see more definitive data from randomized clinical trials.
There is a large amount of hope. We are hoping that these clinical trials will be positive. We are very enthusiastic and we’re also very thrilled to see that Novo Nordisk recently launched a gigantic multisite clinical trial with — I forgot how many sites, but it’s very large across Europe, America, and maybe other continents as well.
Their primary outcome is improvement in alcohol-related liver disease, but they’re also looking at alcohol drinking as a secondary outcome. That’s very important because, unlike in the diabetes field, in the addiction field, we do struggle to build partnership with the private sector because sometimes the addiction field is not seen as an appetitive field from pharma.
We all know that the best success in any medication development story is when you put academia, the government, and pharma together. Think about the COVID-19 vaccine development. That’s unfortunately the exception rather than rule in the addiction field.
With the company doing a large clinical trial in the alcohol field, although they focus more on the liver but they also looked at drinking, I really hope we’ll see more and more companies in the private sector take more and more interest in addiction. Also, I hope to see more and more partnership between the private sector, the government, and academia.
Dr. Jain: Such exciting times, indeed. We can’t wait enough for the results of these and many other trials to come out. Dr. Leggio, it was an absolute delight chatting with you today. Thank you so much for joining us from ADA 2024.
Akshay B. Jain, MD, Clinical Instructor, Department of Endocrinology, University of British Columbia; Endocrinologist, TLC Diabetes and Endocrinology, Vancouver, British Columbia, Canada, has disclosed the following relevant financial relationships: Serve(d) as a speaker or a member of a speakers bureau for: Abbott; Acerus; AstraZeneca; Amgen; Bausch Healthcare; Bayer; Boehringer Ingelheim; Care to Know; CCRN; Connected in Motion; CPD Network; Dexcom; Diabetes Canada; Eli Lilly; GSK; HLS Therapeutics; Janssen; Master Clinician Alliance; MDBriefcase; Merck; Medtronic; Moderna; Novartis; Novo Nordisk; Partners in Progressive Medical Education; Pfizer; Sanofi Aventis; Timed Right; WebMD. Received research grants/research support from: Abbott; Amgen; Novo Nordisk. Received consulting fees from: Abbott; Acerus; AstraZeneca; Amgen; Bausch Healthcare; Bayer; Boehringer Ingelheim; Dexcom; Eli Lilly; Gilead Sciences; GSK; HLS Therapeutics; Insulet; Janssen; Medtronic; Novo Nordisk; Partners in Progressive Medical Education; PocketPills; Roche; Sanofi Aventis; Takeda. Lorenzo Leggio, MD, PhD, Clinical Director, Deputy Scientific Director, National Institute on Drug Abuse Intramural Research Program, National Institutes of Health, Baltimore, Maryland, has disclosed the following relevant financial relationships: Serve(d) as a US federal employee for: National Institutes of Health. He had received income in an amount equal to or greater than $250 from: UK Medical Council on Alcohol for his service as editor-in-chief for Alcohol and Alcoholism and received royalties from Rutledge as an editor for a textbook.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Akshay B. Jain, MD: Today we are very excited to have Dr. Leggio join us all the way from the National Institutes of Health (NIH). He is an addiction physician scientist in the intramural research program at NIH. Welcome, Dr. Leggio. Thanks for joining us.
Lorenzo Leggio, MD, PhD: Thank you so much.
Dr. Jain: We’ll get right into this. Your session was, in my mind, extremely informative. The session looked at glucagon-like peptide 1 receptor agonist (GLP-1 RA) therapy and its potential effects on mitigating alcohol misuse syndrome, so, reduction of alcohol addiction potentially.
We’ve seen in some previous clinical trials, including many from your group, that alcohol use is known to be reduced — the overall risk of incidence, as well as recurrence of alcohol use — in individuals who are on GLP-1 RA therapy.
Can you share more insights about the data already out there?
Dr. Leggio: At the preclinical level, we have a very robust line of studies, experiments, and publications looking at the effect of GLP-1 RAs, starting from exenatide up to, more recently, semaglutide. They show that these GLP-1 RAs do reduce alcohol drinking. They used different animal models of excessive alcohol drinking, using different species — for example, mice, rats, nonhuman primates — models that reflect the excessive alcohol drinking behavior that we see in patients, like physical alcohol dependence or binge-like alcohol drinking, and other behaviors in animal models that reflect the human condition.
In addition to that, we recently have seen an increase in human evidence that GLP-1 RAs may reduce alcohol drinking. For example, there is some anecdotal evidence and some analyses using social media showing that people on GLP-1 RAs report drinking less alcohol.
There are also some pharmacoepidemiology studies which are very intriguing and quite promising. In this case, people have been looking at electronic medical records; they have used the pharmacoepidemiology approaches to match patients on GLP-1 RAs because of diabetes or obesity, and have compared and matched to patients on different drugs as the controls.
A study was recently published Nature Communications by a group in Cleveland in collaboration with Dr. Nora Volkow from the National Institute on Drug Abuse. This study shows the association between being on a GLP-1 RA and the lower incidence of alcohol use disorder and lower drinking.
There is also some promise from prospective randomized clinical trials. In particular, there was one clinical trial from Denmark, a well-known and -conducted clinical trial where they looked at exenatide, and they didn’t see an effect of exenatide compared with placebo in the main analysis. But in a subanalysis, they did see that exenatide reduced alcohol drinking, but only in patients with alcohol use disorder and obesity.
This suggests that these medications may work for some patients and not for other patients. That’s fine, because just like in any other field in medicine, including diabetes, obesity, hypertension, Parkinson’s, and depression, not all medications work for everybody. If these medications will work for alcohol addiction, we do not expect that they will work for everybody.
One ongoing question in the field is to try to identify the phenotypes or the subgroup of people who may be more responsive to these medications.
Dr. Jain: This is such a fascinating field, and all these studies are coming out. In your review of all the literature so far, do you think this is dose dependent? Also, we see that, for instance, with certain individuals, when they take GLP-1 RA therapy, they might have a lot of gastrointestinal (GI) side effects. Recent studies have shown that the rate of these GI side effects does not necessarily correlate with the amount of weight loss. In the alcohol addiction field, do you think that the GI side effects, things like nausea, could also have a potential role in mitigating the alcohol addiction?
Dr. Leggio: This is a great question. They may play a role; they may contribute, too, but we don’t think that they are the driving mechanism of why people drink less, for at least a couple of reasons.
One is that, similar to the obesity field, the data we have so far don’t necessarily show a relationship between the GI side effects and the reduction in drinking. Plus, the reduction in drinking is likely to happen later when many GI side effects are gone or attenuated.
The second reason is from the neuroscience field. We are starting to better understand the mechanism at the brain level as to how these medications work. We don’t see that the nausea or, more generally, not feeling well — malaise, etc. — are driving mechanisms for how these medications work.
Again, it’s not to discount completely that the GI side effects may play a role, but I would say that, if anything, they may be more contributing to. And if they do, that will not be unique to this class of medication. For example, we have three medications approved by the US Food and Drug Administration (FDA) for alcohol use disorder.
One challenge we have in the addiction field is that many people don’t know that these medications exist — many primary care providers don’t know — and they are completely underutilized. Everybody here who is listening to us knows that roughly 85% of people with diabetes receive a medication for diabetes. For alcohol use disorder, the number is 2%. These are medications approved by the FDA.
One of them is naltrexone, which does give GI symptoms — in particular, nausea and vomiting. The other medication is acamprosate, which does give diarrhea.
You have medications approved for alcohol disorder where you do have some GI symptoms, but they are not the mechanism either for how these medications help people to curb craving and reduce alcohol drinking.
Dr. Jain: What about the dose-dependent action? Do you think that GLP-1 RAs, at a lower dose, may not have an effect on alcohol use disorder vs at a higher dose, or is everyone a little different?
Dr. Leggio: That’s a wonderful question. The short answer is, we don’t know, to be honest. Now, in some of the animal studies — my team has been in collaboration with other scientists in the NIH intramural research program, and also with scientists in academia, for example, at Scripps, UCLA — we see a dose response where the higher the dose, the higher the effect of the drug. In this case, semaglutide reduced binge drinking in a rat model of a physical alcohol dependence.
That said, I would be very cautious about claiming, based on the rodent data, that humans will have a dose response. It’s an open question. We really don’t know. Some of the pharmacoepidemiology data suggested that even lower doses — for example, using semaglutide for diabetes without going up to the obesity dose — may be just as effective as a higher dose in reducing the incidence of alcohol use disorder.
It’s important also to keep in mind that the pharmacoepidemiology data are always an association. Reduction in alcohol disorder is associated with the prescription GLP-1 RA, but they don’t really replace the more gold-standard, double-blind, placebo-controlled randomized clinical trial. Nonetheless, with the pharmacoepidemiology data, I think there is an argument to at least hypothesize that people may respond well, even to lower doses.
This also may be important from a safety standpoint.
Basically, we need to wait for results in the next years to come from randomized clinical trials to better unfold the question about doses. For example, just anecdotally, I will tell you that in the clinical trial we are conducting right now at the NIH Intramural Research Program, for which I’m the principal investigator (PI), we are going up to 2.4 mg — the highest dose of semaglutide.
We are collaborating with Kyle Simmons, PhD, from Oklahoma State University. Our two studies are not like a two-site clinical trial, but they are harmonized. In Dr. Simmons’ clinical trial, they’re going up to 1.0 mg. We are excited about this team approach because the trials are slightly different, but they’re harmonized to the point that, once the studies are done, we’ll be able to combine and compare data to better answer the question about dosing, and many other questions.
Dr. Jain: From a clinical perspective, we see that many people who are battling alcohol use disorder may not have obesity. They might actually be on the leaner side, and hence, we may not want to use a high dose of GLP-1 RA therapy. It’ll be very exciting to see when these results come out.
This brings me to the next question. I think everyone would love to know why this happens. Why is GLP-1 RA having this effect on alcohol use disorder? I know that your group has done many animal studies, as you pointed out, and one of the postulated theories was the effect on the GABA neurotransmission pathway.
Can you tell us more about what you feel is the underlying mechanism of action here?
Dr. Leggio: I will start by saying that we don’t fully know. There are many open questions. If I can sidetrack for one second: We come up with the idea that, first of all, alcohol use disorder and substance use disorder are addictive behaviors, addictive disorders. We define addiction as a brain disease.
Granted that addiction is a brain disease, it doesn’t mean that addiction works just in the brain in isolation. As we all know, the brain works in concert with the rest of the body. One specific approach my team has been taking is working on the analogy and the similarities between obesity and addiction to try to understand how the body-brain connection, such as the gut-brain-neuroendocrine pathway, may play a role in patients with addiction.
With that in mind, a large amount of work in my lab in the past 20 years — since I’ve been a PI — has been focused on studying this neuroendocrine pathways related to the gut-brain axis. For example, we have done work on insulin and leptin, primarily; we had done work on ghrelin, and since 2015 on the GLP-1 RAs.
With that in mind, the framework we are working on, which is also substantiated by many studies done by our team and other teams in the neuroscience field, kind of supports the idea that, similar to what we see in obesity, these medications may work by affecting what we call reward processing, or the seeking for addictive drugs, such as alcohol, and also the drugs such as the stimulants, opioids, nicotine, and so on.
The idea is that the mechanism is driven by the ability of the medication — semaglutide and all the GLP-1 RAs — to reduce the rewarding properties of alcohol and drugs. To maybe make the example more pragmatic, what does that mean? It means, for example, that a patient who typically has 10 drinks per day in the afternoon and night, while they are on the medication they may feel the lack of need to drink up to 10 to feel the same reward.
They may be able to stop after two or three drinks, which means a significant harm reduction and a beneficial outcome. This also brings us to another mechanism, which may be related to society. We don’t fully understand how much the society mechanism, including society mechanism related to GI motility, may also play a role.
With that said, we don’t think that the effect of the GLP-1 RAs is merely due to alcohol being a calorie-based nutrient because, in fact, we see alcohol as an addictive drug, not as a nutrient. Also, the GLP-1 RAs, at least in animal models, seem to work on other addictive drugs that don’t have calories, such as nicotine, and possibly with cannabis, opioids, and stimulants.
Then on the molecular level, our team recently showed, in collaboration with Dr. Marisa Roberto from Scripps in La Jolla, California, that semaglutide may in fact change the GABA transmission at the level of some brain regions, such as the amygdala and the prefrontal cortex. These are brain regions that are well-established hubs that play a role in the mechanism underlying addiction.
There are also some very exciting recent data showing how these medications may work not just on GABA or just on dopamine, which is the canonical way we conceive of reward processing, but by working on both by modulating GABA transmission — for example, at the ventral tegmental area and dopamine transmission at the nucleus accumbens.
Bottom line, if I summarize all of this, is that the mechanism is not fully understood, but there is definitely a contribution of this medication to effect and reward processing, possibly by altering the balance between GABA and dopamine. There are still some unknown questions, such as, are these mechanisms all brain driven or are they signaling from the periphery to the brain, or maybe both?
Also, as we all know, there are many differences across all these GLP-1 analogs in brain penetrance. Whether the drug needs to go to the brain to have an effect on alcohol drinking, cocaine seeking, or smoking is really an open question.
Dr. Jain: This is so thought-provoking. I guess the more we uncover, the more mesmerized we get with all the potential crosstalk. There is a large amount of overlap in the brain with each of these different things and how it all interplays with each other.
Speaking of interplay, I’m thinking about how many people prone to having alcohol use disorder can potentially develop complications, one of these being chronic pancreatitis. This is a well-known complication that can occur in people having alcohol addiction. Along that same line, we know that previous history of pancreatitis is considered a use-with-caution, or we don’t want to use GLP-1 RA therapy in people who have had pancreatitis.
Now it becomes this quagmire where people may have chronic pancreatitis, but we may want to consider GLP-1 RA therapy for management of alcohol use disorder. What are your thoughts about this, and the safety, potentially, in using it in these patients?
Dr. Leggio: This is another wonderful question. That’s definitely a top priority in our mind, to address these kinds of questions. For example, our RCT does have, as core primary outcomes, not only the efficacy defined as a reduction in alcohol drinking, but also safety.
The reason is exactly what you just explained. There are many unanswered questions, including whether giving a GLP-1 RA and alcohol together may have synergistic effects and increase the likelihood of having pancreatitis.
The good news is that, so far, based on the published literature, including the RCT done with exenatide in Denmark and published in 2022 and also the ongoing clinical trials — including my own clinical trial, but of course we are blind — pancreatitis has not been coming out as an adverse event.
However, it’s also true that it often happens in clinical medication development. Of course, we screen and select our population well. For example, we do exclude people who have a history of pancreatitis. We exclude people with high lipase or with any of the clinical symptomatology that makes us concerned about these people having pancreatitis.
As often happens when you move a medication from clinical trials to clinical practice, we still need to understand whether this medication works in patients. I’m just speculating, but even if the clinical trials do not raise red flags in terms of increased risk for some side effects such as pancreatitis, I think it will be very important for practitioners to keep a close eye on the death risk regardless.
It’s very interesting that it’s similar to alcohol liver disease. With pancreatitis, not every single patient with alcohol addiction has pancreatitis. We don’t really fully understand why some people develop pancreatitis and some people do not. The point being that there are many patients with alcohol addiction who don’t have pancreatitis and may benefit from these medications if they work. Again, we have to prove that in patients.
On the other side, as we all know, pancreatitis is a potentially life-threatening condition for those people who either have it or are at risk for it. I think we have to be very careful before we consider giving them a GLP-1 RA.
One could argue that alcohol is the leading cause of mortality and morbidity in the world. For example, right now, alcohol is the leading cause of liver disease. It’s the main reason for liver transplantation in our country. Alcohol is affecting thousands of people in terms of death and emergency room visits.
You could argue that the downside is not treating these people and they die because of alcohol addiction. A GLP-1 RA is not going to be for everybody. I will remind everybody that (1) we do have FDA-approved medications for alcohol addiction; and (2) there are also other medications not approved by the FDA, but with a proven efficacy in some clinical trials — for example, topiramate and gabapentin — and they’ve been endorsed by the American Psychiatric Association.
There is also some evidence for another medication, baclofen, which has been endorsed by the American College of Gastroenterology for patients with alcohol addiction and liver disease.
The point I’m making is that it’s not that either we use the GLP-1 RAs or we have no other tools. We have other tools. I think we have to personalize the treatment based on the patient’s profile from a safety standpoint and from a phenotypic standpoint.
Dr. Jain: I love that thought. I think individualization is the key here.
We know that people with diabetes have a higher risk for pancreatitis by virtue of having diabetes. People with obesity also have a higher risk for pancreatitis by virtue of having obesity. These are the two conditions where we are using a large amount of GLP-1 RA therapy. Again, the idea is looking at the person in front of us and then deciding, based on their past medical history and their current risk, whether or not a medication is a right fit for them.
I think more individualization here will come as we start using these medications that might be having potential effects on different organ systems. You mentioned a little bit about the liver, so a thought came in my mind. We know that people with diabetes who have alcohol use disorder are at a higher risk for potential hypoglycemia. If they have events when they have increased consumption of alcohol, there can be more hypoglycemia.
We now could potentially be using semaglutide or other GLP-1 RA therapy for management of alcohol use disorder. In your own experience in the studies that you’ve done or the literature that’s out there, has that been associated with an even higher risk for hypoglycemia?
Dr. Leggio: It’s a wonderful question. I’m not aware of any formal and published report of that association. That said, your thinking from a physiopathologist standpoint makes total sense. I could not agree more. The fact that nothing has been published, at least to my knowledge, doesn’t mean that the death risk doesn’t exist. In fact, I agree with you that it does exist.
Alcohol use disorder is interesting and tricky clinically because chronically, alcohol addiction or alcohol use disorder is associated with an increased risk for diabetes. Acutely, as you point out; and this could be with or without alcohol use disorder. An episode of a high volume of binge drinking may lead to hypoglycemia.
This is one of the reasons why people may show up to the emergency room with intoxication, and one of the symptoms detected at the emergency room is that they also have hypoglycemia in addition to vomiting, nausea, and everything else that we see in patients with acute intoxication.
Similar to the discussion about pancreatitis, as we work on understanding the possible role of GLP-1 RA in patients with alcohol use disorder, we do have to keep a close eye on the risk for hypoglycemia. The short answer is that this is not well established, but based on the simple concept of “first, do no harm,” I think we need to track that very carefully.
In the ongoing clinical trial we’re doing in Maryland in my program at the NIH, we do just that. We are tracking glucose levels. Of course, patients come to clinic weekly, so unless they have symptoms, typically we don’t see anything at the time.
More important, we educate our patients when they go through the consent process. We tell them that this medication per se does not give hypoglycemia. In fact, we’re including people with diabetes, so for people on other medications like metformin, we explain to them that technically such a risk should not exist, but because you’re drinking alcohol in excessive amounts, you do have a potential higher risk. We just don’t know how significant that risk could be.
We do a large amount of education at baseline when they enroll in our study. We also educate our patients on how to recognize early on the potential risk for hypoglycemia, exactly for the reasons you said. We explain to them the unknown potential that the GLP-1 RAs and alcohol together may synergize and give hypoglycemia.
Dr. Jain: I don’t know if you got this feeling at the ADA conference, but I felt, when attending all these sessions, that it seems like GLP-1 RA is the gift that keeps giving. We see the effect on diabetes, obesity, metabolic-associated steatotic liver disease, possibly with Alzheimer’s, chronic obstructive pulmonary disease, and so many things.
Now, of course, there’s potential use in alcohol use disorder. Do you think that using GLP-1 RA therapy is ready for prime time? Do you think we are now ready to prescribe this in people with alcohol use disorder?
Dr. Leggio: I would say we’re not there yet. As I mentioned at the beginning, the evidence keeps on growing. It’s getting stronger and stronger because the positive data keep on coming up. We have data from animal models, including the different species, ranging from rodents to nonhuman primates. We have anecdotal evidence and machine-learning approaches using, for example, big data and social media data. Now we have pharmacoepidemiology data and some small, initial, but still good randomized clinical trials.
What we are missing is the final step of having a substantial number of prospective, double-blind, placebo-controlled clinical trials to really prove or disprove whether these medications work, and to also better understand which patients may respond to these medications.
The good news is that there are many ongoing clinical trials. We are conducting a clinical trial in Maryland at the NIH. Dr. Simmons is doing a clinical trial at Oklahoma State University. Dr. Christian Hendershot at UNC is conducting a study at Chapel Hill. Dr. Josh Gowin is doing a study in Colorado. Dr. Anders Fink-Jensen is doing a study in Denmark. The momentum is very high.
I’m only mentioning those people who are doing alcohol-semaglutide clinical trials. There are also people doing clinical trials on smoking, stimulants, and opioids. There are actually some very fresh, still unpublished data from Penn State that were presented publicly at conferences, showing how these drugs may reduce opioid craving, which is, of course, critically important, given that we’re in the middle of a fentanyl pandemic that is killing one person every 7 minutes, for example, in Baltimore. It’s very alarming and we need more treatments.
The bottom line is that it’s very promising, but we need to wait for these clinical trials to have a definitive answer. I would say that if you have a patient with diabetes, obesity, and also alcohol addiction, and they are on semaglutide or any other GLP-1 RA, and in addition to using the medication for diabetes and obesity, they also have a beneficial effect on their alcohol drinking, then that’s fantastic. At the end of the day, that’s the mission we all share: helping people.
If it’s someone without obesity and diabetes, personally, at this stage, I will go with other medications that either have FDA approval or at least very solid evidence of efficacy from RCTs rather than going with the GLP-1 RA, at least until I see more definitive data from randomized clinical trials.
There is a large amount of hope. We are hoping that these clinical trials will be positive. We are very enthusiastic and we’re also very thrilled to see that Novo Nordisk recently launched a gigantic multisite clinical trial with — I forgot how many sites, but it’s very large across Europe, America, and maybe other continents as well.
Their primary outcome is improvement in alcohol-related liver disease, but they’re also looking at alcohol drinking as a secondary outcome. That’s very important because, unlike in the diabetes field, in the addiction field, we do struggle to build partnership with the private sector because sometimes the addiction field is not seen as an appetitive field from pharma.
We all know that the best success in any medication development story is when you put academia, the government, and pharma together. Think about the COVID-19 vaccine development. That’s unfortunately the exception rather than rule in the addiction field.
With the company doing a large clinical trial in the alcohol field, although they focus more on the liver but they also looked at drinking, I really hope we’ll see more and more companies in the private sector take more and more interest in addiction. Also, I hope to see more and more partnership between the private sector, the government, and academia.
Dr. Jain: Such exciting times, indeed. We can’t wait enough for the results of these and many other trials to come out. Dr. Leggio, it was an absolute delight chatting with you today. Thank you so much for joining us from ADA 2024.
Akshay B. Jain, MD, Clinical Instructor, Department of Endocrinology, University of British Columbia; Endocrinologist, TLC Diabetes and Endocrinology, Vancouver, British Columbia, Canada, has disclosed the following relevant financial relationships: Serve(d) as a speaker or a member of a speakers bureau for: Abbott; Acerus; AstraZeneca; Amgen; Bausch Healthcare; Bayer; Boehringer Ingelheim; Care to Know; CCRN; Connected in Motion; CPD Network; Dexcom; Diabetes Canada; Eli Lilly; GSK; HLS Therapeutics; Janssen; Master Clinician Alliance; MDBriefcase; Merck; Medtronic; Moderna; Novartis; Novo Nordisk; Partners in Progressive Medical Education; Pfizer; Sanofi Aventis; Timed Right; WebMD. Received research grants/research support from: Abbott; Amgen; Novo Nordisk. Received consulting fees from: Abbott; Acerus; AstraZeneca; Amgen; Bausch Healthcare; Bayer; Boehringer Ingelheim; Dexcom; Eli Lilly; Gilead Sciences; GSK; HLS Therapeutics; Insulet; Janssen; Medtronic; Novo Nordisk; Partners in Progressive Medical Education; PocketPills; Roche; Sanofi Aventis; Takeda. Lorenzo Leggio, MD, PhD, Clinical Director, Deputy Scientific Director, National Institute on Drug Abuse Intramural Research Program, National Institutes of Health, Baltimore, Maryland, has disclosed the following relevant financial relationships: Serve(d) as a US federal employee for: National Institutes of Health. He had received income in an amount equal to or greater than $250 from: UK Medical Council on Alcohol for his service as editor-in-chief for Alcohol and Alcoholism and received royalties from Rutledge as an editor for a textbook.
A version of this article first appeared on Medscape.com.
FROM ADA 2024
Wide Regional Variation in Dementia Risk Across the United States
TOPLINE:
The likelihood of receiving a dementia diagnosis in older adults varies significantly by region across the United States, a new study suggests. Rates ranged from 1.7% to 5.4%, with variations more pronounced in those aged 66-74 years and Black or Hispanic individuals.
METHODOLOGY:
- Researchers analyzed newly diagnosed cases of Alzheimer’s disease and related dementias (ADRD) using the 2018-2019 Medicare claims data for 4.8 million older adults across 306 hospital referral regions (HRRs).
- Participants were categorized by age and race or ethnicity to examine variations in diagnosis rates.
- Regional characteristics such as education level and prevalence of obesity, smoking, and diabetes were included to adjust for population risk factors.
- ADRD-specific diagnostic intensity was calculated as the ratio of the observed-to-expected new cases of ADRD in each HRR.
TAKEAWAY:
- Unadjusted analysis for that overall, 3% of older adults received a new ADRD diagnosis in 2019, with rates ranging from 1.7 to 5.4 per 100 individuals across HRRs and varied by age category.
- Regions in the South had the highest unadjusted ADRD case concentration, and the areas in the West/Northwest had the lowest.
- The ADRD-specific diagnosis intensity was 0.69-1.47 and varied the most in Black and Hispanic individuals and those aged 66-74 years.
- Regional differences in ADRD diagnosis rates are not fully explained by population risk factors, indicating potential health system-level differences.
IN PRACTICE:
“From place to place, the likelihood of getting your dementia diagnosed varies, and that may happen because of everything from practice norms for healthcare providers to individual patients’ knowledge and care-seeking behavior. These findings go beyond demographic and population-level differences in risk and indicate that there are health system-level differences that could be targeted and remediated,” lead author Julie P.W. Bynum, MD, MPH, said in a press release.
SOURCE:
The study was led by Dr. Bynum, professor of internal medicine, University of Michigan Medical School, Ann Arbor, Michigan, and published online in Alzheimer’s & Dementia.
LIMITATIONS:
The results may not be generalizable to other groups. The observational design of the study cannot completely negate residual confounding. The measures of population risks are coarser than those used in well-characterized epidemiologic studies, leading to potential imprecision. Finally, the study was not designed to determine whether regional differences in the likelihood of ADRD diagnosis resulted in differences in the population health outcomes.
DISCLOSURES:
The study was supported by a grant from the National Institute on Aging. The authors reported no conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
The likelihood of receiving a dementia diagnosis in older adults varies significantly by region across the United States, a new study suggests. Rates ranged from 1.7% to 5.4%, with variations more pronounced in those aged 66-74 years and Black or Hispanic individuals.
METHODOLOGY:
- Researchers analyzed newly diagnosed cases of Alzheimer’s disease and related dementias (ADRD) using the 2018-2019 Medicare claims data for 4.8 million older adults across 306 hospital referral regions (HRRs).
- Participants were categorized by age and race or ethnicity to examine variations in diagnosis rates.
- Regional characteristics such as education level and prevalence of obesity, smoking, and diabetes were included to adjust for population risk factors.
- ADRD-specific diagnostic intensity was calculated as the ratio of the observed-to-expected new cases of ADRD in each HRR.
TAKEAWAY:
- Unadjusted analysis for that overall, 3% of older adults received a new ADRD diagnosis in 2019, with rates ranging from 1.7 to 5.4 per 100 individuals across HRRs and varied by age category.
- Regions in the South had the highest unadjusted ADRD case concentration, and the areas in the West/Northwest had the lowest.
- The ADRD-specific diagnosis intensity was 0.69-1.47 and varied the most in Black and Hispanic individuals and those aged 66-74 years.
- Regional differences in ADRD diagnosis rates are not fully explained by population risk factors, indicating potential health system-level differences.
IN PRACTICE:
“From place to place, the likelihood of getting your dementia diagnosed varies, and that may happen because of everything from practice norms for healthcare providers to individual patients’ knowledge and care-seeking behavior. These findings go beyond demographic and population-level differences in risk and indicate that there are health system-level differences that could be targeted and remediated,” lead author Julie P.W. Bynum, MD, MPH, said in a press release.
SOURCE:
The study was led by Dr. Bynum, professor of internal medicine, University of Michigan Medical School, Ann Arbor, Michigan, and published online in Alzheimer’s & Dementia.
LIMITATIONS:
The results may not be generalizable to other groups. The observational design of the study cannot completely negate residual confounding. The measures of population risks are coarser than those used in well-characterized epidemiologic studies, leading to potential imprecision. Finally, the study was not designed to determine whether regional differences in the likelihood of ADRD diagnosis resulted in differences in the population health outcomes.
DISCLOSURES:
The study was supported by a grant from the National Institute on Aging. The authors reported no conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
The likelihood of receiving a dementia diagnosis in older adults varies significantly by region across the United States, a new study suggests. Rates ranged from 1.7% to 5.4%, with variations more pronounced in those aged 66-74 years and Black or Hispanic individuals.
METHODOLOGY:
- Researchers analyzed newly diagnosed cases of Alzheimer’s disease and related dementias (ADRD) using the 2018-2019 Medicare claims data for 4.8 million older adults across 306 hospital referral regions (HRRs).
- Participants were categorized by age and race or ethnicity to examine variations in diagnosis rates.
- Regional characteristics such as education level and prevalence of obesity, smoking, and diabetes were included to adjust for population risk factors.
- ADRD-specific diagnostic intensity was calculated as the ratio of the observed-to-expected new cases of ADRD in each HRR.
TAKEAWAY:
- Unadjusted analysis for that overall, 3% of older adults received a new ADRD diagnosis in 2019, with rates ranging from 1.7 to 5.4 per 100 individuals across HRRs and varied by age category.
- Regions in the South had the highest unadjusted ADRD case concentration, and the areas in the West/Northwest had the lowest.
- The ADRD-specific diagnosis intensity was 0.69-1.47 and varied the most in Black and Hispanic individuals and those aged 66-74 years.
- Regional differences in ADRD diagnosis rates are not fully explained by population risk factors, indicating potential health system-level differences.
IN PRACTICE:
“From place to place, the likelihood of getting your dementia diagnosed varies, and that may happen because of everything from practice norms for healthcare providers to individual patients’ knowledge and care-seeking behavior. These findings go beyond demographic and population-level differences in risk and indicate that there are health system-level differences that could be targeted and remediated,” lead author Julie P.W. Bynum, MD, MPH, said in a press release.
SOURCE:
The study was led by Dr. Bynum, professor of internal medicine, University of Michigan Medical School, Ann Arbor, Michigan, and published online in Alzheimer’s & Dementia.
LIMITATIONS:
The results may not be generalizable to other groups. The observational design of the study cannot completely negate residual confounding. The measures of population risks are coarser than those used in well-characterized epidemiologic studies, leading to potential imprecision. Finally, the study was not designed to determine whether regional differences in the likelihood of ADRD diagnosis resulted in differences in the population health outcomes.
DISCLOSURES:
The study was supported by a grant from the National Institute on Aging. The authors reported no conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
Parkinson’s Risk in Women and History of Migraine: New Data
TOPLINE:
A history of migraine is not associated with an elevated risk for Parkinson’s disease (PD) in women, regardless of headache frequency or migraine subtype, a new study suggests.
METHODOLOGY:
- Researchers analyzed data on 39,312 women health professionals aged ≥ 45 years and having no history of PD who enrolled in the Women’s Health Study between 1992 and 1995 and were followed until 2021.
- At baseline, 7321 women (18.6%) had migraine.
- The mean follow-up duration was 22 years.
- The primary outcome was a self-reported, physician-confirmed diagnosis of PD.
TAKEAWAY:
- During the study period, 685 women self-reported a diagnosis of PD.
- Of these, 18.7% of reported cases were in women with any migraine and 81.3% in women without migraine.
- No significant association was found between PD risk and a history of migraine, migraine subtypes (with or without aura), or migraine frequency.
- Migraine was not associated with a higher risk for PD than that of nonmigraine headaches.
IN PRACTICE:
“These results are reassuring for women who have migraine, which itself causes many burdens, that they don’t have to worry about an increased risk of Parkinson’s disease in the future,” study author Tobias Kurth, Charité - Universitätsmedizin Berlin, Germany, said in a press release.
SOURCE:
The study was led by Ricarda S. Schulz, MSc, Charité - Universitätsmedizin Berlin. It was published online in Neurology.
LIMITATIONS:
The study’s findings may not be generalizable to other populations, such as men and non-White individuals. The self-reported data on migraine and PD may be subject to inaccuracies. PD is often not diagnosed until symptoms have reached an advanced stage, potentially leading to cases being underreported. Changes in the status and frequency of migraine over the study period were not accounted for, which may have affected the results.
DISCLOSURES:
The authors did not disclose any specific funding for this work. The Women’s Health Study was supported by the National Cancer Institute and National Heart, Lung, and Blood Institute. Two authors reported having financial ties outside this work. Full disclosures are available in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
A history of migraine is not associated with an elevated risk for Parkinson’s disease (PD) in women, regardless of headache frequency or migraine subtype, a new study suggests.
METHODOLOGY:
- Researchers analyzed data on 39,312 women health professionals aged ≥ 45 years and having no history of PD who enrolled in the Women’s Health Study between 1992 and 1995 and were followed until 2021.
- At baseline, 7321 women (18.6%) had migraine.
- The mean follow-up duration was 22 years.
- The primary outcome was a self-reported, physician-confirmed diagnosis of PD.
TAKEAWAY:
- During the study period, 685 women self-reported a diagnosis of PD.
- Of these, 18.7% of reported cases were in women with any migraine and 81.3% in women without migraine.
- No significant association was found between PD risk and a history of migraine, migraine subtypes (with or without aura), or migraine frequency.
- Migraine was not associated with a higher risk for PD than that of nonmigraine headaches.
IN PRACTICE:
“These results are reassuring for women who have migraine, which itself causes many burdens, that they don’t have to worry about an increased risk of Parkinson’s disease in the future,” study author Tobias Kurth, Charité - Universitätsmedizin Berlin, Germany, said in a press release.
SOURCE:
The study was led by Ricarda S. Schulz, MSc, Charité - Universitätsmedizin Berlin. It was published online in Neurology.
LIMITATIONS:
The study’s findings may not be generalizable to other populations, such as men and non-White individuals. The self-reported data on migraine and PD may be subject to inaccuracies. PD is often not diagnosed until symptoms have reached an advanced stage, potentially leading to cases being underreported. Changes in the status and frequency of migraine over the study period were not accounted for, which may have affected the results.
DISCLOSURES:
The authors did not disclose any specific funding for this work. The Women’s Health Study was supported by the National Cancer Institute and National Heart, Lung, and Blood Institute. Two authors reported having financial ties outside this work. Full disclosures are available in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
A history of migraine is not associated with an elevated risk for Parkinson’s disease (PD) in women, regardless of headache frequency or migraine subtype, a new study suggests.
METHODOLOGY:
- Researchers analyzed data on 39,312 women health professionals aged ≥ 45 years and having no history of PD who enrolled in the Women’s Health Study between 1992 and 1995 and were followed until 2021.
- At baseline, 7321 women (18.6%) had migraine.
- The mean follow-up duration was 22 years.
- The primary outcome was a self-reported, physician-confirmed diagnosis of PD.
TAKEAWAY:
- During the study period, 685 women self-reported a diagnosis of PD.
- Of these, 18.7% of reported cases were in women with any migraine and 81.3% in women without migraine.
- No significant association was found between PD risk and a history of migraine, migraine subtypes (with or without aura), or migraine frequency.
- Migraine was not associated with a higher risk for PD than that of nonmigraine headaches.
IN PRACTICE:
“These results are reassuring for women who have migraine, which itself causes many burdens, that they don’t have to worry about an increased risk of Parkinson’s disease in the future,” study author Tobias Kurth, Charité - Universitätsmedizin Berlin, Germany, said in a press release.
SOURCE:
The study was led by Ricarda S. Schulz, MSc, Charité - Universitätsmedizin Berlin. It was published online in Neurology.
LIMITATIONS:
The study’s findings may not be generalizable to other populations, such as men and non-White individuals. The self-reported data on migraine and PD may be subject to inaccuracies. PD is often not diagnosed until symptoms have reached an advanced stage, potentially leading to cases being underreported. Changes in the status and frequency of migraine over the study period were not accounted for, which may have affected the results.
DISCLOSURES:
The authors did not disclose any specific funding for this work. The Women’s Health Study was supported by the National Cancer Institute and National Heart, Lung, and Blood Institute. Two authors reported having financial ties outside this work. Full disclosures are available in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
The Link Between Vision Impairment and Dementia in Older Adults
TOPLINE:
METHODOLOGY:
- Researchers conducted a cross-sectional analysis using data from the National Health and Aging Trends Study (NHATS).
- The analysis included 2767 US adults aged 71 years or older (54.7% female and 45.3% male).
- Vision impairments were defined using 2019 World Health Organization criteria. Near and distance vision impairments were defined as greater than 0.30 logMAR, and contrast sensitivity impairment was identified by scores below 1.55 logCS.
- Dementia was classified using a standardized algorithm developed in NHATS, which incorporated a series of tests measuring cognition, memory and orientation, reports of Alzheimer’s disease, or a dementia diagnosis from the patient or a proxy, and an informant questionnaire (Ascertain Dementia-8 Dementia Screening Interview).
- The study analyzed data from 2021, with the primary outcome being the population attributable fraction (PAF) of dementia from vision impairment.
TAKEAWAY:
- The PAF of dementia associated with at least one vision impairment was 19% (95% CI, 8.2-29.7).
- Impairment in contrast sensitivity had the highest PAF among all other vision issues, at 15% (95% CI, 6.6-23.6). This figure was higher than that for impairment of near acuity, at 9.7% (95% CI, 2.6-17.0), or distance acuity, at 4.9% (95% CI, 0.1-9.9).
- The highest PAFs for dementia due to vision impairment was among participants aged 71-79 years (24.3%; 95% CI, 6.6-41.8), women (26.8%; 95% CI, 12.2-39.9), and non-Hispanic White participants (22.3%; 95% CI, 9.6-34.5).
IN PRACTICE:
“While not proving a cause-and-effect relationship, these findings support inclusion of multiple objective measures of vision impairments, including contrast sensitivity and visual acuity, to capture the total potential impact of addressing vision impairment on dementia,” study authors wrote.
SOURCE:
This study was led by Jason R. Smith, ScM, of the Department of Epidemiology at the Johns Hopkins Bloomberg School of Public Health in Baltimore. It was published online in JAMA Ophthalmology.
LIMITATIONS:
The limited sample sizes for American Indian, Alaska Native, Asian, and Hispanic groups prevented researchers from calculating PAFs for these populations. The cross-sectional design prevented the researchers from examining the timing of vision impairment in relation to a diagnosis of dementia. The study did not explore links between other measures of vision and dementia. Those with early cognitive impairment may not have updated glasses, affecting visual performance. The findings from the study may not apply to institutionalized older adults.
DISCLOSURES:
Jennifer A. Deal, PhD, MHS, reported receiving personal fees from Frontiers in Epidemiology, Velux Stiftung, and Medical Education Speakers Network outside the submitted work. Nicholas S. Reed, AuD, PhD, reported receiving stock options from Neosensory outside the submitted work. No other disclosures were reported.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Researchers conducted a cross-sectional analysis using data from the National Health and Aging Trends Study (NHATS).
- The analysis included 2767 US adults aged 71 years or older (54.7% female and 45.3% male).
- Vision impairments were defined using 2019 World Health Organization criteria. Near and distance vision impairments were defined as greater than 0.30 logMAR, and contrast sensitivity impairment was identified by scores below 1.55 logCS.
- Dementia was classified using a standardized algorithm developed in NHATS, which incorporated a series of tests measuring cognition, memory and orientation, reports of Alzheimer’s disease, or a dementia diagnosis from the patient or a proxy, and an informant questionnaire (Ascertain Dementia-8 Dementia Screening Interview).
- The study analyzed data from 2021, with the primary outcome being the population attributable fraction (PAF) of dementia from vision impairment.
TAKEAWAY:
- The PAF of dementia associated with at least one vision impairment was 19% (95% CI, 8.2-29.7).
- Impairment in contrast sensitivity had the highest PAF among all other vision issues, at 15% (95% CI, 6.6-23.6). This figure was higher than that for impairment of near acuity, at 9.7% (95% CI, 2.6-17.0), or distance acuity, at 4.9% (95% CI, 0.1-9.9).
- The highest PAFs for dementia due to vision impairment was among participants aged 71-79 years (24.3%; 95% CI, 6.6-41.8), women (26.8%; 95% CI, 12.2-39.9), and non-Hispanic White participants (22.3%; 95% CI, 9.6-34.5).
IN PRACTICE:
“While not proving a cause-and-effect relationship, these findings support inclusion of multiple objective measures of vision impairments, including contrast sensitivity and visual acuity, to capture the total potential impact of addressing vision impairment on dementia,” study authors wrote.
SOURCE:
This study was led by Jason R. Smith, ScM, of the Department of Epidemiology at the Johns Hopkins Bloomberg School of Public Health in Baltimore. It was published online in JAMA Ophthalmology.
LIMITATIONS:
The limited sample sizes for American Indian, Alaska Native, Asian, and Hispanic groups prevented researchers from calculating PAFs for these populations. The cross-sectional design prevented the researchers from examining the timing of vision impairment in relation to a diagnosis of dementia. The study did not explore links between other measures of vision and dementia. Those with early cognitive impairment may not have updated glasses, affecting visual performance. The findings from the study may not apply to institutionalized older adults.
DISCLOSURES:
Jennifer A. Deal, PhD, MHS, reported receiving personal fees from Frontiers in Epidemiology, Velux Stiftung, and Medical Education Speakers Network outside the submitted work. Nicholas S. Reed, AuD, PhD, reported receiving stock options from Neosensory outside the submitted work. No other disclosures were reported.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Researchers conducted a cross-sectional analysis using data from the National Health and Aging Trends Study (NHATS).
- The analysis included 2767 US adults aged 71 years or older (54.7% female and 45.3% male).
- Vision impairments were defined using 2019 World Health Organization criteria. Near and distance vision impairments were defined as greater than 0.30 logMAR, and contrast sensitivity impairment was identified by scores below 1.55 logCS.
- Dementia was classified using a standardized algorithm developed in NHATS, which incorporated a series of tests measuring cognition, memory and orientation, reports of Alzheimer’s disease, or a dementia diagnosis from the patient or a proxy, and an informant questionnaire (Ascertain Dementia-8 Dementia Screening Interview).
- The study analyzed data from 2021, with the primary outcome being the population attributable fraction (PAF) of dementia from vision impairment.
TAKEAWAY:
- The PAF of dementia associated with at least one vision impairment was 19% (95% CI, 8.2-29.7).
- Impairment in contrast sensitivity had the highest PAF among all other vision issues, at 15% (95% CI, 6.6-23.6). This figure was higher than that for impairment of near acuity, at 9.7% (95% CI, 2.6-17.0), or distance acuity, at 4.9% (95% CI, 0.1-9.9).
- The highest PAFs for dementia due to vision impairment was among participants aged 71-79 years (24.3%; 95% CI, 6.6-41.8), women (26.8%; 95% CI, 12.2-39.9), and non-Hispanic White participants (22.3%; 95% CI, 9.6-34.5).
IN PRACTICE:
“While not proving a cause-and-effect relationship, these findings support inclusion of multiple objective measures of vision impairments, including contrast sensitivity and visual acuity, to capture the total potential impact of addressing vision impairment on dementia,” study authors wrote.
SOURCE:
This study was led by Jason R. Smith, ScM, of the Department of Epidemiology at the Johns Hopkins Bloomberg School of Public Health in Baltimore. It was published online in JAMA Ophthalmology.
LIMITATIONS:
The limited sample sizes for American Indian, Alaska Native, Asian, and Hispanic groups prevented researchers from calculating PAFs for these populations. The cross-sectional design prevented the researchers from examining the timing of vision impairment in relation to a diagnosis of dementia. The study did not explore links between other measures of vision and dementia. Those with early cognitive impairment may not have updated glasses, affecting visual performance. The findings from the study may not apply to institutionalized older adults.
DISCLOSURES:
Jennifer A. Deal, PhD, MHS, reported receiving personal fees from Frontiers in Epidemiology, Velux Stiftung, and Medical Education Speakers Network outside the submitted work. Nicholas S. Reed, AuD, PhD, reported receiving stock options from Neosensory outside the submitted work. No other disclosures were reported.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.A version of this article appeared on Medscape.com.
Why More Doctors Are Joining Unions
With huge shifts over the past decade in the way doctors are employed — half of all doctors now work for a health system or large medical group — the idea of unionizing is not only being explored but gaining traction within the profession. In fact, 8% of the physician workforce (or 70,000 physicians) belong to a union, according to statistics gathered in 2022.
Exact numbers are hard to come by, and, interestingly, although the American Medical Association (AMA) “ supports the right of physicians to engage in collective bargaining,” the organization doesn’t track union membership among physicians, according to an AMA spokesperson.
Forming a Union
One challenge is that forming a union is not only time-consuming but also difficult, owing to several barriers. For starters, the laws dictating unionization differ by state, and the rules governing unionization vary if a hospital is public or private. If there’s enough momentum from doctors leading unionization efforts, approval from hospital leaders is required before an official election can be requested from the National Labor Relations Board.
That said, for doctors who are in a union — the two most popular are the Union of American Physicians and Dentists and the Doctors Council branch of the Service Employees International Union (SEIU)—the benefits are immense, especially because union members can focus on what matters, such as providing the best patient care possible.
, reported WBUR in Boston.
Belonging Matters
“When you build a relationship with your patients, it’s special, and that connection isn’t replaceable,” said Nicholas VenOsdel, MD, a pediatrician at Allina Health Primary Care in Hastings, Minnesota, and a union member of the Doctors Council. “However, a lot of us have felt like that hasn’t been respected as the climate of healthcare has changed so fast.”
In fact, autonomy over how much time doctors spend with patients is driving a lot of interest in unionization.
“We don’t necessarily have that autonomy now,” said Amber Higgins, MD, an emergency physician and an obstetrician at ChristianaCare, a hospital network in Newark, Delaware, and a member of the Doctors Council. “There are so many other demands, whether it’s billing, patient documentation, or other demands from the employer, and all of that takes time away from patient care.”
Another primary driver of physician unionization is the physician burnout epidemic. Physicians collectively complain that they spend more time on electronic health record documentation and bureaucratic administration. Yet if unions can improve these working conditions, the benefit to physicians and their patients would be a welcome change.
Union members are bullish and believe that having a cohesive voice will make a difference.
“We need to use our collective voices to get back to focusing on patient care instead of staring at a computer screen for 80% of the day,” Dr. Higgins told this news organization. “So much of medicine involves getting to the correct diagnosis, listening to patients, observing them, and building a relationship with them. We need time to build that.”
With corporate consolidation and a profit-driven mandate by healthcare systems, doctors are increasingly frustrated and feel that their voices haven’t been heard enough when it comes to issues like workplace safety, working hours, and benefits, said Stuart Bussey, MD, JD, a family practice physician and president of the Union of American Physicians and Dentists in Sacramento, California.
However, he adds that urging doctors to join together to fight for a better working environment hasn’t been easy.
“Doctors are individualists, and they don’t know how to work in packs like hospital administrators do,” said Dr. Bussey. “They’re hard to organize, but I want them to understand that unless they join hands, sign petitions, and speak as one voice, they’re going to lose out on an amazing opportunity.”
Overcoming Misperceptions About Unions
One barrier to doctors getting involved is the sentiment that unions might do the opposite of what’s intended — that is, they might further reduce a doctor’s autonomy and work flexibility. Or there may be a perception that the drive to join a union is predicated on making more money.
Though he’s now in a union, Dr. VenOsdel, who has been in a hospital-based practice for 7 years, admits that he initially felt very differently about unions than he does today.
“Even though I have family members in healthcare unions, I had a neutral to even slightly negative view of unions,” said Dr. VenOsdel. “It took me working directly with the Minnesota Nurses Association and the Doctors Council to learn the other side of the story.”
Armed with more information, he began lobbying for stricter rules about how his state’s large healthcare systems were closing hospitals and ending much-needed community services.
“I remember standing at the Capitol in Minnesota and telling one of the members that I once felt negatively about unions,” he added. “I realized then that I only knew what employers were telling me via such things as emails about strikes — that information was all being shared from the employers’ perspective.”
The other misperception is that unions only exist to argue against management, including against colleagues who are also part of the management structure, said Dr. Higgins.
“Some doctors perceive being in a union as ‘how can those same leaders also be in a union,’” she said. She feels that they currently don’t have leadership representing them that can help with such things as restructuring their support teams or getting them help with certain tasks. “That’s another way unions can help.”
Social Justice Plays a Role
For Dr. VenOsdel, being part of a union has helped him return to what he calls the “art” of medicine.
“Philosophically, the union gave me an option for change in what felt like a hopeless situation,” he said. “It wasn’t just that I was tossing the keys to someone else and saying, ‘I can’t fix this.’ Instead, we’re taking the reins back and fixing things ourselves.”
Bussey argues that as the uneven balance between administrators and providers in many healthcare organizations grows, the time to consider forming a union is now.
“We’re in a $4 trillion medical industrial revolution,” he said. “Administrators and bureaucrats are multiplying 30-fold times vs providers, and most of that $4 trillion supports things that don’t contribute to the doctor-patient relationship.”
Furthermore, union proponents say that where a one-on-one relationship between doctor and patient once existed, that has now been “triangulated” to include administrators.
“We’ve lost power in every way,” Dr. Bussey said. “We have the degrees, the liability, and the knowledge — we should have more power to make our workplaces safer and better.”
Ultimately, for some unionized doctors, the very holding of a union card is rooted in supporting social justice issues.
“When doctors realize how powerful a tool a union can be for social justice and change, this will alter perceptions of unions within our profession,” Dr. VenOsdel said. “Our union helps give us a voice to stand up for other staff who aren’t unionized and, most importantly, to stand up for the patients who need us.”
A version of this article first appeared on Medscape.com.
With huge shifts over the past decade in the way doctors are employed — half of all doctors now work for a health system or large medical group — the idea of unionizing is not only being explored but gaining traction within the profession. In fact, 8% of the physician workforce (or 70,000 physicians) belong to a union, according to statistics gathered in 2022.
Exact numbers are hard to come by, and, interestingly, although the American Medical Association (AMA) “ supports the right of physicians to engage in collective bargaining,” the organization doesn’t track union membership among physicians, according to an AMA spokesperson.
Forming a Union
One challenge is that forming a union is not only time-consuming but also difficult, owing to several barriers. For starters, the laws dictating unionization differ by state, and the rules governing unionization vary if a hospital is public or private. If there’s enough momentum from doctors leading unionization efforts, approval from hospital leaders is required before an official election can be requested from the National Labor Relations Board.
That said, for doctors who are in a union — the two most popular are the Union of American Physicians and Dentists and the Doctors Council branch of the Service Employees International Union (SEIU)—the benefits are immense, especially because union members can focus on what matters, such as providing the best patient care possible.
, reported WBUR in Boston.
Belonging Matters
“When you build a relationship with your patients, it’s special, and that connection isn’t replaceable,” said Nicholas VenOsdel, MD, a pediatrician at Allina Health Primary Care in Hastings, Minnesota, and a union member of the Doctors Council. “However, a lot of us have felt like that hasn’t been respected as the climate of healthcare has changed so fast.”
In fact, autonomy over how much time doctors spend with patients is driving a lot of interest in unionization.
“We don’t necessarily have that autonomy now,” said Amber Higgins, MD, an emergency physician and an obstetrician at ChristianaCare, a hospital network in Newark, Delaware, and a member of the Doctors Council. “There are so many other demands, whether it’s billing, patient documentation, or other demands from the employer, and all of that takes time away from patient care.”
Another primary driver of physician unionization is the physician burnout epidemic. Physicians collectively complain that they spend more time on electronic health record documentation and bureaucratic administration. Yet if unions can improve these working conditions, the benefit to physicians and their patients would be a welcome change.
Union members are bullish and believe that having a cohesive voice will make a difference.
“We need to use our collective voices to get back to focusing on patient care instead of staring at a computer screen for 80% of the day,” Dr. Higgins told this news organization. “So much of medicine involves getting to the correct diagnosis, listening to patients, observing them, and building a relationship with them. We need time to build that.”
With corporate consolidation and a profit-driven mandate by healthcare systems, doctors are increasingly frustrated and feel that their voices haven’t been heard enough when it comes to issues like workplace safety, working hours, and benefits, said Stuart Bussey, MD, JD, a family practice physician and president of the Union of American Physicians and Dentists in Sacramento, California.
However, he adds that urging doctors to join together to fight for a better working environment hasn’t been easy.
“Doctors are individualists, and they don’t know how to work in packs like hospital administrators do,” said Dr. Bussey. “They’re hard to organize, but I want them to understand that unless they join hands, sign petitions, and speak as one voice, they’re going to lose out on an amazing opportunity.”
Overcoming Misperceptions About Unions
One barrier to doctors getting involved is the sentiment that unions might do the opposite of what’s intended — that is, they might further reduce a doctor’s autonomy and work flexibility. Or there may be a perception that the drive to join a union is predicated on making more money.
Though he’s now in a union, Dr. VenOsdel, who has been in a hospital-based practice for 7 years, admits that he initially felt very differently about unions than he does today.
“Even though I have family members in healthcare unions, I had a neutral to even slightly negative view of unions,” said Dr. VenOsdel. “It took me working directly with the Minnesota Nurses Association and the Doctors Council to learn the other side of the story.”
Armed with more information, he began lobbying for stricter rules about how his state’s large healthcare systems were closing hospitals and ending much-needed community services.
“I remember standing at the Capitol in Minnesota and telling one of the members that I once felt negatively about unions,” he added. “I realized then that I only knew what employers were telling me via such things as emails about strikes — that information was all being shared from the employers’ perspective.”
The other misperception is that unions only exist to argue against management, including against colleagues who are also part of the management structure, said Dr. Higgins.
“Some doctors perceive being in a union as ‘how can those same leaders also be in a union,’” she said. She feels that they currently don’t have leadership representing them that can help with such things as restructuring their support teams or getting them help with certain tasks. “That’s another way unions can help.”
Social Justice Plays a Role
For Dr. VenOsdel, being part of a union has helped him return to what he calls the “art” of medicine.
“Philosophically, the union gave me an option for change in what felt like a hopeless situation,” he said. “It wasn’t just that I was tossing the keys to someone else and saying, ‘I can’t fix this.’ Instead, we’re taking the reins back and fixing things ourselves.”
Bussey argues that as the uneven balance between administrators and providers in many healthcare organizations grows, the time to consider forming a union is now.
“We’re in a $4 trillion medical industrial revolution,” he said. “Administrators and bureaucrats are multiplying 30-fold times vs providers, and most of that $4 trillion supports things that don’t contribute to the doctor-patient relationship.”
Furthermore, union proponents say that where a one-on-one relationship between doctor and patient once existed, that has now been “triangulated” to include administrators.
“We’ve lost power in every way,” Dr. Bussey said. “We have the degrees, the liability, and the knowledge — we should have more power to make our workplaces safer and better.”
Ultimately, for some unionized doctors, the very holding of a union card is rooted in supporting social justice issues.
“When doctors realize how powerful a tool a union can be for social justice and change, this will alter perceptions of unions within our profession,” Dr. VenOsdel said. “Our union helps give us a voice to stand up for other staff who aren’t unionized and, most importantly, to stand up for the patients who need us.”
A version of this article first appeared on Medscape.com.
With huge shifts over the past decade in the way doctors are employed — half of all doctors now work for a health system or large medical group — the idea of unionizing is not only being explored but gaining traction within the profession. In fact, 8% of the physician workforce (or 70,000 physicians) belong to a union, according to statistics gathered in 2022.
Exact numbers are hard to come by, and, interestingly, although the American Medical Association (AMA) “ supports the right of physicians to engage in collective bargaining,” the organization doesn’t track union membership among physicians, according to an AMA spokesperson.
Forming a Union
One challenge is that forming a union is not only time-consuming but also difficult, owing to several barriers. For starters, the laws dictating unionization differ by state, and the rules governing unionization vary if a hospital is public or private. If there’s enough momentum from doctors leading unionization efforts, approval from hospital leaders is required before an official election can be requested from the National Labor Relations Board.
That said, for doctors who are in a union — the two most popular are the Union of American Physicians and Dentists and the Doctors Council branch of the Service Employees International Union (SEIU)—the benefits are immense, especially because union members can focus on what matters, such as providing the best patient care possible.
, reported WBUR in Boston.
Belonging Matters
“When you build a relationship with your patients, it’s special, and that connection isn’t replaceable,” said Nicholas VenOsdel, MD, a pediatrician at Allina Health Primary Care in Hastings, Minnesota, and a union member of the Doctors Council. “However, a lot of us have felt like that hasn’t been respected as the climate of healthcare has changed so fast.”
In fact, autonomy over how much time doctors spend with patients is driving a lot of interest in unionization.
“We don’t necessarily have that autonomy now,” said Amber Higgins, MD, an emergency physician and an obstetrician at ChristianaCare, a hospital network in Newark, Delaware, and a member of the Doctors Council. “There are so many other demands, whether it’s billing, patient documentation, or other demands from the employer, and all of that takes time away from patient care.”
Another primary driver of physician unionization is the physician burnout epidemic. Physicians collectively complain that they spend more time on electronic health record documentation and bureaucratic administration. Yet if unions can improve these working conditions, the benefit to physicians and their patients would be a welcome change.
Union members are bullish and believe that having a cohesive voice will make a difference.
“We need to use our collective voices to get back to focusing on patient care instead of staring at a computer screen for 80% of the day,” Dr. Higgins told this news organization. “So much of medicine involves getting to the correct diagnosis, listening to patients, observing them, and building a relationship with them. We need time to build that.”
With corporate consolidation and a profit-driven mandate by healthcare systems, doctors are increasingly frustrated and feel that their voices haven’t been heard enough when it comes to issues like workplace safety, working hours, and benefits, said Stuart Bussey, MD, JD, a family practice physician and president of the Union of American Physicians and Dentists in Sacramento, California.
However, he adds that urging doctors to join together to fight for a better working environment hasn’t been easy.
“Doctors are individualists, and they don’t know how to work in packs like hospital administrators do,” said Dr. Bussey. “They’re hard to organize, but I want them to understand that unless they join hands, sign petitions, and speak as one voice, they’re going to lose out on an amazing opportunity.”
Overcoming Misperceptions About Unions
One barrier to doctors getting involved is the sentiment that unions might do the opposite of what’s intended — that is, they might further reduce a doctor’s autonomy and work flexibility. Or there may be a perception that the drive to join a union is predicated on making more money.
Though he’s now in a union, Dr. VenOsdel, who has been in a hospital-based practice for 7 years, admits that he initially felt very differently about unions than he does today.
“Even though I have family members in healthcare unions, I had a neutral to even slightly negative view of unions,” said Dr. VenOsdel. “It took me working directly with the Minnesota Nurses Association and the Doctors Council to learn the other side of the story.”
Armed with more information, he began lobbying for stricter rules about how his state’s large healthcare systems were closing hospitals and ending much-needed community services.
“I remember standing at the Capitol in Minnesota and telling one of the members that I once felt negatively about unions,” he added. “I realized then that I only knew what employers were telling me via such things as emails about strikes — that information was all being shared from the employers’ perspective.”
The other misperception is that unions only exist to argue against management, including against colleagues who are also part of the management structure, said Dr. Higgins.
“Some doctors perceive being in a union as ‘how can those same leaders also be in a union,’” she said. She feels that they currently don’t have leadership representing them that can help with such things as restructuring their support teams or getting them help with certain tasks. “That’s another way unions can help.”
Social Justice Plays a Role
For Dr. VenOsdel, being part of a union has helped him return to what he calls the “art” of medicine.
“Philosophically, the union gave me an option for change in what felt like a hopeless situation,” he said. “It wasn’t just that I was tossing the keys to someone else and saying, ‘I can’t fix this.’ Instead, we’re taking the reins back and fixing things ourselves.”
Bussey argues that as the uneven balance between administrators and providers in many healthcare organizations grows, the time to consider forming a union is now.
“We’re in a $4 trillion medical industrial revolution,” he said. “Administrators and bureaucrats are multiplying 30-fold times vs providers, and most of that $4 trillion supports things that don’t contribute to the doctor-patient relationship.”
Furthermore, union proponents say that where a one-on-one relationship between doctor and patient once existed, that has now been “triangulated” to include administrators.
“We’ve lost power in every way,” Dr. Bussey said. “We have the degrees, the liability, and the knowledge — we should have more power to make our workplaces safer and better.”
Ultimately, for some unionized doctors, the very holding of a union card is rooted in supporting social justice issues.
“When doctors realize how powerful a tool a union can be for social justice and change, this will alter perceptions of unions within our profession,” Dr. VenOsdel said. “Our union helps give us a voice to stand up for other staff who aren’t unionized and, most importantly, to stand up for the patients who need us.”
A version of this article first appeared on Medscape.com.
FDA Rejects MDMA-AT for PTSD, but Lykos, Others, Vow to Push on
The Food and Drug Administration’s (FDA) decision not to approve midomafetamine-assisted therapy (MDMA-AT) for posttraumatic stress disorder (PTSD) puts the therapy’s near-term future in doubt, but officials say the rejection may not knock it out of contention as an eventual therapeutic tool for a variety of conditions.
In August the agency declined to approve the drug with currently available study data and requested that the company conduct an additional phase 3 trial. The agency’s action had potentially devastating consequences for MDMA-AT’s sponsor, Lykos Therapeutics, and was a huge disappointment for researchers, clinicians, and patients who were optimistic that it would be a new option for a condition that affects 13-17 million Americans.
For now, no other company is poised to imminently seek FDA approval for MDMA.
Despite the setback, research into MDMA that combines different psychotherapeutic approaches continues. Currently, there are seven US studies actively recruiting participants, and another 13 are registered with an eye toward starting recruitment, as reported on ClinicalTrials.gov.
The lack of FDA approval “actually increases the opportunity now for us to do trials,” said Michael Ostacher, MD, professor of psychiatry and behavioral sciences at Stanford Medicine in California. Researchers won’t have to be sponsored by Lykos to get access to MDMA.
“There’s a lot of energy and interest in doing these studies,” he said in an interview, adding that philanthropic organizations and Veterans Affairs (VA) are contributing funds to support such studies.
The VA provided a statement saying that it “intends to gather rigorous scientific evidence on the potential efficacy and safety of psychedelic compounds when used in conjunction with psychotherapy.” It also noted that “these studies will be conducted under stringent safety protocols and will mark the first time since the 1960’s that VA is funding research on such compounds.”
Rachel Yehuda, PhD, director of the Center for Psychedelic Therapy Research at Icahn School of Medicine at Mount Sinai in New York City, said in an interview that the FDA rejection “raises questions about how to keep the work going.”
Without the FDA’s imprimatur, MDMA remains a schedule 1 drug, which means it has no valid medical use.
“It’s a lot more complicated and expensive to work with a scheduled compound than to work with a compound that has been approved,” Dr. Yehuda said.
Also, without Lykos or another drug company sponsor, investigators have to find an acceptable MDMA source on their own, said Dr. Yehuda, who was an investigator on a study in which Lykos provided MDMA but was not involved in study design, data collection, analysis, or manuscript preparation.
Lykos in Disarray
Within a week of the FDA’s decision, Lykos announced it was cutting its staff by 75% and that Rick Doblin, PhD, the founder and president of the Multidisciplinary Association for Psychedelic Studies (MAPS) that gave rise to Lykos, had resigned from the Lykos board.
A frequently controversial figure, Doblin has been attempting to legitimize MDMA as a therapy since the mid-1980s. He formed a public benefit corporation (PBC) in 2014 with an eye toward FDA approval. The PBC fully separated from MAPS in 2024 and became Lykos.
Although the FDA has left the door open to approval, Lykos has not released the agency’s complete response letter, so it’s not clear exactly what the FDA is seeking. In a statement, the company said it believes the issues “can be addressed with existing data, postapproval requirements, or through reference to the scientific literature.”
Lykos said in an email that it is working on “securing the meeting with the FDA” and that it “will work with the agency to determine what needs to be done to fulfill their requests.”
Soon after the FDA decision, Lykos was hit with another blow. The journal Psychopharmacology retracted an article that pooled six Lykos phase 2 studies, claiming the paper’s authors knew about unethical conduct before submission but did not inform the publisher.
Lykos said the issues could have been addressed through a correction and that it has filed a complaint with the Committee on Publication Ethics. It also noted that the misconduct at issue was reported to the FDA and Health Canada.
“However, we did not disclose the violations to the journal itself, an additional step we should have taken and regret not doing,” the company said. It added that the efficacy data in the paper were not part of the FDA submission.
Author Allison A. Feduccia, PhD, cofounder of Psychedelic Support, agreed with the retraction but disagreed with the wording. In a post on LinkedIn, she said she and other authors were not informed about the misconduct until years after the study’s submission.
Four authors — including Dr. Doblin — disagreed with the retraction.
Dr. Doblin said in a statement that he’d resigned from Lykos to escape the restrictions that came with being a fiduciary. “Now I can advocate and speak freely,” he said, adding that he could also return to his activist roots.
He predicted that Lykos would eventually gain FDA approval. But if Lykos can’t convince the agency, it have the necessary data already in hand; “potential FDA approval is now at least 2 years away, possibly more,” Dr. Doblin said in his statement.
Research Continues
Lykos is not the only company hoping to commercialize MDMA. Toronto-based Awakn Life Sciences has an MDMA preclinical development program for addiction. In addition, some companies are offering MDMA therapy through clinics, such as Numinus in Utah and Sunstone Therapies in Rockville, Maryland.
But Lykos was the closest to bringing a product to market. The company is still a sponsor of four MDMA-related clinical trials, three of which appear to be on hold. One study at the VA San Diego Healthcare System, San Diego, that is actively recruiting is an open-label trial to assess MDMA-AT in combination with brief Cognitive-Behavioral Conjoint Therapy for PTSD.
Those studies are among 13 US trials listed in ClinicalTrials.gov that have not yet begun recruiting and 7 that are actively recruiting.
Among them is a study of MDMA plus exposure therapy, funded by and conducted at Emory University in Atlanta. One of the Emory principal investigators, Barbara Rothbaum, MD, has also been named to a Lykos’ panel that would help ensure oversight of MDMA-AT post FDA approval.
Dr. Ostacher is an investigator in a study planned at VA Palo Alto Health Care System in California, that will compare MDMA-AT with cognitive processing therapy in veterans with severe PTSD. He said it will be open label in an effort to minimize expectation bias and issues with blinding — both problems that tripped up the Lykos application. Although placebo-controlled trials are the gold standard, it’s not ideal when “the purpose of the drug is for it to change how you see the world and yourself,” Dr. Ostacher said.
The study aims to see whether MDMA-AT is better than “a much shorter, less onerous, but quite evidence-based psychotherapy for PTSD,” he said.
The FDA’s decision is not the end of the road, said Dr. Ostacher. “Even though I think this makes for an obvious delay, I don’t think that it’s a permanent one,” he said.
Dr. Yehuda also said she is not ready to give up.
“We don’t plan on stopping — we plan on finding a way,” she said.
“In our experience, this is a very powerful approach that helps a lot of people that haven’t found help using other approaches, and when it’s in the hands of really trusted, experienced, ethical clinicians in a trusted environment, this could be a real game changer for people who have not been able to find belief by traditional methods,” she said.
Dr. Ostacher reported no relevant financial relationships. Dr. Yahuda is the principal investigator on clinical trials for the Center for Psychedelic Psychotherapy and Trauma Research that are sponsored by the Multidisciplinary Association for Psychedelic Studies and COMPASS Pathways.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration’s (FDA) decision not to approve midomafetamine-assisted therapy (MDMA-AT) for posttraumatic stress disorder (PTSD) puts the therapy’s near-term future in doubt, but officials say the rejection may not knock it out of contention as an eventual therapeutic tool for a variety of conditions.
In August the agency declined to approve the drug with currently available study data and requested that the company conduct an additional phase 3 trial. The agency’s action had potentially devastating consequences for MDMA-AT’s sponsor, Lykos Therapeutics, and was a huge disappointment for researchers, clinicians, and patients who were optimistic that it would be a new option for a condition that affects 13-17 million Americans.
For now, no other company is poised to imminently seek FDA approval for MDMA.
Despite the setback, research into MDMA that combines different psychotherapeutic approaches continues. Currently, there are seven US studies actively recruiting participants, and another 13 are registered with an eye toward starting recruitment, as reported on ClinicalTrials.gov.
The lack of FDA approval “actually increases the opportunity now for us to do trials,” said Michael Ostacher, MD, professor of psychiatry and behavioral sciences at Stanford Medicine in California. Researchers won’t have to be sponsored by Lykos to get access to MDMA.
“There’s a lot of energy and interest in doing these studies,” he said in an interview, adding that philanthropic organizations and Veterans Affairs (VA) are contributing funds to support such studies.
The VA provided a statement saying that it “intends to gather rigorous scientific evidence on the potential efficacy and safety of psychedelic compounds when used in conjunction with psychotherapy.” It also noted that “these studies will be conducted under stringent safety protocols and will mark the first time since the 1960’s that VA is funding research on such compounds.”
Rachel Yehuda, PhD, director of the Center for Psychedelic Therapy Research at Icahn School of Medicine at Mount Sinai in New York City, said in an interview that the FDA rejection “raises questions about how to keep the work going.”
Without the FDA’s imprimatur, MDMA remains a schedule 1 drug, which means it has no valid medical use.
“It’s a lot more complicated and expensive to work with a scheduled compound than to work with a compound that has been approved,” Dr. Yehuda said.
Also, without Lykos or another drug company sponsor, investigators have to find an acceptable MDMA source on their own, said Dr. Yehuda, who was an investigator on a study in which Lykos provided MDMA but was not involved in study design, data collection, analysis, or manuscript preparation.
Lykos in Disarray
Within a week of the FDA’s decision, Lykos announced it was cutting its staff by 75% and that Rick Doblin, PhD, the founder and president of the Multidisciplinary Association for Psychedelic Studies (MAPS) that gave rise to Lykos, had resigned from the Lykos board.
A frequently controversial figure, Doblin has been attempting to legitimize MDMA as a therapy since the mid-1980s. He formed a public benefit corporation (PBC) in 2014 with an eye toward FDA approval. The PBC fully separated from MAPS in 2024 and became Lykos.
Although the FDA has left the door open to approval, Lykos has not released the agency’s complete response letter, so it’s not clear exactly what the FDA is seeking. In a statement, the company said it believes the issues “can be addressed with existing data, postapproval requirements, or through reference to the scientific literature.”
Lykos said in an email that it is working on “securing the meeting with the FDA” and that it “will work with the agency to determine what needs to be done to fulfill their requests.”
Soon after the FDA decision, Lykos was hit with another blow. The journal Psychopharmacology retracted an article that pooled six Lykos phase 2 studies, claiming the paper’s authors knew about unethical conduct before submission but did not inform the publisher.
Lykos said the issues could have been addressed through a correction and that it has filed a complaint with the Committee on Publication Ethics. It also noted that the misconduct at issue was reported to the FDA and Health Canada.
“However, we did not disclose the violations to the journal itself, an additional step we should have taken and regret not doing,” the company said. It added that the efficacy data in the paper were not part of the FDA submission.
Author Allison A. Feduccia, PhD, cofounder of Psychedelic Support, agreed with the retraction but disagreed with the wording. In a post on LinkedIn, she said she and other authors were not informed about the misconduct until years after the study’s submission.
Four authors — including Dr. Doblin — disagreed with the retraction.
Dr. Doblin said in a statement that he’d resigned from Lykos to escape the restrictions that came with being a fiduciary. “Now I can advocate and speak freely,” he said, adding that he could also return to his activist roots.
He predicted that Lykos would eventually gain FDA approval. But if Lykos can’t convince the agency, it have the necessary data already in hand; “potential FDA approval is now at least 2 years away, possibly more,” Dr. Doblin said in his statement.
Research Continues
Lykos is not the only company hoping to commercialize MDMA. Toronto-based Awakn Life Sciences has an MDMA preclinical development program for addiction. In addition, some companies are offering MDMA therapy through clinics, such as Numinus in Utah and Sunstone Therapies in Rockville, Maryland.
But Lykos was the closest to bringing a product to market. The company is still a sponsor of four MDMA-related clinical trials, three of which appear to be on hold. One study at the VA San Diego Healthcare System, San Diego, that is actively recruiting is an open-label trial to assess MDMA-AT in combination with brief Cognitive-Behavioral Conjoint Therapy for PTSD.
Those studies are among 13 US trials listed in ClinicalTrials.gov that have not yet begun recruiting and 7 that are actively recruiting.
Among them is a study of MDMA plus exposure therapy, funded by and conducted at Emory University in Atlanta. One of the Emory principal investigators, Barbara Rothbaum, MD, has also been named to a Lykos’ panel that would help ensure oversight of MDMA-AT post FDA approval.
Dr. Ostacher is an investigator in a study planned at VA Palo Alto Health Care System in California, that will compare MDMA-AT with cognitive processing therapy in veterans with severe PTSD. He said it will be open label in an effort to minimize expectation bias and issues with blinding — both problems that tripped up the Lykos application. Although placebo-controlled trials are the gold standard, it’s not ideal when “the purpose of the drug is for it to change how you see the world and yourself,” Dr. Ostacher said.
The study aims to see whether MDMA-AT is better than “a much shorter, less onerous, but quite evidence-based psychotherapy for PTSD,” he said.
The FDA’s decision is not the end of the road, said Dr. Ostacher. “Even though I think this makes for an obvious delay, I don’t think that it’s a permanent one,” he said.
Dr. Yehuda also said she is not ready to give up.
“We don’t plan on stopping — we plan on finding a way,” she said.
“In our experience, this is a very powerful approach that helps a lot of people that haven’t found help using other approaches, and when it’s in the hands of really trusted, experienced, ethical clinicians in a trusted environment, this could be a real game changer for people who have not been able to find belief by traditional methods,” she said.
Dr. Ostacher reported no relevant financial relationships. Dr. Yahuda is the principal investigator on clinical trials for the Center for Psychedelic Psychotherapy and Trauma Research that are sponsored by the Multidisciplinary Association for Psychedelic Studies and COMPASS Pathways.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration’s (FDA) decision not to approve midomafetamine-assisted therapy (MDMA-AT) for posttraumatic stress disorder (PTSD) puts the therapy’s near-term future in doubt, but officials say the rejection may not knock it out of contention as an eventual therapeutic tool for a variety of conditions.
In August the agency declined to approve the drug with currently available study data and requested that the company conduct an additional phase 3 trial. The agency’s action had potentially devastating consequences for MDMA-AT’s sponsor, Lykos Therapeutics, and was a huge disappointment for researchers, clinicians, and patients who were optimistic that it would be a new option for a condition that affects 13-17 million Americans.
For now, no other company is poised to imminently seek FDA approval for MDMA.
Despite the setback, research into MDMA that combines different psychotherapeutic approaches continues. Currently, there are seven US studies actively recruiting participants, and another 13 are registered with an eye toward starting recruitment, as reported on ClinicalTrials.gov.
The lack of FDA approval “actually increases the opportunity now for us to do trials,” said Michael Ostacher, MD, professor of psychiatry and behavioral sciences at Stanford Medicine in California. Researchers won’t have to be sponsored by Lykos to get access to MDMA.
“There’s a lot of energy and interest in doing these studies,” he said in an interview, adding that philanthropic organizations and Veterans Affairs (VA) are contributing funds to support such studies.
The VA provided a statement saying that it “intends to gather rigorous scientific evidence on the potential efficacy and safety of psychedelic compounds when used in conjunction with psychotherapy.” It also noted that “these studies will be conducted under stringent safety protocols and will mark the first time since the 1960’s that VA is funding research on such compounds.”
Rachel Yehuda, PhD, director of the Center for Psychedelic Therapy Research at Icahn School of Medicine at Mount Sinai in New York City, said in an interview that the FDA rejection “raises questions about how to keep the work going.”
Without the FDA’s imprimatur, MDMA remains a schedule 1 drug, which means it has no valid medical use.
“It’s a lot more complicated and expensive to work with a scheduled compound than to work with a compound that has been approved,” Dr. Yehuda said.
Also, without Lykos or another drug company sponsor, investigators have to find an acceptable MDMA source on their own, said Dr. Yehuda, who was an investigator on a study in which Lykos provided MDMA but was not involved in study design, data collection, analysis, or manuscript preparation.
Lykos in Disarray
Within a week of the FDA’s decision, Lykos announced it was cutting its staff by 75% and that Rick Doblin, PhD, the founder and president of the Multidisciplinary Association for Psychedelic Studies (MAPS) that gave rise to Lykos, had resigned from the Lykos board.
A frequently controversial figure, Doblin has been attempting to legitimize MDMA as a therapy since the mid-1980s. He formed a public benefit corporation (PBC) in 2014 with an eye toward FDA approval. The PBC fully separated from MAPS in 2024 and became Lykos.
Although the FDA has left the door open to approval, Lykos has not released the agency’s complete response letter, so it’s not clear exactly what the FDA is seeking. In a statement, the company said it believes the issues “can be addressed with existing data, postapproval requirements, or through reference to the scientific literature.”
Lykos said in an email that it is working on “securing the meeting with the FDA” and that it “will work with the agency to determine what needs to be done to fulfill their requests.”
Soon after the FDA decision, Lykos was hit with another blow. The journal Psychopharmacology retracted an article that pooled six Lykos phase 2 studies, claiming the paper’s authors knew about unethical conduct before submission but did not inform the publisher.
Lykos said the issues could have been addressed through a correction and that it has filed a complaint with the Committee on Publication Ethics. It also noted that the misconduct at issue was reported to the FDA and Health Canada.
“However, we did not disclose the violations to the journal itself, an additional step we should have taken and regret not doing,” the company said. It added that the efficacy data in the paper were not part of the FDA submission.
Author Allison A. Feduccia, PhD, cofounder of Psychedelic Support, agreed with the retraction but disagreed with the wording. In a post on LinkedIn, she said she and other authors were not informed about the misconduct until years after the study’s submission.
Four authors — including Dr. Doblin — disagreed with the retraction.
Dr. Doblin said in a statement that he’d resigned from Lykos to escape the restrictions that came with being a fiduciary. “Now I can advocate and speak freely,” he said, adding that he could also return to his activist roots.
He predicted that Lykos would eventually gain FDA approval. But if Lykos can’t convince the agency, it have the necessary data already in hand; “potential FDA approval is now at least 2 years away, possibly more,” Dr. Doblin said in his statement.
Research Continues
Lykos is not the only company hoping to commercialize MDMA. Toronto-based Awakn Life Sciences has an MDMA preclinical development program for addiction. In addition, some companies are offering MDMA therapy through clinics, such as Numinus in Utah and Sunstone Therapies in Rockville, Maryland.
But Lykos was the closest to bringing a product to market. The company is still a sponsor of four MDMA-related clinical trials, three of which appear to be on hold. One study at the VA San Diego Healthcare System, San Diego, that is actively recruiting is an open-label trial to assess MDMA-AT in combination with brief Cognitive-Behavioral Conjoint Therapy for PTSD.
Those studies are among 13 US trials listed in ClinicalTrials.gov that have not yet begun recruiting and 7 that are actively recruiting.
Among them is a study of MDMA plus exposure therapy, funded by and conducted at Emory University in Atlanta. One of the Emory principal investigators, Barbara Rothbaum, MD, has also been named to a Lykos’ panel that would help ensure oversight of MDMA-AT post FDA approval.
Dr. Ostacher is an investigator in a study planned at VA Palo Alto Health Care System in California, that will compare MDMA-AT with cognitive processing therapy in veterans with severe PTSD. He said it will be open label in an effort to minimize expectation bias and issues with blinding — both problems that tripped up the Lykos application. Although placebo-controlled trials are the gold standard, it’s not ideal when “the purpose of the drug is for it to change how you see the world and yourself,” Dr. Ostacher said.
The study aims to see whether MDMA-AT is better than “a much shorter, less onerous, but quite evidence-based psychotherapy for PTSD,” he said.
The FDA’s decision is not the end of the road, said Dr. Ostacher. “Even though I think this makes for an obvious delay, I don’t think that it’s a permanent one,” he said.
Dr. Yehuda also said she is not ready to give up.
“We don’t plan on stopping — we plan on finding a way,” she said.
“In our experience, this is a very powerful approach that helps a lot of people that haven’t found help using other approaches, and when it’s in the hands of really trusted, experienced, ethical clinicians in a trusted environment, this could be a real game changer for people who have not been able to find belief by traditional methods,” she said.
Dr. Ostacher reported no relevant financial relationships. Dr. Yahuda is the principal investigator on clinical trials for the Center for Psychedelic Psychotherapy and Trauma Research that are sponsored by the Multidisciplinary Association for Psychedelic Studies and COMPASS Pathways.
A version of this article first appeared on Medscape.com.
Wait, a Health Worker Surplus? Workforce Report Projects Big Surprises
A surprising new report by the Mercer consulting firm projects that the American healthcare workforce will face a small shortfall in 2028 — a shortage of less than 1% of all employees.
Mercer’s projections are rosier than federal workforce projections, which paint a grimmer picture of impending shortages.
“The labor market is a little more stabilized right now, and most healthcare systems are seeing less turnover,” Dan Lezotte, PhD, a partner with Mercer, said in an interview. But he noted “critical shortages” are still expected in some areas.
Mercer last projected workforce numbers in a 2020-2021 report released during the height of the COVID-19 pandemic. Now, “the labor market is drastically different,” Dr. Lezotte said. Health workforce shortages and surpluses have long varied significantly by region across the country.
The report forecasts a small surplus of physicians in 2028 but not in states such as California, New York, and Texas. The upper Midwest states will largely see doctor surpluses while Southern states face shortages. Some states with general physician surpluses may still experience shortages of specialists.
A surplus of nearly 30,000 registered nurses is expected, but New York, New Jersey, and Connecticut are projected to have a combined shortage of 16,000 nurses.
Overall, the report projects a shortage of more than 100,000 healthcare workers nationally by 2028. That’s less than 1% of the entire healthcare workforce of 18.6 million expected by then.
The report also predicts a shortage of nurse practitioners, especially in California and New York, and a shortage of 73,000 nursing assistants, especially in California, New York, and Texas.
“Healthcare systems are having the most difficulty hiring and hanging on to those workers who are supposed to take up the load off physicians and nurses,” Dr. Lezotte said. “They’re competing not only with other healthcare systems but with other industries like Amazon warehouses or McDonald’s in California paying $20 an hour. Healthcare was a little slow to keep up with that. In a lot of healthcare systems, that’s their biggest headache right now.”
On the other hand, the report projects a national surplus of 48,000 home health/personal care aides.
That surprised Bianca K. Frogner, PhD, director of the Center for Health Workforce Studies at the University of Washington, Seattle.
“We are seeing increasing movement of investments toward moving patients out of skilled nursing facilities and keeping them in the home and community, which requires many more home health aides,” Dr. Frogner said. “Given such high turnover in this occupation, it’s hard to know if the surplus is really a surplus or if they will quickly be employed.”
Dr. Frogner receives grants and contracts from not-for-profit entities to investigate issues related to the health workforce.
Dr. Lezotte said the report’s findings are based on data from sources such as public and private databases and job postings. According to the report, “projections were made up to 2028 based on historical data up to 2023,” and “supply projections were derived using a linear autoregressive model based on historical supply within each occupation and geography.”
It’s not clear why some states like New York are expected to have huge shortages, but migration might be a factor, along with a lack of nearby nursing schools, Dr. Lezotte said.
As for shortages, Dr. Lezotte said healthcare systems will have to understand their local workforce situation and adapt. “They’ll need to be more proactive about their employee value proposition” via competitive pay and benefits Flexibility regarding scheduling is also important.
“They’re going to have to figure out how to up their game,” he said.
What about states with surpluses? They might be target-rich environments for states facing shortages, he said.
Positive Outlook Not Shared by Other Researchers
Other workforce projections conflict with Mercer’s, according to Jean Moore, DrPH, and Gaetano Forte, MS, director and assistant director of the Center for Health Workforce Studies, School of Public Health, University at Albany, New York.
The National Center for Health Workforce Analysis projects a 10% shortage of registered nurses and a 13% shortage of physicians in 2031. The agency didn’t make projections for home health aides because that workforce is in flux.
Why are Mercer’s projections so different? Dr. Lezotte said other projections assume that equity efforts will bring healthcare to everyone who needs it. The report assumes this won’t happen, he said. As a result, it expects there will be fewer patients who need to be served by workers.
Other projections expect a shortage of 300,000 registered nurses by 2035, Mr. Forte said. But the number of nurse practitioners in New York is growing quickly, Dr. Moore said.
Dr. Moore said it’s difficult to interpret Mercer’s findings because the company doesn’t provide enough information about its methodology.
“At some level, it’s not particularly useful regarding what the next steps are,” she said. “Projections should make you think about what you should do to change and improve, to create more of what you need.”
The Center for Health Workforce Studies at the University of Albany has provided consulting services to multiple companies that provide healthcare workforce projections. It has no relationship with Mercer.
A version of this article first appeared on Medscape.com.
A surprising new report by the Mercer consulting firm projects that the American healthcare workforce will face a small shortfall in 2028 — a shortage of less than 1% of all employees.
Mercer’s projections are rosier than federal workforce projections, which paint a grimmer picture of impending shortages.
“The labor market is a little more stabilized right now, and most healthcare systems are seeing less turnover,” Dan Lezotte, PhD, a partner with Mercer, said in an interview. But he noted “critical shortages” are still expected in some areas.
Mercer last projected workforce numbers in a 2020-2021 report released during the height of the COVID-19 pandemic. Now, “the labor market is drastically different,” Dr. Lezotte said. Health workforce shortages and surpluses have long varied significantly by region across the country.
The report forecasts a small surplus of physicians in 2028 but not in states such as California, New York, and Texas. The upper Midwest states will largely see doctor surpluses while Southern states face shortages. Some states with general physician surpluses may still experience shortages of specialists.
A surplus of nearly 30,000 registered nurses is expected, but New York, New Jersey, and Connecticut are projected to have a combined shortage of 16,000 nurses.
Overall, the report projects a shortage of more than 100,000 healthcare workers nationally by 2028. That’s less than 1% of the entire healthcare workforce of 18.6 million expected by then.
The report also predicts a shortage of nurse practitioners, especially in California and New York, and a shortage of 73,000 nursing assistants, especially in California, New York, and Texas.
“Healthcare systems are having the most difficulty hiring and hanging on to those workers who are supposed to take up the load off physicians and nurses,” Dr. Lezotte said. “They’re competing not only with other healthcare systems but with other industries like Amazon warehouses or McDonald’s in California paying $20 an hour. Healthcare was a little slow to keep up with that. In a lot of healthcare systems, that’s their biggest headache right now.”
On the other hand, the report projects a national surplus of 48,000 home health/personal care aides.
That surprised Bianca K. Frogner, PhD, director of the Center for Health Workforce Studies at the University of Washington, Seattle.
“We are seeing increasing movement of investments toward moving patients out of skilled nursing facilities and keeping them in the home and community, which requires many more home health aides,” Dr. Frogner said. “Given such high turnover in this occupation, it’s hard to know if the surplus is really a surplus or if they will quickly be employed.”
Dr. Frogner receives grants and contracts from not-for-profit entities to investigate issues related to the health workforce.
Dr. Lezotte said the report’s findings are based on data from sources such as public and private databases and job postings. According to the report, “projections were made up to 2028 based on historical data up to 2023,” and “supply projections were derived using a linear autoregressive model based on historical supply within each occupation and geography.”
It’s not clear why some states like New York are expected to have huge shortages, but migration might be a factor, along with a lack of nearby nursing schools, Dr. Lezotte said.
As for shortages, Dr. Lezotte said healthcare systems will have to understand their local workforce situation and adapt. “They’ll need to be more proactive about their employee value proposition” via competitive pay and benefits Flexibility regarding scheduling is also important.
“They’re going to have to figure out how to up their game,” he said.
What about states with surpluses? They might be target-rich environments for states facing shortages, he said.
Positive Outlook Not Shared by Other Researchers
Other workforce projections conflict with Mercer’s, according to Jean Moore, DrPH, and Gaetano Forte, MS, director and assistant director of the Center for Health Workforce Studies, School of Public Health, University at Albany, New York.
The National Center for Health Workforce Analysis projects a 10% shortage of registered nurses and a 13% shortage of physicians in 2031. The agency didn’t make projections for home health aides because that workforce is in flux.
Why are Mercer’s projections so different? Dr. Lezotte said other projections assume that equity efforts will bring healthcare to everyone who needs it. The report assumes this won’t happen, he said. As a result, it expects there will be fewer patients who need to be served by workers.
Other projections expect a shortage of 300,000 registered nurses by 2035, Mr. Forte said. But the number of nurse practitioners in New York is growing quickly, Dr. Moore said.
Dr. Moore said it’s difficult to interpret Mercer’s findings because the company doesn’t provide enough information about its methodology.
“At some level, it’s not particularly useful regarding what the next steps are,” she said. “Projections should make you think about what you should do to change and improve, to create more of what you need.”
The Center for Health Workforce Studies at the University of Albany has provided consulting services to multiple companies that provide healthcare workforce projections. It has no relationship with Mercer.
A version of this article first appeared on Medscape.com.
A surprising new report by the Mercer consulting firm projects that the American healthcare workforce will face a small shortfall in 2028 — a shortage of less than 1% of all employees.
Mercer’s projections are rosier than federal workforce projections, which paint a grimmer picture of impending shortages.
“The labor market is a little more stabilized right now, and most healthcare systems are seeing less turnover,” Dan Lezotte, PhD, a partner with Mercer, said in an interview. But he noted “critical shortages” are still expected in some areas.
Mercer last projected workforce numbers in a 2020-2021 report released during the height of the COVID-19 pandemic. Now, “the labor market is drastically different,” Dr. Lezotte said. Health workforce shortages and surpluses have long varied significantly by region across the country.
The report forecasts a small surplus of physicians in 2028 but not in states such as California, New York, and Texas. The upper Midwest states will largely see doctor surpluses while Southern states face shortages. Some states with general physician surpluses may still experience shortages of specialists.
A surplus of nearly 30,000 registered nurses is expected, but New York, New Jersey, and Connecticut are projected to have a combined shortage of 16,000 nurses.
Overall, the report projects a shortage of more than 100,000 healthcare workers nationally by 2028. That’s less than 1% of the entire healthcare workforce of 18.6 million expected by then.
The report also predicts a shortage of nurse practitioners, especially in California and New York, and a shortage of 73,000 nursing assistants, especially in California, New York, and Texas.
“Healthcare systems are having the most difficulty hiring and hanging on to those workers who are supposed to take up the load off physicians and nurses,” Dr. Lezotte said. “They’re competing not only with other healthcare systems but with other industries like Amazon warehouses or McDonald’s in California paying $20 an hour. Healthcare was a little slow to keep up with that. In a lot of healthcare systems, that’s their biggest headache right now.”
On the other hand, the report projects a national surplus of 48,000 home health/personal care aides.
That surprised Bianca K. Frogner, PhD, director of the Center for Health Workforce Studies at the University of Washington, Seattle.
“We are seeing increasing movement of investments toward moving patients out of skilled nursing facilities and keeping them in the home and community, which requires many more home health aides,” Dr. Frogner said. “Given such high turnover in this occupation, it’s hard to know if the surplus is really a surplus or if they will quickly be employed.”
Dr. Frogner receives grants and contracts from not-for-profit entities to investigate issues related to the health workforce.
Dr. Lezotte said the report’s findings are based on data from sources such as public and private databases and job postings. According to the report, “projections were made up to 2028 based on historical data up to 2023,” and “supply projections were derived using a linear autoregressive model based on historical supply within each occupation and geography.”
It’s not clear why some states like New York are expected to have huge shortages, but migration might be a factor, along with a lack of nearby nursing schools, Dr. Lezotte said.
As for shortages, Dr. Lezotte said healthcare systems will have to understand their local workforce situation and adapt. “They’ll need to be more proactive about their employee value proposition” via competitive pay and benefits Flexibility regarding scheduling is also important.
“They’re going to have to figure out how to up their game,” he said.
What about states with surpluses? They might be target-rich environments for states facing shortages, he said.
Positive Outlook Not Shared by Other Researchers
Other workforce projections conflict with Mercer’s, according to Jean Moore, DrPH, and Gaetano Forte, MS, director and assistant director of the Center for Health Workforce Studies, School of Public Health, University at Albany, New York.
The National Center for Health Workforce Analysis projects a 10% shortage of registered nurses and a 13% shortage of physicians in 2031. The agency didn’t make projections for home health aides because that workforce is in flux.
Why are Mercer’s projections so different? Dr. Lezotte said other projections assume that equity efforts will bring healthcare to everyone who needs it. The report assumes this won’t happen, he said. As a result, it expects there will be fewer patients who need to be served by workers.
Other projections expect a shortage of 300,000 registered nurses by 2035, Mr. Forte said. But the number of nurse practitioners in New York is growing quickly, Dr. Moore said.
Dr. Moore said it’s difficult to interpret Mercer’s findings because the company doesn’t provide enough information about its methodology.
“At some level, it’s not particularly useful regarding what the next steps are,” she said. “Projections should make you think about what you should do to change and improve, to create more of what you need.”
The Center for Health Workforce Studies at the University of Albany has provided consulting services to multiple companies that provide healthcare workforce projections. It has no relationship with Mercer.
A version of this article first appeared on Medscape.com.