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Physicians shared their views on frequently discussed (and sometimes controversial) topics ranging from romances with patients to age-related competency tests in the latest report from Medscape Medical News.

The report captured data from over 1000 full- or part-time US physicians across more than 29 specialties who were surveyed over a 3-month period in 2024.

Responsibility toward their patients was a clear priority among the doctors surveyed.

While around 6 in 10 physicians said they would immediately discharge a patient who refused to follow their treatment recommendations, 8% said they would wait, and 31% indicated they would keep the patient.

Asked whether physicians should have to undergo competency testing at a certain age, 30% of respondents said yes vs 22% no, and 48% felt it depended on multiple factors.

Most doctors (91%) said they would not accept a gift of substantial monetary or sentimental value from a patient, adhering to the AMA Code of Medical Ethics.

Big gifts “may signal psychological issues, and it is not fair to patients who can’t afford big gifts, since they may encourage better care,” said Jason Doctor, PhD, a senior scholar at the USC Leonard D. Schaeffer Center for Health Policy & Economics in Los Angeles, California. “It also taints the doctor-patient relationship, which should not involve large gifts of expectations of reciprocity.”

The vast majority of doctors said a romantic relationship with a patient still in their care was unacceptable, although 1% felt it would be OK, and 9% said, “it depends.”

When asked if they might withhold information about a patient’s condition if disclosure could do more harm than good, the majority of doctors said no. But 38% said it depended on the situation.

“This is how the profession and public expectations are evolving from the old paternalistic approach,” said Peter Angood, MD, president and CEO of the American Association for Physician Leadership.

Meanwhile, most doctors (62%) said that an annual flu shot should be mandatory for physicians who see patients. And a substantial majority of doctors surveyed agreed that taking care of their physical and mental health amounts to an ethical duty.

Around three in four physicians surveyed said felt periodic bias training was necessary for doctors.

“We all need refreshers about our own bias and how to manage it,” one respondent said. But another physician said, “I think we all know what appropriate behavior is and don’t need to add yet another CME course, ugh.”

Roughly equal shares of doctors surveyed felt some obligation to take at least some Medicaid patients or felt no societal obligation. The remaining 18% were willing to treat Medicaid patients once states streamlined the rules and improved reimbursements.

And finally, nearly all the survey respondents said physicians should advise patients on the risks of marijuana, notwithstanding the number of states and localities that recently have legalized pot or cannabis products.
 

A version of this article first appeared on Medscape.com.

Physicians shared their views on frequently discussed (and sometimes controversial) topics ranging from romances with patients to age-related competency tests in the latest report from Medscape Medical News.

The report captured data from over 1000 full- or part-time US physicians across more than 29 specialties who were surveyed over a 3-month period in 2024.

Responsibility toward their patients was a clear priority among the doctors surveyed.

While around 6 in 10 physicians said they would immediately discharge a patient who refused to follow their treatment recommendations, 8% said they would wait, and 31% indicated they would keep the patient.

Asked whether physicians should have to undergo competency testing at a certain age, 30% of respondents said yes vs 22% no, and 48% felt it depended on multiple factors.

Most doctors (91%) said they would not accept a gift of substantial monetary or sentimental value from a patient, adhering to the AMA Code of Medical Ethics.

Big gifts “may signal psychological issues, and it is not fair to patients who can’t afford big gifts, since they may encourage better care,” said Jason Doctor, PhD, a senior scholar at the USC Leonard D. Schaeffer Center for Health Policy & Economics in Los Angeles, California. “It also taints the doctor-patient relationship, which should not involve large gifts of expectations of reciprocity.”

The vast majority of doctors said a romantic relationship with a patient still in their care was unacceptable, although 1% felt it would be OK, and 9% said, “it depends.”

When asked if they might withhold information about a patient’s condition if disclosure could do more harm than good, the majority of doctors said no. But 38% said it depended on the situation.

“This is how the profession and public expectations are evolving from the old paternalistic approach,” said Peter Angood, MD, president and CEO of the American Association for Physician Leadership.

Meanwhile, most doctors (62%) said that an annual flu shot should be mandatory for physicians who see patients. And a substantial majority of doctors surveyed agreed that taking care of their physical and mental health amounts to an ethical duty.

Around three in four physicians surveyed said felt periodic bias training was necessary for doctors.

“We all need refreshers about our own bias and how to manage it,” one respondent said. But another physician said, “I think we all know what appropriate behavior is and don’t need to add yet another CME course, ugh.”

Roughly equal shares of doctors surveyed felt some obligation to take at least some Medicaid patients or felt no societal obligation. The remaining 18% were willing to treat Medicaid patients once states streamlined the rules and improved reimbursements.

And finally, nearly all the survey respondents said physicians should advise patients on the risks of marijuana, notwithstanding the number of states and localities that recently have legalized pot or cannabis products.
 

A version of this article first appeared on Medscape.com.

Physicians shared their views on frequently discussed (and sometimes controversial) topics ranging from romances with patients to age-related competency tests in the latest report from Medscape Medical News.

The report captured data from over 1000 full- or part-time US physicians across more than 29 specialties who were surveyed over a 3-month period in 2024.

Responsibility toward their patients was a clear priority among the doctors surveyed.

While around 6 in 10 physicians said they would immediately discharge a patient who refused to follow their treatment recommendations, 8% said they would wait, and 31% indicated they would keep the patient.

Asked whether physicians should have to undergo competency testing at a certain age, 30% of respondents said yes vs 22% no, and 48% felt it depended on multiple factors.

Most doctors (91%) said they would not accept a gift of substantial monetary or sentimental value from a patient, adhering to the AMA Code of Medical Ethics.

Big gifts “may signal psychological issues, and it is not fair to patients who can’t afford big gifts, since they may encourage better care,” said Jason Doctor, PhD, a senior scholar at the USC Leonard D. Schaeffer Center for Health Policy & Economics in Los Angeles, California. “It also taints the doctor-patient relationship, which should not involve large gifts of expectations of reciprocity.”

The vast majority of doctors said a romantic relationship with a patient still in their care was unacceptable, although 1% felt it would be OK, and 9% said, “it depends.”

When asked if they might withhold information about a patient’s condition if disclosure could do more harm than good, the majority of doctors said no. But 38% said it depended on the situation.

“This is how the profession and public expectations are evolving from the old paternalistic approach,” said Peter Angood, MD, president and CEO of the American Association for Physician Leadership.

Meanwhile, most doctors (62%) said that an annual flu shot should be mandatory for physicians who see patients. And a substantial majority of doctors surveyed agreed that taking care of their physical and mental health amounts to an ethical duty.

Around three in four physicians surveyed said felt periodic bias training was necessary for doctors.

“We all need refreshers about our own bias and how to manage it,” one respondent said. But another physician said, “I think we all know what appropriate behavior is and don’t need to add yet another CME course, ugh.”

Roughly equal shares of doctors surveyed felt some obligation to take at least some Medicaid patients or felt no societal obligation. The remaining 18% were willing to treat Medicaid patients once states streamlined the rules and improved reimbursements.

And finally, nearly all the survey respondents said physicians should advise patients on the risks of marijuana, notwithstanding the number of states and localities that recently have legalized pot or cannabis products.
 

A version of this article first appeared on Medscape.com.

Primary care doctors and specialists should advise patients who have already experienced a heart attack or stroke that they are at a higher risk for long COVID and need to take steps to avoid contracting the virus, according to new research.

The study, led by researchers at Columbia University, New York City, suggests that anyone with cardiovascular disease (CVD) — defined as having experienced a heart attack or stroke — should consider getting the updated COVID vaccine boosters. They also suggest patients with CVD take other steps to avoid an acute infection, such as avoiding crowded indoor spaces.

There is no specific test or treatment for long COVID, which can become disabling and chronic. Long COVID is defined by the failure to recover from acute COVID-19 in 90 days.

The scientists used data from nearly 5000 people enrolled in 14 established, ongoing research programs, including the 76-year-old Framingham Heart Study. The results of the analysis of the “mega-cohort” were published in JAMA Network Open.

Most of the 14 studies already had 10-20 years of data on the cardiac health of thousands of enrollees, said Norrina B. Allen, one of the authors and a cardiac epidemiologist at Northwestern University Feinberg School of Medicine in Chicago, Illinois.

“This is a particularly strong study that looked at risk factors — or individual health — prior to developing COVID and their impact on the likely of recovering from COVID,” she said.

In addition to those with CVD, women and adults with preexisting chronic illnesses took longer to recover.

More than 20% of those in the large, racially and ethnically diverse US population–based study did not recover from COVID in 90 days. The researchers found that the median self-reported time to recovery from acute infection was 20 days.

While women and those with chronic illness had a higher risk for long COVID, vaccination and infection with the Omicron variant wave were associated with shorter recovery times.

These findings make sense, said Ziyad Al-Aly, MD, chief of research at Veterans Affairs St. Louis Health Care System and clinical epidemiologist at Washington University in St. Louis, Missouri.

“We also see that COVID-19 can lead to new-onset cardiovascular disease,” said Al-Aly, who was not involved in the study. “There is clearly a (link) between COVID and cardiovascular disease. These two seem to be intimately intertwined. In my view, this emphasizes the importance of targeting these individuals for vaccination and potentially antivirals (when they get infected) to help reduce their risk of adverse events and ameliorate their chance of full and fast recovery.”

The study used data from the Collaborative Cohort of Cohorts for COVID-19 Research. The long list of researchers contributing to this study includes epidemiologists, biostatisticians, neurologists, pulmonologists, and cardiologists. The data come from a list of cohorts like the Framingham Heart Study, which identified key risk factors for CVD, including cholesterol levels. Other studies include the Atherosclerosis Risk in Communities study, which began in the mid-1980s. Researchers there recruited a cohort of 15,792 men and women in rural North Carolina and Mississippi and suburban Minneapolis. They enrolled a high number of African American participants, who have been underrepresented in past studies. Other cohorts focused on young adults with CVD and Hispanics, while another focused on people with chronic obstructive pulmonary disease.

Lead author Elizabeth C. Oelsner, MD, of Columbia University Irving Medical Center in New York City, said she was not surprised by the CVD-long COVID link.

“We were aware that individuals with CVD were at higher risk of a more severe acute infection,” she said. “We were also seeing evidence that long and severe infection led to persistent symptoms.”

Oelsner noted that many patients still take more than 3 months to recover, even during the Omicron wave.

“While that has improved over the course of the pandemic, many individuals are taking a very long time to recover, and that can have a huge burden on the patient,” she said.

She encourages healthcare providers to tell patients at higher risk to take steps to avoid the virus, including vaccination and boosters.

A version of this article first appeared on Medscape.com.

Primary care doctors and specialists should advise patients who have already experienced a heart attack or stroke that they are at a higher risk for long COVID and need to take steps to avoid contracting the virus, according to new research.

The study, led by researchers at Columbia University, New York City, suggests that anyone with cardiovascular disease (CVD) — defined as having experienced a heart attack or stroke — should consider getting the updated COVID vaccine boosters. They also suggest patients with CVD take other steps to avoid an acute infection, such as avoiding crowded indoor spaces.

There is no specific test or treatment for long COVID, which can become disabling and chronic. Long COVID is defined by the failure to recover from acute COVID-19 in 90 days.

The scientists used data from nearly 5000 people enrolled in 14 established, ongoing research programs, including the 76-year-old Framingham Heart Study. The results of the analysis of the “mega-cohort” were published in JAMA Network Open.

Most of the 14 studies already had 10-20 years of data on the cardiac health of thousands of enrollees, said Norrina B. Allen, one of the authors and a cardiac epidemiologist at Northwestern University Feinberg School of Medicine in Chicago, Illinois.

“This is a particularly strong study that looked at risk factors — or individual health — prior to developing COVID and their impact on the likely of recovering from COVID,” she said.

In addition to those with CVD, women and adults with preexisting chronic illnesses took longer to recover.

More than 20% of those in the large, racially and ethnically diverse US population–based study did not recover from COVID in 90 days. The researchers found that the median self-reported time to recovery from acute infection was 20 days.

While women and those with chronic illness had a higher risk for long COVID, vaccination and infection with the Omicron variant wave were associated with shorter recovery times.

These findings make sense, said Ziyad Al-Aly, MD, chief of research at Veterans Affairs St. Louis Health Care System and clinical epidemiologist at Washington University in St. Louis, Missouri.

“We also see that COVID-19 can lead to new-onset cardiovascular disease,” said Al-Aly, who was not involved in the study. “There is clearly a (link) between COVID and cardiovascular disease. These two seem to be intimately intertwined. In my view, this emphasizes the importance of targeting these individuals for vaccination and potentially antivirals (when they get infected) to help reduce their risk of adverse events and ameliorate their chance of full and fast recovery.”

The study used data from the Collaborative Cohort of Cohorts for COVID-19 Research. The long list of researchers contributing to this study includes epidemiologists, biostatisticians, neurologists, pulmonologists, and cardiologists. The data come from a list of cohorts like the Framingham Heart Study, which identified key risk factors for CVD, including cholesterol levels. Other studies include the Atherosclerosis Risk in Communities study, which began in the mid-1980s. Researchers there recruited a cohort of 15,792 men and women in rural North Carolina and Mississippi and suburban Minneapolis. They enrolled a high number of African American participants, who have been underrepresented in past studies. Other cohorts focused on young adults with CVD and Hispanics, while another focused on people with chronic obstructive pulmonary disease.

Lead author Elizabeth C. Oelsner, MD, of Columbia University Irving Medical Center in New York City, said she was not surprised by the CVD-long COVID link.

“We were aware that individuals with CVD were at higher risk of a more severe acute infection,” she said. “We were also seeing evidence that long and severe infection led to persistent symptoms.”

Oelsner noted that many patients still take more than 3 months to recover, even during the Omicron wave.

“While that has improved over the course of the pandemic, many individuals are taking a very long time to recover, and that can have a huge burden on the patient,” she said.

She encourages healthcare providers to tell patients at higher risk to take steps to avoid the virus, including vaccination and boosters.

A version of this article first appeared on Medscape.com.

Primary care doctors and specialists should advise patients who have already experienced a heart attack or stroke that they are at a higher risk for long COVID and need to take steps to avoid contracting the virus, according to new research.

The study, led by researchers at Columbia University, New York City, suggests that anyone with cardiovascular disease (CVD) — defined as having experienced a heart attack or stroke — should consider getting the updated COVID vaccine boosters. They also suggest patients with CVD take other steps to avoid an acute infection, such as avoiding crowded indoor spaces.

There is no specific test or treatment for long COVID, which can become disabling and chronic. Long COVID is defined by the failure to recover from acute COVID-19 in 90 days.

The scientists used data from nearly 5000 people enrolled in 14 established, ongoing research programs, including the 76-year-old Framingham Heart Study. The results of the analysis of the “mega-cohort” were published in JAMA Network Open.

Most of the 14 studies already had 10-20 years of data on the cardiac health of thousands of enrollees, said Norrina B. Allen, one of the authors and a cardiac epidemiologist at Northwestern University Feinberg School of Medicine in Chicago, Illinois.

“This is a particularly strong study that looked at risk factors — or individual health — prior to developing COVID and their impact on the likely of recovering from COVID,” she said.

In addition to those with CVD, women and adults with preexisting chronic illnesses took longer to recover.

More than 20% of those in the large, racially and ethnically diverse US population–based study did not recover from COVID in 90 days. The researchers found that the median self-reported time to recovery from acute infection was 20 days.

While women and those with chronic illness had a higher risk for long COVID, vaccination and infection with the Omicron variant wave were associated with shorter recovery times.

These findings make sense, said Ziyad Al-Aly, MD, chief of research at Veterans Affairs St. Louis Health Care System and clinical epidemiologist at Washington University in St. Louis, Missouri.

“We also see that COVID-19 can lead to new-onset cardiovascular disease,” said Al-Aly, who was not involved in the study. “There is clearly a (link) between COVID and cardiovascular disease. These two seem to be intimately intertwined. In my view, this emphasizes the importance of targeting these individuals for vaccination and potentially antivirals (when they get infected) to help reduce their risk of adverse events and ameliorate their chance of full and fast recovery.”

The study used data from the Collaborative Cohort of Cohorts for COVID-19 Research. The long list of researchers contributing to this study includes epidemiologists, biostatisticians, neurologists, pulmonologists, and cardiologists. The data come from a list of cohorts like the Framingham Heart Study, which identified key risk factors for CVD, including cholesterol levels. Other studies include the Atherosclerosis Risk in Communities study, which began in the mid-1980s. Researchers there recruited a cohort of 15,792 men and women in rural North Carolina and Mississippi and suburban Minneapolis. They enrolled a high number of African American participants, who have been underrepresented in past studies. Other cohorts focused on young adults with CVD and Hispanics, while another focused on people with chronic obstructive pulmonary disease.

Lead author Elizabeth C. Oelsner, MD, of Columbia University Irving Medical Center in New York City, said she was not surprised by the CVD-long COVID link.

“We were aware that individuals with CVD were at higher risk of a more severe acute infection,” she said. “We were also seeing evidence that long and severe infection led to persistent symptoms.”

Oelsner noted that many patients still take more than 3 months to recover, even during the Omicron wave.

“While that has improved over the course of the pandemic, many individuals are taking a very long time to recover, and that can have a huge burden on the patient,” she said.

She encourages healthcare providers to tell patients at higher risk to take steps to avoid the virus, including vaccination and boosters.

A version of this article first appeared on Medscape.com.

TOPLINE:

Genetic predisposition to gout, unfavorable lifestyle habits, and poor metabolic health are associated with an increased risk for cardiovascular disease (CVD); however, adherence to a healthy lifestyle can reduce this risk by up to 62%, even in individuals with high genetic risk.

METHODOLOGY:

• Researchers investigated the association between genetic predisposition to gout, combined with lifestyle habits, and the risk for CVD in two diverse prospective cohorts from different ancestral backgrounds.
• They analyzed the data of 224,689 participants of European descent from the UK Biobank (mean age, 57.0 years; 56.1% women) and 50,364 participants of East Asian descent from the Korean Genome and Epidemiology Study (KoGES; mean age, 53.7 years; 66.0% women).
• The genetic predisposition to gout was evaluated using a polygenic risk score (PRS) derived from a metagenome-wide association study, and the participants were categorized into low, intermediate, and high genetic risk groups based on their PRS for gout.
• A favorable lifestyle was defined as having ≥ 3 healthy lifestyle factors, and 0-1 metabolic syndrome factor defined the ideal metabolic health status.
• The incident CVD risk was evaluated according to genetic risk, lifestyle habits, and metabolic syndrome.

TAKEAWAY:

• Individuals in the high genetic risk group had a higher risk for CVD than those in the low genetic risk group in both the UK Biobank (adjusted hazard ratio [aHR], 1.10; P < .001) and KoGES (aHR, 1.31; P = .024) cohorts.
• In the UK Biobank cohort, individuals with a high genetic risk for gout and unfavorable lifestyle choices had a 1.99 times higher risk for incident CVD than those with low genetic risk (aHR, 1.99; P < .001); similar outcomes were observed in the KoGES cohort.
• Similarly, individuals with a high genetic risk for gout and poor metabolic health in the UK Biobank cohort had a 2.16 times higher risk for CVD than those with low genetic risk (aHR, 2.16; P < .001 for both); outcomes were no different in the KoGES cohort.
• Improving metabolic health and adhering to a healthy lifestyle reduced the risk for CVD by 62% in individuals with high genetic risk and by 46% in those with low genetic risk (P < .001 for both).

IN PRACTICE:

“PRS for gout can be used for preventing not only gout but also CVD. It is possible to identify individuals with high genetic risk for gout and strongly recommend modifying lifestyle habits. Weight reduction, smoking cessation, regular exercise, and eating healthy food are effective strategies to prevent gout and CVD,” the authors wrote.

SOURCE:

This study was led by Ki Won Moon, MD, PhD, Department of Internal Medicine, Kangwon National University School of Medicine, Chuncheon, Republic of Korea, and SangHyuk Jung, PhD, University of Pennsylvania, Philadelphia, and was published online on October 8, 2024, in RMD Open.

LIMITATIONS: 

The definitions of lifestyle and metabolic syndrome were different in each cohort, which may have affected the findings. Data on lifestyle behaviors and metabolic health statuses were collected at enrollment, but these variables may have changed during the follow-up period, which potentially introduced bias into the results. This study was not able to establish causality between genetic predisposition to gout and the incident risk for CVD.

DISCLOSURES:

This study was supported by the National Institute of General Medical Sciences and the National Research Foundation of Korea. The authors declared no competing interests.

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:

Genetic predisposition to gout, unfavorable lifestyle habits, and poor metabolic health are associated with an increased risk for cardiovascular disease (CVD); however, adherence to a healthy lifestyle can reduce this risk by up to 62%, even in individuals with high genetic risk.

METHODOLOGY:

• Researchers investigated the association between genetic predisposition to gout, combined with lifestyle habits, and the risk for CVD in two diverse prospective cohorts from different ancestral backgrounds.
• They analyzed the data of 224,689 participants of European descent from the UK Biobank (mean age, 57.0 years; 56.1% women) and 50,364 participants of East Asian descent from the Korean Genome and Epidemiology Study (KoGES; mean age, 53.7 years; 66.0% women).
• The genetic predisposition to gout was evaluated using a polygenic risk score (PRS) derived from a metagenome-wide association study, and the participants were categorized into low, intermediate, and high genetic risk groups based on their PRS for gout.
• A favorable lifestyle was defined as having ≥ 3 healthy lifestyle factors, and 0-1 metabolic syndrome factor defined the ideal metabolic health status.
• The incident CVD risk was evaluated according to genetic risk, lifestyle habits, and metabolic syndrome.

TAKEAWAY:

• Individuals in the high genetic risk group had a higher risk for CVD than those in the low genetic risk group in both the UK Biobank (adjusted hazard ratio [aHR], 1.10; P < .001) and KoGES (aHR, 1.31; P = .024) cohorts.
• In the UK Biobank cohort, individuals with a high genetic risk for gout and unfavorable lifestyle choices had a 1.99 times higher risk for incident CVD than those with low genetic risk (aHR, 1.99; P < .001); similar outcomes were observed in the KoGES cohort.
• Similarly, individuals with a high genetic risk for gout and poor metabolic health in the UK Biobank cohort had a 2.16 times higher risk for CVD than those with low genetic risk (aHR, 2.16; P < .001 for both); outcomes were no different in the KoGES cohort.
• Improving metabolic health and adhering to a healthy lifestyle reduced the risk for CVD by 62% in individuals with high genetic risk and by 46% in those with low genetic risk (P < .001 for both).

IN PRACTICE:

“PRS for gout can be used for preventing not only gout but also CVD. It is possible to identify individuals with high genetic risk for gout and strongly recommend modifying lifestyle habits. Weight reduction, smoking cessation, regular exercise, and eating healthy food are effective strategies to prevent gout and CVD,” the authors wrote.

SOURCE:

This study was led by Ki Won Moon, MD, PhD, Department of Internal Medicine, Kangwon National University School of Medicine, Chuncheon, Republic of Korea, and SangHyuk Jung, PhD, University of Pennsylvania, Philadelphia, and was published online on October 8, 2024, in RMD Open.

LIMITATIONS: 

The definitions of lifestyle and metabolic syndrome were different in each cohort, which may have affected the findings. Data on lifestyle behaviors and metabolic health statuses were collected at enrollment, but these variables may have changed during the follow-up period, which potentially introduced bias into the results. This study was not able to establish causality between genetic predisposition to gout and the incident risk for CVD.

DISCLOSURES:

This study was supported by the National Institute of General Medical Sciences and the National Research Foundation of Korea. The authors declared no competing interests.

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:

Genetic predisposition to gout, unfavorable lifestyle habits, and poor metabolic health are associated with an increased risk for cardiovascular disease (CVD); however, adherence to a healthy lifestyle can reduce this risk by up to 62%, even in individuals with high genetic risk.

METHODOLOGY:

• Researchers investigated the association between genetic predisposition to gout, combined with lifestyle habits, and the risk for CVD in two diverse prospective cohorts from different ancestral backgrounds.
• They analyzed the data of 224,689 participants of European descent from the UK Biobank (mean age, 57.0 years; 56.1% women) and 50,364 participants of East Asian descent from the Korean Genome and Epidemiology Study (KoGES; mean age, 53.7 years; 66.0% women).
• The genetic predisposition to gout was evaluated using a polygenic risk score (PRS) derived from a metagenome-wide association study, and the participants were categorized into low, intermediate, and high genetic risk groups based on their PRS for gout.
• A favorable lifestyle was defined as having ≥ 3 healthy lifestyle factors, and 0-1 metabolic syndrome factor defined the ideal metabolic health status.
• The incident CVD risk was evaluated according to genetic risk, lifestyle habits, and metabolic syndrome.

TAKEAWAY:

• Individuals in the high genetic risk group had a higher risk for CVD than those in the low genetic risk group in both the UK Biobank (adjusted hazard ratio [aHR], 1.10; P < .001) and KoGES (aHR, 1.31; P = .024) cohorts.
• In the UK Biobank cohort, individuals with a high genetic risk for gout and unfavorable lifestyle choices had a 1.99 times higher risk for incident CVD than those with low genetic risk (aHR, 1.99; P < .001); similar outcomes were observed in the KoGES cohort.
• Similarly, individuals with a high genetic risk for gout and poor metabolic health in the UK Biobank cohort had a 2.16 times higher risk for CVD than those with low genetic risk (aHR, 2.16; P < .001 for both); outcomes were no different in the KoGES cohort.
• Improving metabolic health and adhering to a healthy lifestyle reduced the risk for CVD by 62% in individuals with high genetic risk and by 46% in those with low genetic risk (P < .001 for both).

IN PRACTICE:

“PRS for gout can be used for preventing not only gout but also CVD. It is possible to identify individuals with high genetic risk for gout and strongly recommend modifying lifestyle habits. Weight reduction, smoking cessation, regular exercise, and eating healthy food are effective strategies to prevent gout and CVD,” the authors wrote.

SOURCE:

This study was led by Ki Won Moon, MD, PhD, Department of Internal Medicine, Kangwon National University School of Medicine, Chuncheon, Republic of Korea, and SangHyuk Jung, PhD, University of Pennsylvania, Philadelphia, and was published online on October 8, 2024, in RMD Open.

LIMITATIONS: 

The definitions of lifestyle and metabolic syndrome were different in each cohort, which may have affected the findings. Data on lifestyle behaviors and metabolic health statuses were collected at enrollment, but these variables may have changed during the follow-up period, which potentially introduced bias into the results. This study was not able to establish causality between genetic predisposition to gout and the incident risk for CVD.

DISCLOSURES:

This study was supported by the National Institute of General Medical Sciences and the National Research Foundation of Korea. The authors declared no competing interests.

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.

Depending on one’s perspective, “mast cell activation syndrome (MCAS)” is either a relatively rare, narrowly defined severe allergic condition or a vastly underrecognized underlying cause of multiple chronic inflammatory conditions that affect roughly 17% of the entire population. 

Inappropriate activation of mast cells — now termed mast cell activation disease (MCAD) — has long been known to underlie allergic symptoms and inflammation, and far less commonly, neoplasias such as mastocytosis. The concept of chronic, persistent MCAS associated with aberrant growth and dystrophism is more recent, emerging only in the last couple of decades as a separate entity under the MCAD heading. 

Observational studies and clinical experience have linked signs and symptoms of MCAS with other inflammatory chronic conditions such as hypermobile Ehlers-Danlos Syndrome (EDS), postural orthostatic tachycardia syndrome (POTS), myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), and recently, long COVID. However, those conditions themselves are diagnostically challenging, and as yet there is no proof of causation.

The idea that MCAS is the entity — or at least, a key one — at the center of “a confoundingly, extraordinarily heterogeneous chronic multisystem polymorbidity” was the theme of a recent 4-day meeting of a professional group informally dubbed “Masterminds.” Since their first meeting in 2018, the group has grown from about 35 to nearly 650 multidisciplinary professionals. 

Stephanie L. Grach, MD, assistant professor of medicine at the Mayo Clinic, Rochester, Minnesota, gave an introductory talk about the importance of changing “the medical paradigm around complex chronic illness.” Much of the rest of the meeting was devoted to sharing approaches for managing MCAS comorbidities, including dysautonomia, hypermobility, and associated craniocervical dysfunction, and various other multi-system conditions characterized by chronic pain and/or fatigue. Several talks covered the use of agents that block mast cell activity as potential treatment. 

In an interview, Grach said “the meeting was an exciting example of how not only research, but also medicine, is moving forward, and it’s really cool to see that people are independently coming to very similar conclusions about shared pathologies, and because of that, the importance of overlap amongst complex medical conditions that historically have really been poorly addressed.”

She added, “mast cell activation, or mast cell hyperactivity, is one part of the greater picture. What’s important about the mast cell component is that of the multiple different targetable pathologies, it’s one that currently has potential available therapies that can be explored, some of them relatively easily.”

But Christopher Chang, MD, PhD, chief of the Pediatric Allergy and Immunology program, Joe DiMaggio Children’s Hospital, Hollywood, Florida, sees it differently. In an interview, he noted that the reason for disagreement over what constitutes MCAS is that “it doesn’t have a lot of objective findings that we can identify. ... We know that mast cells are important immune cells, just like all immune cells are important. It seems like whenever someone has unexplained symptoms, people try to blame it on mast cells. But it’s very hard to prove that.” 
 

Two Definitions Characterize the Illness Differently

One proposed “consensus” MCAS definition was first published in 2011 by a group led by hematologist Peter Valent, MD, of the Medical University of Vienna in Austria. It has been revised since, and similar versions adopted by medical societies, including the American Academy of Allergy, Asthma & Immunology (AAAAI). The most recent versions propose three core MCAS criteria: 

• Typical clinical signs of severe, recurrent (episodic) systemic (at least two organ systems) MCA are present (often in the form of anaphylaxis).
• The involvement of mast cells (MCs) is documented by biochemical studies, preferably an increase in serum tryptase levels from the individual’s baseline to plus 20% + 2 ng/mL.
• Response of symptoms to therapy with MC-stabilizing agents, drugs directed against MC mediator production, or drugs blocking mediator release or effects of MC-derived mediators.

The following year, a separate publication authored by Gerhard J. Molderings, MD, University of Bonn in Germany, and colleagues proposed a much broader MCAS definition. Also revised since, the latest “consensus-2” was published in 2020. This definition consists of one major criterion: “A constellation of clinical complaints attributable to pathologically increased MC activity, ie, MC mediator release syndrome.” This “constellation” involves conditions of nearly every organ system that, taken together, are estimated to affect up to 17% of the entire population. These are just a few examples: 

• Constitutional: Chronic fatigue, flushing, or sweats
• Dermatologic: Rashes or lesions
• Ophthalmologic: dry eyes
• Oral: Burning or itching in mouth
• Pulmonary: Airway inflammation at any/all levels
• Cardiovascular: Blood pressure lability or codiagnosis of POTS is common
• Gastrointestinal: Reflux, dysphagia, or malabsorption
• Genitourinary: Endometriosis, dysmenorrhea, or dyspareunia
• Musculoskeletal/connective tissue: Fibromyalgia or diagnosis of hypermobile EDS is common
• Neurologic: Headaches or sensory neuropathies
• Psychiatric: Depression or anxiety
• Endocrinologic: Thyroid disease or dyslipidemia
• Hematologic: Polycythemia or anemia (after ruling out other causes)

The diagnosis is made by fulfilling that major criterion, plus at least one objective assessment of pathologically increased release of MC mediators, including infiltrates, abnormal MC morphology, or MC genetic changes shown to increase MC activity. Other alternatives include evidence of above-normal levels of MC mediators, including tryptase, histamine or its metabolites, heparin, or chromatin A, in whole blood, serum, plasma, or urine. Symptomatic response to MC activation inhibitors can also be used but isn’t required as it is in the other definition. 
 

Underdiagnosis vs Overdiagnosis

Lawrence B. Afrin, MD, senior consultant in hematology/oncology at the AIM Center for Personalized Medicine, Westchester, New York, and lead author of the 2020 update of the broader “consensus-2” criteria, said in an interview, “we now know MCAS exists, and it’s prevalent, even though, for understandable and forgivable reasons, we’ve been missing it all along. ... If you see a patient who has this chronic, multisystem unwellness with general themes of inflammation plus or minus allergic issues and you can’t find some other rational explanation that better accounts for what’s going on ... then it’s reasonable to think to include MCAS in the differential diagnosis. If the patient happens not to fit the diagnostic criteria being advanced by one group, that doesn’t necessarily rule out the possibility that this is still going on.”

Afrin, along with his coauthors, faulted the narrower “consensus-1” definition for lacking data to support the “20% + 2” criteria for requiring the difficult determination of a patient’s “baseline” and for requiring evidence of response to treatment prior to making the diagnosis. Not all patients will respond to a given histamine blocker, he noted. 

But Lawrence B. Schwartz, MD, PhD, an author on both the Valent and AAAAI criteria, disagreed, noting that the narrower criteria “appear to have a high degree of specificity and sensitivity when the reaction is systemic and involves hypotension. Less severe clinical events, particularly involving the gastrointestinal or central nervous systems, do not have precise clinical or biomarker criteria for identifying mast cell involvement.” 

Added Schwartz, who is professor of medicine and chair of the Division of Rheumatology, Allergy, and Immunology and program director of Allergy and Immunology, Virginia Commonwealth University (VCU), Richmond, “when mast cell activation events occur only in the skin, we refer to it as chronic urticaria and in the airways or conjunctiva of allergic individuals as allergic asthma, rhinitis, and/or conjunctivitis. The absence of specific criteria for mast cell activation in the GI [gastrointestinal] tract or CNS [central nervous system] neither rules in mast cell involvement nor does it rule out mast cell involvement. Thus, more research is needed to find better diagnostic criteria.”

Schwartz also pointed to a recent paper reporting the use of artificial intelligence models to “quantify diagnostic precision and specificity” of “alternative” MCAS definitions. The conclusion was a “lack of specificity is pronounced in relation to multiple control criteria, raising the concern that alternative criteria could disproportionately contribute to MCAS overdiagnosis, to the exclusion of more appropriate diagnoses.”

During the meeting, Afrin acknowledged that the broader view risks overdiagnosis of MCAS. However, he also referenced Occam’s razor, the principle that the simplest explanation is probably the best one. “Which scenario is more likely? Multiple diagnoses and problems that are all independent of each other vs one diagnosis that’s biologically capable of causing most or all of the findings, ie, the simplest solution even if it’s not the most immediately obvious solution?”

He said in an interview: “Do we have any proof that MCAS is what’s underlying hypermobile Ehlers-Danlos or POTS or chronic fatigue? No, we don’t have any proof, not because anybody has done studies that have shown there to be no connection but simply because we’re so early in our awareness that the disease even exists that the necessary studies haven’t even been done yet.”

At the meeting, Afrin introduced proposals to turn the “Masterminds” group into a formal professional society and to launch a journal. He also gave an update on progress in developing a symptom assessment tool both for clinical use and to enable clinical trials of new drugs to target mast cells or their mediators. The plan is to field test the tool in 2025 and publish those results in 2026. 

Grach, Afrin, and Chang had no disclosures. Schwartz discovered tryptase and invented the Thermo Fisher tryptase assay, for which his institution (VCU) receives royalties that are shared with him. He also invented monoclonal antibodies used for detecting mast cells or basophils, for which VCU receives royalties from several companies, including Millipore, Santa Cruz, BioLegend, and Hycult Biotech, that are also shared with him. He is a paid consultant for Blueprint Medicines, Celldex Therapeutics, Invea, Third Harmonic Bio, HYCOR Biomedical, Jasper, TerSera Therapeutics, and GLG. He also serves on an AstraZeneca data safety monitoring board for a clinical trial involving benralizumab treatment of hypereosinophilic syndrome and receives royalties from UpToDate (biomarkers for anaphylaxis) and Goldman-Cecil Medicine (anaphylaxis).

A version of this article first appeared on Medscape.com.

Depending on one’s perspective, “mast cell activation syndrome (MCAS)” is either a relatively rare, narrowly defined severe allergic condition or a vastly underrecognized underlying cause of multiple chronic inflammatory conditions that affect roughly 17% of the entire population. 

Inappropriate activation of mast cells — now termed mast cell activation disease (MCAD) — has long been known to underlie allergic symptoms and inflammation, and far less commonly, neoplasias such as mastocytosis. The concept of chronic, persistent MCAS associated with aberrant growth and dystrophism is more recent, emerging only in the last couple of decades as a separate entity under the MCAD heading. 

Observational studies and clinical experience have linked signs and symptoms of MCAS with other inflammatory chronic conditions such as hypermobile Ehlers-Danlos Syndrome (EDS), postural orthostatic tachycardia syndrome (POTS), myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), and recently, long COVID. However, those conditions themselves are diagnostically challenging, and as yet there is no proof of causation.

The idea that MCAS is the entity — or at least, a key one — at the center of “a confoundingly, extraordinarily heterogeneous chronic multisystem polymorbidity” was the theme of a recent 4-day meeting of a professional group informally dubbed “Masterminds.” Since their first meeting in 2018, the group has grown from about 35 to nearly 650 multidisciplinary professionals. 

Stephanie L. Grach, MD, assistant professor of medicine at the Mayo Clinic, Rochester, Minnesota, gave an introductory talk about the importance of changing “the medical paradigm around complex chronic illness.” Much of the rest of the meeting was devoted to sharing approaches for managing MCAS comorbidities, including dysautonomia, hypermobility, and associated craniocervical dysfunction, and various other multi-system conditions characterized by chronic pain and/or fatigue. Several talks covered the use of agents that block mast cell activity as potential treatment. 

In an interview, Grach said “the meeting was an exciting example of how not only research, but also medicine, is moving forward, and it’s really cool to see that people are independently coming to very similar conclusions about shared pathologies, and because of that, the importance of overlap amongst complex medical conditions that historically have really been poorly addressed.”

She added, “mast cell activation, or mast cell hyperactivity, is one part of the greater picture. What’s important about the mast cell component is that of the multiple different targetable pathologies, it’s one that currently has potential available therapies that can be explored, some of them relatively easily.”

But Christopher Chang, MD, PhD, chief of the Pediatric Allergy and Immunology program, Joe DiMaggio Children’s Hospital, Hollywood, Florida, sees it differently. In an interview, he noted that the reason for disagreement over what constitutes MCAS is that “it doesn’t have a lot of objective findings that we can identify. ... We know that mast cells are important immune cells, just like all immune cells are important. It seems like whenever someone has unexplained symptoms, people try to blame it on mast cells. But it’s very hard to prove that.” 
 

Two Definitions Characterize the Illness Differently

One proposed “consensus” MCAS definition was first published in 2011 by a group led by hematologist Peter Valent, MD, of the Medical University of Vienna in Austria. It has been revised since, and similar versions adopted by medical societies, including the American Academy of Allergy, Asthma & Immunology (AAAAI). The most recent versions propose three core MCAS criteria: 

• Typical clinical signs of severe, recurrent (episodic) systemic (at least two organ systems) MCA are present (often in the form of anaphylaxis).
• The involvement of mast cells (MCs) is documented by biochemical studies, preferably an increase in serum tryptase levels from the individual’s baseline to plus 20% + 2 ng/mL.
• Response of symptoms to therapy with MC-stabilizing agents, drugs directed against MC mediator production, or drugs blocking mediator release or effects of MC-derived mediators.

The following year, a separate publication authored by Gerhard J. Molderings, MD, University of Bonn in Germany, and colleagues proposed a much broader MCAS definition. Also revised since, the latest “consensus-2” was published in 2020. This definition consists of one major criterion: “A constellation of clinical complaints attributable to pathologically increased MC activity, ie, MC mediator release syndrome.” This “constellation” involves conditions of nearly every organ system that, taken together, are estimated to affect up to 17% of the entire population. These are just a few examples: 

• Constitutional: Chronic fatigue, flushing, or sweats
• Dermatologic: Rashes or lesions
• Ophthalmologic: dry eyes
• Oral: Burning or itching in mouth
• Pulmonary: Airway inflammation at any/all levels
• Cardiovascular: Blood pressure lability or codiagnosis of POTS is common
• Gastrointestinal: Reflux, dysphagia, or malabsorption
• Genitourinary: Endometriosis, dysmenorrhea, or dyspareunia
• Musculoskeletal/connective tissue: Fibromyalgia or diagnosis of hypermobile EDS is common
• Neurologic: Headaches or sensory neuropathies
• Psychiatric: Depression or anxiety
• Endocrinologic: Thyroid disease or dyslipidemia
• Hematologic: Polycythemia or anemia (after ruling out other causes)

The diagnosis is made by fulfilling that major criterion, plus at least one objective assessment of pathologically increased release of MC mediators, including infiltrates, abnormal MC morphology, or MC genetic changes shown to increase MC activity. Other alternatives include evidence of above-normal levels of MC mediators, including tryptase, histamine or its metabolites, heparin, or chromatin A, in whole blood, serum, plasma, or urine. Symptomatic response to MC activation inhibitors can also be used but isn’t required as it is in the other definition. 
 

Underdiagnosis vs Overdiagnosis

Lawrence B. Afrin, MD, senior consultant in hematology/oncology at the AIM Center for Personalized Medicine, Westchester, New York, and lead author of the 2020 update of the broader “consensus-2” criteria, said in an interview, “we now know MCAS exists, and it’s prevalent, even though, for understandable and forgivable reasons, we’ve been missing it all along. ... If you see a patient who has this chronic, multisystem unwellness with general themes of inflammation plus or minus allergic issues and you can’t find some other rational explanation that better accounts for what’s going on ... then it’s reasonable to think to include MCAS in the differential diagnosis. If the patient happens not to fit the diagnostic criteria being advanced by one group, that doesn’t necessarily rule out the possibility that this is still going on.”

Afrin, along with his coauthors, faulted the narrower “consensus-1” definition for lacking data to support the “20% + 2” criteria for requiring the difficult determination of a patient’s “baseline” and for requiring evidence of response to treatment prior to making the diagnosis. Not all patients will respond to a given histamine blocker, he noted. 

But Lawrence B. Schwartz, MD, PhD, an author on both the Valent and AAAAI criteria, disagreed, noting that the narrower criteria “appear to have a high degree of specificity and sensitivity when the reaction is systemic and involves hypotension. Less severe clinical events, particularly involving the gastrointestinal or central nervous systems, do not have precise clinical or biomarker criteria for identifying mast cell involvement.” 

Added Schwartz, who is professor of medicine and chair of the Division of Rheumatology, Allergy, and Immunology and program director of Allergy and Immunology, Virginia Commonwealth University (VCU), Richmond, “when mast cell activation events occur only in the skin, we refer to it as chronic urticaria and in the airways or conjunctiva of allergic individuals as allergic asthma, rhinitis, and/or conjunctivitis. The absence of specific criteria for mast cell activation in the GI [gastrointestinal] tract or CNS [central nervous system] neither rules in mast cell involvement nor does it rule out mast cell involvement. Thus, more research is needed to find better diagnostic criteria.”

Schwartz also pointed to a recent paper reporting the use of artificial intelligence models to “quantify diagnostic precision and specificity” of “alternative” MCAS definitions. The conclusion was a “lack of specificity is pronounced in relation to multiple control criteria, raising the concern that alternative criteria could disproportionately contribute to MCAS overdiagnosis, to the exclusion of more appropriate diagnoses.”

During the meeting, Afrin acknowledged that the broader view risks overdiagnosis of MCAS. However, he also referenced Occam’s razor, the principle that the simplest explanation is probably the best one. “Which scenario is more likely? Multiple diagnoses and problems that are all independent of each other vs one diagnosis that’s biologically capable of causing most or all of the findings, ie, the simplest solution even if it’s not the most immediately obvious solution?”

He said in an interview: “Do we have any proof that MCAS is what’s underlying hypermobile Ehlers-Danlos or POTS or chronic fatigue? No, we don’t have any proof, not because anybody has done studies that have shown there to be no connection but simply because we’re so early in our awareness that the disease even exists that the necessary studies haven’t even been done yet.”

At the meeting, Afrin introduced proposals to turn the “Masterminds” group into a formal professional society and to launch a journal. He also gave an update on progress in developing a symptom assessment tool both for clinical use and to enable clinical trials of new drugs to target mast cells or their mediators. The plan is to field test the tool in 2025 and publish those results in 2026. 

Grach, Afrin, and Chang had no disclosures. Schwartz discovered tryptase and invented the Thermo Fisher tryptase assay, for which his institution (VCU) receives royalties that are shared with him. He also invented monoclonal antibodies used for detecting mast cells or basophils, for which VCU receives royalties from several companies, including Millipore, Santa Cruz, BioLegend, and Hycult Biotech, that are also shared with him. He is a paid consultant for Blueprint Medicines, Celldex Therapeutics, Invea, Third Harmonic Bio, HYCOR Biomedical, Jasper, TerSera Therapeutics, and GLG. He also serves on an AstraZeneca data safety monitoring board for a clinical trial involving benralizumab treatment of hypereosinophilic syndrome and receives royalties from UpToDate (biomarkers for anaphylaxis) and Goldman-Cecil Medicine (anaphylaxis).

A version of this article first appeared on Medscape.com.

Depending on one’s perspective, “mast cell activation syndrome (MCAS)” is either a relatively rare, narrowly defined severe allergic condition or a vastly underrecognized underlying cause of multiple chronic inflammatory conditions that affect roughly 17% of the entire population. 

Inappropriate activation of mast cells — now termed mast cell activation disease (MCAD) — has long been known to underlie allergic symptoms and inflammation, and far less commonly, neoplasias such as mastocytosis. The concept of chronic, persistent MCAS associated with aberrant growth and dystrophism is more recent, emerging only in the last couple of decades as a separate entity under the MCAD heading. 

Observational studies and clinical experience have linked signs and symptoms of MCAS with other inflammatory chronic conditions such as hypermobile Ehlers-Danlos Syndrome (EDS), postural orthostatic tachycardia syndrome (POTS), myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), and recently, long COVID. However, those conditions themselves are diagnostically challenging, and as yet there is no proof of causation.

The idea that MCAS is the entity — or at least, a key one — at the center of “a confoundingly, extraordinarily heterogeneous chronic multisystem polymorbidity” was the theme of a recent 4-day meeting of a professional group informally dubbed “Masterminds.” Since their first meeting in 2018, the group has grown from about 35 to nearly 650 multidisciplinary professionals. 

Stephanie L. Grach, MD, assistant professor of medicine at the Mayo Clinic, Rochester, Minnesota, gave an introductory talk about the importance of changing “the medical paradigm around complex chronic illness.” Much of the rest of the meeting was devoted to sharing approaches for managing MCAS comorbidities, including dysautonomia, hypermobility, and associated craniocervical dysfunction, and various other multi-system conditions characterized by chronic pain and/or fatigue. Several talks covered the use of agents that block mast cell activity as potential treatment. 

In an interview, Grach said “the meeting was an exciting example of how not only research, but also medicine, is moving forward, and it’s really cool to see that people are independently coming to very similar conclusions about shared pathologies, and because of that, the importance of overlap amongst complex medical conditions that historically have really been poorly addressed.”

She added, “mast cell activation, or mast cell hyperactivity, is one part of the greater picture. What’s important about the mast cell component is that of the multiple different targetable pathologies, it’s one that currently has potential available therapies that can be explored, some of them relatively easily.”

But Christopher Chang, MD, PhD, chief of the Pediatric Allergy and Immunology program, Joe DiMaggio Children’s Hospital, Hollywood, Florida, sees it differently. In an interview, he noted that the reason for disagreement over what constitutes MCAS is that “it doesn’t have a lot of objective findings that we can identify. ... We know that mast cells are important immune cells, just like all immune cells are important. It seems like whenever someone has unexplained symptoms, people try to blame it on mast cells. But it’s very hard to prove that.” 
 

Two Definitions Characterize the Illness Differently

One proposed “consensus” MCAS definition was first published in 2011 by a group led by hematologist Peter Valent, MD, of the Medical University of Vienna in Austria. It has been revised since, and similar versions adopted by medical societies, including the American Academy of Allergy, Asthma & Immunology (AAAAI). The most recent versions propose three core MCAS criteria: 

• Typical clinical signs of severe, recurrent (episodic) systemic (at least two organ systems) MCA are present (often in the form of anaphylaxis).
• The involvement of mast cells (MCs) is documented by biochemical studies, preferably an increase in serum tryptase levels from the individual’s baseline to plus 20% + 2 ng/mL.
• Response of symptoms to therapy with MC-stabilizing agents, drugs directed against MC mediator production, or drugs blocking mediator release or effects of MC-derived mediators.

The following year, a separate publication authored by Gerhard J. Molderings, MD, University of Bonn in Germany, and colleagues proposed a much broader MCAS definition. Also revised since, the latest “consensus-2” was published in 2020. This definition consists of one major criterion: “A constellation of clinical complaints attributable to pathologically increased MC activity, ie, MC mediator release syndrome.” This “constellation” involves conditions of nearly every organ system that, taken together, are estimated to affect up to 17% of the entire population. These are just a few examples: 

• Constitutional: Chronic fatigue, flushing, or sweats
• Dermatologic: Rashes or lesions
• Ophthalmologic: dry eyes
• Oral: Burning or itching in mouth
• Pulmonary: Airway inflammation at any/all levels
• Cardiovascular: Blood pressure lability or codiagnosis of POTS is common
• Gastrointestinal: Reflux, dysphagia, or malabsorption
• Genitourinary: Endometriosis, dysmenorrhea, or dyspareunia
• Musculoskeletal/connective tissue: Fibromyalgia or diagnosis of hypermobile EDS is common
• Neurologic: Headaches or sensory neuropathies
• Psychiatric: Depression or anxiety
• Endocrinologic: Thyroid disease or dyslipidemia
• Hematologic: Polycythemia or anemia (after ruling out other causes)

The diagnosis is made by fulfilling that major criterion, plus at least one objective assessment of pathologically increased release of MC mediators, including infiltrates, abnormal MC morphology, or MC genetic changes shown to increase MC activity. Other alternatives include evidence of above-normal levels of MC mediators, including tryptase, histamine or its metabolites, heparin, or chromatin A, in whole blood, serum, plasma, or urine. Symptomatic response to MC activation inhibitors can also be used but isn’t required as it is in the other definition. 
 

Underdiagnosis vs Overdiagnosis

Lawrence B. Afrin, MD, senior consultant in hematology/oncology at the AIM Center for Personalized Medicine, Westchester, New York, and lead author of the 2020 update of the broader “consensus-2” criteria, said in an interview, “we now know MCAS exists, and it’s prevalent, even though, for understandable and forgivable reasons, we’ve been missing it all along. ... If you see a patient who has this chronic, multisystem unwellness with general themes of inflammation plus or minus allergic issues and you can’t find some other rational explanation that better accounts for what’s going on ... then it’s reasonable to think to include MCAS in the differential diagnosis. If the patient happens not to fit the diagnostic criteria being advanced by one group, that doesn’t necessarily rule out the possibility that this is still going on.”

Afrin, along with his coauthors, faulted the narrower “consensus-1” definition for lacking data to support the “20% + 2” criteria for requiring the difficult determination of a patient’s “baseline” and for requiring evidence of response to treatment prior to making the diagnosis. Not all patients will respond to a given histamine blocker, he noted. 

But Lawrence B. Schwartz, MD, PhD, an author on both the Valent and AAAAI criteria, disagreed, noting that the narrower criteria “appear to have a high degree of specificity and sensitivity when the reaction is systemic and involves hypotension. Less severe clinical events, particularly involving the gastrointestinal or central nervous systems, do not have precise clinical or biomarker criteria for identifying mast cell involvement.” 

Added Schwartz, who is professor of medicine and chair of the Division of Rheumatology, Allergy, and Immunology and program director of Allergy and Immunology, Virginia Commonwealth University (VCU), Richmond, “when mast cell activation events occur only in the skin, we refer to it as chronic urticaria and in the airways or conjunctiva of allergic individuals as allergic asthma, rhinitis, and/or conjunctivitis. The absence of specific criteria for mast cell activation in the GI [gastrointestinal] tract or CNS [central nervous system] neither rules in mast cell involvement nor does it rule out mast cell involvement. Thus, more research is needed to find better diagnostic criteria.”

Schwartz also pointed to a recent paper reporting the use of artificial intelligence models to “quantify diagnostic precision and specificity” of “alternative” MCAS definitions. The conclusion was a “lack of specificity is pronounced in relation to multiple control criteria, raising the concern that alternative criteria could disproportionately contribute to MCAS overdiagnosis, to the exclusion of more appropriate diagnoses.”

During the meeting, Afrin acknowledged that the broader view risks overdiagnosis of MCAS. However, he also referenced Occam’s razor, the principle that the simplest explanation is probably the best one. “Which scenario is more likely? Multiple diagnoses and problems that are all independent of each other vs one diagnosis that’s biologically capable of causing most or all of the findings, ie, the simplest solution even if it’s not the most immediately obvious solution?”

He said in an interview: “Do we have any proof that MCAS is what’s underlying hypermobile Ehlers-Danlos or POTS or chronic fatigue? No, we don’t have any proof, not because anybody has done studies that have shown there to be no connection but simply because we’re so early in our awareness that the disease even exists that the necessary studies haven’t even been done yet.”

At the meeting, Afrin introduced proposals to turn the “Masterminds” group into a formal professional society and to launch a journal. He also gave an update on progress in developing a symptom assessment tool both for clinical use and to enable clinical trials of new drugs to target mast cells or their mediators. The plan is to field test the tool in 2025 and publish those results in 2026. 

Grach, Afrin, and Chang had no disclosures. Schwartz discovered tryptase and invented the Thermo Fisher tryptase assay, for which his institution (VCU) receives royalties that are shared with him. He also invented monoclonal antibodies used for detecting mast cells or basophils, for which VCU receives royalties from several companies, including Millipore, Santa Cruz, BioLegend, and Hycult Biotech, that are also shared with him. He is a paid consultant for Blueprint Medicines, Celldex Therapeutics, Invea, Third Harmonic Bio, HYCOR Biomedical, Jasper, TerSera Therapeutics, and GLG. He also serves on an AstraZeneca data safety monitoring board for a clinical trial involving benralizumab treatment of hypereosinophilic syndrome and receives royalties from UpToDate (biomarkers for anaphylaxis) and Goldman-Cecil Medicine (anaphylaxis).

A version of this article first appeared on Medscape.com.

TOPLINE:

Deprescribing antihypertensive medications is associated with a 12% lower likelihood of cognitive decline in older nursing home residents, a new study suggests. The association was strongest among those with dementia.

METHODOLOGY:

• The cohort study included 12,644 long-term care residents (mean age, 77.7 years; 97% men; 17.5% Black) with stays of at least 12 weeks from 2006 to 2019.
• Residents who experienced either a reduction in the total number of antihypertensive medications or a sustained 30% decrease in dosage for at least 2 weeks were classified as deprescribing users (n = 1290). Those with no medication changes were considered stable users (n = 11,354).
• The primary outcome was cognitive impairment assessed using the four-point Cognitive Function Scale (CFS), with the score proportional to the severity of impairment.
• The median follow-up duration was 23 weeks for the deprescribing users and 21 weeks for the stable users.

TAKEAWAY:

• Deprescribing antihypertensives was associated with a 12% lower likelihood of progressing to a worse CFS score per 12-week period (odds ratio [OR], 0.88; 95% CI, 0.78-0.99), compared with stable users.
• Among residents with dementia, deprescribing was associated with a 16% reduced likelihood of cognitive decline per 12-week period (OR, 0.84; 95% CI, 0.72-0.98).
• At the end of follow-up, 12% of residents had a higher CFS score and 7.7% had a lower CFS score.
• In the intention-to-treat analysis, the association between deprescribing antihypertensive medications and reduced cognitive decline remained consistent (OR, 0.94; 95% CI, 0.90-0.98).

IN PRACTICE:

“This work highlights the need for patient-centered approaches to deprescribing, ensuring that medication regimens for older adults are optimized to preserve cognitive function and minimize potential harms,” the study authors wrote.

SOURCE:

The study was led by Bocheng Jing, MS, Department of Medicine, University of California, San Francisco. It was published online in JAMA Internal Medicine.

LIMITATIONS:

The study population included predominantly men and White individuals, limiting the generalizability of the results to women and other racial and ethnic groups. The findings may not be applicable to patients with heart failure owing to their noninclusion. The specificity of dementia diagnosis was limited, as this study combined various forms of dementia, making it challenging to differentiate the impacts among subgroups.

DISCLOSURES:

This study was supported by the US National Institute on Aging. Two authors reported receiving grants, honoraria, consulting fees, or royalties from various sources. Details are provided 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:

Deprescribing antihypertensive medications is associated with a 12% lower likelihood of cognitive decline in older nursing home residents, a new study suggests. The association was strongest among those with dementia.

METHODOLOGY:

• The cohort study included 12,644 long-term care residents (mean age, 77.7 years; 97% men; 17.5% Black) with stays of at least 12 weeks from 2006 to 2019.
• Residents who experienced either a reduction in the total number of antihypertensive medications or a sustained 30% decrease in dosage for at least 2 weeks were classified as deprescribing users (n = 1290). Those with no medication changes were considered stable users (n = 11,354).
• The primary outcome was cognitive impairment assessed using the four-point Cognitive Function Scale (CFS), with the score proportional to the severity of impairment.
• The median follow-up duration was 23 weeks for the deprescribing users and 21 weeks for the stable users.

TAKEAWAY:

• Deprescribing antihypertensives was associated with a 12% lower likelihood of progressing to a worse CFS score per 12-week period (odds ratio [OR], 0.88; 95% CI, 0.78-0.99), compared with stable users.
• Among residents with dementia, deprescribing was associated with a 16% reduced likelihood of cognitive decline per 12-week period (OR, 0.84; 95% CI, 0.72-0.98).
• At the end of follow-up, 12% of residents had a higher CFS score and 7.7% had a lower CFS score.
• In the intention-to-treat analysis, the association between deprescribing antihypertensive medications and reduced cognitive decline remained consistent (OR, 0.94; 95% CI, 0.90-0.98).

IN PRACTICE:

“This work highlights the need for patient-centered approaches to deprescribing, ensuring that medication regimens for older adults are optimized to preserve cognitive function and minimize potential harms,” the study authors wrote.

SOURCE:

The study was led by Bocheng Jing, MS, Department of Medicine, University of California, San Francisco. It was published online in JAMA Internal Medicine.

LIMITATIONS:

The study population included predominantly men and White individuals, limiting the generalizability of the results to women and other racial and ethnic groups. The findings may not be applicable to patients with heart failure owing to their noninclusion. The specificity of dementia diagnosis was limited, as this study combined various forms of dementia, making it challenging to differentiate the impacts among subgroups.

DISCLOSURES:

This study was supported by the US National Institute on Aging. Two authors reported receiving grants, honoraria, consulting fees, or royalties from various sources. Details are provided 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:

Deprescribing antihypertensive medications is associated with a 12% lower likelihood of cognitive decline in older nursing home residents, a new study suggests. The association was strongest among those with dementia.

METHODOLOGY:

• The cohort study included 12,644 long-term care residents (mean age, 77.7 years; 97% men; 17.5% Black) with stays of at least 12 weeks from 2006 to 2019.
• Residents who experienced either a reduction in the total number of antihypertensive medications or a sustained 30% decrease in dosage for at least 2 weeks were classified as deprescribing users (n = 1290). Those with no medication changes were considered stable users (n = 11,354).
• The primary outcome was cognitive impairment assessed using the four-point Cognitive Function Scale (CFS), with the score proportional to the severity of impairment.
• The median follow-up duration was 23 weeks for the deprescribing users and 21 weeks for the stable users.

TAKEAWAY:

• Deprescribing antihypertensives was associated with a 12% lower likelihood of progressing to a worse CFS score per 12-week period (odds ratio [OR], 0.88; 95% CI, 0.78-0.99), compared with stable users.
• Among residents with dementia, deprescribing was associated with a 16% reduced likelihood of cognitive decline per 12-week period (OR, 0.84; 95% CI, 0.72-0.98).
• At the end of follow-up, 12% of residents had a higher CFS score and 7.7% had a lower CFS score.
• In the intention-to-treat analysis, the association between deprescribing antihypertensive medications and reduced cognitive decline remained consistent (OR, 0.94; 95% CI, 0.90-0.98).

IN PRACTICE:

“This work highlights the need for patient-centered approaches to deprescribing, ensuring that medication regimens for older adults are optimized to preserve cognitive function and minimize potential harms,” the study authors wrote.

SOURCE:

The study was led by Bocheng Jing, MS, Department of Medicine, University of California, San Francisco. It was published online in JAMA Internal Medicine.

LIMITATIONS:

The study population included predominantly men and White individuals, limiting the generalizability of the results to women and other racial and ethnic groups. The findings may not be applicable to patients with heart failure owing to their noninclusion. The specificity of dementia diagnosis was limited, as this study combined various forms of dementia, making it challenging to differentiate the impacts among subgroups.

DISCLOSURES:

This study was supported by the US National Institute on Aging. Two authors reported receiving grants, honoraria, consulting fees, or royalties from various sources. Details are provided 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.

Coffee and tea are among the plants that are highest in caffeine. Their use as beverages makes caffeine the most consumed psychoactive agent in the world. Coffee is commonly used to increase alertness and work productivity. Synthetic caffeine is added to soft drinks, energy drinks, and products intended to reduce fatigue or promote weight loss.

The caffeine content varies with the type of drink: It is high in coffee, energy drinks, and caffeine tablets; intermediate in tea; and low in soft drinks. Coffee is the predominant source of the caffeine ingested by adults. The evidence for caffeine’s effects on people is ambiguous, and some risks and benefits deserve special attention because of the impact they may have on our health.
 

Characteristics of Caffeine

Caffeine is a methylxanthine that is completely absorbed 45 minutes after ingestion, peaking between 15 minutes and 2 hours. The half-life of caffeine varies according to age. In adults, it is 2.5-4.5 hours; in newborns, 80 hours; in children older than 6 months, it remains stable over time with respect to weight. Smoking accelerates caffeine metabolism by reducing the half-life by 50%. Oral contraceptives, however, double caffeine’s half-life. Caffeine metabolism is reduced during pregnancy (it is greater in the first trimester), with a half-life of more than 15 hours. Caffeine clearance can be slowed by several classes of drugs (eg, quinolones, cardiovascular drugs, bronchodilators, and antidepressants) that increase its half-life because they are metabolized by the same liver enzymes.

Caffeine passes the blood-brain barrier and, having an adenosine-like structure, inhibits adenosine’s effects by binding to adenosine receptors. In the brain, caffeine reduces fatigue, increases alertness, reduces reaction times, may reduce the risk for depression, and increases the effectiveness of nonsteroidal anti-inflammatory drugs in treating headaches and other types of pain.
 

Caffeine and Chronic Diseases

The evidence available on the relationship between caffeine and health has several methodological limitations. Observations of the acute effects of caffeine may not reflect long-term effects because tolerance to caffeine’s effects may develop over time. Smoking and unhealthy lifestyles are confounding factors in epidemiological studies of caffeine intake. In addition, the estimate of the amount and frequency of caffeine intake is often inaccurate because it is mainly based on self-assessment systems. Finally, prospective studies of caffeine consumption are mainly based on coffee and tea consumption, but it is unclear how much the observed outcomes can be translated to intake of other beverages such as energy drinks.

Considering the very high prevalence of arterial hypertension worldwide (31.1% of adults), many questions have been raised about the influence of coffee consumption on blood pressure (BP) and the risk for arterial hypertension. Administration of 200-300 mg caffeine is shown to induce a mean increase of 8.1 mm Hg systolic BP and 5.7 mm Hg diastolic BP. The increase is observed in the first hour after caffeine intake and lasts no longer than 3 hours.

Yet, the moderate and usual consumption of coffee does not increase, but may even reduce, the risk of developing high BP. In contrast, occasional coffee consumption can have hypertensive effects, and moderate and usual consumption in patients with high BP does not appear to increase the risk for uncontrolled BP and can reduce the risk for death from any cause. The inverse association between coffee consumption and hypertension risk was confirmed in a review and meta-analysis of cross-sectional and cohort studies.

With respect to lipid metabolism, cholesterol levels may increase after caffeine consumption because of cafestol. Concentrations of cafestol are high in unfiltered coffee, intermediate in espresso and moka pot coffee, and negligible in instant or filtered coffee. Studies on the impact of coffee on lipid levels have led to inconsistent results, however. Data have shown that people who drink more coffee have higher triglycerides, total cholesterol, and low-density lipoprotein cholesterol (LDL-C) levels. Other data have shown that caffeine promotes LDL receptor expression and clearance of LDL cholesterol.

Experimental and cohort studies have not shown an association between coffee consumption and atrial fibrillation (AF). In fact, evidence suggests that coffee consumption tends to reduce the risk for AF in a dose-response relationship. Similarly, coffee consumption is not associated with increased risk for cardiovascular events in the general population or among patients with a history of hypertension, diabetes, or cardiovascular disease.

The Coffee and Real-Time Atrial and Ventricular Ectopy study evaluated the acute effects of coffee consumption on cardiac ectopy using wearable sensors with continuous recording. It did not demonstrate any increase in daily premature atrial contractions with coffee consumption, compared with abstaining from caffeine. 

In patients with type 2 diabetes, a study performed in Japan showed that coffee consumption was associated with reduced all-cause mortality. The results suggested a dose-response relationship, and drinking coffee and green tea appeared to reduce mortality risk further. The results were not generalizable, however, because of the study population’s ethnic homogeneity.
 

Dose and Toxicity

Caffeine at high doses (> 400 mg daily) and in susceptible patients can induce anxiety, but the effects of caffeine on sleep and anxiety can differ from patient to patient. This variation reflects differences in caffeine metabolism rate and adenosine receptor gene variants.

High caffeine intake can stimulate diuresis, but without causing damaging effects on hydration when taking moderate doses of caffeine (≤ 400 mg daily) for long periods. Stopping caffeine suddenly, in a regular consumer, can lead to withdrawal symptoms such as headache, asthenia, decreased attention, depressed mood, and flu-like symptoms.

The toxic effects of caffeine occur with intake > 1.2 g. A dose of 10-14 g is considered fatal. Caffeine overdose is rare when considering traditional methods of intake (coffee and tea) because 70-100 cups of coffee should be sufficient for caffeine poisoning. Severe events can occur following the use of caffeine tablets or as energy drinks for the following reasons:

• The episodic consumption of caffeine does not allow for tolerance to develop.
• Young people are more vulnerable to the effects of caffeine.
• Caffeine has a synergistic effect in combination with other components in energy drinks.
• Taking caffeine in combination with alcohol or intense exertion causes serious, even fatal, outcomes.

Products Containing Caffeine

Evidence supports the relationship between high consumption (approximately 1 L) of energy drinks with a caffeine content of 320 mg and short-term cardiovascular adverse events, such as increased BP, QT-segment prolongation corrected for heart rate, and palpitations. These tests prompt the recommendation to avoid consuming these beverages in high quantities and in association with alcohol.

Weight loss products generally contain caffeine coupled with herbal extracts that are expected to improve fat metabolism, lipolysis, and oxidation. These products, because of their easy availability, presumed benefits, and high caffeine concentration, may be more susceptible to misuse because they can be taken in larger portions than recommended. The combination of multiple ingredients, concentrated amounts of caffeine, and excessive consumption increases the likelihood of adverse effects.

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.

Coffee and tea are among the plants that are highest in caffeine. Their use as beverages makes caffeine the most consumed psychoactive agent in the world. Coffee is commonly used to increase alertness and work productivity. Synthetic caffeine is added to soft drinks, energy drinks, and products intended to reduce fatigue or promote weight loss.

The caffeine content varies with the type of drink: It is high in coffee, energy drinks, and caffeine tablets; intermediate in tea; and low in soft drinks. Coffee is the predominant source of the caffeine ingested by adults. The evidence for caffeine’s effects on people is ambiguous, and some risks and benefits deserve special attention because of the impact they may have on our health.
 

Characteristics of Caffeine

Caffeine is a methylxanthine that is completely absorbed 45 minutes after ingestion, peaking between 15 minutes and 2 hours. The half-life of caffeine varies according to age. In adults, it is 2.5-4.5 hours; in newborns, 80 hours; in children older than 6 months, it remains stable over time with respect to weight. Smoking accelerates caffeine metabolism by reducing the half-life by 50%. Oral contraceptives, however, double caffeine’s half-life. Caffeine metabolism is reduced during pregnancy (it is greater in the first trimester), with a half-life of more than 15 hours. Caffeine clearance can be slowed by several classes of drugs (eg, quinolones, cardiovascular drugs, bronchodilators, and antidepressants) that increase its half-life because they are metabolized by the same liver enzymes.

Caffeine passes the blood-brain barrier and, having an adenosine-like structure, inhibits adenosine’s effects by binding to adenosine receptors. In the brain, caffeine reduces fatigue, increases alertness, reduces reaction times, may reduce the risk for depression, and increases the effectiveness of nonsteroidal anti-inflammatory drugs in treating headaches and other types of pain.
 

Caffeine and Chronic Diseases

The evidence available on the relationship between caffeine and health has several methodological limitations. Observations of the acute effects of caffeine may not reflect long-term effects because tolerance to caffeine’s effects may develop over time. Smoking and unhealthy lifestyles are confounding factors in epidemiological studies of caffeine intake. In addition, the estimate of the amount and frequency of caffeine intake is often inaccurate because it is mainly based on self-assessment systems. Finally, prospective studies of caffeine consumption are mainly based on coffee and tea consumption, but it is unclear how much the observed outcomes can be translated to intake of other beverages such as energy drinks.

Considering the very high prevalence of arterial hypertension worldwide (31.1% of adults), many questions have been raised about the influence of coffee consumption on blood pressure (BP) and the risk for arterial hypertension. Administration of 200-300 mg caffeine is shown to induce a mean increase of 8.1 mm Hg systolic BP and 5.7 mm Hg diastolic BP. The increase is observed in the first hour after caffeine intake and lasts no longer than 3 hours.

Yet, the moderate and usual consumption of coffee does not increase, but may even reduce, the risk of developing high BP. In contrast, occasional coffee consumption can have hypertensive effects, and moderate and usual consumption in patients with high BP does not appear to increase the risk for uncontrolled BP and can reduce the risk for death from any cause. The inverse association between coffee consumption and hypertension risk was confirmed in a review and meta-analysis of cross-sectional and cohort studies.

With respect to lipid metabolism, cholesterol levels may increase after caffeine consumption because of cafestol. Concentrations of cafestol are high in unfiltered coffee, intermediate in espresso and moka pot coffee, and negligible in instant or filtered coffee. Studies on the impact of coffee on lipid levels have led to inconsistent results, however. Data have shown that people who drink more coffee have higher triglycerides, total cholesterol, and low-density lipoprotein cholesterol (LDL-C) levels. Other data have shown that caffeine promotes LDL receptor expression and clearance of LDL cholesterol.

Experimental and cohort studies have not shown an association between coffee consumption and atrial fibrillation (AF). In fact, evidence suggests that coffee consumption tends to reduce the risk for AF in a dose-response relationship. Similarly, coffee consumption is not associated with increased risk for cardiovascular events in the general population or among patients with a history of hypertension, diabetes, or cardiovascular disease.

The Coffee and Real-Time Atrial and Ventricular Ectopy study evaluated the acute effects of coffee consumption on cardiac ectopy using wearable sensors with continuous recording. It did not demonstrate any increase in daily premature atrial contractions with coffee consumption, compared with abstaining from caffeine. 

In patients with type 2 diabetes, a study performed in Japan showed that coffee consumption was associated with reduced all-cause mortality. The results suggested a dose-response relationship, and drinking coffee and green tea appeared to reduce mortality risk further. The results were not generalizable, however, because of the study population’s ethnic homogeneity.
 

Dose and Toxicity

Caffeine at high doses (> 400 mg daily) and in susceptible patients can induce anxiety, but the effects of caffeine on sleep and anxiety can differ from patient to patient. This variation reflects differences in caffeine metabolism rate and adenosine receptor gene variants.

High caffeine intake can stimulate diuresis, but without causing damaging effects on hydration when taking moderate doses of caffeine (≤ 400 mg daily) for long periods. Stopping caffeine suddenly, in a regular consumer, can lead to withdrawal symptoms such as headache, asthenia, decreased attention, depressed mood, and flu-like symptoms.

The toxic effects of caffeine occur with intake > 1.2 g. A dose of 10-14 g is considered fatal. Caffeine overdose is rare when considering traditional methods of intake (coffee and tea) because 70-100 cups of coffee should be sufficient for caffeine poisoning. Severe events can occur following the use of caffeine tablets or as energy drinks for the following reasons:

• The episodic consumption of caffeine does not allow for tolerance to develop.
• Young people are more vulnerable to the effects of caffeine.
• Caffeine has a synergistic effect in combination with other components in energy drinks.
• Taking caffeine in combination with alcohol or intense exertion causes serious, even fatal, outcomes.

Products Containing Caffeine

Evidence supports the relationship between high consumption (approximately 1 L) of energy drinks with a caffeine content of 320 mg and short-term cardiovascular adverse events, such as increased BP, QT-segment prolongation corrected for heart rate, and palpitations. These tests prompt the recommendation to avoid consuming these beverages in high quantities and in association with alcohol.

Weight loss products generally contain caffeine coupled with herbal extracts that are expected to improve fat metabolism, lipolysis, and oxidation. These products, because of their easy availability, presumed benefits, and high caffeine concentration, may be more susceptible to misuse because they can be taken in larger portions than recommended. The combination of multiple ingredients, concentrated amounts of caffeine, and excessive consumption increases the likelihood of adverse effects.

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.

Coffee and tea are among the plants that are highest in caffeine. Their use as beverages makes caffeine the most consumed psychoactive agent in the world. Coffee is commonly used to increase alertness and work productivity. Synthetic caffeine is added to soft drinks, energy drinks, and products intended to reduce fatigue or promote weight loss.

The caffeine content varies with the type of drink: It is high in coffee, energy drinks, and caffeine tablets; intermediate in tea; and low in soft drinks. Coffee is the predominant source of the caffeine ingested by adults. The evidence for caffeine’s effects on people is ambiguous, and some risks and benefits deserve special attention because of the impact they may have on our health.
 

Characteristics of Caffeine

Caffeine is a methylxanthine that is completely absorbed 45 minutes after ingestion, peaking between 15 minutes and 2 hours. The half-life of caffeine varies according to age. In adults, it is 2.5-4.5 hours; in newborns, 80 hours; in children older than 6 months, it remains stable over time with respect to weight. Smoking accelerates caffeine metabolism by reducing the half-life by 50%. Oral contraceptives, however, double caffeine’s half-life. Caffeine metabolism is reduced during pregnancy (it is greater in the first trimester), with a half-life of more than 15 hours. Caffeine clearance can be slowed by several classes of drugs (eg, quinolones, cardiovascular drugs, bronchodilators, and antidepressants) that increase its half-life because they are metabolized by the same liver enzymes.

Caffeine passes the blood-brain barrier and, having an adenosine-like structure, inhibits adenosine’s effects by binding to adenosine receptors. In the brain, caffeine reduces fatigue, increases alertness, reduces reaction times, may reduce the risk for depression, and increases the effectiveness of nonsteroidal anti-inflammatory drugs in treating headaches and other types of pain.
 

Caffeine and Chronic Diseases

The evidence available on the relationship between caffeine and health has several methodological limitations. Observations of the acute effects of caffeine may not reflect long-term effects because tolerance to caffeine’s effects may develop over time. Smoking and unhealthy lifestyles are confounding factors in epidemiological studies of caffeine intake. In addition, the estimate of the amount and frequency of caffeine intake is often inaccurate because it is mainly based on self-assessment systems. Finally, prospective studies of caffeine consumption are mainly based on coffee and tea consumption, but it is unclear how much the observed outcomes can be translated to intake of other beverages such as energy drinks.

Considering the very high prevalence of arterial hypertension worldwide (31.1% of adults), many questions have been raised about the influence of coffee consumption on blood pressure (BP) and the risk for arterial hypertension. Administration of 200-300 mg caffeine is shown to induce a mean increase of 8.1 mm Hg systolic BP and 5.7 mm Hg diastolic BP. The increase is observed in the first hour after caffeine intake and lasts no longer than 3 hours.

Yet, the moderate and usual consumption of coffee does not increase, but may even reduce, the risk of developing high BP. In contrast, occasional coffee consumption can have hypertensive effects, and moderate and usual consumption in patients with high BP does not appear to increase the risk for uncontrolled BP and can reduce the risk for death from any cause. The inverse association between coffee consumption and hypertension risk was confirmed in a review and meta-analysis of cross-sectional and cohort studies.

With respect to lipid metabolism, cholesterol levels may increase after caffeine consumption because of cafestol. Concentrations of cafestol are high in unfiltered coffee, intermediate in espresso and moka pot coffee, and negligible in instant or filtered coffee. Studies on the impact of coffee on lipid levels have led to inconsistent results, however. Data have shown that people who drink more coffee have higher triglycerides, total cholesterol, and low-density lipoprotein cholesterol (LDL-C) levels. Other data have shown that caffeine promotes LDL receptor expression and clearance of LDL cholesterol.

Experimental and cohort studies have not shown an association between coffee consumption and atrial fibrillation (AF). In fact, evidence suggests that coffee consumption tends to reduce the risk for AF in a dose-response relationship. Similarly, coffee consumption is not associated with increased risk for cardiovascular events in the general population or among patients with a history of hypertension, diabetes, or cardiovascular disease.

The Coffee and Real-Time Atrial and Ventricular Ectopy study evaluated the acute effects of coffee consumption on cardiac ectopy using wearable sensors with continuous recording. It did not demonstrate any increase in daily premature atrial contractions with coffee consumption, compared with abstaining from caffeine. 

In patients with type 2 diabetes, a study performed in Japan showed that coffee consumption was associated with reduced all-cause mortality. The results suggested a dose-response relationship, and drinking coffee and green tea appeared to reduce mortality risk further. The results were not generalizable, however, because of the study population’s ethnic homogeneity.
 

Dose and Toxicity

Caffeine at high doses (> 400 mg daily) and in susceptible patients can induce anxiety, but the effects of caffeine on sleep and anxiety can differ from patient to patient. This variation reflects differences in caffeine metabolism rate and adenosine receptor gene variants.

High caffeine intake can stimulate diuresis, but without causing damaging effects on hydration when taking moderate doses of caffeine (≤ 400 mg daily) for long periods. Stopping caffeine suddenly, in a regular consumer, can lead to withdrawal symptoms such as headache, asthenia, decreased attention, depressed mood, and flu-like symptoms.

The toxic effects of caffeine occur with intake > 1.2 g. A dose of 10-14 g is considered fatal. Caffeine overdose is rare when considering traditional methods of intake (coffee and tea) because 70-100 cups of coffee should be sufficient for caffeine poisoning. Severe events can occur following the use of caffeine tablets or as energy drinks for the following reasons:

• The episodic consumption of caffeine does not allow for tolerance to develop.
• Young people are more vulnerable to the effects of caffeine.
• Caffeine has a synergistic effect in combination with other components in energy drinks.
• Taking caffeine in combination with alcohol or intense exertion causes serious, even fatal, outcomes.

Products Containing Caffeine

Evidence supports the relationship between high consumption (approximately 1 L) of energy drinks with a caffeine content of 320 mg and short-term cardiovascular adverse events, such as increased BP, QT-segment prolongation corrected for heart rate, and palpitations. These tests prompt the recommendation to avoid consuming these beverages in high quantities and in association with alcohol.

Weight loss products generally contain caffeine coupled with herbal extracts that are expected to improve fat metabolism, lipolysis, and oxidation. These products, because of their easy availability, presumed benefits, and high caffeine concentration, may be more susceptible to misuse because they can be taken in larger portions than recommended. The combination of multiple ingredients, concentrated amounts of caffeine, and excessive consumption increases the likelihood of adverse effects.

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.

A new scanner can provide three-dimensional (3D) photoacoustic images of millimeter-scale veins and arteries in seconds.

The scanner, developed by researchers at University College London (UCL) in England, could help clinicians better visualize and track microvascular changes for a wide range of diseases, including cancer, rheumatoid arthritis (RA), and peripheral vascular disease (PVD).

In exploratory case studies, researchers demonstrated how the scanner visualized vessels with a corkscrew-like structure in patients with suspected PVD and mapped new blood vessel formation driven by inflammation in patients with RA.

The case studies “illustrate potential areas of application that warrant future, more comprehensive clinical studies,” the authors wrote. “Moreover, they demonstrate the feasibility of using the scanner on a real-world patient cohort where imaging is more challenging due to frailty, comorbidity, or pain that may limit their ability to tolerate prolonged scan times.”

The work was published online in Nature Biomedical Engineering.
 

Improving Photoacoustic Imaging

PAT works using the photoacoustic effect, a phenomenon where sound waves are generated when light is absorbed by a material. When pulsed light from a laser is directed at tissue, some of that light is absorbed and causes an increase in heat in the targeted area. This localized heat also increases pressure, which generates ultrasound waves that can be detected by specialized sensors.

While previous PAT scanners translated these sound waves to electric signals directly to generate imaging, UCL engineers developed a sensor in the early 2000s that can detect these ultrasound waves using light. The result was much clearer, 3D images.

“That was great, but the problem was it was very slow, and it would take 5 minutes to get an image,” explained Paul Beard, PhD, professor of biomedical photoacoustics at UCL and senior author of the study. “That’s fine if you’re imaging a dead mouse or an anesthetized mouse, but not so useful for human imaging,” he continued, where motion would blur the image.

In this new paper, Beard and colleagues outlined how they cut scanning times to an order of seconds (or fraction of a second) rather than minutes. While previous iterations could detect only acoustic waves from one point at a time, this new scanner can detect waves from multiple points simultaneously. The scanner can visualize veins and arteries up to 15 mm deep in human tissue and can also provide dynamic, 3D images of “time-varying tissue perfusion and other hemodynamic events,” the authors wrote.

With these types of scanners, there is always a trade-off between imaging quality and imaging speed, explained Srivalleesha Mallidi, PhD, an assistant professor of biomedical engineering at Tufts University in Medford, Massachusetts. She was not involved with the work.

“With the resolution that [the authors] are providing and the depth at which they are seeing the signals, it is one of the fastest systems,” she said.
 

Clinical Utility

Beard and colleagues also tested the scanner to visualize blood vessels in participants with RA, suspected PVD, and skin inflammation. The scanning images “illustrated how vascular abnormalities such as increased vessel tortuosity, which has previously been linked to PVD, and the neovascularization associated with inflammation can be visualized and quantified,” the authors wrote.

The next step, Beard noted, is testing whether these characteristics can be used as a marker for the progression of disease.

Nehal Mehta, MD, a cardiologist and professor of medicine at the George Washington University, Washington, DC, agreed that more longitudinal research is needed to understand how the abnormalities captured in these images can inform detection and diagnosis of various diseases.

“You don’t know whether these images look bad because of reverse causation — the disease is doing this — or true causation — that this is actually detecting the root cause of the disease,” he explained. “Until we have a bank of normal and abnormal scans, we don’t know what any of these things mean.”

Though still some time away from entering the clinic, Mehta likened the technology to the introduction of optical coherence tomography in the 1980s. Before being adapted for clinical use, researchers first needed to visualize differences between normal coronary vasculature and myocardial infarction.

“I think this is an amazingly strong first proof of concept,” Mehta said. “This technology is showing a true promise in the field imaging.”

The work was funded by grants from Cancer Research UK, the Engineering & Physical Sciences Research Council, Wellcome Trust, the European Research Council, and the National Institute for Health and Care Research University College London Hospitals Biomedical Research Centre. Beard and two coauthors are shareholders of DeepColor Imaging to which the intellectual property associated with the new scanner has been licensed, but the company was not involved in any of this research. Mallidi and Mehta had no relevant disclosures.

A version of this article first appeared on Medscape.com.

A new scanner can provide three-dimensional (3D) photoacoustic images of millimeter-scale veins and arteries in seconds.

The scanner, developed by researchers at University College London (UCL) in England, could help clinicians better visualize and track microvascular changes for a wide range of diseases, including cancer, rheumatoid arthritis (RA), and peripheral vascular disease (PVD).

In exploratory case studies, researchers demonstrated how the scanner visualized vessels with a corkscrew-like structure in patients with suspected PVD and mapped new blood vessel formation driven by inflammation in patients with RA.

The case studies “illustrate potential areas of application that warrant future, more comprehensive clinical studies,” the authors wrote. “Moreover, they demonstrate the feasibility of using the scanner on a real-world patient cohort where imaging is more challenging due to frailty, comorbidity, or pain that may limit their ability to tolerate prolonged scan times.”

The work was published online in Nature Biomedical Engineering.
 

Improving Photoacoustic Imaging

PAT works using the photoacoustic effect, a phenomenon where sound waves are generated when light is absorbed by a material. When pulsed light from a laser is directed at tissue, some of that light is absorbed and causes an increase in heat in the targeted area. This localized heat also increases pressure, which generates ultrasound waves that can be detected by specialized sensors.

While previous PAT scanners translated these sound waves to electric signals directly to generate imaging, UCL engineers developed a sensor in the early 2000s that can detect these ultrasound waves using light. The result was much clearer, 3D images.

“That was great, but the problem was it was very slow, and it would take 5 minutes to get an image,” explained Paul Beard, PhD, professor of biomedical photoacoustics at UCL and senior author of the study. “That’s fine if you’re imaging a dead mouse or an anesthetized mouse, but not so useful for human imaging,” he continued, where motion would blur the image.

In this new paper, Beard and colleagues outlined how they cut scanning times to an order of seconds (or fraction of a second) rather than minutes. While previous iterations could detect only acoustic waves from one point at a time, this new scanner can detect waves from multiple points simultaneously. The scanner can visualize veins and arteries up to 15 mm deep in human tissue and can also provide dynamic, 3D images of “time-varying tissue perfusion and other hemodynamic events,” the authors wrote.

With these types of scanners, there is always a trade-off between imaging quality and imaging speed, explained Srivalleesha Mallidi, PhD, an assistant professor of biomedical engineering at Tufts University in Medford, Massachusetts. She was not involved with the work.

“With the resolution that [the authors] are providing and the depth at which they are seeing the signals, it is one of the fastest systems,” she said.
 

Clinical Utility

Beard and colleagues also tested the scanner to visualize blood vessels in participants with RA, suspected PVD, and skin inflammation. The scanning images “illustrated how vascular abnormalities such as increased vessel tortuosity, which has previously been linked to PVD, and the neovascularization associated with inflammation can be visualized and quantified,” the authors wrote.

The next step, Beard noted, is testing whether these characteristics can be used as a marker for the progression of disease.

Nehal Mehta, MD, a cardiologist and professor of medicine at the George Washington University, Washington, DC, agreed that more longitudinal research is needed to understand how the abnormalities captured in these images can inform detection and diagnosis of various diseases.

“You don’t know whether these images look bad because of reverse causation — the disease is doing this — or true causation — that this is actually detecting the root cause of the disease,” he explained. “Until we have a bank of normal and abnormal scans, we don’t know what any of these things mean.”

Though still some time away from entering the clinic, Mehta likened the technology to the introduction of optical coherence tomography in the 1980s. Before being adapted for clinical use, researchers first needed to visualize differences between normal coronary vasculature and myocardial infarction.

“I think this is an amazingly strong first proof of concept,” Mehta said. “This technology is showing a true promise in the field imaging.”

The work was funded by grants from Cancer Research UK, the Engineering & Physical Sciences Research Council, Wellcome Trust, the European Research Council, and the National Institute for Health and Care Research University College London Hospitals Biomedical Research Centre. Beard and two coauthors are shareholders of DeepColor Imaging to which the intellectual property associated with the new scanner has been licensed, but the company was not involved in any of this research. Mallidi and Mehta had no relevant disclosures.

A version of this article first appeared on Medscape.com.

A new scanner can provide three-dimensional (3D) photoacoustic images of millimeter-scale veins and arteries in seconds.

The scanner, developed by researchers at University College London (UCL) in England, could help clinicians better visualize and track microvascular changes for a wide range of diseases, including cancer, rheumatoid arthritis (RA), and peripheral vascular disease (PVD).

In exploratory case studies, researchers demonstrated how the scanner visualized vessels with a corkscrew-like structure in patients with suspected PVD and mapped new blood vessel formation driven by inflammation in patients with RA.

The case studies “illustrate potential areas of application that warrant future, more comprehensive clinical studies,” the authors wrote. “Moreover, they demonstrate the feasibility of using the scanner on a real-world patient cohort where imaging is more challenging due to frailty, comorbidity, or pain that may limit their ability to tolerate prolonged scan times.”

The work was published online in Nature Biomedical Engineering.
 

Improving Photoacoustic Imaging

PAT works using the photoacoustic effect, a phenomenon where sound waves are generated when light is absorbed by a material. When pulsed light from a laser is directed at tissue, some of that light is absorbed and causes an increase in heat in the targeted area. This localized heat also increases pressure, which generates ultrasound waves that can be detected by specialized sensors.

While previous PAT scanners translated these sound waves to electric signals directly to generate imaging, UCL engineers developed a sensor in the early 2000s that can detect these ultrasound waves using light. The result was much clearer, 3D images.

“That was great, but the problem was it was very slow, and it would take 5 minutes to get an image,” explained Paul Beard, PhD, professor of biomedical photoacoustics at UCL and senior author of the study. “That’s fine if you’re imaging a dead mouse or an anesthetized mouse, but not so useful for human imaging,” he continued, where motion would blur the image.

In this new paper, Beard and colleagues outlined how they cut scanning times to an order of seconds (or fraction of a second) rather than minutes. While previous iterations could detect only acoustic waves from one point at a time, this new scanner can detect waves from multiple points simultaneously. The scanner can visualize veins and arteries up to 15 mm deep in human tissue and can also provide dynamic, 3D images of “time-varying tissue perfusion and other hemodynamic events,” the authors wrote.

With these types of scanners, there is always a trade-off between imaging quality and imaging speed, explained Srivalleesha Mallidi, PhD, an assistant professor of biomedical engineering at Tufts University in Medford, Massachusetts. She was not involved with the work.

“With the resolution that [the authors] are providing and the depth at which they are seeing the signals, it is one of the fastest systems,” she said.
 

Clinical Utility

Beard and colleagues also tested the scanner to visualize blood vessels in participants with RA, suspected PVD, and skin inflammation. The scanning images “illustrated how vascular abnormalities such as increased vessel tortuosity, which has previously been linked to PVD, and the neovascularization associated with inflammation can be visualized and quantified,” the authors wrote.

The next step, Beard noted, is testing whether these characteristics can be used as a marker for the progression of disease.

Nehal Mehta, MD, a cardiologist and professor of medicine at the George Washington University, Washington, DC, agreed that more longitudinal research is needed to understand how the abnormalities captured in these images can inform detection and diagnosis of various diseases.

“You don’t know whether these images look bad because of reverse causation — the disease is doing this — or true causation — that this is actually detecting the root cause of the disease,” he explained. “Until we have a bank of normal and abnormal scans, we don’t know what any of these things mean.”

Though still some time away from entering the clinic, Mehta likened the technology to the introduction of optical coherence tomography in the 1980s. Before being adapted for clinical use, researchers first needed to visualize differences between normal coronary vasculature and myocardial infarction.

“I think this is an amazingly strong first proof of concept,” Mehta said. “This technology is showing a true promise in the field imaging.”

The work was funded by grants from Cancer Research UK, the Engineering & Physical Sciences Research Council, Wellcome Trust, the European Research Council, and the National Institute for Health and Care Research University College London Hospitals Biomedical Research Centre. Beard and two coauthors are shareholders of DeepColor Imaging to which the intellectual property associated with the new scanner has been licensed, but the company was not involved in any of this research. Mallidi and Mehta had no relevant disclosures.

A version of this article first appeared on Medscape.com.

A first stroke in older adults is associated with substantial immediate and accelerated long-term cognitive decline, suggested a new study that underscores the need for continuous cognitive monitoring in this patient population.

Results from the study, which included 14 international cohorts of older adults, showed that stroke was associated with a significant acute decline in global cognition and a small, but significant, acceleration in the rate of cognitive decline over time.

Cognitive assessments in primary care are “crucial, especially since cognitive impairment is frequently missed or undiagnosed in hospitals,” lead author Jessica Lo, MSc, biostatistician and research associate with the Center for Healthy Brain Aging, University of New South Wales, Sydney, Australia, told this news organization.

She suggested clinicians incorporate long-term cognitive assessments into care plans, using more sensitive neuropsychological tests in primary care to detect early signs of cognitive impairment. “Early detection would enable timely interventions to improve outcomes,” Lo said.

She also noted that poststroke care typically includes physical rehabilitation but not cognitive rehabilitation, which many rehabilitation centers aren’t equipped to provide.

The study was published online in JAMA Network Open.
 

Mapping Cognitive Decline Trajectory

Cognitive impairment after stroke is common, but the trajectory of cognitive decline following a first stroke, relative to prestroke cognitive function, remains unclear.

The investigators leveraged data from 14 population-based cohort studies of 20,860 adults (mean age, 73 years; 59% women) to map the trajectory of cognitive function before and after a first stroke.

The primary outcome was global cognition, defined as the standardized average of four cognitive domains (language, memory, processing speed, and executive function).

During a mean follow-up of 7.5 years, 1041 (5%) adults (mean age, 79 years) experienced a first stroke, a mean of 4.5 years after study entry.

In adjusted analyses, stroke was associated with a significant acute decline of 0.25 SD in global cognition and a “small but significant” acceleration in the rate of decline of −0.038 SD per year, the authors reported.

Stroke was also associated with acute decline in all individual cognitive domains except for memory, with effect sizes ranging from −0.17 to −0.22 SD. Poststroke declines in Mini-Mental State Examination scores (−0.36 SD) were also noted.

In terms of cognitive trajectory, the rate of decline before stroke in survivors was similar to that seen in peers who didn’t have a stroke (−0.048 and −0.049 SD per year in global cognition, respectively).

The researchers did not identify any vascular risk factors moderating cognitive decline following a stroke, consistent with prior research. However, cognitive decline was significantly more rapid in individuals without stroke, regardless of any future stroke, who had a history of diabetes, hypertension, high cholesterol, cardiovascular disease, depression, smoking, or were APOE4 carriers.

“Targeting modifiable vascular risk factors at an early stage may reduce the risk of stroke but also subsequent risk of stroke-related cognitive decline and cognitive impairment,” the researchers noted.
 

A ‘Major Step’ in the Right Direction

As previously reported by this news organization, in 2023 the American Heart Association (AHA) issued a statement noting that screening for cognitive impairment should be part of multidisciplinary care for stroke survivors.

Commenting for this news organization, Mitchell Elkind, MD, MS, AHA chief clinical science officer, said these new data are consistent with current AHA guidelines and statements that “support screening for cognitive and functional decline in patients both acutely and over the long term after stroke.”

Elkind noted that the 2022 guideline for intracerebral hemorrhage states that cognitive screening should occur “across the continuum of inpatient care and at intervals in the outpatient setting” and provides recommendations for cognitive therapy.

“Our 2021 scientific statement on the primary care of patients after stroke also recommends screening for both depression and cognitive impairment over both the short- and long-term,” said Elkind, professor of neurology and epidemiology at Columbia University Irving Medical Center in New York City.

“These documents recognize the fact that function and cognition can continue to decline years after stroke and that patients’ rehabilitation and support needs may therefore change over time after stroke,” Elkind added.

The authors of an accompanying commentary called it a “major step” in the right direction for the future of long-term stroke outcome assessment.

“As we develop new devices, indications, and time windows for stroke treatment, it may perhaps be wise to ensure trials steer away from simpler outcomes to more complex, granular ones,” wrote Yasmin Sadigh, MSc, and Victor Volovici, MD, PhD, with Erasmus University Medical Center, Rotterdam, the Netherlands.

The study had no commercial funding. The authors and commentary writers and Elkind have declared no conflicts of interest.

A version of this article first appeared on Medscape.com.

A first stroke in older adults is associated with substantial immediate and accelerated long-term cognitive decline, suggested a new study that underscores the need for continuous cognitive monitoring in this patient population.

Results from the study, which included 14 international cohorts of older adults, showed that stroke was associated with a significant acute decline in global cognition and a small, but significant, acceleration in the rate of cognitive decline over time.

Cognitive assessments in primary care are “crucial, especially since cognitive impairment is frequently missed or undiagnosed in hospitals,” lead author Jessica Lo, MSc, biostatistician and research associate with the Center for Healthy Brain Aging, University of New South Wales, Sydney, Australia, told this news organization.

She suggested clinicians incorporate long-term cognitive assessments into care plans, using more sensitive neuropsychological tests in primary care to detect early signs of cognitive impairment. “Early detection would enable timely interventions to improve outcomes,” Lo said.

She also noted that poststroke care typically includes physical rehabilitation but not cognitive rehabilitation, which many rehabilitation centers aren’t equipped to provide.

The study was published online in JAMA Network Open.
 

Mapping Cognitive Decline Trajectory

Cognitive impairment after stroke is common, but the trajectory of cognitive decline following a first stroke, relative to prestroke cognitive function, remains unclear.

The investigators leveraged data from 14 population-based cohort studies of 20,860 adults (mean age, 73 years; 59% women) to map the trajectory of cognitive function before and after a first stroke.

The primary outcome was global cognition, defined as the standardized average of four cognitive domains (language, memory, processing speed, and executive function).

During a mean follow-up of 7.5 years, 1041 (5%) adults (mean age, 79 years) experienced a first stroke, a mean of 4.5 years after study entry.

In adjusted analyses, stroke was associated with a significant acute decline of 0.25 SD in global cognition and a “small but significant” acceleration in the rate of decline of −0.038 SD per year, the authors reported.

Stroke was also associated with acute decline in all individual cognitive domains except for memory, with effect sizes ranging from −0.17 to −0.22 SD. Poststroke declines in Mini-Mental State Examination scores (−0.36 SD) were also noted.

In terms of cognitive trajectory, the rate of decline before stroke in survivors was similar to that seen in peers who didn’t have a stroke (−0.048 and −0.049 SD per year in global cognition, respectively).

The researchers did not identify any vascular risk factors moderating cognitive decline following a stroke, consistent with prior research. However, cognitive decline was significantly more rapid in individuals without stroke, regardless of any future stroke, who had a history of diabetes, hypertension, high cholesterol, cardiovascular disease, depression, smoking, or were APOE4 carriers.

“Targeting modifiable vascular risk factors at an early stage may reduce the risk of stroke but also subsequent risk of stroke-related cognitive decline and cognitive impairment,” the researchers noted.
 

A ‘Major Step’ in the Right Direction

As previously reported by this news organization, in 2023 the American Heart Association (AHA) issued a statement noting that screening for cognitive impairment should be part of multidisciplinary care for stroke survivors.

Commenting for this news organization, Mitchell Elkind, MD, MS, AHA chief clinical science officer, said these new data are consistent with current AHA guidelines and statements that “support screening for cognitive and functional decline in patients both acutely and over the long term after stroke.”

Elkind noted that the 2022 guideline for intracerebral hemorrhage states that cognitive screening should occur “across the continuum of inpatient care and at intervals in the outpatient setting” and provides recommendations for cognitive therapy.

“Our 2021 scientific statement on the primary care of patients after stroke also recommends screening for both depression and cognitive impairment over both the short- and long-term,” said Elkind, professor of neurology and epidemiology at Columbia University Irving Medical Center in New York City.

“These documents recognize the fact that function and cognition can continue to decline years after stroke and that patients’ rehabilitation and support needs may therefore change over time after stroke,” Elkind added.

The authors of an accompanying commentary called it a “major step” in the right direction for the future of long-term stroke outcome assessment.

“As we develop new devices, indications, and time windows for stroke treatment, it may perhaps be wise to ensure trials steer away from simpler outcomes to more complex, granular ones,” wrote Yasmin Sadigh, MSc, and Victor Volovici, MD, PhD, with Erasmus University Medical Center, Rotterdam, the Netherlands.

The study had no commercial funding. The authors and commentary writers and Elkind have declared no conflicts of interest.

A version of this article first appeared on Medscape.com.

A first stroke in older adults is associated with substantial immediate and accelerated long-term cognitive decline, suggested a new study that underscores the need for continuous cognitive monitoring in this patient population.

Results from the study, which included 14 international cohorts of older adults, showed that stroke was associated with a significant acute decline in global cognition and a small, but significant, acceleration in the rate of cognitive decline over time.

Cognitive assessments in primary care are “crucial, especially since cognitive impairment is frequently missed or undiagnosed in hospitals,” lead author Jessica Lo, MSc, biostatistician and research associate with the Center for Healthy Brain Aging, University of New South Wales, Sydney, Australia, told this news organization.

She suggested clinicians incorporate long-term cognitive assessments into care plans, using more sensitive neuropsychological tests in primary care to detect early signs of cognitive impairment. “Early detection would enable timely interventions to improve outcomes,” Lo said.

She also noted that poststroke care typically includes physical rehabilitation but not cognitive rehabilitation, which many rehabilitation centers aren’t equipped to provide.

The study was published online in JAMA Network Open.
 

Mapping Cognitive Decline Trajectory

Cognitive impairment after stroke is common, but the trajectory of cognitive decline following a first stroke, relative to prestroke cognitive function, remains unclear.

The investigators leveraged data from 14 population-based cohort studies of 20,860 adults (mean age, 73 years; 59% women) to map the trajectory of cognitive function before and after a first stroke.

The primary outcome was global cognition, defined as the standardized average of four cognitive domains (language, memory, processing speed, and executive function).

During a mean follow-up of 7.5 years, 1041 (5%) adults (mean age, 79 years) experienced a first stroke, a mean of 4.5 years after study entry.

In adjusted analyses, stroke was associated with a significant acute decline of 0.25 SD in global cognition and a “small but significant” acceleration in the rate of decline of −0.038 SD per year, the authors reported.

Stroke was also associated with acute decline in all individual cognitive domains except for memory, with effect sizes ranging from −0.17 to −0.22 SD. Poststroke declines in Mini-Mental State Examination scores (−0.36 SD) were also noted.

In terms of cognitive trajectory, the rate of decline before stroke in survivors was similar to that seen in peers who didn’t have a stroke (−0.048 and −0.049 SD per year in global cognition, respectively).

The researchers did not identify any vascular risk factors moderating cognitive decline following a stroke, consistent with prior research. However, cognitive decline was significantly more rapid in individuals without stroke, regardless of any future stroke, who had a history of diabetes, hypertension, high cholesterol, cardiovascular disease, depression, smoking, or were APOE4 carriers.

“Targeting modifiable vascular risk factors at an early stage may reduce the risk of stroke but also subsequent risk of stroke-related cognitive decline and cognitive impairment,” the researchers noted.
 

A ‘Major Step’ in the Right Direction

As previously reported by this news organization, in 2023 the American Heart Association (AHA) issued a statement noting that screening for cognitive impairment should be part of multidisciplinary care for stroke survivors.

Commenting for this news organization, Mitchell Elkind, MD, MS, AHA chief clinical science officer, said these new data are consistent with current AHA guidelines and statements that “support screening for cognitive and functional decline in patients both acutely and over the long term after stroke.”

Elkind noted that the 2022 guideline for intracerebral hemorrhage states that cognitive screening should occur “across the continuum of inpatient care and at intervals in the outpatient setting” and provides recommendations for cognitive therapy.

“Our 2021 scientific statement on the primary care of patients after stroke also recommends screening for both depression and cognitive impairment over both the short- and long-term,” said Elkind, professor of neurology and epidemiology at Columbia University Irving Medical Center in New York City.

“These documents recognize the fact that function and cognition can continue to decline years after stroke and that patients’ rehabilitation and support needs may therefore change over time after stroke,” Elkind added.

The authors of an accompanying commentary called it a “major step” in the right direction for the future of long-term stroke outcome assessment.

“As we develop new devices, indications, and time windows for stroke treatment, it may perhaps be wise to ensure trials steer away from simpler outcomes to more complex, granular ones,” wrote Yasmin Sadigh, MSc, and Victor Volovici, MD, PhD, with Erasmus University Medical Center, Rotterdam, the Netherlands.

The study had no commercial funding. The authors and commentary writers and Elkind have declared no conflicts of interest.

A version of this article first appeared on Medscape.com.

TOPLINE:

Maternal serum folate levels during early to midpregnancy show a U-shaped association with congenital heart disease (CHD) risk in offspring. Both low and high folate levels are linked to an increased risk, with vitamin B12 deficiency and elevated homocysteine levels further exacerbating this risk.

METHODOLOGY:

• Researchers conducted a case-control study with 129 participants with CHD and 516 matched control participants from Guangdong Provincial People’s Hospital in China between 2015 and 2018.
• Maternal serum levels of folate, vitamin B12, and homocysteine were measured at around 16 weeks of gestation using a chemiluminescence microparticle immunoassay.
• CHD was confirmed using echocardiography, and the participants were matched by maternal age at a ratio of 1:4.
• Covariates included periconceptional folic acid supplementation, maternal education, occupation, parity, abortion history, pregnancy complications, and genetic polymorphisms related to folate metabolism.
• Conditional logistic regression was used to assess the associations, with adjustments for various covariates and sensitivity analyses excluding participants with missing genetic data.

TAKEAWAY:

• A U-shaped association was found between maternal serum folate levels and CHD risk in offspring, with both low and high levels linked to increased risk (P < .001).
• Low maternal folate levels were associated with an adjusted odds ratio (aOR) of 3.09 (95% CI, 1.88-5.08) for CHD risk, whereas high levels had an aOR of 1.81 (95% CI, 1.07-3.06).
• Using World Health Organization criteria, folate deficiency (< 5.9 ng/mL) had an aOR of 18.97 (95% CI, 3.87-93.11) and elevated levels (> 20 ng/mL) had an aOR of 5.71 (95% CI, 2.72-11.98) for CHD risk.
• Vitamin B12 deficiency and elevated homocysteine levels further increased the risk associated with both low and high maternal folate levels.

IN PRACTICE:

“Insufficient folate and vitamin B12 can lead to increased homocysteine levels, which is harmful to the cardiovascular system. Thus, homocysteine might act as a central mediator in the relationships between deficiencies in folate and vitamin B12 and the risk of CHD. Additionally, the role of folate extends beyond homocysteine mediation, contributing independently to placental implantation and vascular remodeling, irrespective of vitamin B12 and homocysteine levels,” the authors wrote.

SOURCE:

The study was led by Yanji Qu, PhD, and Jie Li, PhD, Global Health Research Center, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China. It was published online in JAMA Network Open.

LIMITATIONS:

The study’s limitations included the measurement of maternal serum folate levels at a single time point, which may not reflect preconception and early postconception periods. The study’s findings may not be generalizable to other populations as participants were recruited from a single cardiac referral center in Southern China. Additionally, the lack of dietary intake data limited the ability to account for related biases. The sample size, while relatively large for CHD research, may lack sufficient power for stratified analyses.

DISCLOSURES:

One coauthor reported receiving personal fees from Guangdong Cardiovascular Institute outside the submitted work. Additional disclosures are noted 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:

Maternal serum folate levels during early to midpregnancy show a U-shaped association with congenital heart disease (CHD) risk in offspring. Both low and high folate levels are linked to an increased risk, with vitamin B12 deficiency and elevated homocysteine levels further exacerbating this risk.

METHODOLOGY:

• Researchers conducted a case-control study with 129 participants with CHD and 516 matched control participants from Guangdong Provincial People’s Hospital in China between 2015 and 2018.
• Maternal serum levels of folate, vitamin B12, and homocysteine were measured at around 16 weeks of gestation using a chemiluminescence microparticle immunoassay.
• CHD was confirmed using echocardiography, and the participants were matched by maternal age at a ratio of 1:4.
• Covariates included periconceptional folic acid supplementation, maternal education, occupation, parity, abortion history, pregnancy complications, and genetic polymorphisms related to folate metabolism.
• Conditional logistic regression was used to assess the associations, with adjustments for various covariates and sensitivity analyses excluding participants with missing genetic data.

TAKEAWAY:

• A U-shaped association was found between maternal serum folate levels and CHD risk in offspring, with both low and high levels linked to increased risk (P < .001).
• Low maternal folate levels were associated with an adjusted odds ratio (aOR) of 3.09 (95% CI, 1.88-5.08) for CHD risk, whereas high levels had an aOR of 1.81 (95% CI, 1.07-3.06).
• Using World Health Organization criteria, folate deficiency (< 5.9 ng/mL) had an aOR of 18.97 (95% CI, 3.87-93.11) and elevated levels (> 20 ng/mL) had an aOR of 5.71 (95% CI, 2.72-11.98) for CHD risk.
• Vitamin B12 deficiency and elevated homocysteine levels further increased the risk associated with both low and high maternal folate levels.

IN PRACTICE:

“Insufficient folate and vitamin B12 can lead to increased homocysteine levels, which is harmful to the cardiovascular system. Thus, homocysteine might act as a central mediator in the relationships between deficiencies in folate and vitamin B12 and the risk of CHD. Additionally, the role of folate extends beyond homocysteine mediation, contributing independently to placental implantation and vascular remodeling, irrespective of vitamin B12 and homocysteine levels,” the authors wrote.

SOURCE:

The study was led by Yanji Qu, PhD, and Jie Li, PhD, Global Health Research Center, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China. It was published online in JAMA Network Open.

LIMITATIONS:

The study’s limitations included the measurement of maternal serum folate levels at a single time point, which may not reflect preconception and early postconception periods. The study’s findings may not be generalizable to other populations as participants were recruited from a single cardiac referral center in Southern China. Additionally, the lack of dietary intake data limited the ability to account for related biases. The sample size, while relatively large for CHD research, may lack sufficient power for stratified analyses.

DISCLOSURES:

One coauthor reported receiving personal fees from Guangdong Cardiovascular Institute outside the submitted work. Additional disclosures are noted 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:

Maternal serum folate levels during early to midpregnancy show a U-shaped association with congenital heart disease (CHD) risk in offspring. Both low and high folate levels are linked to an increased risk, with vitamin B12 deficiency and elevated homocysteine levels further exacerbating this risk.

METHODOLOGY:

• Researchers conducted a case-control study with 129 participants with CHD and 516 matched control participants from Guangdong Provincial People’s Hospital in China between 2015 and 2018.
• Maternal serum levels of folate, vitamin B12, and homocysteine were measured at around 16 weeks of gestation using a chemiluminescence microparticle immunoassay.
• CHD was confirmed using echocardiography, and the participants were matched by maternal age at a ratio of 1:4.
• Covariates included periconceptional folic acid supplementation, maternal education, occupation, parity, abortion history, pregnancy complications, and genetic polymorphisms related to folate metabolism.
• Conditional logistic regression was used to assess the associations, with adjustments for various covariates and sensitivity analyses excluding participants with missing genetic data.

TAKEAWAY:

• A U-shaped association was found between maternal serum folate levels and CHD risk in offspring, with both low and high levels linked to increased risk (P < .001).
• Low maternal folate levels were associated with an adjusted odds ratio (aOR) of 3.09 (95% CI, 1.88-5.08) for CHD risk, whereas high levels had an aOR of 1.81 (95% CI, 1.07-3.06).
• Using World Health Organization criteria, folate deficiency (< 5.9 ng/mL) had an aOR of 18.97 (95% CI, 3.87-93.11) and elevated levels (> 20 ng/mL) had an aOR of 5.71 (95% CI, 2.72-11.98) for CHD risk.
• Vitamin B12 deficiency and elevated homocysteine levels further increased the risk associated with both low and high maternal folate levels.

IN PRACTICE:

“Insufficient folate and vitamin B12 can lead to increased homocysteine levels, which is harmful to the cardiovascular system. Thus, homocysteine might act as a central mediator in the relationships between deficiencies in folate and vitamin B12 and the risk of CHD. Additionally, the role of folate extends beyond homocysteine mediation, contributing independently to placental implantation and vascular remodeling, irrespective of vitamin B12 and homocysteine levels,” the authors wrote.

SOURCE:

The study was led by Yanji Qu, PhD, and Jie Li, PhD, Global Health Research Center, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China. It was published online in JAMA Network Open.

LIMITATIONS:

The study’s limitations included the measurement of maternal serum folate levels at a single time point, which may not reflect preconception and early postconception periods. The study’s findings may not be generalizable to other populations as participants were recruited from a single cardiac referral center in Southern China. Additionally, the lack of dietary intake data limited the ability to account for related biases. The sample size, while relatively large for CHD research, may lack sufficient power for stratified analyses.

DISCLOSURES:

One coauthor reported receiving personal fees from Guangdong Cardiovascular Institute outside the submitted work. Additional disclosures are noted 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.

While Kellie Lease Stecher, MD, was working as an ob.gyn. in Minneapolis, Minnesota, a patient confided in her a sexual assault allegation about one of Stecher’s male colleagues. Stecher shared the allegation with her supervisor, who told Stecher not to file a report and chose not to address the issue with the patient. Stecher weighed how to do the right thing: Should she speak up? What were the ethical and legal implications of speaking up vs staying silent?

After seeking advice from her mentors, Stecher felt it was her moral and legal duty to report the allegation to the Minnesota Medical Board. Once she did, her supervisor chastised her repeatedly for reporting the allegation. Stecher soon found herself in a hostile work environment where she was regularly singled out and silenced by her supervisor and colleagues.

“I got to a point where I felt like I couldn’t say anything at any meetings without somehow being targeted after the meeting. There was an individual who was even allowed to fat-shame me with no consequences,” Stecher said. “[Being bullied at work is] a struggle because you have no voice, you have no opportunities, and there’s someone who is intentionally making your life uncomfortable.”

Stecher’s experience is not unusual. Mistreatment is a common issue among healthcare workers, ranging from rudeness to bullying and harassment and permeating every level and specialty of the medical profession. A 2019 research review estimated that 26.3% of healthcare workers had experienced bullying and found bullying in healthcare to be associated with mental health problems such as burnout and depression, physical health problems such as insomnia and headaches, and physicians taking more sick leave.

The Medscape Physician Workplace Culture Report 2024 found similarly bleak results:

• 38% said workplace culture is declining.
• 70% don’t see a big commitment from employers for positive culture.
• 48% said staff isn’t committed to positive culture.

Toxicity’s ripple effects contribute to several issues in healthcare, including staffing shortages, physician attrition, inadequate leadership, and even suicide rates.

The irony, of course, is that most physicians enter the field to care for people. As individuals go from medical school to residency and on with the rest of their careers, they often experience a rude awakening.
 

It’s Everywhere

Noticing the prevalence of workplace bullying in the medical field, endocrinologist Farah Khan, MD, at UW Medicine in Seattle, Washington, decided to conduct a survey on the issue.

Khan collected 122 responses from colleagues, friends, and acquaintances in the field. When asked if they had ever been bullied in medicine, 68% of respondents said yes. But here’s the fascinating part: She tried to pinpoint one particular area or source of toxicity in the progression of a physician’s career — and couldn’t because it existed at all levels.

More than one third of respondents said their worst bullying experiences occurred in residency, while 30% said mistreatment was worst in medical school, and 24% indicated their worst experience had occurred once they became an attending.

The litany of experiences included being belittled, excluded, yelled at, criticized, shamed, unfairly blamed, threatened, sexually harassed, subjected to bigotry and slurs, and humiliated.

“What surprised me the most was how widespread this problem is and the many different layers of healthcare it permeates through, from operating room staff to medical students to hospital HR to residents and attendings,” Khan said of her findings.
 

Who Cares for the Caregivers?

When hematologist Mikkael Sekeres, MD, was in medical school, he seriously considered a career as a surgeon. Following success in his surgical rotations, he scrubbed in with a cardiothoracic surgeon who was well known for both his status as a surgeon and his fiery temper. Sekeres witnessed the surgeon yelling at whoever was nearby: Medical students, fellows, residents, operating room nurses.

“At the end of that experience, any passing thoughts I had of going into cardiothoracic surgery were gone,” Sekeres said. “Some of the people I met in surgery were truly wonderful. Some were unhappy people.”

He has clear ideas why. Mental health struggles that are all too common among physicians can be caused or exacerbated by mistreatment and can also lead a physician to mistreat others.

“People bully when they themselves are hurting,” Sekeres said. “It begs the question, why are people hurting? What’s driving them to be bullies? I think part of the reason is that they’re working really hard and they’re tired, and nobody’s caring for them. It’s hard to care for others when you feel as if you’re hurting more than they are.”

Gail Gazelle, MD, experienced something like this. In her case, the pressure to please and to be a perfect professional and mother affected how she interacted with those around her. While working as a hospice medical director and an academician and clinician at Harvard Medical School, Boston, Massachusetts, she found herself feeling exhausted and burnt out but simultaneously guilty for not doing enough at work or at home.

Guess what happened? She became irritable, lashing out at her son and not putting her best foot forward with coworkers or patients.

After trying traditional therapy and self-help through books and podcasts, Gazelle found her solution in life coaching. “I realized just how harsh I was being on myself and found ways to reverse that pattern,” she said. “I learned ways of regulating myself emotionally that I definitely didn’t learn in my training.”

Today, Gazelle works as a life coach herself, guiding physicians through common challenges of the profession — particularly bullying, which she sees often. She remembers one client, an oncologist, who was being targeted by a nurse practitioner she was training. The nurse practitioner began talking back to the oncologist, as well as gossiping and bad-mouthing her to the nurses in the practice. The nurses then began excluding the oncologist from their cafeteria table at lunchtime, which felt blatant in such a small practice.

A core component of Gazelle’s coaching strategy was helping the client reclaim her self-esteem by focusing on her strengths. She instructed the client to write down what went well that day each night rather than lying in bed ruminating. Such self-care strategies can not only help bullied physicians but also prevent some of the challenges that might cause a physician to bully or lash out at another in the first place.

Such strategies, along with the recent influx of wellness programs available in healthcare facilities, can help physicians cope with the mental health impacts of bullying and the job in general. But even life coaches like Gazelle acknowledge that they are often band-aids on the system’s deeper wounds. Bullying in healthcare is not an individual issue; at its core, it’s an institutional one.
 

Negative Hierarchies in Healthcare

When Stecher’s contract expired, she was fired by the supervisor who had been bullying her. Stecher has since filed a lawsuit, claiming sexual discrimination, defamation, and wrongful termination.

The medical field has a long history of hierarchy, and while this rigidity has softened over time, negative hierarchical dynamics are often perpetuated by leaders. Phenomena like cronyism and cliques and behaviors like petty gossip, lunchroom exclusion (which in the worst cases can mimic high school dynamics), and targeting can be at play in the healthcare workplace.

The classic examples, Stecher said, can usually be spotted: “If you threaten the status quo or offer different ideas, you are seen as a threat. Cronyism ... strict hierarchies ... people who elevate individuals in their social arena into leadership positions. Physicians don’t get the leadership training that they really need; they are often just dumped into roles with no previous experience because they’re someone’s golfing buddy.”

The question is how to get workplace culture momentum moving in a positive direction. When Gazelle’s clients are hesitant to voice concerns, she emphasizes doing so can and should benefit leadership, as well as patients and the wider healthcare system.

“The win-win is that you have a healthy culture of respect and dignity and civility rather than the opposite,” she said. “The leader will actually have more staff retention, which everybody’s concerned about, given the shortage of healthcare workers.”

And that’s a key incentive that may not be discussed as much: Talent drain from toxicity. The Medscape Workplace Culture Report asked about culture as it applies to physicians looking to join up. Notably, 93% of doctors say culture is important when mulling a job offer, 70% said culture is equal to money, and 18% ranked it as more important than money, and 46% say a positive atmosphere is the top priority.

Ultimately, it comes down to who is willing to step in and stand up. Respondents to Khan’s survey counted anonymous reporting systems, more supportive administration teams, and zero-tolerance policies as potential remedies. Gazelle, Sekeres, and Stecher all emphasize the need for zero-tolerance policies for bullying and mistreatment.

“We can’t afford to have things going on like this that just destroy the fabric of the healthcare endeavor,” Gazelle said. “They come out sideways eventually. They come out in terms of poor patient care because there are greater errors. There’s a lack of respect for patients. There’s anger and irritability and so much spillover. We have to have zero-tolerance policies from the top down.”

A version of this article appeared on Medscape.com.

While Kellie Lease Stecher, MD, was working as an ob.gyn. in Minneapolis, Minnesota, a patient confided in her a sexual assault allegation about one of Stecher’s male colleagues. Stecher shared the allegation with her supervisor, who told Stecher not to file a report and chose not to address the issue with the patient. Stecher weighed how to do the right thing: Should she speak up? What were the ethical and legal implications of speaking up vs staying silent?

After seeking advice from her mentors, Stecher felt it was her moral and legal duty to report the allegation to the Minnesota Medical Board. Once she did, her supervisor chastised her repeatedly for reporting the allegation. Stecher soon found herself in a hostile work environment where she was regularly singled out and silenced by her supervisor and colleagues.

“I got to a point where I felt like I couldn’t say anything at any meetings without somehow being targeted after the meeting. There was an individual who was even allowed to fat-shame me with no consequences,” Stecher said. “[Being bullied at work is] a struggle because you have no voice, you have no opportunities, and there’s someone who is intentionally making your life uncomfortable.”

Stecher’s experience is not unusual. Mistreatment is a common issue among healthcare workers, ranging from rudeness to bullying and harassment and permeating every level and specialty of the medical profession. A 2019 research review estimated that 26.3% of healthcare workers had experienced bullying and found bullying in healthcare to be associated with mental health problems such as burnout and depression, physical health problems such as insomnia and headaches, and physicians taking more sick leave.

The Medscape Physician Workplace Culture Report 2024 found similarly bleak results:

• 38% said workplace culture is declining.
• 70% don’t see a big commitment from employers for positive culture.
• 48% said staff isn’t committed to positive culture.

Toxicity’s ripple effects contribute to several issues in healthcare, including staffing shortages, physician attrition, inadequate leadership, and even suicide rates.

The irony, of course, is that most physicians enter the field to care for people. As individuals go from medical school to residency and on with the rest of their careers, they often experience a rude awakening.
 

It’s Everywhere

Noticing the prevalence of workplace bullying in the medical field, endocrinologist Farah Khan, MD, at UW Medicine in Seattle, Washington, decided to conduct a survey on the issue.

Khan collected 122 responses from colleagues, friends, and acquaintances in the field. When asked if they had ever been bullied in medicine, 68% of respondents said yes. But here’s the fascinating part: She tried to pinpoint one particular area or source of toxicity in the progression of a physician’s career — and couldn’t because it existed at all levels.

More than one third of respondents said their worst bullying experiences occurred in residency, while 30% said mistreatment was worst in medical school, and 24% indicated their worst experience had occurred once they became an attending.

The litany of experiences included being belittled, excluded, yelled at, criticized, shamed, unfairly blamed, threatened, sexually harassed, subjected to bigotry and slurs, and humiliated.

“What surprised me the most was how widespread this problem is and the many different layers of healthcare it permeates through, from operating room staff to medical students to hospital HR to residents and attendings,” Khan said of her findings.
 

Who Cares for the Caregivers?

When hematologist Mikkael Sekeres, MD, was in medical school, he seriously considered a career as a surgeon. Following success in his surgical rotations, he scrubbed in with a cardiothoracic surgeon who was well known for both his status as a surgeon and his fiery temper. Sekeres witnessed the surgeon yelling at whoever was nearby: Medical students, fellows, residents, operating room nurses.

“At the end of that experience, any passing thoughts I had of going into cardiothoracic surgery were gone,” Sekeres said. “Some of the people I met in surgery were truly wonderful. Some were unhappy people.”

He has clear ideas why. Mental health struggles that are all too common among physicians can be caused or exacerbated by mistreatment and can also lead a physician to mistreat others.

“People bully when they themselves are hurting,” Sekeres said. “It begs the question, why are people hurting? What’s driving them to be bullies? I think part of the reason is that they’re working really hard and they’re tired, and nobody’s caring for them. It’s hard to care for others when you feel as if you’re hurting more than they are.”

Gail Gazelle, MD, experienced something like this. In her case, the pressure to please and to be a perfect professional and mother affected how she interacted with those around her. While working as a hospice medical director and an academician and clinician at Harvard Medical School, Boston, Massachusetts, she found herself feeling exhausted and burnt out but simultaneously guilty for not doing enough at work or at home.

Guess what happened? She became irritable, lashing out at her son and not putting her best foot forward with coworkers or patients.

After trying traditional therapy and self-help through books and podcasts, Gazelle found her solution in life coaching. “I realized just how harsh I was being on myself and found ways to reverse that pattern,” she said. “I learned ways of regulating myself emotionally that I definitely didn’t learn in my training.”

Today, Gazelle works as a life coach herself, guiding physicians through common challenges of the profession — particularly bullying, which she sees often. She remembers one client, an oncologist, who was being targeted by a nurse practitioner she was training. The nurse practitioner began talking back to the oncologist, as well as gossiping and bad-mouthing her to the nurses in the practice. The nurses then began excluding the oncologist from their cafeteria table at lunchtime, which felt blatant in such a small practice.

A core component of Gazelle’s coaching strategy was helping the client reclaim her self-esteem by focusing on her strengths. She instructed the client to write down what went well that day each night rather than lying in bed ruminating. Such self-care strategies can not only help bullied physicians but also prevent some of the challenges that might cause a physician to bully or lash out at another in the first place.

Such strategies, along with the recent influx of wellness programs available in healthcare facilities, can help physicians cope with the mental health impacts of bullying and the job in general. But even life coaches like Gazelle acknowledge that they are often band-aids on the system’s deeper wounds. Bullying in healthcare is not an individual issue; at its core, it’s an institutional one.
 

Negative Hierarchies in Healthcare

When Stecher’s contract expired, she was fired by the supervisor who had been bullying her. Stecher has since filed a lawsuit, claiming sexual discrimination, defamation, and wrongful termination.

The medical field has a long history of hierarchy, and while this rigidity has softened over time, negative hierarchical dynamics are often perpetuated by leaders. Phenomena like cronyism and cliques and behaviors like petty gossip, lunchroom exclusion (which in the worst cases can mimic high school dynamics), and targeting can be at play in the healthcare workplace.

The classic examples, Stecher said, can usually be spotted: “If you threaten the status quo or offer different ideas, you are seen as a threat. Cronyism ... strict hierarchies ... people who elevate individuals in their social arena into leadership positions. Physicians don’t get the leadership training that they really need; they are often just dumped into roles with no previous experience because they’re someone’s golfing buddy.”

The question is how to get workplace culture momentum moving in a positive direction. When Gazelle’s clients are hesitant to voice concerns, she emphasizes doing so can and should benefit leadership, as well as patients and the wider healthcare system.

“The win-win is that you have a healthy culture of respect and dignity and civility rather than the opposite,” she said. “The leader will actually have more staff retention, which everybody’s concerned about, given the shortage of healthcare workers.”

And that’s a key incentive that may not be discussed as much: Talent drain from toxicity. The Medscape Workplace Culture Report asked about culture as it applies to physicians looking to join up. Notably, 93% of doctors say culture is important when mulling a job offer, 70% said culture is equal to money, and 18% ranked it as more important than money, and 46% say a positive atmosphere is the top priority.

Ultimately, it comes down to who is willing to step in and stand up. Respondents to Khan’s survey counted anonymous reporting systems, more supportive administration teams, and zero-tolerance policies as potential remedies. Gazelle, Sekeres, and Stecher all emphasize the need for zero-tolerance policies for bullying and mistreatment.

“We can’t afford to have things going on like this that just destroy the fabric of the healthcare endeavor,” Gazelle said. “They come out sideways eventually. They come out in terms of poor patient care because there are greater errors. There’s a lack of respect for patients. There’s anger and irritability and so much spillover. We have to have zero-tolerance policies from the top down.”

A version of this article appeared on Medscape.com.

While Kellie Lease Stecher, MD, was working as an ob.gyn. in Minneapolis, Minnesota, a patient confided in her a sexual assault allegation about one of Stecher’s male colleagues. Stecher shared the allegation with her supervisor, who told Stecher not to file a report and chose not to address the issue with the patient. Stecher weighed how to do the right thing: Should she speak up? What were the ethical and legal implications of speaking up vs staying silent?

After seeking advice from her mentors, Stecher felt it was her moral and legal duty to report the allegation to the Minnesota Medical Board. Once she did, her supervisor chastised her repeatedly for reporting the allegation. Stecher soon found herself in a hostile work environment where she was regularly singled out and silenced by her supervisor and colleagues.

“I got to a point where I felt like I couldn’t say anything at any meetings without somehow being targeted after the meeting. There was an individual who was even allowed to fat-shame me with no consequences,” Stecher said. “[Being bullied at work is] a struggle because you have no voice, you have no opportunities, and there’s someone who is intentionally making your life uncomfortable.”

Stecher’s experience is not unusual. Mistreatment is a common issue among healthcare workers, ranging from rudeness to bullying and harassment and permeating every level and specialty of the medical profession. A 2019 research review estimated that 26.3% of healthcare workers had experienced bullying and found bullying in healthcare to be associated with mental health problems such as burnout and depression, physical health problems such as insomnia and headaches, and physicians taking more sick leave.

The Medscape Physician Workplace Culture Report 2024 found similarly bleak results:

• 38% said workplace culture is declining.
• 70% don’t see a big commitment from employers for positive culture.
• 48% said staff isn’t committed to positive culture.

Toxicity’s ripple effects contribute to several issues in healthcare, including staffing shortages, physician attrition, inadequate leadership, and even suicide rates.

The irony, of course, is that most physicians enter the field to care for people. As individuals go from medical school to residency and on with the rest of their careers, they often experience a rude awakening.
 

It’s Everywhere

Noticing the prevalence of workplace bullying in the medical field, endocrinologist Farah Khan, MD, at UW Medicine in Seattle, Washington, decided to conduct a survey on the issue.

Khan collected 122 responses from colleagues, friends, and acquaintances in the field. When asked if they had ever been bullied in medicine, 68% of respondents said yes. But here’s the fascinating part: She tried to pinpoint one particular area or source of toxicity in the progression of a physician’s career — and couldn’t because it existed at all levels.

More than one third of respondents said their worst bullying experiences occurred in residency, while 30% said mistreatment was worst in medical school, and 24% indicated their worst experience had occurred once they became an attending.

The litany of experiences included being belittled, excluded, yelled at, criticized, shamed, unfairly blamed, threatened, sexually harassed, subjected to bigotry and slurs, and humiliated.

“What surprised me the most was how widespread this problem is and the many different layers of healthcare it permeates through, from operating room staff to medical students to hospital HR to residents and attendings,” Khan said of her findings.
 

Who Cares for the Caregivers?

When hematologist Mikkael Sekeres, MD, was in medical school, he seriously considered a career as a surgeon. Following success in his surgical rotations, he scrubbed in with a cardiothoracic surgeon who was well known for both his status as a surgeon and his fiery temper. Sekeres witnessed the surgeon yelling at whoever was nearby: Medical students, fellows, residents, operating room nurses.

“At the end of that experience, any passing thoughts I had of going into cardiothoracic surgery were gone,” Sekeres said. “Some of the people I met in surgery were truly wonderful. Some were unhappy people.”

He has clear ideas why. Mental health struggles that are all too common among physicians can be caused or exacerbated by mistreatment and can also lead a physician to mistreat others.

“People bully when they themselves are hurting,” Sekeres said. “It begs the question, why are people hurting? What’s driving them to be bullies? I think part of the reason is that they’re working really hard and they’re tired, and nobody’s caring for them. It’s hard to care for others when you feel as if you’re hurting more than they are.”

Gail Gazelle, MD, experienced something like this. In her case, the pressure to please and to be a perfect professional and mother affected how she interacted with those around her. While working as a hospice medical director and an academician and clinician at Harvard Medical School, Boston, Massachusetts, she found herself feeling exhausted and burnt out but simultaneously guilty for not doing enough at work or at home.

Guess what happened? She became irritable, lashing out at her son and not putting her best foot forward with coworkers or patients.

After trying traditional therapy and self-help through books and podcasts, Gazelle found her solution in life coaching. “I realized just how harsh I was being on myself and found ways to reverse that pattern,” she said. “I learned ways of regulating myself emotionally that I definitely didn’t learn in my training.”

Today, Gazelle works as a life coach herself, guiding physicians through common challenges of the profession — particularly bullying, which she sees often. She remembers one client, an oncologist, who was being targeted by a nurse practitioner she was training. The nurse practitioner began talking back to the oncologist, as well as gossiping and bad-mouthing her to the nurses in the practice. The nurses then began excluding the oncologist from their cafeteria table at lunchtime, which felt blatant in such a small practice.

A core component of Gazelle’s coaching strategy was helping the client reclaim her self-esteem by focusing on her strengths. She instructed the client to write down what went well that day each night rather than lying in bed ruminating. Such self-care strategies can not only help bullied physicians but also prevent some of the challenges that might cause a physician to bully or lash out at another in the first place.

Such strategies, along with the recent influx of wellness programs available in healthcare facilities, can help physicians cope with the mental health impacts of bullying and the job in general. But even life coaches like Gazelle acknowledge that they are often band-aids on the system’s deeper wounds. Bullying in healthcare is not an individual issue; at its core, it’s an institutional one.
 

Negative Hierarchies in Healthcare

When Stecher’s contract expired, she was fired by the supervisor who had been bullying her. Stecher has since filed a lawsuit, claiming sexual discrimination, defamation, and wrongful termination.

The medical field has a long history of hierarchy, and while this rigidity has softened over time, negative hierarchical dynamics are often perpetuated by leaders. Phenomena like cronyism and cliques and behaviors like petty gossip, lunchroom exclusion (which in the worst cases can mimic high school dynamics), and targeting can be at play in the healthcare workplace.

The classic examples, Stecher said, can usually be spotted: “If you threaten the status quo or offer different ideas, you are seen as a threat. Cronyism ... strict hierarchies ... people who elevate individuals in their social arena into leadership positions. Physicians don’t get the leadership training that they really need; they are often just dumped into roles with no previous experience because they’re someone’s golfing buddy.”

The question is how to get workplace culture momentum moving in a positive direction. When Gazelle’s clients are hesitant to voice concerns, she emphasizes doing so can and should benefit leadership, as well as patients and the wider healthcare system.

“The win-win is that you have a healthy culture of respect and dignity and civility rather than the opposite,” she said. “The leader will actually have more staff retention, which everybody’s concerned about, given the shortage of healthcare workers.”

And that’s a key incentive that may not be discussed as much: Talent drain from toxicity. The Medscape Workplace Culture Report asked about culture as it applies to physicians looking to join up. Notably, 93% of doctors say culture is important when mulling a job offer, 70% said culture is equal to money, and 18% ranked it as more important than money, and 46% say a positive atmosphere is the top priority.

Ultimately, it comes down to who is willing to step in and stand up. Respondents to Khan’s survey counted anonymous reporting systems, more supportive administration teams, and zero-tolerance policies as potential remedies. Gazelle, Sekeres, and Stecher all emphasize the need for zero-tolerance policies for bullying and mistreatment.

“We can’t afford to have things going on like this that just destroy the fabric of the healthcare endeavor,” Gazelle said. “They come out sideways eventually. They come out in terms of poor patient care because there are greater errors. There’s a lack of respect for patients. There’s anger and irritability and so much spillover. We have to have zero-tolerance policies from the top down.”

A version of this article appeared on Medscape.com.