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A federal sting operation led to the recent conviction of a Texas physician assistant on charges of illegally prescribing a total of $3 million in drugs to patients at two “pill mill” clinics in Houston and helping others do the same.

The May 20 conviction of Charles Thompson, 76, of Houston, was based on charges of distributing more than 1.2 million opioid pills to thousands of individuals posing as patients at two pain management clinics, according to the U.S. Department of Justice.

Thompson’s conviction was the latest legal action in a string of cases involving the operation, including a doctor convicted in March who worked with Thompson at the West Parker Medical Clinic. Internist James Pierre, MD, 52, faces charges of unlawfully prescribing more than $1 million worth of opioid hydrocodone, according to federal officials.

Thompson also worked at Priority Wellness Clinic. Six people have pled guilty in connection with their conduct at West Parker or Priority Wellness, the justice department reported.

From June 2015 through July 2016, while Thompson was at West Parker, he helped Dr. Pierre unlawfully prescribe hydrocodone and the muscle relaxant carisoprodol, a combination of controlled substances for pain management known as the “Las Vegas cocktail,” to people in the sting operations pretending to be patients, authorities stated.

Thompson also distributed unlawful prescriptions for carisoprodol. So-called “runners” brought numerous people to pose as patients at West Parker and paid the clinic about $220 to $500 in cash for each visit that resulted in prescriptions for dangerous drugs. Throughout the scheme, West Parker pocketed about $1.75 million from prescriptions; Thompson was paid more than $208,000.

According to authorities, Thompson also helped others illegally prescribe controlled substances, including hydrocodone and oxycodone, from May to July 2017 at Priority Wellness, which opened in December 2016 after West Parker closed.

Priority Wellness reportedly operated as a pill mill similar to West Parker’s. Runners brought people posing as patients to Priority Wellness and paid the clinic between $300 and $600. The cost depended on whether the purported patient received a prescription for hydrocodone or oxycodone, almost always prescribed in combination with carisoprodol, authorities said. Throughout the scheme, Priority Wellness made about $1.1 million, and Thompson made between $700 and $900 a day.

He was convicted of one count of conspiracy to unlawfully distribute and dispense controlled substances and seven counts of unlawfully distributing and dispensing controlled substances in connection with his conduct at West Parker. For his conduct at Priority Wellness, he was convicted of one count of conspiracy to unlawfully distribute and dispense controlled substances and one count of unlawfully distributing and dispensing controlled substances.

He faces up to 20 years in prison for each count of conviction with sentencing scheduled for Oct. 3.

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

A federal sting operation led to the recent conviction of a Texas physician assistant on charges of illegally prescribing a total of $3 million in drugs to patients at two “pill mill” clinics in Houston and helping others do the same.

The May 20 conviction of Charles Thompson, 76, of Houston, was based on charges of distributing more than 1.2 million opioid pills to thousands of individuals posing as patients at two pain management clinics, according to the U.S. Department of Justice.

Thompson’s conviction was the latest legal action in a string of cases involving the operation, including a doctor convicted in March who worked with Thompson at the West Parker Medical Clinic. Internist James Pierre, MD, 52, faces charges of unlawfully prescribing more than $1 million worth of opioid hydrocodone, according to federal officials.

Thompson also worked at Priority Wellness Clinic. Six people have pled guilty in connection with their conduct at West Parker or Priority Wellness, the justice department reported.

From June 2015 through July 2016, while Thompson was at West Parker, he helped Dr. Pierre unlawfully prescribe hydrocodone and the muscle relaxant carisoprodol, a combination of controlled substances for pain management known as the “Las Vegas cocktail,” to people in the sting operations pretending to be patients, authorities stated.

Thompson also distributed unlawful prescriptions for carisoprodol. So-called “runners” brought numerous people to pose as patients at West Parker and paid the clinic about $220 to $500 in cash for each visit that resulted in prescriptions for dangerous drugs. Throughout the scheme, West Parker pocketed about $1.75 million from prescriptions; Thompson was paid more than $208,000.

According to authorities, Thompson also helped others illegally prescribe controlled substances, including hydrocodone and oxycodone, from May to July 2017 at Priority Wellness, which opened in December 2016 after West Parker closed.

Priority Wellness reportedly operated as a pill mill similar to West Parker’s. Runners brought people posing as patients to Priority Wellness and paid the clinic between $300 and $600. The cost depended on whether the purported patient received a prescription for hydrocodone or oxycodone, almost always prescribed in combination with carisoprodol, authorities said. Throughout the scheme, Priority Wellness made about $1.1 million, and Thompson made between $700 and $900 a day.

He was convicted of one count of conspiracy to unlawfully distribute and dispense controlled substances and seven counts of unlawfully distributing and dispensing controlled substances in connection with his conduct at West Parker. For his conduct at Priority Wellness, he was convicted of one count of conspiracy to unlawfully distribute and dispense controlled substances and one count of unlawfully distributing and dispensing controlled substances.

He faces up to 20 years in prison for each count of conviction with sentencing scheduled for Oct. 3.

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

A federal sting operation led to the recent conviction of a Texas physician assistant on charges of illegally prescribing a total of $3 million in drugs to patients at two “pill mill” clinics in Houston and helping others do the same.

The May 20 conviction of Charles Thompson, 76, of Houston, was based on charges of distributing more than 1.2 million opioid pills to thousands of individuals posing as patients at two pain management clinics, according to the U.S. Department of Justice.

Thompson’s conviction was the latest legal action in a string of cases involving the operation, including a doctor convicted in March who worked with Thompson at the West Parker Medical Clinic. Internist James Pierre, MD, 52, faces charges of unlawfully prescribing more than $1 million worth of opioid hydrocodone, according to federal officials.

Thompson also worked at Priority Wellness Clinic. Six people have pled guilty in connection with their conduct at West Parker or Priority Wellness, the justice department reported.

From June 2015 through July 2016, while Thompson was at West Parker, he helped Dr. Pierre unlawfully prescribe hydrocodone and the muscle relaxant carisoprodol, a combination of controlled substances for pain management known as the “Las Vegas cocktail,” to people in the sting operations pretending to be patients, authorities stated.

Thompson also distributed unlawful prescriptions for carisoprodol. So-called “runners” brought numerous people to pose as patients at West Parker and paid the clinic about $220 to $500 in cash for each visit that resulted in prescriptions for dangerous drugs. Throughout the scheme, West Parker pocketed about $1.75 million from prescriptions; Thompson was paid more than $208,000.

According to authorities, Thompson also helped others illegally prescribe controlled substances, including hydrocodone and oxycodone, from May to July 2017 at Priority Wellness, which opened in December 2016 after West Parker closed.

Priority Wellness reportedly operated as a pill mill similar to West Parker’s. Runners brought people posing as patients to Priority Wellness and paid the clinic between $300 and $600. The cost depended on whether the purported patient received a prescription for hydrocodone or oxycodone, almost always prescribed in combination with carisoprodol, authorities said. Throughout the scheme, Priority Wellness made about $1.1 million, and Thompson made between $700 and $900 a day.

He was convicted of one count of conspiracy to unlawfully distribute and dispense controlled substances and seven counts of unlawfully distributing and dispensing controlled substances in connection with his conduct at West Parker. For his conduct at Priority Wellness, he was convicted of one count of conspiracy to unlawfully distribute and dispense controlled substances and one count of unlawfully distributing and dispensing controlled substances.

He faces up to 20 years in prison for each count of conviction with sentencing scheduled for Oct. 3.

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

Nearly half of all U.S. adults aged 45 and older have modifiable risk factors for Alzheimer’s disease and related dementias (ADRD), including hypertension, low levels of physical activity, and obesity, new research shows.

Data from the Centers for Disease Control and Prevention reveal that among nearly 162,000 adults aged 45 and older who were surveyed in 2019 as part of the Behavioral Risk Factor Surveillance System (BRFSS), nearly half had high blood pressure and did not achieve aerobic physical activity recommendations. These were the two most common modifiable risk factors for ADRD.

In addition, more than one-third (35%) of adults were obese, 19% had diabetes, 18% had depression, 15% were smokers, 11% had hearing loss, and 10% were binge drinkers.

The findings were published online in the CDC’s Morbidity and Mortality Weekly Report.
 

A missed prevention opportunity

More than 1 in 10 (11.3%) adults surveyed reported subjective cognitive decline (SCD), an early indicator of possible future ADRD. 

The prevalence of SCD increased from about 4% among adults with no modifiable risk factors for ADRD to 25% for those with four or more risk factors.

Adults with SCD were more apt to report having almost all modifiable risk factors and were more likely to report four or more risk factors (34%) than were peers without SCD (13%)

The prevalence of SCD ranged from a high of about 29% in those with depression and 25% in those with hearing loss to 11% in those who reported binge drinking.

In line with previous research, the findings indicate that American Indian or Alaska Native, Black or African American, and Hispanic populations were more likely to have modifiable risk factors for ADRD than other racial groups, the researchers reported.

The CDC’s National Healthy Brain Initiative supports culturally tailored interventions that address ADRD risk factors specifically in these populations.

In 2021, the federal government’s National Plan to Address Alzheimer’s Disease was updated to include a new goal to reduce risk factors for ADRD.

“Given the prevalence of modifiable risk factors for ADRD and anticipated growth of the older adult population and those with ADRD, this new goal has the potential to benefit a large proportion of U.S. adults,” the investigators wrote.

“In addition to helping patients discuss concerns about memory loss, health care professionals should also screen patients for modifiable risk factors, counsel patients with risk factors, and refer them to effective programs and interventions where recommended,” they advised.

A recent report from the Lancet Commission on Dementia Prevention, Intervention, and Care found that modifying 12 risk factors over the life course could delay or prevent 40% of dementia cases.

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

Nearly half of all U.S. adults aged 45 and older have modifiable risk factors for Alzheimer’s disease and related dementias (ADRD), including hypertension, low levels of physical activity, and obesity, new research shows.

Data from the Centers for Disease Control and Prevention reveal that among nearly 162,000 adults aged 45 and older who were surveyed in 2019 as part of the Behavioral Risk Factor Surveillance System (BRFSS), nearly half had high blood pressure and did not achieve aerobic physical activity recommendations. These were the two most common modifiable risk factors for ADRD.

In addition, more than one-third (35%) of adults were obese, 19% had diabetes, 18% had depression, 15% were smokers, 11% had hearing loss, and 10% were binge drinkers.

The findings were published online in the CDC’s Morbidity and Mortality Weekly Report.
 

A missed prevention opportunity

More than 1 in 10 (11.3%) adults surveyed reported subjective cognitive decline (SCD), an early indicator of possible future ADRD. 

The prevalence of SCD increased from about 4% among adults with no modifiable risk factors for ADRD to 25% for those with four or more risk factors.

Adults with SCD were more apt to report having almost all modifiable risk factors and were more likely to report four or more risk factors (34%) than were peers without SCD (13%)

The prevalence of SCD ranged from a high of about 29% in those with depression and 25% in those with hearing loss to 11% in those who reported binge drinking.

In line with previous research, the findings indicate that American Indian or Alaska Native, Black or African American, and Hispanic populations were more likely to have modifiable risk factors for ADRD than other racial groups, the researchers reported.

The CDC’s National Healthy Brain Initiative supports culturally tailored interventions that address ADRD risk factors specifically in these populations.

In 2021, the federal government’s National Plan to Address Alzheimer’s Disease was updated to include a new goal to reduce risk factors for ADRD.

“Given the prevalence of modifiable risk factors for ADRD and anticipated growth of the older adult population and those with ADRD, this new goal has the potential to benefit a large proportion of U.S. adults,” the investigators wrote.

“In addition to helping patients discuss concerns about memory loss, health care professionals should also screen patients for modifiable risk factors, counsel patients with risk factors, and refer them to effective programs and interventions where recommended,” they advised.

A recent report from the Lancet Commission on Dementia Prevention, Intervention, and Care found that modifying 12 risk factors over the life course could delay or prevent 40% of dementia cases.

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

Nearly half of all U.S. adults aged 45 and older have modifiable risk factors for Alzheimer’s disease and related dementias (ADRD), including hypertension, low levels of physical activity, and obesity, new research shows.

Data from the Centers for Disease Control and Prevention reveal that among nearly 162,000 adults aged 45 and older who were surveyed in 2019 as part of the Behavioral Risk Factor Surveillance System (BRFSS), nearly half had high blood pressure and did not achieve aerobic physical activity recommendations. These were the two most common modifiable risk factors for ADRD.

In addition, more than one-third (35%) of adults were obese, 19% had diabetes, 18% had depression, 15% were smokers, 11% had hearing loss, and 10% were binge drinkers.

The findings were published online in the CDC’s Morbidity and Mortality Weekly Report.
 

A missed prevention opportunity

More than 1 in 10 (11.3%) adults surveyed reported subjective cognitive decline (SCD), an early indicator of possible future ADRD. 

The prevalence of SCD increased from about 4% among adults with no modifiable risk factors for ADRD to 25% for those with four or more risk factors.

Adults with SCD were more apt to report having almost all modifiable risk factors and were more likely to report four or more risk factors (34%) than were peers without SCD (13%)

The prevalence of SCD ranged from a high of about 29% in those with depression and 25% in those with hearing loss to 11% in those who reported binge drinking.

In line with previous research, the findings indicate that American Indian or Alaska Native, Black or African American, and Hispanic populations were more likely to have modifiable risk factors for ADRD than other racial groups, the researchers reported.

The CDC’s National Healthy Brain Initiative supports culturally tailored interventions that address ADRD risk factors specifically in these populations.

In 2021, the federal government’s National Plan to Address Alzheimer’s Disease was updated to include a new goal to reduce risk factors for ADRD.

“Given the prevalence of modifiable risk factors for ADRD and anticipated growth of the older adult population and those with ADRD, this new goal has the potential to benefit a large proportion of U.S. adults,” the investigators wrote.

“In addition to helping patients discuss concerns about memory loss, health care professionals should also screen patients for modifiable risk factors, counsel patients with risk factors, and refer them to effective programs and interventions where recommended,” they advised.

A recent report from the Lancet Commission on Dementia Prevention, Intervention, and Care found that modifying 12 risk factors over the life course could delay or prevent 40% of dementia cases.

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

The diverse effects of obesity on lung health and disease are increasingly being teased apart, with researchers honing in on the impact of metabolic dysfunction, circulating inflammatory factors produced by adipose tissue, lipid handling, and other factors – in addition to body mass index – that are associated with the obese state.

“The bird’s eye view is that obesity completely changes lung health. It’s something we’ve only recently begun to appreciate,” said Anne E. Dixon, MA, BM, BCh, director of the Vermont Lung Center at the University of Vermont, Burlington, who is focused on the research field of obesity and lung disease.

OSA and OHS

“With sleep apnea we tend to focus on anatomic considerations, but there may be relationships or interactions between obesity and neuromuscular function and neuroventilatory control,” Susheel P. Patil, MD, PhD, director of the sleep medicine program for University Hospitals and assistant professor at Case Western Reserve University, Cleveland, said in an interview.

Some studies suggest, for instance, that TNF-alpha can increase obstructive sleep apnea (OSA) susceptibility and severity through its neuroventilatory modulating properties during sleep. And the potential for additional proinflammatory cytokines produced by adipose tissue to similarly affect upper airway neuroventilatory control is an “intriguing line” of inquiry for researchers in the sleep apnea space, he said.

Leptin is of interest particularly in obesity hypoventilation syndrome (OHS), which is characterized by chronic daytime hypercapnia. Best known as a satiety hormone, leptin is produced by adipose tissue and suppresses appetite at the central nervous system level. But it has long been known that leptin also affects ventilation and the control of breathing.

When transported across the blood-brain barrier, leptin increases the hypercapnic ventilatory response, Babak Mokhlesi, MD, MSc, codirector of the Rush Lung Center and chief of pulmonary, critical care, and sleep medicine at Rush University Medical Center in Chicago, said in an interview.

Research suggests that patients with OHS may have resistance to leptin at the central nervous system level – with leptin not reaching the sites of ventilatory control. This is a “prevailing theory” and could explain why these patients “do not augment their ventilation to maintain homeostasis, normal levels of CO₂,” Dr. Mokhlesi said.

“Why some patients with severe obesity develop CO₂ retention while others do not is not fully understood,” he said, noting that patients with OHS can normalize their CO₂ quickly when instructed to take deep breaths. “What we know is that the centers in the brain responsible for augmenting ventilation when CO₂ goes up are somehow blunted.”

In a study of obese mice led by Vsevolod Y. Polotsky, MD, PhD, of Johns Hopkins University, Baltimore – and highlighted by Dr. Mokhlesi as an example of important, recent research – leptin delivered intranasally alleviated hypoventilation (and upper-airway obstruction), while intraperitoneally administered leptin did not, seemingly overcoming “central leptin deficiency.” (Am J Respir Crit Care Med. 2019;199[6]:773-83).

“This proved that there is some level of resistance in this animal model ... and has potential for therapeutics in the future,” Dr. Mokhlesi said.

Understanding the role of insulin resistance in OSA is another research focus. Some data suggest that insulin resistance, which is more common in obesity, is more prevalent in populations with OSA, Dr. Patil said. Researchers have discussed a bidirectional relationship for years, but it’s likely that insulin resistance is a precursor, he said.

In a mechanistic study published in 2016, Dr. Patil and his coinvestigators found that obese individuals with insulin resistance but without frank diabetes or sleep apnea demonstrated preclinical elevations in pharyngeal collapsibility during sleep. The findings suggest that insulin resistance could play a causal role in OSA pathogenesis by “generating requisite elevations in pharyngeal collapsibility,” they wrote (Eur. Respir J. 2016;47[6]:1718-26).

More recently, Dr. Patil noted in the interview, there is increasing appreciation in academia that the type of fat may be important to predicting OSA. “Visceral fat has a completely different cytokine-secretion profile than subcutaneous fat ... it is the more metabolically active fat that may secondarily impact upper airway function though a neuroinflammatory mechanism,” he said. “That is one of the working hypotheses today.”
 

Asthma

Research has so roundly suggested that metabolic dysfunction contributes to severe, poorly controlled asthma that there’s recent and growing interest in targeting metabolic dysfunction as part of the treatment of obese asthma, said Dr. Dixon, whose own research in obesity and lung disease has focused on asthma.

Data from animal models and some epidemiologic studies have suggested that drugs used to treat type 2 diabetes mellitus, such as glucagon-like peptide receptor-1 (GLPR-1) agonists and metformin, may help control asthma. In one recent study – cited by Dr. Dixon in a 2022 review of obesity and asthma – people with obesity and asthma who were prescribed GLPR-1 agonists for diabetes had fewer asthma exacerbations compared with those who took other medications for diabetes (Semin Respir Crit Care Med. 2022 Feb 17. doi: 10.1055/s-0042-1742384).

There is also research interest in targeting the pro-inflammatory adipokine interleukin 6 (IL-6), since increased circulating levels of IL-6 correlate with asthma severity, and in addressing oxidative stress in asthma through treatment with a mitochondrially targeted antioxidant, she said. Oxidative stress is increased in the airways of people with obesity, and researchers believe it may contribute to the pathophysiology of obese asthma through effects on airway nitric oxide levels.

(Her own research work at the University of Vermont has found associations between poor asthma control and high levels of leptin, and similar associations involving low levels of adiponectin, an anti-inflammatory adipokine that has been shown to downregulate eosinophil recruitment in the airways.)

Weight loss has been shown in mostly small, single-center studies to improve asthma control, but short of weight loss, researchers are also investigating the role of poor dietary quality. Thus far, data suggest that it’s the composition of the diet, and not just its contribution to weight gain, that could be impactful, Dr. Dixon said.

More basic research questions cited by Dr. Dixon include the extent to which adipose tissue inflammation causes inflammation in the lungs. “It’s a little unclear whether all the metabolic dysfunction associated with poor asthma control is causing inflammation in the lungs,” she said, though “we’ve done some work here that shows mediators produced by the adipose tissue could be impacting production of inflammatory mediators by the airway epithelium.”

Overall, she said, “the big questions [in asthma] are, how does adipose tissue affect the airway? Is it through direct effects? Through effects on the immune system? And obesity is affected by diet and the gut microbiome – how can these be [impacting] the airway?”

Obesity “is associated with so many changes – the gut, the immune system, and metabolic dysfunction, in addition to airway mechanics,” she said, “that I no longer think, as I did when I came to this, that it’s just one thing. It’s probably all of these things together.”

In the meantime, questions about potential shared pathways for the development of obesity and asthma remain. “Obesity is a risk factor for developing asthma, but it’s also entirely possible that asthma is a risk factor for developing obesity,” she said. (Some data from pediatric populations, she noted, suggest that nonobese children with asthma are at increased risk of developing obesity.)

Also important, Dr. Dixon said, is “emerging literature in the last 5-10 years” that suggests that people with obesity are more susceptible to the effects of air pollution. Research involving inner-city schoolchildren with asthma, for instance, has shown that those with obesity had worse symptoms with air pollution exposure than did those who were not obese.
 

Pulmonary arterial hypertension

Some research has looked at adipose tissue–produced substances in PAH, but the most well-established association in obesity and PAH involves insulin resistance.

“I don’t think we’re certain as a community that obesity [in general] is the problem – it’s not itself considered a risk factor for PAH,” Anna R. Hemnes, MD, associate professor of medicine at Vanderbilt University Medical Center in Nashville, Tenn., said in an interview. She noted that it’s “hard to dissect obesity” apart.

Researchers are “more confident,” she said, “that insulin resistance – one feature of obesity [in some people] – is associated with worse outcomes in PAH.” Metabolic disease resembling insulin resistance is common in PAH and is believed to contribute to pulmonary vascular disease and right ventricular (RV) failure – the main cause of mortality in PAH – at least in part because of increased oxidative stress.

Dr. Hemnes led a mechanistic phase II clinical trial of metformin in PAH in which the drug was associated with improved RV fractional area change and reduced RV lipid deposition (J Am Heart Assoc. 2020;9[22]:e018349), and she’s now leading a National Institutes of Health–funded multicenter trial looking at the impact of metformin and an exercise intervention on 6-minute walk distance and World Health Organization functional class in PAH.

At the Rush Lung Center, in the meantime, Dr. Mokhlesi is utilizing animal models of OSA and OHS to explore the effect of hypoxia and nighttime hypercapnia on the development of PAH. “I think the jury is still out as to whether obesity itself is a major risk factor, but if so, by what mechanism?” he said. “Is it worsening [sleep-disordered breathing], which then worsens PAH?”
 

COPD

The focus in COPD has traditionally been on underweight, but the relationship between obesity and COPD has increasingly been recognized in the last 10-15 years, said Frits M. E. Franssen, MD, PhD, of CIRO, a research institute in Horn, the Netherlands, that treats COPD and other chronic lung diseases, and of the department of respiratory medicine at Maastricht University.

Researchers like Dr. Franssen are trying, for one, to understand obesity’s impact on COPD pathophysiology and to tease apart the impact of both conditions on disease severity and patient-related outcomes such as exercise capacity and exercise-related symptoms.

When Dr. Franssen’s group compared responses to weight-bearing exercise (6-min. walk test) and weight-supported exercise (cycling) in obese and normal weight COPD patients matched for age, gender, and degree of airflow limitation, the researchers found that walking capacity was significantly reduced while cycling capacity was preserved in the obese group (Respirology. 2016;21[3]:483-8).

Exercise-related symptoms (dyspnea and leg fatigue) were largely comparable between the obese and normal-weight COPD patients in both exercise modalities. However, in other studies, dyspnea ratings during cycling – at any given level of ventilation – have been lower in obese patients, indicating that “additional fat mass may have a beneficial effect on lung functioning [in non–weight-bearing exercise],” he said in an interview.

Dr. Franssen’s group also has assessed body composition in overweight and obese patients with COPD and found that a significant number have low muscle mass. These patients had worse lung function, exercise tolerance, and muscle strength compared to patients with comparable BMI and normal muscle mass (Respir Res. 2021 Mar 25. doi: 10.1186/s12931-021-01689-w).

“We’d always thought that obese patients have normal muscle mass ... but now we know it can be dramatically low,” he said. In assessing obesity and formulating any weight loss plans, “we’re now interested not only in weight but in the distribution of fat mass and fat-free mass ... and in maintaining muscle mass in patients who are [prescribed dietary interventions].”

Paradoxically, in patients with severe COPD, obesity is associated with prolonged survival, while in patients with mild to moderate COPD, obesity is associated with increased mortality risk, he noted.

The impact of adipose tissue and the chronic inflammation and metabolic disturbances that characterize obesity are currently largely unexplored, he said. Researchers have not yet studied what optimal weights may be for patients with COPD. “And we’re interested in the questions, are body weight and body composition the result of the disease, or [are they] determining the type of COPD one will get?” Dr. Franssen said.

Patients with COPD who are obese have “more of the phenotype of chronic bronchitis,” he noted, “while typical emphysema patients are normally underweight.”

The diverse effects of obesity on lung health and disease are increasingly being teased apart, with researchers honing in on the impact of metabolic dysfunction, circulating inflammatory factors produced by adipose tissue, lipid handling, and other factors – in addition to body mass index – that are associated with the obese state.

“The bird’s eye view is that obesity completely changes lung health. It’s something we’ve only recently begun to appreciate,” said Anne E. Dixon, MA, BM, BCh, director of the Vermont Lung Center at the University of Vermont, Burlington, who is focused on the research field of obesity and lung disease.

OSA and OHS

“With sleep apnea we tend to focus on anatomic considerations, but there may be relationships or interactions between obesity and neuromuscular function and neuroventilatory control,” Susheel P. Patil, MD, PhD, director of the sleep medicine program for University Hospitals and assistant professor at Case Western Reserve University, Cleveland, said in an interview.

Some studies suggest, for instance, that TNF-alpha can increase obstructive sleep apnea (OSA) susceptibility and severity through its neuroventilatory modulating properties during sleep. And the potential for additional proinflammatory cytokines produced by adipose tissue to similarly affect upper airway neuroventilatory control is an “intriguing line” of inquiry for researchers in the sleep apnea space, he said.

Leptin is of interest particularly in obesity hypoventilation syndrome (OHS), which is characterized by chronic daytime hypercapnia. Best known as a satiety hormone, leptin is produced by adipose tissue and suppresses appetite at the central nervous system level. But it has long been known that leptin also affects ventilation and the control of breathing.

When transported across the blood-brain barrier, leptin increases the hypercapnic ventilatory response, Babak Mokhlesi, MD, MSc, codirector of the Rush Lung Center and chief of pulmonary, critical care, and sleep medicine at Rush University Medical Center in Chicago, said in an interview.

Research suggests that patients with OHS may have resistance to leptin at the central nervous system level – with leptin not reaching the sites of ventilatory control. This is a “prevailing theory” and could explain why these patients “do not augment their ventilation to maintain homeostasis, normal levels of CO₂,” Dr. Mokhlesi said.

“Why some patients with severe obesity develop CO₂ retention while others do not is not fully understood,” he said, noting that patients with OHS can normalize their CO₂ quickly when instructed to take deep breaths. “What we know is that the centers in the brain responsible for augmenting ventilation when CO₂ goes up are somehow blunted.”

In a study of obese mice led by Vsevolod Y. Polotsky, MD, PhD, of Johns Hopkins University, Baltimore – and highlighted by Dr. Mokhlesi as an example of important, recent research – leptin delivered intranasally alleviated hypoventilation (and upper-airway obstruction), while intraperitoneally administered leptin did not, seemingly overcoming “central leptin deficiency.” (Am J Respir Crit Care Med. 2019;199[6]:773-83).

“This proved that there is some level of resistance in this animal model ... and has potential for therapeutics in the future,” Dr. Mokhlesi said.

Understanding the role of insulin resistance in OSA is another research focus. Some data suggest that insulin resistance, which is more common in obesity, is more prevalent in populations with OSA, Dr. Patil said. Researchers have discussed a bidirectional relationship for years, but it’s likely that insulin resistance is a precursor, he said.

In a mechanistic study published in 2016, Dr. Patil and his coinvestigators found that obese individuals with insulin resistance but without frank diabetes or sleep apnea demonstrated preclinical elevations in pharyngeal collapsibility during sleep. The findings suggest that insulin resistance could play a causal role in OSA pathogenesis by “generating requisite elevations in pharyngeal collapsibility,” they wrote (Eur. Respir J. 2016;47[6]:1718-26).

More recently, Dr. Patil noted in the interview, there is increasing appreciation in academia that the type of fat may be important to predicting OSA. “Visceral fat has a completely different cytokine-secretion profile than subcutaneous fat ... it is the more metabolically active fat that may secondarily impact upper airway function though a neuroinflammatory mechanism,” he said. “That is one of the working hypotheses today.”
 

Asthma

Research has so roundly suggested that metabolic dysfunction contributes to severe, poorly controlled asthma that there’s recent and growing interest in targeting metabolic dysfunction as part of the treatment of obese asthma, said Dr. Dixon, whose own research in obesity and lung disease has focused on asthma.

Data from animal models and some epidemiologic studies have suggested that drugs used to treat type 2 diabetes mellitus, such as glucagon-like peptide receptor-1 (GLPR-1) agonists and metformin, may help control asthma. In one recent study – cited by Dr. Dixon in a 2022 review of obesity and asthma – people with obesity and asthma who were prescribed GLPR-1 agonists for diabetes had fewer asthma exacerbations compared with those who took other medications for diabetes (Semin Respir Crit Care Med. 2022 Feb 17. doi: 10.1055/s-0042-1742384).

There is also research interest in targeting the pro-inflammatory adipokine interleukin 6 (IL-6), since increased circulating levels of IL-6 correlate with asthma severity, and in addressing oxidative stress in asthma through treatment with a mitochondrially targeted antioxidant, she said. Oxidative stress is increased in the airways of people with obesity, and researchers believe it may contribute to the pathophysiology of obese asthma through effects on airway nitric oxide levels.

(Her own research work at the University of Vermont has found associations between poor asthma control and high levels of leptin, and similar associations involving low levels of adiponectin, an anti-inflammatory adipokine that has been shown to downregulate eosinophil recruitment in the airways.)

Weight loss has been shown in mostly small, single-center studies to improve asthma control, but short of weight loss, researchers are also investigating the role of poor dietary quality. Thus far, data suggest that it’s the composition of the diet, and not just its contribution to weight gain, that could be impactful, Dr. Dixon said.

More basic research questions cited by Dr. Dixon include the extent to which adipose tissue inflammation causes inflammation in the lungs. “It’s a little unclear whether all the metabolic dysfunction associated with poor asthma control is causing inflammation in the lungs,” she said, though “we’ve done some work here that shows mediators produced by the adipose tissue could be impacting production of inflammatory mediators by the airway epithelium.”

Overall, she said, “the big questions [in asthma] are, how does adipose tissue affect the airway? Is it through direct effects? Through effects on the immune system? And obesity is affected by diet and the gut microbiome – how can these be [impacting] the airway?”

Obesity “is associated with so many changes – the gut, the immune system, and metabolic dysfunction, in addition to airway mechanics,” she said, “that I no longer think, as I did when I came to this, that it’s just one thing. It’s probably all of these things together.”

In the meantime, questions about potential shared pathways for the development of obesity and asthma remain. “Obesity is a risk factor for developing asthma, but it’s also entirely possible that asthma is a risk factor for developing obesity,” she said. (Some data from pediatric populations, she noted, suggest that nonobese children with asthma are at increased risk of developing obesity.)

Also important, Dr. Dixon said, is “emerging literature in the last 5-10 years” that suggests that people with obesity are more susceptible to the effects of air pollution. Research involving inner-city schoolchildren with asthma, for instance, has shown that those with obesity had worse symptoms with air pollution exposure than did those who were not obese.
 

Pulmonary arterial hypertension

Some research has looked at adipose tissue–produced substances in PAH, but the most well-established association in obesity and PAH involves insulin resistance.

“I don’t think we’re certain as a community that obesity [in general] is the problem – it’s not itself considered a risk factor for PAH,” Anna R. Hemnes, MD, associate professor of medicine at Vanderbilt University Medical Center in Nashville, Tenn., said in an interview. She noted that it’s “hard to dissect obesity” apart.

Researchers are “more confident,” she said, “that insulin resistance – one feature of obesity [in some people] – is associated with worse outcomes in PAH.” Metabolic disease resembling insulin resistance is common in PAH and is believed to contribute to pulmonary vascular disease and right ventricular (RV) failure – the main cause of mortality in PAH – at least in part because of increased oxidative stress.

Dr. Hemnes led a mechanistic phase II clinical trial of metformin in PAH in which the drug was associated with improved RV fractional area change and reduced RV lipid deposition (J Am Heart Assoc. 2020;9[22]:e018349), and she’s now leading a National Institutes of Health–funded multicenter trial looking at the impact of metformin and an exercise intervention on 6-minute walk distance and World Health Organization functional class in PAH.

At the Rush Lung Center, in the meantime, Dr. Mokhlesi is utilizing animal models of OSA and OHS to explore the effect of hypoxia and nighttime hypercapnia on the development of PAH. “I think the jury is still out as to whether obesity itself is a major risk factor, but if so, by what mechanism?” he said. “Is it worsening [sleep-disordered breathing], which then worsens PAH?”
 

COPD

The focus in COPD has traditionally been on underweight, but the relationship between obesity and COPD has increasingly been recognized in the last 10-15 years, said Frits M. E. Franssen, MD, PhD, of CIRO, a research institute in Horn, the Netherlands, that treats COPD and other chronic lung diseases, and of the department of respiratory medicine at Maastricht University.

Researchers like Dr. Franssen are trying, for one, to understand obesity’s impact on COPD pathophysiology and to tease apart the impact of both conditions on disease severity and patient-related outcomes such as exercise capacity and exercise-related symptoms.

When Dr. Franssen’s group compared responses to weight-bearing exercise (6-min. walk test) and weight-supported exercise (cycling) in obese and normal weight COPD patients matched for age, gender, and degree of airflow limitation, the researchers found that walking capacity was significantly reduced while cycling capacity was preserved in the obese group (Respirology. 2016;21[3]:483-8).

Exercise-related symptoms (dyspnea and leg fatigue) were largely comparable between the obese and normal-weight COPD patients in both exercise modalities. However, in other studies, dyspnea ratings during cycling – at any given level of ventilation – have been lower in obese patients, indicating that “additional fat mass may have a beneficial effect on lung functioning [in non–weight-bearing exercise],” he said in an interview.

Dr. Franssen’s group also has assessed body composition in overweight and obese patients with COPD and found that a significant number have low muscle mass. These patients had worse lung function, exercise tolerance, and muscle strength compared to patients with comparable BMI and normal muscle mass (Respir Res. 2021 Mar 25. doi: 10.1186/s12931-021-01689-w).

“We’d always thought that obese patients have normal muscle mass ... but now we know it can be dramatically low,” he said. In assessing obesity and formulating any weight loss plans, “we’re now interested not only in weight but in the distribution of fat mass and fat-free mass ... and in maintaining muscle mass in patients who are [prescribed dietary interventions].”

Paradoxically, in patients with severe COPD, obesity is associated with prolonged survival, while in patients with mild to moderate COPD, obesity is associated with increased mortality risk, he noted.

The impact of adipose tissue and the chronic inflammation and metabolic disturbances that characterize obesity are currently largely unexplored, he said. Researchers have not yet studied what optimal weights may be for patients with COPD. “And we’re interested in the questions, are body weight and body composition the result of the disease, or [are they] determining the type of COPD one will get?” Dr. Franssen said.

Patients with COPD who are obese have “more of the phenotype of chronic bronchitis,” he noted, “while typical emphysema patients are normally underweight.”

The diverse effects of obesity on lung health and disease are increasingly being teased apart, with researchers honing in on the impact of metabolic dysfunction, circulating inflammatory factors produced by adipose tissue, lipid handling, and other factors – in addition to body mass index – that are associated with the obese state.

“The bird’s eye view is that obesity completely changes lung health. It’s something we’ve only recently begun to appreciate,” said Anne E. Dixon, MA, BM, BCh, director of the Vermont Lung Center at the University of Vermont, Burlington, who is focused on the research field of obesity and lung disease.

OSA and OHS

“With sleep apnea we tend to focus on anatomic considerations, but there may be relationships or interactions between obesity and neuromuscular function and neuroventilatory control,” Susheel P. Patil, MD, PhD, director of the sleep medicine program for University Hospitals and assistant professor at Case Western Reserve University, Cleveland, said in an interview.

Some studies suggest, for instance, that TNF-alpha can increase obstructive sleep apnea (OSA) susceptibility and severity through its neuroventilatory modulating properties during sleep. And the potential for additional proinflammatory cytokines produced by adipose tissue to similarly affect upper airway neuroventilatory control is an “intriguing line” of inquiry for researchers in the sleep apnea space, he said.

Leptin is of interest particularly in obesity hypoventilation syndrome (OHS), which is characterized by chronic daytime hypercapnia. Best known as a satiety hormone, leptin is produced by adipose tissue and suppresses appetite at the central nervous system level. But it has long been known that leptin also affects ventilation and the control of breathing.

When transported across the blood-brain barrier, leptin increases the hypercapnic ventilatory response, Babak Mokhlesi, MD, MSc, codirector of the Rush Lung Center and chief of pulmonary, critical care, and sleep medicine at Rush University Medical Center in Chicago, said in an interview.

Research suggests that patients with OHS may have resistance to leptin at the central nervous system level – with leptin not reaching the sites of ventilatory control. This is a “prevailing theory” and could explain why these patients “do not augment their ventilation to maintain homeostasis, normal levels of CO₂,” Dr. Mokhlesi said.

“Why some patients with severe obesity develop CO₂ retention while others do not is not fully understood,” he said, noting that patients with OHS can normalize their CO₂ quickly when instructed to take deep breaths. “What we know is that the centers in the brain responsible for augmenting ventilation when CO₂ goes up are somehow blunted.”

In a study of obese mice led by Vsevolod Y. Polotsky, MD, PhD, of Johns Hopkins University, Baltimore – and highlighted by Dr. Mokhlesi as an example of important, recent research – leptin delivered intranasally alleviated hypoventilation (and upper-airway obstruction), while intraperitoneally administered leptin did not, seemingly overcoming “central leptin deficiency.” (Am J Respir Crit Care Med. 2019;199[6]:773-83).

“This proved that there is some level of resistance in this animal model ... and has potential for therapeutics in the future,” Dr. Mokhlesi said.

Understanding the role of insulin resistance in OSA is another research focus. Some data suggest that insulin resistance, which is more common in obesity, is more prevalent in populations with OSA, Dr. Patil said. Researchers have discussed a bidirectional relationship for years, but it’s likely that insulin resistance is a precursor, he said.

In a mechanistic study published in 2016, Dr. Patil and his coinvestigators found that obese individuals with insulin resistance but without frank diabetes or sleep apnea demonstrated preclinical elevations in pharyngeal collapsibility during sleep. The findings suggest that insulin resistance could play a causal role in OSA pathogenesis by “generating requisite elevations in pharyngeal collapsibility,” they wrote (Eur. Respir J. 2016;47[6]:1718-26).

More recently, Dr. Patil noted in the interview, there is increasing appreciation in academia that the type of fat may be important to predicting OSA. “Visceral fat has a completely different cytokine-secretion profile than subcutaneous fat ... it is the more metabolically active fat that may secondarily impact upper airway function though a neuroinflammatory mechanism,” he said. “That is one of the working hypotheses today.”
 

Asthma

Research has so roundly suggested that metabolic dysfunction contributes to severe, poorly controlled asthma that there’s recent and growing interest in targeting metabolic dysfunction as part of the treatment of obese asthma, said Dr. Dixon, whose own research in obesity and lung disease has focused on asthma.

Data from animal models and some epidemiologic studies have suggested that drugs used to treat type 2 diabetes mellitus, such as glucagon-like peptide receptor-1 (GLPR-1) agonists and metformin, may help control asthma. In one recent study – cited by Dr. Dixon in a 2022 review of obesity and asthma – people with obesity and asthma who were prescribed GLPR-1 agonists for diabetes had fewer asthma exacerbations compared with those who took other medications for diabetes (Semin Respir Crit Care Med. 2022 Feb 17. doi: 10.1055/s-0042-1742384).

There is also research interest in targeting the pro-inflammatory adipokine interleukin 6 (IL-6), since increased circulating levels of IL-6 correlate with asthma severity, and in addressing oxidative stress in asthma through treatment with a mitochondrially targeted antioxidant, she said. Oxidative stress is increased in the airways of people with obesity, and researchers believe it may contribute to the pathophysiology of obese asthma through effects on airway nitric oxide levels.

(Her own research work at the University of Vermont has found associations between poor asthma control and high levels of leptin, and similar associations involving low levels of adiponectin, an anti-inflammatory adipokine that has been shown to downregulate eosinophil recruitment in the airways.)

Weight loss has been shown in mostly small, single-center studies to improve asthma control, but short of weight loss, researchers are also investigating the role of poor dietary quality. Thus far, data suggest that it’s the composition of the diet, and not just its contribution to weight gain, that could be impactful, Dr. Dixon said.

More basic research questions cited by Dr. Dixon include the extent to which adipose tissue inflammation causes inflammation in the lungs. “It’s a little unclear whether all the metabolic dysfunction associated with poor asthma control is causing inflammation in the lungs,” she said, though “we’ve done some work here that shows mediators produced by the adipose tissue could be impacting production of inflammatory mediators by the airway epithelium.”

Overall, she said, “the big questions [in asthma] are, how does adipose tissue affect the airway? Is it through direct effects? Through effects on the immune system? And obesity is affected by diet and the gut microbiome – how can these be [impacting] the airway?”

Obesity “is associated with so many changes – the gut, the immune system, and metabolic dysfunction, in addition to airway mechanics,” she said, “that I no longer think, as I did when I came to this, that it’s just one thing. It’s probably all of these things together.”

In the meantime, questions about potential shared pathways for the development of obesity and asthma remain. “Obesity is a risk factor for developing asthma, but it’s also entirely possible that asthma is a risk factor for developing obesity,” she said. (Some data from pediatric populations, she noted, suggest that nonobese children with asthma are at increased risk of developing obesity.)

Also important, Dr. Dixon said, is “emerging literature in the last 5-10 years” that suggests that people with obesity are more susceptible to the effects of air pollution. Research involving inner-city schoolchildren with asthma, for instance, has shown that those with obesity had worse symptoms with air pollution exposure than did those who were not obese.
 

Pulmonary arterial hypertension

Some research has looked at adipose tissue–produced substances in PAH, but the most well-established association in obesity and PAH involves insulin resistance.

“I don’t think we’re certain as a community that obesity [in general] is the problem – it’s not itself considered a risk factor for PAH,” Anna R. Hemnes, MD, associate professor of medicine at Vanderbilt University Medical Center in Nashville, Tenn., said in an interview. She noted that it’s “hard to dissect obesity” apart.

Researchers are “more confident,” she said, “that insulin resistance – one feature of obesity [in some people] – is associated with worse outcomes in PAH.” Metabolic disease resembling insulin resistance is common in PAH and is believed to contribute to pulmonary vascular disease and right ventricular (RV) failure – the main cause of mortality in PAH – at least in part because of increased oxidative stress.

Dr. Hemnes led a mechanistic phase II clinical trial of metformin in PAH in which the drug was associated with improved RV fractional area change and reduced RV lipid deposition (J Am Heart Assoc. 2020;9[22]:e018349), and she’s now leading a National Institutes of Health–funded multicenter trial looking at the impact of metformin and an exercise intervention on 6-minute walk distance and World Health Organization functional class in PAH.

At the Rush Lung Center, in the meantime, Dr. Mokhlesi is utilizing animal models of OSA and OHS to explore the effect of hypoxia and nighttime hypercapnia on the development of PAH. “I think the jury is still out as to whether obesity itself is a major risk factor, but if so, by what mechanism?” he said. “Is it worsening [sleep-disordered breathing], which then worsens PAH?”
 

COPD

The focus in COPD has traditionally been on underweight, but the relationship between obesity and COPD has increasingly been recognized in the last 10-15 years, said Frits M. E. Franssen, MD, PhD, of CIRO, a research institute in Horn, the Netherlands, that treats COPD and other chronic lung diseases, and of the department of respiratory medicine at Maastricht University.

Researchers like Dr. Franssen are trying, for one, to understand obesity’s impact on COPD pathophysiology and to tease apart the impact of both conditions on disease severity and patient-related outcomes such as exercise capacity and exercise-related symptoms.

When Dr. Franssen’s group compared responses to weight-bearing exercise (6-min. walk test) and weight-supported exercise (cycling) in obese and normal weight COPD patients matched for age, gender, and degree of airflow limitation, the researchers found that walking capacity was significantly reduced while cycling capacity was preserved in the obese group (Respirology. 2016;21[3]:483-8).

Exercise-related symptoms (dyspnea and leg fatigue) were largely comparable between the obese and normal-weight COPD patients in both exercise modalities. However, in other studies, dyspnea ratings during cycling – at any given level of ventilation – have been lower in obese patients, indicating that “additional fat mass may have a beneficial effect on lung functioning [in non–weight-bearing exercise],” he said in an interview.

Dr. Franssen’s group also has assessed body composition in overweight and obese patients with COPD and found that a significant number have low muscle mass. These patients had worse lung function, exercise tolerance, and muscle strength compared to patients with comparable BMI and normal muscle mass (Respir Res. 2021 Mar 25. doi: 10.1186/s12931-021-01689-w).

“We’d always thought that obese patients have normal muscle mass ... but now we know it can be dramatically low,” he said. In assessing obesity and formulating any weight loss plans, “we’re now interested not only in weight but in the distribution of fat mass and fat-free mass ... and in maintaining muscle mass in patients who are [prescribed dietary interventions].”

Paradoxically, in patients with severe COPD, obesity is associated with prolonged survival, while in patients with mild to moderate COPD, obesity is associated with increased mortality risk, he noted.

The impact of adipose tissue and the chronic inflammation and metabolic disturbances that characterize obesity are currently largely unexplored, he said. Researchers have not yet studied what optimal weights may be for patients with COPD. “And we’re interested in the questions, are body weight and body composition the result of the disease, or [are they] determining the type of COPD one will get?” Dr. Franssen said.

Patients with COPD who are obese have “more of the phenotype of chronic bronchitis,” he noted, “while typical emphysema patients are normally underweight.”

SAN FRANCISCO – It may be time to move beyond relying largely on spirometry to distinguish between healthy and abnormal lung function in diverse populations.

That conclusion comes from investigators who looked at patients with ostensibly normal spirometry values in a large population-based study and found that using standard equations to adjust for racial differences in lung-function measures appeared to miss emphysema in a significant proportion of Black patients.

“Our traditional measures of lung health based on spirometry may be under-recognizing impaired respiratory health in Black adults and particularly Black men,” said lead author Gabrielle Liu, MD, a fellow in the division of pulmonary and critical care medicine at the Northwestern University Feinberg School of Medicine, Chicago.

“CT imaging may be useful in the evaluation of those with suspected impaired respiratory health and normal spirometry,” she said in an oral abstract session at the American Thoracic Society International Conference 2022.

Dr. Liu and colleagues studied the association between self-identified race and visually identified emphysema among 2,674 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study. The patients had CT scans at a mean age of 50 and spirometry at a mean age of 55.
 

Racial differences

The investigators found that among men with forced expiratory volume in 1 second (FEV1) ranging from 100% to 120% of predicted according to race-adjusted formulas, 14.6% of Black men had emphysema, compared with only 1.7% of White men (P < .001). Respective emphysema rates in Black women and White women were 3.8% and 1.9%; this difference was not statistically significant.

Among patients with FEV1 80% to 99% of predicted according to race-specific measures, 15.5% of Black men had emphysema, compared with 4% of White men (P < .001). Respective rates of emphysema were 6.9% for Black women versus 3.2% for White women (P = .025).

When the investigators applied race-neutral spirometry reference equations to the same population, they found that it attenuated but did not completely eliminate the racial disparity in emphysema prevalence among patients with FEV1, ranging from 80% to 120% of predicted.
 

Relic of the past

The results suggest that race-based adjustments of spirometry measures are a relic of less enlightened times, said Adam Gaffney, MD, MPH, assistant professor of medicine at Harvard Medical School, Boston, and a pulmonologist and critical care physician at Cambridge Health Alliance, Massachusetts.

“If the average lower lung function of Black people is being driven by adversity, structural racism, and deprivation, that means that race-specific equations are normalizing that adversity,” he said in an interview.

“In my opinion, it is time to move beyond race-based equations in clinical pulmonary medicine, particularly in the context of patients with established lung disease in whom use of race-based equations might actually lead to undertreatment,” said Dr. Gaffney, who was not involved in the study.

Dr. Liu agreed that it’s time to move to race-neutral measures and that the whole concept of race-based differences is flawed.

“The long-standing structural inequities in health likely made the reference populations have lower lung function than among Whites,” she told this news organization.

Dr. Liu said that evaluation of lung function should not rely on spirometry alone, but should also include – when appropriate – CT scans, as well as improved understanding of how symptoms may be predictive for poor outcomes.

The study was supported by grants from the National Institutes of Health. Dr. Liu and Dr. Gaffney have disclosed no relevant financial relationships.

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

SAN FRANCISCO – It may be time to move beyond relying largely on spirometry to distinguish between healthy and abnormal lung function in diverse populations.

That conclusion comes from investigators who looked at patients with ostensibly normal spirometry values in a large population-based study and found that using standard equations to adjust for racial differences in lung-function measures appeared to miss emphysema in a significant proportion of Black patients.

“Our traditional measures of lung health based on spirometry may be under-recognizing impaired respiratory health in Black adults and particularly Black men,” said lead author Gabrielle Liu, MD, a fellow in the division of pulmonary and critical care medicine at the Northwestern University Feinberg School of Medicine, Chicago.

“CT imaging may be useful in the evaluation of those with suspected impaired respiratory health and normal spirometry,” she said in an oral abstract session at the American Thoracic Society International Conference 2022.

Dr. Liu and colleagues studied the association between self-identified race and visually identified emphysema among 2,674 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study. The patients had CT scans at a mean age of 50 and spirometry at a mean age of 55.
 

Racial differences

The investigators found that among men with forced expiratory volume in 1 second (FEV1) ranging from 100% to 120% of predicted according to race-adjusted formulas, 14.6% of Black men had emphysema, compared with only 1.7% of White men (P < .001). Respective emphysema rates in Black women and White women were 3.8% and 1.9%; this difference was not statistically significant.

Among patients with FEV1 80% to 99% of predicted according to race-specific measures, 15.5% of Black men had emphysema, compared with 4% of White men (P < .001). Respective rates of emphysema were 6.9% for Black women versus 3.2% for White women (P = .025).

When the investigators applied race-neutral spirometry reference equations to the same population, they found that it attenuated but did not completely eliminate the racial disparity in emphysema prevalence among patients with FEV1, ranging from 80% to 120% of predicted.
 

Relic of the past

The results suggest that race-based adjustments of spirometry measures are a relic of less enlightened times, said Adam Gaffney, MD, MPH, assistant professor of medicine at Harvard Medical School, Boston, and a pulmonologist and critical care physician at Cambridge Health Alliance, Massachusetts.

“If the average lower lung function of Black people is being driven by adversity, structural racism, and deprivation, that means that race-specific equations are normalizing that adversity,” he said in an interview.

“In my opinion, it is time to move beyond race-based equations in clinical pulmonary medicine, particularly in the context of patients with established lung disease in whom use of race-based equations might actually lead to undertreatment,” said Dr. Gaffney, who was not involved in the study.

Dr. Liu agreed that it’s time to move to race-neutral measures and that the whole concept of race-based differences is flawed.

“The long-standing structural inequities in health likely made the reference populations have lower lung function than among Whites,” she told this news organization.

Dr. Liu said that evaluation of lung function should not rely on spirometry alone, but should also include – when appropriate – CT scans, as well as improved understanding of how symptoms may be predictive for poor outcomes.

The study was supported by grants from the National Institutes of Health. Dr. Liu and Dr. Gaffney have disclosed no relevant financial relationships.

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

SAN FRANCISCO – It may be time to move beyond relying largely on spirometry to distinguish between healthy and abnormal lung function in diverse populations.

That conclusion comes from investigators who looked at patients with ostensibly normal spirometry values in a large population-based study and found that using standard equations to adjust for racial differences in lung-function measures appeared to miss emphysema in a significant proportion of Black patients.

“Our traditional measures of lung health based on spirometry may be under-recognizing impaired respiratory health in Black adults and particularly Black men,” said lead author Gabrielle Liu, MD, a fellow in the division of pulmonary and critical care medicine at the Northwestern University Feinberg School of Medicine, Chicago.

“CT imaging may be useful in the evaluation of those with suspected impaired respiratory health and normal spirometry,” she said in an oral abstract session at the American Thoracic Society International Conference 2022.

Dr. Liu and colleagues studied the association between self-identified race and visually identified emphysema among 2,674 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study. The patients had CT scans at a mean age of 50 and spirometry at a mean age of 55.
 

Racial differences

The investigators found that among men with forced expiratory volume in 1 second (FEV1) ranging from 100% to 120% of predicted according to race-adjusted formulas, 14.6% of Black men had emphysema, compared with only 1.7% of White men (P < .001). Respective emphysema rates in Black women and White women were 3.8% and 1.9%; this difference was not statistically significant.

Among patients with FEV1 80% to 99% of predicted according to race-specific measures, 15.5% of Black men had emphysema, compared with 4% of White men (P < .001). Respective rates of emphysema were 6.9% for Black women versus 3.2% for White women (P = .025).

When the investigators applied race-neutral spirometry reference equations to the same population, they found that it attenuated but did not completely eliminate the racial disparity in emphysema prevalence among patients with FEV1, ranging from 80% to 120% of predicted.
 

Relic of the past

The results suggest that race-based adjustments of spirometry measures are a relic of less enlightened times, said Adam Gaffney, MD, MPH, assistant professor of medicine at Harvard Medical School, Boston, and a pulmonologist and critical care physician at Cambridge Health Alliance, Massachusetts.

“If the average lower lung function of Black people is being driven by adversity, structural racism, and deprivation, that means that race-specific equations are normalizing that adversity,” he said in an interview.

“In my opinion, it is time to move beyond race-based equations in clinical pulmonary medicine, particularly in the context of patients with established lung disease in whom use of race-based equations might actually lead to undertreatment,” said Dr. Gaffney, who was not involved in the study.

Dr. Liu agreed that it’s time to move to race-neutral measures and that the whole concept of race-based differences is flawed.

“The long-standing structural inequities in health likely made the reference populations have lower lung function than among Whites,” she told this news organization.

Dr. Liu said that evaluation of lung function should not rely on spirometry alone, but should also include – when appropriate – CT scans, as well as improved understanding of how symptoms may be predictive for poor outcomes.

The study was supported by grants from the National Institutes of Health. Dr. Liu and Dr. Gaffney have disclosed no relevant financial relationships.

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

Advocates and users of electroconvulsive therapy (ECT) have received further scientific backing: a retrospective cohort study has provided further evidence that ECT can prevent suicide among severely depressed patients.

The patient cohort comprised 27,231 men and 40,096 women who had been treated as inpatients. The average age was 45.1 years (range: 18-103 years), and 4,982 patients received ECT. The primary endpoint was death by suicide within 365 days of hospital discharge. The secondary endpoints were death not by suicide and total mortality. The cause-specific hazard ratio (csHR) was calculated for patients with ECT, compared with patients without ECT.

In the propensity score-weighted analysis, ECT was linked to a significantly reduced suicide risk (csHR: 0.53; 95% confidence interval, 0.31-0.92). According to the calculations, ECT was associated with a significantly decreased total mortality risk (hazard ratio, 0.75; 95% CI, 0.58-0.97). However, this was not the case for death from causes other than suicide.

The authors, led by Tyler S. Kaster, PhD, a psychiatrist at Temerty Centre for Therapeutic Brain Intervention, Centre for Addiction and Mental Health, Toronto, concluded that this study underlines the importance of ECT, in particular for people with severe depression.
 

A well-tested therapy

ECT has been used for decades as a substantial tool for the treatment of patients with severe mental illnesses. Over the past 15 years, new methods for the treatment of severely depressed patients have been tested, such as vagus nerve stimulation, transcranial magnetic stimulation, and intranasal administration of esketamine. However, in a recent review paper in the New England Journal of Medicine, American psychiatrists Randall T. Espinoza, MD, MPH, University of California, Los Angeles, and Charles H. Kellner, MD, University of South Carolina, Charleston, reported that none of these therapies had proven to be an indisputable substitute for ECT for people with severe depression.

Significant clinical benefits

According to these American psychiatrists, the benefit of ECT has been proven many times, and several studies demonstrate the effect on the risk for suicide. Moreover, quality of life is improved, and the rate of new hospital admissions is lowered. ECT can rapidly improve depressive, psychotic, and catatonic symptoms and reduce suicidal urges for certain patient groups.

Studies on ECT involving patients with treatment-refractory depression have shown response rates of 60%-80% and pooled remission rates of 50%-60%. High response rates for ECT have even been reported for patients with psychotic depression or catatonia. In one study that recruited patients with treatment-refractory schizophrenia, the ECT efficacy rates were between 40% and 70%. In some Asian countries, schizophrenia is the main indication for ECT.
 

Good safety profile

Overall, the psychiatrists consider ECT to be a safe and tolerable therapy. The estimated death rate is around 2.1 deaths per 100,000 treatments. The most common complications are acute cardiopulmonary events, which are estimated to occur in less than 1% of treatments. Rare serious adverse events linked to ECT are arrhythmias, shortness of breath, aspiration, and prolonged seizures. The common but mild side effects are headaches, jaw pain, myalgia, nausea, and vomiting after the procedure, as well as fatigue.

Concerns regarding cognitive impairment still represent an obstacle for the use of ECT. However, in today’s practice, ECT leads to fewer cognitive side effects than previous treatments. The authors stated that it is not possible to predict how an individual patient will be affected, but most patients have only mild or moderate cognitive side effects that generally abate days to weeks after an ECT course has ended.

However, retrograde amnesia linked to ECT can last over a year. In rare cases, acute confusion or delirium can develop that requires interruption or discontinuation of treatment. No indications of structural brain damage after ECT have been detected in neuropathological testing. A Danish cohort study involving 168,015 patients with depression, of whom 3.1% had at least one ECT treatment, did not find a link between ECT with a mean period of almost 5 years and increased onset of dementia.
 

Bad reputation

Dr. Espinoza and Dr. Kellner criticized the fact that, despite its proven efficacy and safety, ECT is used too little. This judgment is nothing new. Psychiatrists have been complaining for years that this procedure is used too little, including Eric Slade, MD, from the University of Baltimore, in 2017 and German professors Andreas Fallgatter, MD, and Urban Wiesing, MD, PhD, in 2018. Dr. Wiesing and Dr. Fallgatter attribute the low level of use to the fact that ECT is labor-intensive, compared with pharmacotherapy.

Another reason is clearly the bad reputation of this method. However, ECT’s poor image, which has only increased over time, is not a convincing argument to forego today’s ECT as a treatment for patients with severe mental illnesses. According to Dr. Fallgatter and Dr. Wiesing, even the risk of misuse of this method is “not a sufficient argument for categorical refusal, rather for caution at best.” They argued that otherwise, “modern medicine would have to renounce many more therapies.”  

This article was translated from Univadis Germany.

Advocates and users of electroconvulsive therapy (ECT) have received further scientific backing: a retrospective cohort study has provided further evidence that ECT can prevent suicide among severely depressed patients.

The patient cohort comprised 27,231 men and 40,096 women who had been treated as inpatients. The average age was 45.1 years (range: 18-103 years), and 4,982 patients received ECT. The primary endpoint was death by suicide within 365 days of hospital discharge. The secondary endpoints were death not by suicide and total mortality. The cause-specific hazard ratio (csHR) was calculated for patients with ECT, compared with patients without ECT.

In the propensity score-weighted analysis, ECT was linked to a significantly reduced suicide risk (csHR: 0.53; 95% confidence interval, 0.31-0.92). According to the calculations, ECT was associated with a significantly decreased total mortality risk (hazard ratio, 0.75; 95% CI, 0.58-0.97). However, this was not the case for death from causes other than suicide.

The authors, led by Tyler S. Kaster, PhD, a psychiatrist at Temerty Centre for Therapeutic Brain Intervention, Centre for Addiction and Mental Health, Toronto, concluded that this study underlines the importance of ECT, in particular for people with severe depression.
 

A well-tested therapy

ECT has been used for decades as a substantial tool for the treatment of patients with severe mental illnesses. Over the past 15 years, new methods for the treatment of severely depressed patients have been tested, such as vagus nerve stimulation, transcranial magnetic stimulation, and intranasal administration of esketamine. However, in a recent review paper in the New England Journal of Medicine, American psychiatrists Randall T. Espinoza, MD, MPH, University of California, Los Angeles, and Charles H. Kellner, MD, University of South Carolina, Charleston, reported that none of these therapies had proven to be an indisputable substitute for ECT for people with severe depression.

Significant clinical benefits

According to these American psychiatrists, the benefit of ECT has been proven many times, and several studies demonstrate the effect on the risk for suicide. Moreover, quality of life is improved, and the rate of new hospital admissions is lowered. ECT can rapidly improve depressive, psychotic, and catatonic symptoms and reduce suicidal urges for certain patient groups.

Studies on ECT involving patients with treatment-refractory depression have shown response rates of 60%-80% and pooled remission rates of 50%-60%. High response rates for ECT have even been reported for patients with psychotic depression or catatonia. In one study that recruited patients with treatment-refractory schizophrenia, the ECT efficacy rates were between 40% and 70%. In some Asian countries, schizophrenia is the main indication for ECT.
 

Good safety profile

Overall, the psychiatrists consider ECT to be a safe and tolerable therapy. The estimated death rate is around 2.1 deaths per 100,000 treatments. The most common complications are acute cardiopulmonary events, which are estimated to occur in less than 1% of treatments. Rare serious adverse events linked to ECT are arrhythmias, shortness of breath, aspiration, and prolonged seizures. The common but mild side effects are headaches, jaw pain, myalgia, nausea, and vomiting after the procedure, as well as fatigue.

Concerns regarding cognitive impairment still represent an obstacle for the use of ECT. However, in today’s practice, ECT leads to fewer cognitive side effects than previous treatments. The authors stated that it is not possible to predict how an individual patient will be affected, but most patients have only mild or moderate cognitive side effects that generally abate days to weeks after an ECT course has ended.

However, retrograde amnesia linked to ECT can last over a year. In rare cases, acute confusion or delirium can develop that requires interruption or discontinuation of treatment. No indications of structural brain damage after ECT have been detected in neuropathological testing. A Danish cohort study involving 168,015 patients with depression, of whom 3.1% had at least one ECT treatment, did not find a link between ECT with a mean period of almost 5 years and increased onset of dementia.
 

Bad reputation

Dr. Espinoza and Dr. Kellner criticized the fact that, despite its proven efficacy and safety, ECT is used too little. This judgment is nothing new. Psychiatrists have been complaining for years that this procedure is used too little, including Eric Slade, MD, from the University of Baltimore, in 2017 and German professors Andreas Fallgatter, MD, and Urban Wiesing, MD, PhD, in 2018. Dr. Wiesing and Dr. Fallgatter attribute the low level of use to the fact that ECT is labor-intensive, compared with pharmacotherapy.

Another reason is clearly the bad reputation of this method. However, ECT’s poor image, which has only increased over time, is not a convincing argument to forego today’s ECT as a treatment for patients with severe mental illnesses. According to Dr. Fallgatter and Dr. Wiesing, even the risk of misuse of this method is “not a sufficient argument for categorical refusal, rather for caution at best.” They argued that otherwise, “modern medicine would have to renounce many more therapies.”  

This article was translated from Univadis Germany.

Advocates and users of electroconvulsive therapy (ECT) have received further scientific backing: a retrospective cohort study has provided further evidence that ECT can prevent suicide among severely depressed patients.

The patient cohort comprised 27,231 men and 40,096 women who had been treated as inpatients. The average age was 45.1 years (range: 18-103 years), and 4,982 patients received ECT. The primary endpoint was death by suicide within 365 days of hospital discharge. The secondary endpoints were death not by suicide and total mortality. The cause-specific hazard ratio (csHR) was calculated for patients with ECT, compared with patients without ECT.

In the propensity score-weighted analysis, ECT was linked to a significantly reduced suicide risk (csHR: 0.53; 95% confidence interval, 0.31-0.92). According to the calculations, ECT was associated with a significantly decreased total mortality risk (hazard ratio, 0.75; 95% CI, 0.58-0.97). However, this was not the case for death from causes other than suicide.

The authors, led by Tyler S. Kaster, PhD, a psychiatrist at Temerty Centre for Therapeutic Brain Intervention, Centre for Addiction and Mental Health, Toronto, concluded that this study underlines the importance of ECT, in particular for people with severe depression.
 

A well-tested therapy

ECT has been used for decades as a substantial tool for the treatment of patients with severe mental illnesses. Over the past 15 years, new methods for the treatment of severely depressed patients have been tested, such as vagus nerve stimulation, transcranial magnetic stimulation, and intranasal administration of esketamine. However, in a recent review paper in the New England Journal of Medicine, American psychiatrists Randall T. Espinoza, MD, MPH, University of California, Los Angeles, and Charles H. Kellner, MD, University of South Carolina, Charleston, reported that none of these therapies had proven to be an indisputable substitute for ECT for people with severe depression.

Significant clinical benefits

According to these American psychiatrists, the benefit of ECT has been proven many times, and several studies demonstrate the effect on the risk for suicide. Moreover, quality of life is improved, and the rate of new hospital admissions is lowered. ECT can rapidly improve depressive, psychotic, and catatonic symptoms and reduce suicidal urges for certain patient groups.

Studies on ECT involving patients with treatment-refractory depression have shown response rates of 60%-80% and pooled remission rates of 50%-60%. High response rates for ECT have even been reported for patients with psychotic depression or catatonia. In one study that recruited patients with treatment-refractory schizophrenia, the ECT efficacy rates were between 40% and 70%. In some Asian countries, schizophrenia is the main indication for ECT.
 

Good safety profile

Overall, the psychiatrists consider ECT to be a safe and tolerable therapy. The estimated death rate is around 2.1 deaths per 100,000 treatments. The most common complications are acute cardiopulmonary events, which are estimated to occur in less than 1% of treatments. Rare serious adverse events linked to ECT are arrhythmias, shortness of breath, aspiration, and prolonged seizures. The common but mild side effects are headaches, jaw pain, myalgia, nausea, and vomiting after the procedure, as well as fatigue.

Concerns regarding cognitive impairment still represent an obstacle for the use of ECT. However, in today’s practice, ECT leads to fewer cognitive side effects than previous treatments. The authors stated that it is not possible to predict how an individual patient will be affected, but most patients have only mild or moderate cognitive side effects that generally abate days to weeks after an ECT course has ended.

However, retrograde amnesia linked to ECT can last over a year. In rare cases, acute confusion or delirium can develop that requires interruption or discontinuation of treatment. No indications of structural brain damage after ECT have been detected in neuropathological testing. A Danish cohort study involving 168,015 patients with depression, of whom 3.1% had at least one ECT treatment, did not find a link between ECT with a mean period of almost 5 years and increased onset of dementia.
 

Bad reputation

Dr. Espinoza and Dr. Kellner criticized the fact that, despite its proven efficacy and safety, ECT is used too little. This judgment is nothing new. Psychiatrists have been complaining for years that this procedure is used too little, including Eric Slade, MD, from the University of Baltimore, in 2017 and German professors Andreas Fallgatter, MD, and Urban Wiesing, MD, PhD, in 2018. Dr. Wiesing and Dr. Fallgatter attribute the low level of use to the fact that ECT is labor-intensive, compared with pharmacotherapy.

Another reason is clearly the bad reputation of this method. However, ECT’s poor image, which has only increased over time, is not a convincing argument to forego today’s ECT as a treatment for patients with severe mental illnesses. According to Dr. Fallgatter and Dr. Wiesing, even the risk of misuse of this method is “not a sufficient argument for categorical refusal, rather for caution at best.” They argued that otherwise, “modern medicine would have to renounce many more therapies.”  

This article was translated from Univadis Germany.

A new study questions the conventional wisdom of using steroids and anti-inflammatory drugs like ibuprofen to treat low back pain if exercise and other nondrug therapies don’t work right away.

Those medications offer relief from acute pain but may actually increase a person’s chances of developing chronic pain, said the investigators for a study published in Science Translational Medicine. The study results indicate that inflammation is a normal part of recovering from a painful injury and that inhibiting inflammation may result in more-difficult-to-treat chronic pain.

“For many decades it’s been standard medical practice to treat pain with anti-inflammatory drugs,” Jeffrey Mogil, PhD, a psychology professor at McGill University, Montreal, said in a school news release. “But we found that this short-term fix could lead to longer-term problems.”

Researchers looked at low back pain because it’s so common, with 25% of U.S. adults saying they had low back pain in the previous 3 months, according to the Centers for Disease Control and Prevention. Acute back pain is defined as lasting less than 4 weeks while chronic back pain lasts more than 12 weeks.

By examining blood samples, researchers discovered that people whose low back pain was resolved had high inflammation driven by neutrophils, a type of white blood cell that helps the body fight infection, the study said.

“Neutrophils dominate the early stages of inflammation and set the stage for repair of tissue damage. Inflammation occurs for a reason, and it looks like it’s dangerous to interfere with it,” Dr. Mogil said in the news release.

The research team found that blocking neutrophils in mice prolonged pain in the animals up to 10-fold. Pain also was prolonged when the mice were given anti-inflammatory drugs and steroids, the news release says.

McGill University said other studies support the findings. The school cited an analysis of 500,000 people in the United Kingdom. The analysis found that those taking anti-inflammatory drugs for pain were more likely to have pain 2 to 10 years later.

While saying the study suggests it’s time to reconsider how pain is treated, the researchers called for clinical trials on humans, not just observations of people with low back pain.

Experts warned about accepting the results without further investigation.

“It’s intriguing but requires further study,” Steven J. Atlas, MD, director of the Primary Care Research & Quality Improvement Network at Massachusetts General Hospital, Boston, told The New York Times.

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

A new study questions the conventional wisdom of using steroids and anti-inflammatory drugs like ibuprofen to treat low back pain if exercise and other nondrug therapies don’t work right away.

Those medications offer relief from acute pain but may actually increase a person’s chances of developing chronic pain, said the investigators for a study published in Science Translational Medicine. The study results indicate that inflammation is a normal part of recovering from a painful injury and that inhibiting inflammation may result in more-difficult-to-treat chronic pain.

“For many decades it’s been standard medical practice to treat pain with anti-inflammatory drugs,” Jeffrey Mogil, PhD, a psychology professor at McGill University, Montreal, said in a school news release. “But we found that this short-term fix could lead to longer-term problems.”

Researchers looked at low back pain because it’s so common, with 25% of U.S. adults saying they had low back pain in the previous 3 months, according to the Centers for Disease Control and Prevention. Acute back pain is defined as lasting less than 4 weeks while chronic back pain lasts more than 12 weeks.

By examining blood samples, researchers discovered that people whose low back pain was resolved had high inflammation driven by neutrophils, a type of white blood cell that helps the body fight infection, the study said.

“Neutrophils dominate the early stages of inflammation and set the stage for repair of tissue damage. Inflammation occurs for a reason, and it looks like it’s dangerous to interfere with it,” Dr. Mogil said in the news release.

The research team found that blocking neutrophils in mice prolonged pain in the animals up to 10-fold. Pain also was prolonged when the mice were given anti-inflammatory drugs and steroids, the news release says.

McGill University said other studies support the findings. The school cited an analysis of 500,000 people in the United Kingdom. The analysis found that those taking anti-inflammatory drugs for pain were more likely to have pain 2 to 10 years later.

While saying the study suggests it’s time to reconsider how pain is treated, the researchers called for clinical trials on humans, not just observations of people with low back pain.

Experts warned about accepting the results without further investigation.

“It’s intriguing but requires further study,” Steven J. Atlas, MD, director of the Primary Care Research & Quality Improvement Network at Massachusetts General Hospital, Boston, told The New York Times.

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

A new study questions the conventional wisdom of using steroids and anti-inflammatory drugs like ibuprofen to treat low back pain if exercise and other nondrug therapies don’t work right away.

Those medications offer relief from acute pain but may actually increase a person’s chances of developing chronic pain, said the investigators for a study published in Science Translational Medicine. The study results indicate that inflammation is a normal part of recovering from a painful injury and that inhibiting inflammation may result in more-difficult-to-treat chronic pain.

“For many decades it’s been standard medical practice to treat pain with anti-inflammatory drugs,” Jeffrey Mogil, PhD, a psychology professor at McGill University, Montreal, said in a school news release. “But we found that this short-term fix could lead to longer-term problems.”

Researchers looked at low back pain because it’s so common, with 25% of U.S. adults saying they had low back pain in the previous 3 months, according to the Centers for Disease Control and Prevention. Acute back pain is defined as lasting less than 4 weeks while chronic back pain lasts more than 12 weeks.

By examining blood samples, researchers discovered that people whose low back pain was resolved had high inflammation driven by neutrophils, a type of white blood cell that helps the body fight infection, the study said.

“Neutrophils dominate the early stages of inflammation and set the stage for repair of tissue damage. Inflammation occurs for a reason, and it looks like it’s dangerous to interfere with it,” Dr. Mogil said in the news release.

The research team found that blocking neutrophils in mice prolonged pain in the animals up to 10-fold. Pain also was prolonged when the mice were given anti-inflammatory drugs and steroids, the news release says.

McGill University said other studies support the findings. The school cited an analysis of 500,000 people in the United Kingdom. The analysis found that those taking anti-inflammatory drugs for pain were more likely to have pain 2 to 10 years later.

While saying the study suggests it’s time to reconsider how pain is treated, the researchers called for clinical trials on humans, not just observations of people with low back pain.

Experts warned about accepting the results without further investigation.

“It’s intriguing but requires further study,” Steven J. Atlas, MD, director of the Primary Care Research & Quality Improvement Network at Massachusetts General Hospital, Boston, told The New York Times.

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

The annual cost of Lyme disease in the United States could be nearly $970 million, according to new research. But not all cases of Lyme disease are equally costly. Costs for patients with disseminated Lyme disease were more than twice as high as those for patients with localized disease.

CDC/ Dr. Amanda Loftis, Dr. William Nicholson, Dr. Will Reeves, Dr. Chris Paddock

“These findings emphasize the importance of early and accurate diagnosis to reduce both illness and its associated personal and societal costs,” the study’s authors write. The analysis was published  in Emerging Infectious Diseases. The authors are from the Centers for Disease Control and Prevention, the Yale School of Public Health, and the Departments of Health of Minnesota, Maryland, and New York State.

Lyme disease is the most reported vector-borne disease in the United States; an estimated 476,000 Americans are diagnosed with the infection every year. Though the highest incidences are in the Northeast and in Minnesota and Wisconsin, the CDC has recorded cases in all 50 states. Over the past 20 years, estimates of the total cost of treating Lyme disease have varied from $203 million to nearly $1.3 billion. A major limitation to these studies, however, is that they may not accurately identify patients with Lyme disease or capture many of the nonmedical costs associated with treatment, the authors write, such as costs associated with time taken off work and travel to appointments.

To better capture the comprehensive cost of Lyme disease in the United States, researchers conducted a prospective study from September 2014 to January 2016 and followed reported cases in four states with high rates of Lyme disease: Connecticut, Maryland, Minnesota, and New York. The team conducted monthly patient surveys and queried billing codes from participants’ clinicians to estimate both the personal expenses and societal costs – such as total costs to the health care system – of Lyme disease.

Participants were variously assigned to one of three categories: those with confirmed local disease (such as patients with erythema migrans); those with confirmed disseminated disease, with symptoms including arthritis, lymphocytic meningitis, and encephalomyelitis; and those with probable cases with reported symptoms.

The researchers surveyed 901 participants with clinician-diagnosed Lyme disease: 402 with localized disease, 238 with disseminated disease, and 261 with probable cases. Nearly all participants (94%) were White, 57% were men, and 71% had an annual household income above $60,000. About 28% of participants were younger than 18 years, 16% were aged 18-45 years, 36% were aged 46-65, and 19% were older than 65 years. For most participants (68%), complete medical cost data were available. Those data were used to calculate societal costs.

Costs per patient varied dramatically, from $0.46 to $30,628. On average, patients spent $1,252 during the study period on expenses related to Lyme disease treatment, including expenses associated with travel and time taken off work. The median cost to patients was notably smaller, at $244. Patients with disseminated disease had the highest median ($358) and mean ($1,692) costs, followed by participants with probable disease (median, $315; mean, $1,277). Participants with localized disease had the lowest median ($170) and mean ($1,070) costs.

Societal costs ranged from $54 to $122,766 per patient; the median was $690, and the mean was $2,032. Multiplying these numbers by the estimated cases diagnosed nationally each year, researchers determined that the total cost of Lyme disease in the United States is between $345 million and $968 million.

The study “pointed out the tremendous variability in costs” associated with Lyme disease treatment, Brian Fallon, MD, MPH, director of the Lyme and Tick-Borne Diseases Research Center at the Columbia University Irving Medical Center, New York, told this news organization. He was not involved with the research. Some patients continued having health expenses after the end of the study, which means their costs would be even higher, he noted. Though most patients fully recovered after 1 year, about 4% still reported symptoms, and 3% were still incurring costs.

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

The annual cost of Lyme disease in the United States could be nearly $970 million, according to new research. But not all cases of Lyme disease are equally costly. Costs for patients with disseminated Lyme disease were more than twice as high as those for patients with localized disease.

CDC/ Dr. Amanda Loftis, Dr. William Nicholson, Dr. Will Reeves, Dr. Chris Paddock

“These findings emphasize the importance of early and accurate diagnosis to reduce both illness and its associated personal and societal costs,” the study’s authors write. The analysis was published  in Emerging Infectious Diseases. The authors are from the Centers for Disease Control and Prevention, the Yale School of Public Health, and the Departments of Health of Minnesota, Maryland, and New York State.

Lyme disease is the most reported vector-borne disease in the United States; an estimated 476,000 Americans are diagnosed with the infection every year. Though the highest incidences are in the Northeast and in Minnesota and Wisconsin, the CDC has recorded cases in all 50 states. Over the past 20 years, estimates of the total cost of treating Lyme disease have varied from $203 million to nearly $1.3 billion. A major limitation to these studies, however, is that they may not accurately identify patients with Lyme disease or capture many of the nonmedical costs associated with treatment, the authors write, such as costs associated with time taken off work and travel to appointments.

To better capture the comprehensive cost of Lyme disease in the United States, researchers conducted a prospective study from September 2014 to January 2016 and followed reported cases in four states with high rates of Lyme disease: Connecticut, Maryland, Minnesota, and New York. The team conducted monthly patient surveys and queried billing codes from participants’ clinicians to estimate both the personal expenses and societal costs – such as total costs to the health care system – of Lyme disease.

Participants were variously assigned to one of three categories: those with confirmed local disease (such as patients with erythema migrans); those with confirmed disseminated disease, with symptoms including arthritis, lymphocytic meningitis, and encephalomyelitis; and those with probable cases with reported symptoms.

The researchers surveyed 901 participants with clinician-diagnosed Lyme disease: 402 with localized disease, 238 with disseminated disease, and 261 with probable cases. Nearly all participants (94%) were White, 57% were men, and 71% had an annual household income above $60,000. About 28% of participants were younger than 18 years, 16% were aged 18-45 years, 36% were aged 46-65, and 19% were older than 65 years. For most participants (68%), complete medical cost data were available. Those data were used to calculate societal costs.

Costs per patient varied dramatically, from $0.46 to $30,628. On average, patients spent $1,252 during the study period on expenses related to Lyme disease treatment, including expenses associated with travel and time taken off work. The median cost to patients was notably smaller, at $244. Patients with disseminated disease had the highest median ($358) and mean ($1,692) costs, followed by participants with probable disease (median, $315; mean, $1,277). Participants with localized disease had the lowest median ($170) and mean ($1,070) costs.

Societal costs ranged from $54 to $122,766 per patient; the median was $690, and the mean was $2,032. Multiplying these numbers by the estimated cases diagnosed nationally each year, researchers determined that the total cost of Lyme disease in the United States is between $345 million and $968 million.

The study “pointed out the tremendous variability in costs” associated with Lyme disease treatment, Brian Fallon, MD, MPH, director of the Lyme and Tick-Borne Diseases Research Center at the Columbia University Irving Medical Center, New York, told this news organization. He was not involved with the research. Some patients continued having health expenses after the end of the study, which means their costs would be even higher, he noted. Though most patients fully recovered after 1 year, about 4% still reported symptoms, and 3% were still incurring costs.

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

The annual cost of Lyme disease in the United States could be nearly $970 million, according to new research. But not all cases of Lyme disease are equally costly. Costs for patients with disseminated Lyme disease were more than twice as high as those for patients with localized disease.

CDC/ Dr. Amanda Loftis, Dr. William Nicholson, Dr. Will Reeves, Dr. Chris Paddock

“These findings emphasize the importance of early and accurate diagnosis to reduce both illness and its associated personal and societal costs,” the study’s authors write. The analysis was published  in Emerging Infectious Diseases. The authors are from the Centers for Disease Control and Prevention, the Yale School of Public Health, and the Departments of Health of Minnesota, Maryland, and New York State.

Lyme disease is the most reported vector-borne disease in the United States; an estimated 476,000 Americans are diagnosed with the infection every year. Though the highest incidences are in the Northeast and in Minnesota and Wisconsin, the CDC has recorded cases in all 50 states. Over the past 20 years, estimates of the total cost of treating Lyme disease have varied from $203 million to nearly $1.3 billion. A major limitation to these studies, however, is that they may not accurately identify patients with Lyme disease or capture many of the nonmedical costs associated with treatment, the authors write, such as costs associated with time taken off work and travel to appointments.

To better capture the comprehensive cost of Lyme disease in the United States, researchers conducted a prospective study from September 2014 to January 2016 and followed reported cases in four states with high rates of Lyme disease: Connecticut, Maryland, Minnesota, and New York. The team conducted monthly patient surveys and queried billing codes from participants’ clinicians to estimate both the personal expenses and societal costs – such as total costs to the health care system – of Lyme disease.

Participants were variously assigned to one of three categories: those with confirmed local disease (such as patients with erythema migrans); those with confirmed disseminated disease, with symptoms including arthritis, lymphocytic meningitis, and encephalomyelitis; and those with probable cases with reported symptoms.

The researchers surveyed 901 participants with clinician-diagnosed Lyme disease: 402 with localized disease, 238 with disseminated disease, and 261 with probable cases. Nearly all participants (94%) were White, 57% were men, and 71% had an annual household income above $60,000. About 28% of participants were younger than 18 years, 16% were aged 18-45 years, 36% were aged 46-65, and 19% were older than 65 years. For most participants (68%), complete medical cost data were available. Those data were used to calculate societal costs.

Costs per patient varied dramatically, from $0.46 to $30,628. On average, patients spent $1,252 during the study period on expenses related to Lyme disease treatment, including expenses associated with travel and time taken off work. The median cost to patients was notably smaller, at $244. Patients with disseminated disease had the highest median ($358) and mean ($1,692) costs, followed by participants with probable disease (median, $315; mean, $1,277). Participants with localized disease had the lowest median ($170) and mean ($1,070) costs.

Societal costs ranged from $54 to $122,766 per patient; the median was $690, and the mean was $2,032. Multiplying these numbers by the estimated cases diagnosed nationally each year, researchers determined that the total cost of Lyme disease in the United States is between $345 million and $968 million.

The study “pointed out the tremendous variability in costs” associated with Lyme disease treatment, Brian Fallon, MD, MPH, director of the Lyme and Tick-Borne Diseases Research Center at the Columbia University Irving Medical Center, New York, told this news organization. He was not involved with the research. Some patients continued having health expenses after the end of the study, which means their costs would be even higher, he noted. Though most patients fully recovered after 1 year, about 4% still reported symptoms, and 3% were still incurring costs.

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

People with nonalcoholic fatty liver disease (NAFLD) and a lean or healthy body mass index are at increased risk for peripheral vascular disease, stroke, and cardiovascular disease, a surprise finding from a new study reveals.

“Our team had expected to see that those with a normal BMI would have a lower prevalence of any metabolic or cardiovascular conditions,” lead researcher Karn Wijarnpreecha, MD, MPH, said during a media briefing that previewed select research for Digestive Disease Week^® (DDW) 2022. “So, we were very surprised to find this link to cardiovascular disease.”

The investigators saw this increased risk of cardiovascular disease despite this group having a lower prevalence of atherosclerotic risk factors and metabolic disease.

This first study of its kind suggests physicians should consider the risk of cardiovascular disease in all patients with NAFLD, not just in those who are overweight or living with obesity – groups traditionally thought to carry more risk.

NAFLD in lean individuals is not a benign disease.

“NAFLD patients with a normal BMI are often overlooked because we assume that the risk for more serious conditions is lower than for those who are overweight or obese. But this way of thinking may be putting these patients at risk,” added Dr. Wijarnpreecha, who is a transplant hepatology fellow at the University of Michigan, Ann Arbor.

Key findings

Approximately 25% of U.S. adults live with NAFLD, an umbrella term for liver conditions in people who drink little to no alcohol. It is characterized by too much fat stored in the liver. Although most people have no symptoms, the condition can lead to other dangerous conditions, such as diabetes, cardiovascular disease, and cirrhosis of the liver, Dr. Wijarnpreecha said.

The investigators retrospectively studied a cohort of 18,793 adults diagnosed with NAFLD at the University of Michigan Hospital from 2012-2021. One aim was to compare the prevalence of cirrhosis, cardiovascular disease, metabolic diseases, and chronic kidney disease in relation to BMI.

They also classified people into four BMI categories: lean, overweight, obesity class 1, and obesity class 2-3.

Compared with non-lean patients, lean patients had a higher prevalence of peripheral arterial disease and stroke and a similar rate of cardiovascular disease based on identification of ICD codes.

Almost 6% of lean patients had peripheral arterial disease, compared with rates of approximately 4%-5% in overweight people and people with obesity. Similarly, more than 6% of the lean group experienced a stroke compared with 5% or less of the other BMI groups.

“We found that lean patients with NAFLD also had a significant higher prevalence of cardiovascular disease, independent of age, sex, race, smoking status, diabetes, hypertension, and dyslipidemia,” Dr. Wijarnpreecha said.

At the same time, compared with non-lean patients, lean patients had a lower prevalence of cirrhosis, diabetes mellitus, hypertension, dyslipidemia, and chronic kidney disease in an analysis that adjusted for confounders.
 

Exploring the unknown

Researchers now have a mystery on their hands: What is causing this unexpected higher risk of cardiovascular disease in lean people with NAFLD?

Loren Laine, MD, chief of the section of digestive diseases at Yale University School of Medicine, New Haven, Conn., and moderator of the media briefing, asked Wijarnpreecha for his leading theory behind this connection.

“We think that could be from a difference in lifestyle, diet, exercise, genetics, or even gut microbiota,” Dr. Wijarnpreecha replied. “But these are factors that we did not capture from this current study.”

“We are preparing to conduct additional research with longitudinal data to better understand NAFLD in lean patients,” Dr. Wijarnpreecha added.

“It’s an interesting finding, but there are some questions from this retrospective study,” said Arun J. Sanyal, MD, when asked to comment on the study.

Identifying and quantifying any alcohol use, smoking, or hypertension that could also have contributed to increased cardiovascular risk would be useful. Another question relates to how the population with NAFLD was identified. Was NAFLD an incidental finding in their diagnosis, asked Dr. Sanyal, director of the Stravitz-Sanyal Institute for Liver Disease & Metabolic Health at Virginia Commonwealth University, Richmond.

“I’m not dissing the study,” he said, “But like all the observations like this, I think we have to kick the tires.”

It’s an “important new observation” that requires further study to fully understand what it means and what the therapeutic implications might be. It is also important to assess any possible confounders and any causal relationship among these factors, Dr. Sanyal added.

“There’s no question it is important to continue to do these types of studies,” he added. “Through this kind of research we find new things that lead to the science that can then significantly change how we approach these issues.”

A version of this article first appeared on Medscape.com. This article was updated on May 18, 2022.

People with nonalcoholic fatty liver disease (NAFLD) and a lean or healthy body mass index are at increased risk for peripheral vascular disease, stroke, and cardiovascular disease, a surprise finding from a new study reveals.

“Our team had expected to see that those with a normal BMI would have a lower prevalence of any metabolic or cardiovascular conditions,” lead researcher Karn Wijarnpreecha, MD, MPH, said during a media briefing that previewed select research for Digestive Disease Week^® (DDW) 2022. “So, we were very surprised to find this link to cardiovascular disease.”

The investigators saw this increased risk of cardiovascular disease despite this group having a lower prevalence of atherosclerotic risk factors and metabolic disease.

This first study of its kind suggests physicians should consider the risk of cardiovascular disease in all patients with NAFLD, not just in those who are overweight or living with obesity – groups traditionally thought to carry more risk.

NAFLD in lean individuals is not a benign disease.

“NAFLD patients with a normal BMI are often overlooked because we assume that the risk for more serious conditions is lower than for those who are overweight or obese. But this way of thinking may be putting these patients at risk,” added Dr. Wijarnpreecha, who is a transplant hepatology fellow at the University of Michigan, Ann Arbor.

Key findings

Approximately 25% of U.S. adults live with NAFLD, an umbrella term for liver conditions in people who drink little to no alcohol. It is characterized by too much fat stored in the liver. Although most people have no symptoms, the condition can lead to other dangerous conditions, such as diabetes, cardiovascular disease, and cirrhosis of the liver, Dr. Wijarnpreecha said.

The investigators retrospectively studied a cohort of 18,793 adults diagnosed with NAFLD at the University of Michigan Hospital from 2012-2021. One aim was to compare the prevalence of cirrhosis, cardiovascular disease, metabolic diseases, and chronic kidney disease in relation to BMI.

They also classified people into four BMI categories: lean, overweight, obesity class 1, and obesity class 2-3.

Compared with non-lean patients, lean patients had a higher prevalence of peripheral arterial disease and stroke and a similar rate of cardiovascular disease based on identification of ICD codes.

Almost 6% of lean patients had peripheral arterial disease, compared with rates of approximately 4%-5% in overweight people and people with obesity. Similarly, more than 6% of the lean group experienced a stroke compared with 5% or less of the other BMI groups.

“We found that lean patients with NAFLD also had a significant higher prevalence of cardiovascular disease, independent of age, sex, race, smoking status, diabetes, hypertension, and dyslipidemia,” Dr. Wijarnpreecha said.

At the same time, compared with non-lean patients, lean patients had a lower prevalence of cirrhosis, diabetes mellitus, hypertension, dyslipidemia, and chronic kidney disease in an analysis that adjusted for confounders.
 

Exploring the unknown

Researchers now have a mystery on their hands: What is causing this unexpected higher risk of cardiovascular disease in lean people with NAFLD?

Loren Laine, MD, chief of the section of digestive diseases at Yale University School of Medicine, New Haven, Conn., and moderator of the media briefing, asked Wijarnpreecha for his leading theory behind this connection.

“We think that could be from a difference in lifestyle, diet, exercise, genetics, or even gut microbiota,” Dr. Wijarnpreecha replied. “But these are factors that we did not capture from this current study.”

“We are preparing to conduct additional research with longitudinal data to better understand NAFLD in lean patients,” Dr. Wijarnpreecha added.

“It’s an interesting finding, but there are some questions from this retrospective study,” said Arun J. Sanyal, MD, when asked to comment on the study.

Identifying and quantifying any alcohol use, smoking, or hypertension that could also have contributed to increased cardiovascular risk would be useful. Another question relates to how the population with NAFLD was identified. Was NAFLD an incidental finding in their diagnosis, asked Dr. Sanyal, director of the Stravitz-Sanyal Institute for Liver Disease & Metabolic Health at Virginia Commonwealth University, Richmond.

“I’m not dissing the study,” he said, “But like all the observations like this, I think we have to kick the tires.”

It’s an “important new observation” that requires further study to fully understand what it means and what the therapeutic implications might be. It is also important to assess any possible confounders and any causal relationship among these factors, Dr. Sanyal added.

“There’s no question it is important to continue to do these types of studies,” he added. “Through this kind of research we find new things that lead to the science that can then significantly change how we approach these issues.”

A version of this article first appeared on Medscape.com. This article was updated on May 18, 2022.

People with nonalcoholic fatty liver disease (NAFLD) and a lean or healthy body mass index are at increased risk for peripheral vascular disease, stroke, and cardiovascular disease, a surprise finding from a new study reveals.

“Our team had expected to see that those with a normal BMI would have a lower prevalence of any metabolic or cardiovascular conditions,” lead researcher Karn Wijarnpreecha, MD, MPH, said during a media briefing that previewed select research for Digestive Disease Week^® (DDW) 2022. “So, we were very surprised to find this link to cardiovascular disease.”

The investigators saw this increased risk of cardiovascular disease despite this group having a lower prevalence of atherosclerotic risk factors and metabolic disease.

This first study of its kind suggests physicians should consider the risk of cardiovascular disease in all patients with NAFLD, not just in those who are overweight or living with obesity – groups traditionally thought to carry more risk.

NAFLD in lean individuals is not a benign disease.

“NAFLD patients with a normal BMI are often overlooked because we assume that the risk for more serious conditions is lower than for those who are overweight or obese. But this way of thinking may be putting these patients at risk,” added Dr. Wijarnpreecha, who is a transplant hepatology fellow at the University of Michigan, Ann Arbor.

Key findings

Approximately 25% of U.S. adults live with NAFLD, an umbrella term for liver conditions in people who drink little to no alcohol. It is characterized by too much fat stored in the liver. Although most people have no symptoms, the condition can lead to other dangerous conditions, such as diabetes, cardiovascular disease, and cirrhosis of the liver, Dr. Wijarnpreecha said.

The investigators retrospectively studied a cohort of 18,793 adults diagnosed with NAFLD at the University of Michigan Hospital from 2012-2021. One aim was to compare the prevalence of cirrhosis, cardiovascular disease, metabolic diseases, and chronic kidney disease in relation to BMI.

They also classified people into four BMI categories: lean, overweight, obesity class 1, and obesity class 2-3.

Compared with non-lean patients, lean patients had a higher prevalence of peripheral arterial disease and stroke and a similar rate of cardiovascular disease based on identification of ICD codes.

Almost 6% of lean patients had peripheral arterial disease, compared with rates of approximately 4%-5% in overweight people and people with obesity. Similarly, more than 6% of the lean group experienced a stroke compared with 5% or less of the other BMI groups.

“We found that lean patients with NAFLD also had a significant higher prevalence of cardiovascular disease, independent of age, sex, race, smoking status, diabetes, hypertension, and dyslipidemia,” Dr. Wijarnpreecha said.

At the same time, compared with non-lean patients, lean patients had a lower prevalence of cirrhosis, diabetes mellitus, hypertension, dyslipidemia, and chronic kidney disease in an analysis that adjusted for confounders.
 

Exploring the unknown

Researchers now have a mystery on their hands: What is causing this unexpected higher risk of cardiovascular disease in lean people with NAFLD?

Loren Laine, MD, chief of the section of digestive diseases at Yale University School of Medicine, New Haven, Conn., and moderator of the media briefing, asked Wijarnpreecha for his leading theory behind this connection.

“We think that could be from a difference in lifestyle, diet, exercise, genetics, or even gut microbiota,” Dr. Wijarnpreecha replied. “But these are factors that we did not capture from this current study.”

“We are preparing to conduct additional research with longitudinal data to better understand NAFLD in lean patients,” Dr. Wijarnpreecha added.

“It’s an interesting finding, but there are some questions from this retrospective study,” said Arun J. Sanyal, MD, when asked to comment on the study.

Identifying and quantifying any alcohol use, smoking, or hypertension that could also have contributed to increased cardiovascular risk would be useful. Another question relates to how the population with NAFLD was identified. Was NAFLD an incidental finding in their diagnosis, asked Dr. Sanyal, director of the Stravitz-Sanyal Institute for Liver Disease & Metabolic Health at Virginia Commonwealth University, Richmond.

“I’m not dissing the study,” he said, “But like all the observations like this, I think we have to kick the tires.”

It’s an “important new observation” that requires further study to fully understand what it means and what the therapeutic implications might be. It is also important to assess any possible confounders and any causal relationship among these factors, Dr. Sanyal added.

“There’s no question it is important to continue to do these types of studies,” he added. “Through this kind of research we find new things that lead to the science that can then significantly change how we approach these issues.”

A version of this article first appeared on Medscape.com. This article was updated on May 18, 2022.

Thousands of military veterans who are sick after being exposed to toxic smoke and dust while on duty are facing a Senate roadblock to ambitious legislation designed to provide them care.

The Senate could start work as soon as this week on a bipartisan bill, called the Honoring Our PACT Act, that passed the House of Representatives in March. It would make it much easier for veterans to get health care and benefits from the Veterans Health Administration if they get sick because of the air they breathed around massive, open-air incineration pits. The military used those pits in war zones around the globe — sometimes the size of football fields — to burn anything from human and medical waste to plastics and munitions, setting it alight with jet fuel.

As it stands now, more than three-quarters of all veterans who submit claims for cancer, breathing disorders, and other illnesses that they believe are caused by inhaling poisonous burn pit smoke have their claims denied, according to estimates from the Department of Veterans Affairs and service organizations.

The reason so few are approved is that the military and VA require injured war fighters to prove an illness is directly connected to their service — something that is extremely difficult when it comes to toxic exposures. The House’s PACT Act would make that easier by declaring that any of the 3.5 million veterans who served in the global war on terror — including operations in Afghanistan, Iraq, and the Persian Gulf — would be presumed eligible for benefits if they come down with any of 23 ailments linked to the burn pits.

Although 34 Republicans voted with Democrats to pass the bill in the House, only one Republican, Sen. Marco Rubio of Florida, has signaled support for the measure. At least 10 GOP members would have to join all Democrats to avoid the threat of a filibuster in the Senate and allow the bill to advance to President Joe Biden’s desk. Biden called on Congress to pass such legislation in his State of the Union address, citing the death of his son Beau Biden, who served in Iraq in 2008 and died in 2015 of glioblastoma, a brain cancer included on the bill’s list of qualifying conditions.

Senate Republicans are raising concerns about the measure, however, suggesting it won’t be paid for, that it is too big, too ambitious, and could end up promising more than the government can deliver.

The Congressional Budget Office estimates the bill would cost more than $300 billion over 10 years, and the VA already has struggled for years to meet surging demand from troops serving deployments since the 2001 terror attacks on America, with a backlog of delayed claims running into the hundreds of thousands. Besides addressing burn pits, the bill would expand benefits for veterans who served at certain nuclear sites, and cover more conditions related to Agent Orange exposure in Vietnam, among several other issues.

While the bill phases in coverage for new groups of beneficiaries over 10 years, some Republicans involved in writing legislation about burn pits fear it is all too much.

Sen. Mike Rounds (R-S.D.), a member of the Veterans’ Affairs Committee, summed up the concern as stemming from promising lots of assistance “that might look really good,” but the bottom line is that those “who really need the care would never get into a VA facility.”

Sen. Thom Tillis (R-N.C.), another member of the panel, agreed. “What we’re concerned with is that you’ve got a backlog of 222,000 cases now, and if you implement, by legislative fiat, the 23 presumptions, we’re gonna go to a million and a half to two and a half million backlog,” he said. Tillis has advanced his own burn pits bill that would leave it to the military and VA to determine which illnesses automatically were presumed to be service-connected. That tally is likely to cover fewer people. “So the question we have is, while making a new promise, are we going to be breaking a promise for all those veterans that need care today?”

Republicans have insisted they want to do something to help veterans who are increasingly getting sick with illnesses that appear related to toxic exposure. About 300,000 veterans have signed up with the VA’s burn pits registry.

Sen. Jerry Moran from Kansas, the top Republican on the Veterans’ Affairs Committee, held a press conference in February with Sen. Jon Tester (D-Mont.), the committee chairman, advocating a more gradual process to expand access to benefits and define the illnesses that would qualify.

The event was designed to show what would easily gain bipartisan support in the Senate while the House was still working on its bill.

Veterans’ service organizations, which try to avoid taking partisan positions, have praised such efforts. But they’ve also made clear they like the House bill. More than 40 of the groups endorsed the PACT Act before it passed the lower chamber.

Aleks Morosky, a governmental affairs specialist for the Wounded Warrior Project, plans to meet with senators this month in hope of advancing the PACT Act.

“This is an urgent issue. I mean, people are dying,” Morosky said.

He added that he believes some minor changes and input from the VA would eliminate the sorts of problems senators are raising.

“This bill was meticulously put together, and these are the provisions that veterans need,” Morosky said. “The VA is telling us that they can implement it the way they’ve implemented large numbers of people coming into the system in the past.”

He pointed to the recent expansion of Agent Orange benefits to Navy veterans and to VA Secretary Denis McDonough’s testimony to the Senate Veterans’ Affairs committee in March. McDonough largely supported the legislation but said the VA would need new leasing authority to ensure it had adequate facilities, as well as more say over adding illnesses to be covered.

Senate Republicans are not so sure about the VA’s ability to absorb such a large group of new patients. Tillis and Rounds suggested one solution would be to greatly expand the access to care veterans can seek outside the VA. They pointed to the Mission Act, a law passed in 2018 that was meant to grant veterans access to private health care. Some critics say it has not lived up to its promise. It’s also been expensive, requiring emergency appropriations from Congress.

“You better think about having community care — because there’s no way you’re going to be able to ramp up the medical infrastructure to provide that purely through the VA,” Tillis said.

Tester said in a statement that the committee was working on McDonough’s requests — and could have a modified bill for a vote before Memorial Day.

“In addition to delivering historic reform for all generations of toxic-exposed veterans, I’m working to ensure this legislation provides VA with additional resources and authorities to hire more staff, establish new facilities, and make critical investments to better ensure it can meet the current and future needs of our nation’s veterans,” Tester said.

Whether or not those changes satisfy enough Republicans remains to be seen.

Sen. Kirsten Gillibrand (D-N.Y.), who chairs the Armed Services subcommittee on personnel and earlier wrote a burn pits bill, said neither cost nor fears about problems on implementation should get in the way of passing the bill. Her proposal was incorporated into the House’s PACT Act.

“To deny service because of a lack of resources or a lack of personnel is an outrageous statement,” Gillibrand said. “We promised these men and women when they went to war that when they came back, we would protect them. And that is our solemn obligation. And if it needs more resources, we will get them more resources.”

She predicted Republicans would come along to help pass a bill.

“I’m optimistic, actually. I think we just need a little more time to talk to more Republicans to get everybody on board,” she said.

Thousands of military veterans who are sick after being exposed to toxic smoke and dust while on duty are facing a Senate roadblock to ambitious legislation designed to provide them care.

The Senate could start work as soon as this week on a bipartisan bill, called the Honoring Our PACT Act, that passed the House of Representatives in March. It would make it much easier for veterans to get health care and benefits from the Veterans Health Administration if they get sick because of the air they breathed around massive, open-air incineration pits. The military used those pits in war zones around the globe — sometimes the size of football fields — to burn anything from human and medical waste to plastics and munitions, setting it alight with jet fuel.

As it stands now, more than three-quarters of all veterans who submit claims for cancer, breathing disorders, and other illnesses that they believe are caused by inhaling poisonous burn pit smoke have their claims denied, according to estimates from the Department of Veterans Affairs and service organizations.

The reason so few are approved is that the military and VA require injured war fighters to prove an illness is directly connected to their service — something that is extremely difficult when it comes to toxic exposures. The House’s PACT Act would make that easier by declaring that any of the 3.5 million veterans who served in the global war on terror — including operations in Afghanistan, Iraq, and the Persian Gulf — would be presumed eligible for benefits if they come down with any of 23 ailments linked to the burn pits.

Although 34 Republicans voted with Democrats to pass the bill in the House, only one Republican, Sen. Marco Rubio of Florida, has signaled support for the measure. At least 10 GOP members would have to join all Democrats to avoid the threat of a filibuster in the Senate and allow the bill to advance to President Joe Biden’s desk. Biden called on Congress to pass such legislation in his State of the Union address, citing the death of his son Beau Biden, who served in Iraq in 2008 and died in 2015 of glioblastoma, a brain cancer included on the bill’s list of qualifying conditions.

Senate Republicans are raising concerns about the measure, however, suggesting it won’t be paid for, that it is too big, too ambitious, and could end up promising more than the government can deliver.

The Congressional Budget Office estimates the bill would cost more than $300 billion over 10 years, and the VA already has struggled for years to meet surging demand from troops serving deployments since the 2001 terror attacks on America, with a backlog of delayed claims running into the hundreds of thousands. Besides addressing burn pits, the bill would expand benefits for veterans who served at certain nuclear sites, and cover more conditions related to Agent Orange exposure in Vietnam, among several other issues.

While the bill phases in coverage for new groups of beneficiaries over 10 years, some Republicans involved in writing legislation about burn pits fear it is all too much.

Sen. Mike Rounds (R-S.D.), a member of the Veterans’ Affairs Committee, summed up the concern as stemming from promising lots of assistance “that might look really good,” but the bottom line is that those “who really need the care would never get into a VA facility.”

Sen. Thom Tillis (R-N.C.), another member of the panel, agreed. “What we’re concerned with is that you’ve got a backlog of 222,000 cases now, and if you implement, by legislative fiat, the 23 presumptions, we’re gonna go to a million and a half to two and a half million backlog,” he said. Tillis has advanced his own burn pits bill that would leave it to the military and VA to determine which illnesses automatically were presumed to be service-connected. That tally is likely to cover fewer people. “So the question we have is, while making a new promise, are we going to be breaking a promise for all those veterans that need care today?”

Republicans have insisted they want to do something to help veterans who are increasingly getting sick with illnesses that appear related to toxic exposure. About 300,000 veterans have signed up with the VA’s burn pits registry.

Sen. Jerry Moran from Kansas, the top Republican on the Veterans’ Affairs Committee, held a press conference in February with Sen. Jon Tester (D-Mont.), the committee chairman, advocating a more gradual process to expand access to benefits and define the illnesses that would qualify.

The event was designed to show what would easily gain bipartisan support in the Senate while the House was still working on its bill.

Veterans’ service organizations, which try to avoid taking partisan positions, have praised such efforts. But they’ve also made clear they like the House bill. More than 40 of the groups endorsed the PACT Act before it passed the lower chamber.

Aleks Morosky, a governmental affairs specialist for the Wounded Warrior Project, plans to meet with senators this month in hope of advancing the PACT Act.

“This is an urgent issue. I mean, people are dying,” Morosky said.

He added that he believes some minor changes and input from the VA would eliminate the sorts of problems senators are raising.

“This bill was meticulously put together, and these are the provisions that veterans need,” Morosky said. “The VA is telling us that they can implement it the way they’ve implemented large numbers of people coming into the system in the past.”

He pointed to the recent expansion of Agent Orange benefits to Navy veterans and to VA Secretary Denis McDonough’s testimony to the Senate Veterans’ Affairs committee in March. McDonough largely supported the legislation but said the VA would need new leasing authority to ensure it had adequate facilities, as well as more say over adding illnesses to be covered.

Senate Republicans are not so sure about the VA’s ability to absorb such a large group of new patients. Tillis and Rounds suggested one solution would be to greatly expand the access to care veterans can seek outside the VA. They pointed to the Mission Act, a law passed in 2018 that was meant to grant veterans access to private health care. Some critics say it has not lived up to its promise. It’s also been expensive, requiring emergency appropriations from Congress.

“You better think about having community care — because there’s no way you’re going to be able to ramp up the medical infrastructure to provide that purely through the VA,” Tillis said.

Tester said in a statement that the committee was working on McDonough’s requests — and could have a modified bill for a vote before Memorial Day.

“In addition to delivering historic reform for all generations of toxic-exposed veterans, I’m working to ensure this legislation provides VA with additional resources and authorities to hire more staff, establish new facilities, and make critical investments to better ensure it can meet the current and future needs of our nation’s veterans,” Tester said.

Whether or not those changes satisfy enough Republicans remains to be seen.

Sen. Kirsten Gillibrand (D-N.Y.), who chairs the Armed Services subcommittee on personnel and earlier wrote a burn pits bill, said neither cost nor fears about problems on implementation should get in the way of passing the bill. Her proposal was incorporated into the House’s PACT Act.

“To deny service because of a lack of resources or a lack of personnel is an outrageous statement,” Gillibrand said. “We promised these men and women when they went to war that when they came back, we would protect them. And that is our solemn obligation. And if it needs more resources, we will get them more resources.”

She predicted Republicans would come along to help pass a bill.

“I’m optimistic, actually. I think we just need a little more time to talk to more Republicans to get everybody on board,” she said.

Thousands of military veterans who are sick after being exposed to toxic smoke and dust while on duty are facing a Senate roadblock to ambitious legislation designed to provide them care.

The Senate could start work as soon as this week on a bipartisan bill, called the Honoring Our PACT Act, that passed the House of Representatives in March. It would make it much easier for veterans to get health care and benefits from the Veterans Health Administration if they get sick because of the air they breathed around massive, open-air incineration pits. The military used those pits in war zones around the globe — sometimes the size of football fields — to burn anything from human and medical waste to plastics and munitions, setting it alight with jet fuel.

As it stands now, more than three-quarters of all veterans who submit claims for cancer, breathing disorders, and other illnesses that they believe are caused by inhaling poisonous burn pit smoke have their claims denied, according to estimates from the Department of Veterans Affairs and service organizations.

The reason so few are approved is that the military and VA require injured war fighters to prove an illness is directly connected to their service — something that is extremely difficult when it comes to toxic exposures. The House’s PACT Act would make that easier by declaring that any of the 3.5 million veterans who served in the global war on terror — including operations in Afghanistan, Iraq, and the Persian Gulf — would be presumed eligible for benefits if they come down with any of 23 ailments linked to the burn pits.

Although 34 Republicans voted with Democrats to pass the bill in the House, only one Republican, Sen. Marco Rubio of Florida, has signaled support for the measure. At least 10 GOP members would have to join all Democrats to avoid the threat of a filibuster in the Senate and allow the bill to advance to President Joe Biden’s desk. Biden called on Congress to pass such legislation in his State of the Union address, citing the death of his son Beau Biden, who served in Iraq in 2008 and died in 2015 of glioblastoma, a brain cancer included on the bill’s list of qualifying conditions.

Senate Republicans are raising concerns about the measure, however, suggesting it won’t be paid for, that it is too big, too ambitious, and could end up promising more than the government can deliver.

The Congressional Budget Office estimates the bill would cost more than $300 billion over 10 years, and the VA already has struggled for years to meet surging demand from troops serving deployments since the 2001 terror attacks on America, with a backlog of delayed claims running into the hundreds of thousands. Besides addressing burn pits, the bill would expand benefits for veterans who served at certain nuclear sites, and cover more conditions related to Agent Orange exposure in Vietnam, among several other issues.

While the bill phases in coverage for new groups of beneficiaries over 10 years, some Republicans involved in writing legislation about burn pits fear it is all too much.

Sen. Mike Rounds (R-S.D.), a member of the Veterans’ Affairs Committee, summed up the concern as stemming from promising lots of assistance “that might look really good,” but the bottom line is that those “who really need the care would never get into a VA facility.”

Sen. Thom Tillis (R-N.C.), another member of the panel, agreed. “What we’re concerned with is that you’ve got a backlog of 222,000 cases now, and if you implement, by legislative fiat, the 23 presumptions, we’re gonna go to a million and a half to two and a half million backlog,” he said. Tillis has advanced his own burn pits bill that would leave it to the military and VA to determine which illnesses automatically were presumed to be service-connected. That tally is likely to cover fewer people. “So the question we have is, while making a new promise, are we going to be breaking a promise for all those veterans that need care today?”

Republicans have insisted they want to do something to help veterans who are increasingly getting sick with illnesses that appear related to toxic exposure. About 300,000 veterans have signed up with the VA’s burn pits registry.

Sen. Jerry Moran from Kansas, the top Republican on the Veterans’ Affairs Committee, held a press conference in February with Sen. Jon Tester (D-Mont.), the committee chairman, advocating a more gradual process to expand access to benefits and define the illnesses that would qualify.

The event was designed to show what would easily gain bipartisan support in the Senate while the House was still working on its bill.

Veterans’ service organizations, which try to avoid taking partisan positions, have praised such efforts. But they’ve also made clear they like the House bill. More than 40 of the groups endorsed the PACT Act before it passed the lower chamber.

Aleks Morosky, a governmental affairs specialist for the Wounded Warrior Project, plans to meet with senators this month in hope of advancing the PACT Act.

“This is an urgent issue. I mean, people are dying,” Morosky said.

He added that he believes some minor changes and input from the VA would eliminate the sorts of problems senators are raising.

“This bill was meticulously put together, and these are the provisions that veterans need,” Morosky said. “The VA is telling us that they can implement it the way they’ve implemented large numbers of people coming into the system in the past.”

He pointed to the recent expansion of Agent Orange benefits to Navy veterans and to VA Secretary Denis McDonough’s testimony to the Senate Veterans’ Affairs committee in March. McDonough largely supported the legislation but said the VA would need new leasing authority to ensure it had adequate facilities, as well as more say over adding illnesses to be covered.

Senate Republicans are not so sure about the VA’s ability to absorb such a large group of new patients. Tillis and Rounds suggested one solution would be to greatly expand the access to care veterans can seek outside the VA. They pointed to the Mission Act, a law passed in 2018 that was meant to grant veterans access to private health care. Some critics say it has not lived up to its promise. It’s also been expensive, requiring emergency appropriations from Congress.

“You better think about having community care — because there’s no way you’re going to be able to ramp up the medical infrastructure to provide that purely through the VA,” Tillis said.

Tester said in a statement that the committee was working on McDonough’s requests — and could have a modified bill for a vote before Memorial Day.

“In addition to delivering historic reform for all generations of toxic-exposed veterans, I’m working to ensure this legislation provides VA with additional resources and authorities to hire more staff, establish new facilities, and make critical investments to better ensure it can meet the current and future needs of our nation’s veterans,” Tester said.

Whether or not those changes satisfy enough Republicans remains to be seen.

Sen. Kirsten Gillibrand (D-N.Y.), who chairs the Armed Services subcommittee on personnel and earlier wrote a burn pits bill, said neither cost nor fears about problems on implementation should get in the way of passing the bill. Her proposal was incorporated into the House’s PACT Act.

“To deny service because of a lack of resources or a lack of personnel is an outrageous statement,” Gillibrand said. “We promised these men and women when they went to war that when they came back, we would protect them. And that is our solemn obligation. And if it needs more resources, we will get them more resources.”

She predicted Republicans would come along to help pass a bill.

“I’m optimistic, actually. I think we just need a little more time to talk to more Republicans to get everybody on board,” she said.

A recent article on Medscape entitled “Online Reviews Most Important Factor in Choosing a Doctor: Survey” really got me thinking about my online presence. According to the results of a new Press Ganey survey, online reviews and star ratings are the most important factor for consumers when choosing a new health care provider, even more so than the recommendation of another doctor. Almost 85% of the survey respondents said they wouldn’t make an appointment with a referred provider if they had a rating of less than 4 stars.

To be honest, I’ve rarely thought about my ratings or online reviews, and I almost never enter my own name into a web browser to see what might emerge. I don’t use most popular social media apps, I don’t have a professional website, and I was completely late in joining LinkedIn. After considering the Press Ganey survey results, though, I’m wondering how many patients (or potential patients) have found me online. And what exactly did they see?

So, I just searched online for my ratings and reviews. There weren’t many direct hits (although I’m not sure if that is a good thing or not). One of the results listed me as a “Fibromyalgia Doctor” at www.lymeforums.org. To be clear, I’m a locum tenens infectious diseases provider with a focus on inpatient consultations and teaching. I couldn’t find any reviews for myself on WebMD, but I had one rating on the Healthgrades website – I was pleased to see someone gave me 5 stars (though there weren’t any comments) until I realized the site listed my address at an ob.gyn. office; I’m not even sure if that rating was meant for me.

Use of the Internet to assess my qualities as a physician is clearly limited, and much of the online information about my specialty and practice sites is completely inaccurate. Yet, according to the Press Ganey survey, the average consumer uses three different websites and reads more than five online reviews before making a provider decision. Once they’ve seen a provider, though, patients rank practice customer service and communication as more important than “bedside manner” when considering a 5-star review. So, it appears that many physician reviews and ratings probably reflect the performance of the office staff, not the provider.

Given the few hits that I encountered when searching my own name, I’m not convinced I need to do anything differently about my online presence; essentially, I don’t really have one. However, there were certainly a lot of other physicians with the same last name as mine who did have impressive numbers of reviews and ratings. One doctor of cosmetic surgery had more than 200 reviews on multiple sites; almost all were positive, but a few patients rated him at 1 or 2 (out of 5) stars, suggesting that patients should find a new surgeon. What does one do about those outliers?

Medicine is indeed a business and patients behave as consumers when searching the web for a health care provider. Another survey has suggested that just one negative review may cause a business to risk losing 22% of its customers, and that multiple bad ratings are even worse – nearly 60% of customers will avoid a business with three or more negative online reviews.

A few years ago, The Washington Post published an article about doctors who were fighting back against bad reviews. Unfortunately, while trying to directly combat inaccuracies, some providers divulged sensitive patient information and suffered the consequences of HIPAA violations. Many legal experts suggest that, in most cases, physicians should restrain from responding publicly to negative online reviews, however tempting it may be to react.

If a negative review is attributed to a specific patient, some lawyers recommend contacting them privately by phone to address their concerns; this may clear the air enough to result in a withdrawal of the negative review or rating. Flagging and reporting fake or unsubstantiated negative reviews (or reviews that violate the Terms of Service of a specific platform) can be done. Consultation with an Internet defamation attorney might be helpful in some circumstances, though hopefully, legal action such as a lawsuit or a cease-and-desist letter can be avoided.

For physicians who do maintain an online presence, engaging with an online reputation management service can help suppress fake or negative reviews while offering strategies for building a better reputation. As for me, I think that I’m grateful my name hasn’t attracted a lot of attention at physician ranking and review sites. I guess we’ll see if it stays that way.

Dr. Devlin is president of Locum Infectious Disease Services, and an independent contractor for Weatherby Healthcare. She has disclosed no relevant financial relationships. A version of this article first appeared on Medscape.com.

A recent article on Medscape entitled “Online Reviews Most Important Factor in Choosing a Doctor: Survey” really got me thinking about my online presence. According to the results of a new Press Ganey survey, online reviews and star ratings are the most important factor for consumers when choosing a new health care provider, even more so than the recommendation of another doctor. Almost 85% of the survey respondents said they wouldn’t make an appointment with a referred provider if they had a rating of less than 4 stars.

To be honest, I’ve rarely thought about my ratings or online reviews, and I almost never enter my own name into a web browser to see what might emerge. I don’t use most popular social media apps, I don’t have a professional website, and I was completely late in joining LinkedIn. After considering the Press Ganey survey results, though, I’m wondering how many patients (or potential patients) have found me online. And what exactly did they see?

So, I just searched online for my ratings and reviews. There weren’t many direct hits (although I’m not sure if that is a good thing or not). One of the results listed me as a “Fibromyalgia Doctor” at www.lymeforums.org. To be clear, I’m a locum tenens infectious diseases provider with a focus on inpatient consultations and teaching. I couldn’t find any reviews for myself on WebMD, but I had one rating on the Healthgrades website – I was pleased to see someone gave me 5 stars (though there weren’t any comments) until I realized the site listed my address at an ob.gyn. office; I’m not even sure if that rating was meant for me.

Use of the Internet to assess my qualities as a physician is clearly limited, and much of the online information about my specialty and practice sites is completely inaccurate. Yet, according to the Press Ganey survey, the average consumer uses three different websites and reads more than five online reviews before making a provider decision. Once they’ve seen a provider, though, patients rank practice customer service and communication as more important than “bedside manner” when considering a 5-star review. So, it appears that many physician reviews and ratings probably reflect the performance of the office staff, not the provider.

Given the few hits that I encountered when searching my own name, I’m not convinced I need to do anything differently about my online presence; essentially, I don’t really have one. However, there were certainly a lot of other physicians with the same last name as mine who did have impressive numbers of reviews and ratings. One doctor of cosmetic surgery had more than 200 reviews on multiple sites; almost all were positive, but a few patients rated him at 1 or 2 (out of 5) stars, suggesting that patients should find a new surgeon. What does one do about those outliers?

Medicine is indeed a business and patients behave as consumers when searching the web for a health care provider. Another survey has suggested that just one negative review may cause a business to risk losing 22% of its customers, and that multiple bad ratings are even worse – nearly 60% of customers will avoid a business with three or more negative online reviews.

A few years ago, The Washington Post published an article about doctors who were fighting back against bad reviews. Unfortunately, while trying to directly combat inaccuracies, some providers divulged sensitive patient information and suffered the consequences of HIPAA violations. Many legal experts suggest that, in most cases, physicians should restrain from responding publicly to negative online reviews, however tempting it may be to react.

If a negative review is attributed to a specific patient, some lawyers recommend contacting them privately by phone to address their concerns; this may clear the air enough to result in a withdrawal of the negative review or rating. Flagging and reporting fake or unsubstantiated negative reviews (or reviews that violate the Terms of Service of a specific platform) can be done. Consultation with an Internet defamation attorney might be helpful in some circumstances, though hopefully, legal action such as a lawsuit or a cease-and-desist letter can be avoided.

For physicians who do maintain an online presence, engaging with an online reputation management service can help suppress fake or negative reviews while offering strategies for building a better reputation. As for me, I think that I’m grateful my name hasn’t attracted a lot of attention at physician ranking and review sites. I guess we’ll see if it stays that way.

Dr. Devlin is president of Locum Infectious Disease Services, and an independent contractor for Weatherby Healthcare. She has disclosed no relevant financial relationships. A version of this article first appeared on Medscape.com.

A recent article on Medscape entitled “Online Reviews Most Important Factor in Choosing a Doctor: Survey” really got me thinking about my online presence. According to the results of a new Press Ganey survey, online reviews and star ratings are the most important factor for consumers when choosing a new health care provider, even more so than the recommendation of another doctor. Almost 85% of the survey respondents said they wouldn’t make an appointment with a referred provider if they had a rating of less than 4 stars.

To be honest, I’ve rarely thought about my ratings or online reviews, and I almost never enter my own name into a web browser to see what might emerge. I don’t use most popular social media apps, I don’t have a professional website, and I was completely late in joining LinkedIn. After considering the Press Ganey survey results, though, I’m wondering how many patients (or potential patients) have found me online. And what exactly did they see?

So, I just searched online for my ratings and reviews. There weren’t many direct hits (although I’m not sure if that is a good thing or not). One of the results listed me as a “Fibromyalgia Doctor” at www.lymeforums.org. To be clear, I’m a locum tenens infectious diseases provider with a focus on inpatient consultations and teaching. I couldn’t find any reviews for myself on WebMD, but I had one rating on the Healthgrades website – I was pleased to see someone gave me 5 stars (though there weren’t any comments) until I realized the site listed my address at an ob.gyn. office; I’m not even sure if that rating was meant for me.

Use of the Internet to assess my qualities as a physician is clearly limited, and much of the online information about my specialty and practice sites is completely inaccurate. Yet, according to the Press Ganey survey, the average consumer uses three different websites and reads more than five online reviews before making a provider decision. Once they’ve seen a provider, though, patients rank practice customer service and communication as more important than “bedside manner” when considering a 5-star review. So, it appears that many physician reviews and ratings probably reflect the performance of the office staff, not the provider.

Given the few hits that I encountered when searching my own name, I’m not convinced I need to do anything differently about my online presence; essentially, I don’t really have one. However, there were certainly a lot of other physicians with the same last name as mine who did have impressive numbers of reviews and ratings. One doctor of cosmetic surgery had more than 200 reviews on multiple sites; almost all were positive, but a few patients rated him at 1 or 2 (out of 5) stars, suggesting that patients should find a new surgeon. What does one do about those outliers?

Medicine is indeed a business and patients behave as consumers when searching the web for a health care provider. Another survey has suggested that just one negative review may cause a business to risk losing 22% of its customers, and that multiple bad ratings are even worse – nearly 60% of customers will avoid a business with three or more negative online reviews.

A few years ago, The Washington Post published an article about doctors who were fighting back against bad reviews. Unfortunately, while trying to directly combat inaccuracies, some providers divulged sensitive patient information and suffered the consequences of HIPAA violations. Many legal experts suggest that, in most cases, physicians should restrain from responding publicly to negative online reviews, however tempting it may be to react.

If a negative review is attributed to a specific patient, some lawyers recommend contacting them privately by phone to address their concerns; this may clear the air enough to result in a withdrawal of the negative review or rating. Flagging and reporting fake or unsubstantiated negative reviews (or reviews that violate the Terms of Service of a specific platform) can be done. Consultation with an Internet defamation attorney might be helpful in some circumstances, though hopefully, legal action such as a lawsuit or a cease-and-desist letter can be avoided.

For physicians who do maintain an online presence, engaging with an online reputation management service can help suppress fake or negative reviews while offering strategies for building a better reputation. As for me, I think that I’m grateful my name hasn’t attracted a lot of attention at physician ranking and review sites. I guess we’ll see if it stays that way.

Dr. Devlin is president of Locum Infectious Disease Services, and an independent contractor for Weatherby Healthcare. She has disclosed no relevant financial relationships. A version of this article first appeared on Medscape.com.