Key clinical point: Pneumonia Severity Index (PSI) and the confusion, urea, respiratory rate, and blood pressure (CURB)-65 score are as effective at predicting in-hospital mortality in patients with SARS-CoV-2 community-acquired pneumonia (CAP) as they are in those with non-SARS-CoV-2 CAP.

Main finding: The area under the receiver operating characteristic curve in patients with SARS-CoV-2 CAP and non-SARS-CoV-2 CAP for PSI was 0.82 (95% Bayesian credible interval [bCI] 0.78-0.86) and 0.79 (95% bCI 0.77-0.80) and that for CURB-65 was 0.79 (95% bCI 0.75-0.84) and 0.75 (95% bCI 0.73-0.77), respectively.

Study details: This was a secondary analysis of 8,081 patients from 2 population-based cohort studies, each of which included adults hospitalized for either SARS-CoV-2 CAP or non-SARS-CoV-2 CAP.

Disclosures: The study was supported by the Center for Excellence for Research in Infectious Diseases at the University of Louisville. None of the authors declared any potential conflict of interests.

Source: Bradley J et al. Chest. 2021 (Nov 2). Doi: 10.1016/j.chest.2021.10.031.

Key clinical point: Pneumonia Severity Index (PSI) and the confusion, urea, respiratory rate, and blood pressure (CURB)-65 score are as effective at predicting in-hospital mortality in patients with SARS-CoV-2 community-acquired pneumonia (CAP) as they are in those with non-SARS-CoV-2 CAP.

Main finding: The area under the receiver operating characteristic curve in patients with SARS-CoV-2 CAP and non-SARS-CoV-2 CAP for PSI was 0.82 (95% Bayesian credible interval [bCI] 0.78-0.86) and 0.79 (95% bCI 0.77-0.80) and that for CURB-65 was 0.79 (95% bCI 0.75-0.84) and 0.75 (95% bCI 0.73-0.77), respectively.

Study details: This was a secondary analysis of 8,081 patients from 2 population-based cohort studies, each of which included adults hospitalized for either SARS-CoV-2 CAP or non-SARS-CoV-2 CAP.

Disclosures: The study was supported by the Center for Excellence for Research in Infectious Diseases at the University of Louisville. None of the authors declared any potential conflict of interests.

Source: Bradley J et al. Chest. 2021 (Nov 2). Doi: 10.1016/j.chest.2021.10.031.

Key clinical point: Pneumonia Severity Index (PSI) and the confusion, urea, respiratory rate, and blood pressure (CURB)-65 score are as effective at predicting in-hospital mortality in patients with SARS-CoV-2 community-acquired pneumonia (CAP) as they are in those with non-SARS-CoV-2 CAP.

Main finding: The area under the receiver operating characteristic curve in patients with SARS-CoV-2 CAP and non-SARS-CoV-2 CAP for PSI was 0.82 (95% Bayesian credible interval [bCI] 0.78-0.86) and 0.79 (95% bCI 0.77-0.80) and that for CURB-65 was 0.79 (95% bCI 0.75-0.84) and 0.75 (95% bCI 0.73-0.77), respectively.

Study details: This was a secondary analysis of 8,081 patients from 2 population-based cohort studies, each of which included adults hospitalized for either SARS-CoV-2 CAP or non-SARS-CoV-2 CAP.

Disclosures: The study was supported by the Center for Excellence for Research in Infectious Diseases at the University of Louisville. None of the authors declared any potential conflict of interests.

Source: Bradley J et al. Chest. 2021 (Nov 2). Doi: 10.1016/j.chest.2021.10.031.

Key clinical point: In patients with moderately severe community-acquired pneumonia (CAP) who reached clinical stability after 3 days of antibiotic treatment, male sex and age were the main risk factors for treatment failure.

Main finding: After excluding the Pneumonia Severity Index score and urea level at day 0, male sex (odds ratio [OR] 1.92; 95% CI 1.08-3.49) and age per year (OR 1.02; 95% CI 1.00-1.05) showed a significant association with treatment failure at day 15.

Study details: This was a secondary analysis including 291 of the 310 patients from the Pneumonia Short Treatment trial who were hospitalized for moderately severe CAP and were clinically stable after 3 days of receiving β-lactams, which is when they were randomly assigned to receive oral amoxicillin-clavulanate or placebo for 5 further days.

Disclosures: The study was supported by the French Ministry of Health and DRCI of Versailles. Dr. Crémieux reported receiving grants from an additional source outside the study.

Source: Dinh A et al. JAMA Netw Open. 2021;4(10):e2129566 (Oct 15). Doi: 10.1001/jamanetworkopen.2021.29566.

Key clinical point: In patients with moderately severe community-acquired pneumonia (CAP) who reached clinical stability after 3 days of antibiotic treatment, male sex and age were the main risk factors for treatment failure.

Main finding: After excluding the Pneumonia Severity Index score and urea level at day 0, male sex (odds ratio [OR] 1.92; 95% CI 1.08-3.49) and age per year (OR 1.02; 95% CI 1.00-1.05) showed a significant association with treatment failure at day 15.

Study details: This was a secondary analysis including 291 of the 310 patients from the Pneumonia Short Treatment trial who were hospitalized for moderately severe CAP and were clinically stable after 3 days of receiving β-lactams, which is when they were randomly assigned to receive oral amoxicillin-clavulanate or placebo for 5 further days.

Disclosures: The study was supported by the French Ministry of Health and DRCI of Versailles. Dr. Crémieux reported receiving grants from an additional source outside the study.

Source: Dinh A et al. JAMA Netw Open. 2021;4(10):e2129566 (Oct 15). Doi: 10.1001/jamanetworkopen.2021.29566.

Key clinical point: In patients with moderately severe community-acquired pneumonia (CAP) who reached clinical stability after 3 days of antibiotic treatment, male sex and age were the main risk factors for treatment failure.

Main finding: After excluding the Pneumonia Severity Index score and urea level at day 0, male sex (odds ratio [OR] 1.92; 95% CI 1.08-3.49) and age per year (OR 1.02; 95% CI 1.00-1.05) showed a significant association with treatment failure at day 15.

Study details: This was a secondary analysis including 291 of the 310 patients from the Pneumonia Short Treatment trial who were hospitalized for moderately severe CAP and were clinically stable after 3 days of receiving β-lactams, which is when they were randomly assigned to receive oral amoxicillin-clavulanate or placebo for 5 further days.

Disclosures: The study was supported by the French Ministry of Health and DRCI of Versailles. Dr. Crémieux reported receiving grants from an additional source outside the study.

Source: Dinh A et al. JAMA Netw Open. 2021;4(10):e2129566 (Oct 15). Doi: 10.1001/jamanetworkopen.2021.29566.

Key clinical point: In children with community-acquired pneumonia (CAP) discharged from emergency departments or inpatient wards, further outpatient treatment with amoxicillin at a lower dose was not inferior to a higher dose, and a 3-day treatment course was not inferior to a 7-day treatment course.

Main finding: Antibiotic retreatment rates in the 4-week period after hospital discharge in the lower dose vs. the higher dose group were 12.6% vs. 12.4% (difference 0.2%; 95% CI –∞ to 4.0%) and those in the shorter duration vs. the longer duration group were 12.5% vs. 12.5% (difference 0.1%; 95% CI –∞ to 3.9%).

Study details: Findings are from the CAP-IT trial including 814 children > 6 months old with CAP who were randomly assigned 1:1 after hospital discharge to receive the 4 possible combinations of amoxicillin dose (35-50 or 70-90 mg/kg) and duration (3 or 7 days).

Disclosures: The trial was funded by the National Institute of Health Research (NIHR) Health Technology Assessment (HTA) Program and Antimicrobial Resistance Themed Call. Some of the authors including the lead author reported receiving research grants from the NIHR/HTA.

Source: Bielicki JA et al. JAMA. 2021;326(17):1713-1724 (Nov 2). Doi: 10.1001/jama.2021.17843.

Key clinical point: In children with community-acquired pneumonia (CAP) discharged from emergency departments or inpatient wards, further outpatient treatment with amoxicillin at a lower dose was not inferior to a higher dose, and a 3-day treatment course was not inferior to a 7-day treatment course.

Main finding: Antibiotic retreatment rates in the 4-week period after hospital discharge in the lower dose vs. the higher dose group were 12.6% vs. 12.4% (difference 0.2%; 95% CI –∞ to 4.0%) and those in the shorter duration vs. the longer duration group were 12.5% vs. 12.5% (difference 0.1%; 95% CI –∞ to 3.9%).

Study details: Findings are from the CAP-IT trial including 814 children > 6 months old with CAP who were randomly assigned 1:1 after hospital discharge to receive the 4 possible combinations of amoxicillin dose (35-50 or 70-90 mg/kg) and duration (3 or 7 days).

Disclosures: The trial was funded by the National Institute of Health Research (NIHR) Health Technology Assessment (HTA) Program and Antimicrobial Resistance Themed Call. Some of the authors including the lead author reported receiving research grants from the NIHR/HTA.

Source: Bielicki JA et al. JAMA. 2021;326(17):1713-1724 (Nov 2). Doi: 10.1001/jama.2021.17843.

Key clinical point: In children with community-acquired pneumonia (CAP) discharged from emergency departments or inpatient wards, further outpatient treatment with amoxicillin at a lower dose was not inferior to a higher dose, and a 3-day treatment course was not inferior to a 7-day treatment course.

Main finding: Antibiotic retreatment rates in the 4-week period after hospital discharge in the lower dose vs. the higher dose group were 12.6% vs. 12.4% (difference 0.2%; 95% CI –∞ to 4.0%) and those in the shorter duration vs. the longer duration group were 12.5% vs. 12.5% (difference 0.1%; 95% CI –∞ to 3.9%).

Study details: Findings are from the CAP-IT trial including 814 children > 6 months old with CAP who were randomly assigned 1:1 after hospital discharge to receive the 4 possible combinations of amoxicillin dose (35-50 or 70-90 mg/kg) and duration (3 or 7 days).

Disclosures: The trial was funded by the National Institute of Health Research (NIHR) Health Technology Assessment (HTA) Program and Antimicrobial Resistance Themed Call. Some of the authors including the lead author reported receiving research grants from the NIHR/HTA.

Source: Bielicki JA et al. JAMA. 2021;326(17):1713-1724 (Nov 2). Doi: 10.1001/jama.2021.17843.

Key clinical point: Antimicrobial stewardship intervention emerged successful in advocating a shift from broad-spectrum to narrow-spectrum antibiotics for treating moderately severe community-acquired pneumonia (CAP) while averting any safety concerns.

Main finding: Antimicrobial stewardship intervention effectuated a decrease in the adjusted mean broad-spectrum days of therapy per patient from 6.5 days to 4.8 days, with an adjusted relative reduction of 26.6% (95% CI 18.0%-35.3%). The adjusted risk difference of 0.4% (90% CI –2.7% to 2.4%) indicated noninferiority.

Study details: The data come from the investigator-initiated, noninferiority, CAP-PACT trial including 4,084 adult patients receiving antibiotics for moderately severe CAP post admission to a non-ICU hospital ward, of whom 2,235 patients were admitted during the control period and 1,849 during the intervention period.

Disclosures: The authors received no financial support for the study. CH van Werkhoven reported receiving grants, personal fees, and nonfinancial support from a few sources outside the study, in addition to obtaining a patent for the prediction of clinical manifestations of gut microbiota.

Source: Schweitzer VA et al. Lancet Infect Dis. 2021(Oct 7). Doi: 10.1016/S1473-3099(21)00255-3.

Key clinical point: Antimicrobial stewardship intervention emerged successful in advocating a shift from broad-spectrum to narrow-spectrum antibiotics for treating moderately severe community-acquired pneumonia (CAP) while averting any safety concerns.

Main finding: Antimicrobial stewardship intervention effectuated a decrease in the adjusted mean broad-spectrum days of therapy per patient from 6.5 days to 4.8 days, with an adjusted relative reduction of 26.6% (95% CI 18.0%-35.3%). The adjusted risk difference of 0.4% (90% CI –2.7% to 2.4%) indicated noninferiority.

Study details: The data come from the investigator-initiated, noninferiority, CAP-PACT trial including 4,084 adult patients receiving antibiotics for moderately severe CAP post admission to a non-ICU hospital ward, of whom 2,235 patients were admitted during the control period and 1,849 during the intervention period.

Disclosures: The authors received no financial support for the study. CH van Werkhoven reported receiving grants, personal fees, and nonfinancial support from a few sources outside the study, in addition to obtaining a patent for the prediction of clinical manifestations of gut microbiota.

Source: Schweitzer VA et al. Lancet Infect Dis. 2021(Oct 7). Doi: 10.1016/S1473-3099(21)00255-3.

Key clinical point: Antimicrobial stewardship intervention emerged successful in advocating a shift from broad-spectrum to narrow-spectrum antibiotics for treating moderately severe community-acquired pneumonia (CAP) while averting any safety concerns.

Main finding: Antimicrobial stewardship intervention effectuated a decrease in the adjusted mean broad-spectrum days of therapy per patient from 6.5 days to 4.8 days, with an adjusted relative reduction of 26.6% (95% CI 18.0%-35.3%). The adjusted risk difference of 0.4% (90% CI –2.7% to 2.4%) indicated noninferiority.

Study details: The data come from the investigator-initiated, noninferiority, CAP-PACT trial including 4,084 adult patients receiving antibiotics for moderately severe CAP post admission to a non-ICU hospital ward, of whom 2,235 patients were admitted during the control period and 1,849 during the intervention period.

Disclosures: The authors received no financial support for the study. CH van Werkhoven reported receiving grants, personal fees, and nonfinancial support from a few sources outside the study, in addition to obtaining a patent for the prediction of clinical manifestations of gut microbiota.

Source: Schweitzer VA et al. Lancet Infect Dis. 2021(Oct 7). Doi: 10.1016/S1473-3099(21)00255-3.

A French population-based study provides further evidence that the BNT162b2 Pfizer-BioNTech mRNA COVID-19 vaccine does not increase the short-term risk for serious cardiovascular adverse events in older people.

The study showed no increased risk of myocardial infarction (MI), stroke, or pulmonary embolism (PE) following vaccination in adults aged 75 years or older in the 14 days following vaccination.

“These findings regarding the BNT162b2 vaccine’s short-term cardiovascular safety profile in older people are reassuring. They should be taken into account by doctors when considering implementing a third dose of the vaccine in older people,” Marie Joelle Jabagi, PharmD, PhD, with the French National Agency for Medicines and Health Products Safety, Saint-Denis, France, said in an interview.

Ridofranz/Getty Images

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

A French population-based study provides further evidence that the BNT162b2 Pfizer-BioNTech mRNA COVID-19 vaccine does not increase the short-term risk for serious cardiovascular adverse events in older people.

The study showed no increased risk of myocardial infarction (MI), stroke, or pulmonary embolism (PE) following vaccination in adults aged 75 years or older in the 14 days following vaccination.

“These findings regarding the BNT162b2 vaccine’s short-term cardiovascular safety profile in older people are reassuring. They should be taken into account by doctors when considering implementing a third dose of the vaccine in older people,” Marie Joelle Jabagi, PharmD, PhD, with the French National Agency for Medicines and Health Products Safety, Saint-Denis, France, said in an interview.

Ridofranz/Getty Images

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

A French population-based study provides further evidence that the BNT162b2 Pfizer-BioNTech mRNA COVID-19 vaccine does not increase the short-term risk for serious cardiovascular adverse events in older people.

The study showed no increased risk of myocardial infarction (MI), stroke, or pulmonary embolism (PE) following vaccination in adults aged 75 years or older in the 14 days following vaccination.

“These findings regarding the BNT162b2 vaccine’s short-term cardiovascular safety profile in older people are reassuring. They should be taken into account by doctors when considering implementing a third dose of the vaccine in older people,” Marie Joelle Jabagi, PharmD, PhD, with the French National Agency for Medicines and Health Products Safety, Saint-Denis, France, said in an interview.

Ridofranz/Getty Images

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

According to an analysis by the Pew Research Center and a report by the National Women’s Law Center, women were earning approximately $0.83-$0.84 for every $1.00 earned by their male counterparts in 2020. Accordingly, women would need to work an additional 42 days to receive compensation for earnings by men during that year. Moreover, these gaps exist with respect to race inequalities. For example, Black and Latinx women who are working full-time were reported to earn approximately $0.64 and $0.57, respectively, for every $1.00 compared with their white, non-Hispanic male counterparts. Striking, isn’t it?

The gender pay gap also affects physicians. A 2021 Medscape survey found that male physicians earn 35% more than female physicians. The biggest gap seems to be between male and female specialists, with men earning $376,000 and women $283,000.
 

Gender inequality and COVID-19

In addition to workplace responsibilities, women are more likely to take on unpaid positions in the informal care economy – examples of these tasks include cleaning, grocery shopping, and child care. In fact, the COVID-19 pandemic has increased the burden of unpaid care work among women, which often incurs a significant impact on their participation in the paid economy.

A study in the United States evaluating the impact of gender inequality during COVID-19 suggested that the rise in unemployment among women during this time may be related to decreased occupational flexibility. Accordingly, the closure of schools and caregiving facilities has translated into increased responsibilities as the informal caregiver, and a decreased ability to fulfill work obligations. Consequently, women may be overwhelmed and unable to maintain their employment status, are limited in their work opportunities, and/or are furloughed or passed over for promotions.
 

Gendered pay gaps affect mental health

A study by Platt and colleagues investigated the relationship between gendered wage gaps and gendered disparities in depression and anxiety disorders. Researchers found that females with a lower income compared with their matched male counterparts were more likely to experience depression and generalized anxiety disorders (i.e., they were 2.4 times more likely to experience depression and 4 times more likely to experience anxiety), while women who earned more than men did not report a significant difference in depression there were reduced gaps in the prevalence of anxiety disorders. As such, it has been suggested that wage gap inequalities are a contributing factor to gendered mental health disparities.

Reduced pay is not only a signifier of reduced returns on human capital. It may also have implications for one’s role in the care economy (e.g., greater time allocation as a result of reduced return), and may result in a higher likelihood for relocation as it relates to a partner’s work, overqualification for a position, inflexible work schedules, and reduced work autonomy.

Wage inequalities may act as a proxy for workplace inequalities such as promotions, prestigious projects, limited upward mobility, and internalized negative workplace experiences, all of which may contribute to increased sleep loss, stress, and related mental health stressors.

One might say, “A few cents, so what?” In addition to income itself, there’s a broader theme at play, which is gender discrimination and inequality. We should encourage conversations around the gender pay gap and develop strategies to combat this economic and social disparity.
 

Ms. Lui completed an HBSc global health specialist degree at the University of Toronto, where she is now an MSc candidate. She has received income from Braxia Scientific Corp. A version of this article first appeared on Medscape.com.

According to an analysis by the Pew Research Center and a report by the National Women’s Law Center, women were earning approximately $0.83-$0.84 for every $1.00 earned by their male counterparts in 2020. Accordingly, women would need to work an additional 42 days to receive compensation for earnings by men during that year. Moreover, these gaps exist with respect to race inequalities. For example, Black and Latinx women who are working full-time were reported to earn approximately $0.64 and $0.57, respectively, for every $1.00 compared with their white, non-Hispanic male counterparts. Striking, isn’t it?

The gender pay gap also affects physicians. A 2021 Medscape survey found that male physicians earn 35% more than female physicians. The biggest gap seems to be between male and female specialists, with men earning $376,000 and women $283,000.
 

Gender inequality and COVID-19

In addition to workplace responsibilities, women are more likely to take on unpaid positions in the informal care economy – examples of these tasks include cleaning, grocery shopping, and child care. In fact, the COVID-19 pandemic has increased the burden of unpaid care work among women, which often incurs a significant impact on their participation in the paid economy.

A study in the United States evaluating the impact of gender inequality during COVID-19 suggested that the rise in unemployment among women during this time may be related to decreased occupational flexibility. Accordingly, the closure of schools and caregiving facilities has translated into increased responsibilities as the informal caregiver, and a decreased ability to fulfill work obligations. Consequently, women may be overwhelmed and unable to maintain their employment status, are limited in their work opportunities, and/or are furloughed or passed over for promotions.
 

Gendered pay gaps affect mental health

A study by Platt and colleagues investigated the relationship between gendered wage gaps and gendered disparities in depression and anxiety disorders. Researchers found that females with a lower income compared with their matched male counterparts were more likely to experience depression and generalized anxiety disorders (i.e., they were 2.4 times more likely to experience depression and 4 times more likely to experience anxiety), while women who earned more than men did not report a significant difference in depression there were reduced gaps in the prevalence of anxiety disorders. As such, it has been suggested that wage gap inequalities are a contributing factor to gendered mental health disparities.

Reduced pay is not only a signifier of reduced returns on human capital. It may also have implications for one’s role in the care economy (e.g., greater time allocation as a result of reduced return), and may result in a higher likelihood for relocation as it relates to a partner’s work, overqualification for a position, inflexible work schedules, and reduced work autonomy.

Wage inequalities may act as a proxy for workplace inequalities such as promotions, prestigious projects, limited upward mobility, and internalized negative workplace experiences, all of which may contribute to increased sleep loss, stress, and related mental health stressors.

One might say, “A few cents, so what?” In addition to income itself, there’s a broader theme at play, which is gender discrimination and inequality. We should encourage conversations around the gender pay gap and develop strategies to combat this economic and social disparity.
 

Ms. Lui completed an HBSc global health specialist degree at the University of Toronto, where she is now an MSc candidate. She has received income from Braxia Scientific Corp. A version of this article first appeared on Medscape.com.

According to an analysis by the Pew Research Center and a report by the National Women’s Law Center, women were earning approximately $0.83-$0.84 for every $1.00 earned by their male counterparts in 2020. Accordingly, women would need to work an additional 42 days to receive compensation for earnings by men during that year. Moreover, these gaps exist with respect to race inequalities. For example, Black and Latinx women who are working full-time were reported to earn approximately $0.64 and $0.57, respectively, for every $1.00 compared with their white, non-Hispanic male counterparts. Striking, isn’t it?

The gender pay gap also affects physicians. A 2021 Medscape survey found that male physicians earn 35% more than female physicians. The biggest gap seems to be between male and female specialists, with men earning $376,000 and women $283,000.
 

Gender inequality and COVID-19

In addition to workplace responsibilities, women are more likely to take on unpaid positions in the informal care economy – examples of these tasks include cleaning, grocery shopping, and child care. In fact, the COVID-19 pandemic has increased the burden of unpaid care work among women, which often incurs a significant impact on their participation in the paid economy.

A study in the United States evaluating the impact of gender inequality during COVID-19 suggested that the rise in unemployment among women during this time may be related to decreased occupational flexibility. Accordingly, the closure of schools and caregiving facilities has translated into increased responsibilities as the informal caregiver, and a decreased ability to fulfill work obligations. Consequently, women may be overwhelmed and unable to maintain their employment status, are limited in their work opportunities, and/or are furloughed or passed over for promotions.
 

Gendered pay gaps affect mental health

A study by Platt and colleagues investigated the relationship between gendered wage gaps and gendered disparities in depression and anxiety disorders. Researchers found that females with a lower income compared with their matched male counterparts were more likely to experience depression and generalized anxiety disorders (i.e., they were 2.4 times more likely to experience depression and 4 times more likely to experience anxiety), while women who earned more than men did not report a significant difference in depression there were reduced gaps in the prevalence of anxiety disorders. As such, it has been suggested that wage gap inequalities are a contributing factor to gendered mental health disparities.

Reduced pay is not only a signifier of reduced returns on human capital. It may also have implications for one’s role in the care economy (e.g., greater time allocation as a result of reduced return), and may result in a higher likelihood for relocation as it relates to a partner’s work, overqualification for a position, inflexible work schedules, and reduced work autonomy.

Wage inequalities may act as a proxy for workplace inequalities such as promotions, prestigious projects, limited upward mobility, and internalized negative workplace experiences, all of which may contribute to increased sleep loss, stress, and related mental health stressors.

One might say, “A few cents, so what?” In addition to income itself, there’s a broader theme at play, which is gender discrimination and inequality. We should encourage conversations around the gender pay gap and develop strategies to combat this economic and social disparity.
 

Ms. Lui completed an HBSc global health specialist degree at the University of Toronto, where she is now an MSc candidate. She has received income from Braxia Scientific Corp. A version of this article first appeared on Medscape.com.

A new lipid-lowering agent in a class that had been written off by many is being developed by a group of academic experts, with new data showing large LDL reductions on top of high-intensity statins.

Obicetrapib is a member of the cholesteryl ester transfer protein (CETP) inhibitor class, which had fallen out of favor after several disappointments with previous drugs in this class.

These agents were initially developed for their ability to raise HDL cholesterol, which was thought to be beneficial. But that approach has now been virtually abandoned after several studies failed to show a link between raising HDL and a reduction in subsequent cardiovascular events.

However, obicetrapib, which is said to be the most potent CETP inhibitor to date, has been shown to produce impressive LDL reductions, and it’s this important data that has caused several lipid experts to want to continue its development.

New data, presented at the recent American Heart Association scientific sessions, show that obicetrapib reduces LDL by 50% when given in addition to high-intensity statins, which could place it as competition for PCSK9 inhibitors or the new agent, inclisiran, but with the advantage of oral dosing.

The drug was in development by Amgen, but the company decided to discontinue its development in 2017 after disappointing results had been seen with several other CETP inhibitors and interest in this class of agent was waning.

But academic experts in the lipid field, led by John Kastelein, MD, PhD, professor of medicine at the Academic Medical Center, University of Amsterdam, and Michael Davidson, MD, clinical professor of medicine at University of Chicago, believed the drug had potential and have acquired obicetrapib from Amgen.

Dr. Kastelein and Dr. Davidson have set up a new company – New Amsterdam Pharma – to further develop obicetrapib, and have raised $200 million from venture capital funding to complete phase 2 and phase 3 studies.

The company has a heavyweight academic advisory board including Stephen Nicholls, MD, Monash University, Clayton, Australia; Kausik Ray, MD, Imperial College London; and Christie Ballantyne, MD, Baylor College of Medicine, Houston.

“We wanted to develop obicetrapib further because of its amazing LDL-lowering properties,” Dr. Kastelein said in an interview.

“No one has paid much attention to CETP inhibitors after the HDL hypothesis was disregarded, as everyone thought these drugs were just about raising HDL. But actually, they can also lower LDL, and this particular agent reduces LDL very effectively,” Dr. Kastelein said.
 

ROSE study

Dr. Nicholls presented the latest data on obicetrapib at the AHA meeting.

“Despite the use of high-intensity statins, two-thirds of patients do not reach their target LDL level, so we have a need for new therapies that lower LDL and can be used in combination with high-intensity statins,” he explained.

He noted that earlier studies with obicetrapib showed a 45% lowering of LDL with monotherapy.

Dr. Nicholls reported that recent evidence has emerged that increases interest in inhibiting CETP to be potentially cardioprotective.

To begin, genetic studies have shown that genetic polymorphisms associated with lower levels of CETP appear to be cardioprotective, and this is associated with lower levels of LDL rather than higher levels of HDL. 

Furthermore, the REVEAL cardiovascular outcomes trial with anacetrapib (also a CETP inhibitor) in 2017 showed a significant 9% reduction in major adverse cardiac events (MACE) after 4 years of follow-up. “This was exactly predicted by the 11 mg/dL drop in absolute LDL cholesterol level. It was not predicted or associated with the increase in HDL level observed with that agent,” Dr. Nicholls said.

The objective of the current ROSE study was to evaluate the lipid-lowering ability, safety, and tolerability of obicetrapib in patients on high-intensity statins.

The study included 120 patients who had been treated on a stable dose of high-intensity statins (atorvastatin at a dose of at least 40 mg daily or rosuvastatin at a dose of 20 mg daily) for at least 8 weeks. All patients were required to have a fasting LDL of at least 70 mg/dL and the median baseline LDL was 90 mg/dL. They were randomly assigned to obicetrapib (5 mg or 10 mg daily) or placebo.

The primary endpoint was the difference between groups in percentage change in LDL from baseline to week 8, with LDL levels measured by two different techniques.

Results showed a “robust” 51% reduction in LDL with the 10-mg dose of obicetrapib, and a 42% reduction with the 5-mg dose, Dr. Nicholls reported.

These effects were comparable regardless of baseline LDL and were similar with both methods of LDL measurement. 

Almost all patients demonstrated some degree of LDL cholesterol lowering, with only three patients on the 5-mg dose and one patient on the 10-mg dose not showing any reduction in LDL.

Other results showed a dose-dependent lowering of Apo B of up to 30%, and a reduction of non-HDL cholesterol of up to 44%.

“Predictably, there were also increases of HDL cholesterol,” Dr. Nicholls said. “At the 10-mg dose, we see a 165% increase in HDL levels. That is associated with a 48% increase in Apo A1 levels. This is very consistent with findings from the previous monotherapy study.”  

There was a 56% reduction in Lp(a) levels, and a modest 11% reduction in triglycerides.

Both doses of obicetrapib were well tolerated, with no increase in the rate of adverse events. Only one patient discontinued the study drug because of an adverse event and that patient was in the placebo group, Dr. Nicholls noted.  

“Blood pressure is an important adverse event to look at in the CETP class given the challenges seen with the first CETP evaluated – torcetrapib,” Dr. Nicholls said. “But in the three clinical trials with obicetrapib conducted to date, reassuringly, we see no increase in either systolic or diastolic blood pressure with either the 5-mg or 10-mg dose.”

He concluded that obicetrapib “could be a valuable addition to high-risk patients with atherosclerotic cardiovascular disease who do not achieve their target LDL level despite use of high-intensity statin therapy.”
 

Differences from other CETP inhibitors

Asked how obicetrapib differs from other agents in the CETP inhibitor class, Dr. Nicholls replied that obicetrapib is much more potent, as shown by the large lipid changes seen with very small quantities of this drug, 5 mg or 10 mg, whereas prior CETP inhibitors showed smaller changes with much higher doses.

“We are giving very small amounts of obicetrapib and seeing very robust effects on both atherogenic and lipid parameters,” he said.  

“The other major point with this class of agent is that the first drug, torcetrapib, had toxicity, which resulted in increased cardiovascular events. But it has now been established that torcetrapib had a number of off-target effects that have not been seen with subsequent agents in this class,” he said.

Studies so far show that obicetrapib does not have torcetrapib-like effects. “That is encouraging. This, and the impressive LDL lowering effects, certainly lay the foundation for larger studies moving forward,” he added.

“This has been an intriguing field to many of us involved from the start. We started with a very disappointing result with torcetrapib. Then a couple of studies looked to be clinically futile, but we were encouraged by the REVEAL study which suggested that there might be benefit,” Dr. Nicholls said.

“If we combined the REVEAL results with the genetic data, it has actually flipped the whole CETP story upside down. We started thinking that inhibiting CETP was all about raising HDL, but it turns out that it is about LDL lowering,” he said. “And that is not only important in terms of the lipid effects but also the trials and the way they are designed.

“I think you’ll find that the future trials in this class and with this agent will have LDL very much in mind and that will very much influence the study design,” he said, adding that a larger cardiovascular outcome trial is now being planned. 

“The regulatory perspective is that LDL is a pretty trusted surrogate ... but I think an outcomes trial will be important to reinforce and reassure on safety and outline cost-effectiveness, which will help us understand where the sweet spot for using this agent in the clinic will be,” Dr. Nicholls noted.  

Dr. Kastelein explained that it has taken some time to realize that CETP inhibitors may be valuable for reducing LDL.   

“The first agent, torcetrapib, had an off-target toxicity that led to increased blood pressure but a specific part of the torcetrapib molecule was subsequently identified that was responsible for that, and subsequent agents in the CETP inhibitor class did not have such adverse effects,” he said.  

“The next agent, dalcetrapib (Roche), raised HDL but didn’t move LDL, and an outcomes trial with evacetrapib (Lilly) was stopped after 2 years because of futility, but we now believe that lipid lowering trials need longer term follow-up – up to 5 years – to see a benefit,” he noted.  

Dr. Kastelein reports that anacetrapib (Merck) has been the most powerful CETP inhibitor until now, giving an LDL reduction of about 20%, which was associated with a 10% reduction in cardiovascular events in first 4 years of follow-up. 

“Oxford academic researchers decided to continue follow-up in this trial without Merck and showed a 20% reduction in cardiovascular events by 6 years. This has been the strongest rationale for our investors,” Dr. Kastelein said.   

He pointed out that obicetrapib is much more potent than anacetrapib. “Obicetrapib reduces LDL by 50% at just a 10-mg dose, whereas anacetrapib was used at a dose of 100 mg to give a 17%-20% LDL reduction.”
 

Could HDL increase be beneficial after all?

Although increasing HDL is currently not thought to bring about a direct reduction in cardiovascular events, there is new evidence emerging that increasing HDL may confer some benefit in protecting against the development of type 2 diabetes, Dr. Kastelein noted.

“We know that statins can increase risk of developing type 2 diabetes, and post hoc analyses of previous trials with CETP inhibitors suggest that these drugs have the opposite effect,” he said. “We will investigate this protectively in our phase 3 outcomes trial. If this is a true effect, it should eventually translate into a reduction in cardiovascular outcomes, but this could take a longer time to see than the benefits of lowering LDL.”

Commenting on the current data, Steven Nissen, MD, of Cleveland Clinic, said: “The results are truly impressive – a nearly 50% LDL reduction on a background of statins with a once-daily oral agent. While PCSK9 inhibitors can achieve similar results, they are injectable and costly.

“Since anacetrapib, a much weaker CETP inhibitor, was successful at reducing major adverse cardiac events, the likelihood that obicetrapib would reduce MACE even more substantially is very high,” he added.

Dr. Nissen said he has been aware of this drug for some time and has advised the company about development options and regulatory strategy. “I have encouraged this company to develop this very promising drug,” he said.

The current study was funded by New Amsterdam Pharma. Dr. Nicholls reports grants from AstraZeneca, Amgen, Anthera, Eli Lilly, Esperion, Novartis, Cerenis, The Medicines Company, Resverlogix, Infraredx, Roche, Sanofi-Regeneron and LipoScience, and honoraria from New Amsterdam Pharma, AstraZeneca, Akcea, Eli Lilly, Anthera, Omthera, Merck, Takeda, Resverlogix, Sanofi-Regeneron, CSL Behring, Esperion, and Boehringer Ingelheim. Dr. Kastelein is chief scientific officer of New Amsterdam Pharma.  

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

A new lipid-lowering agent in a class that had been written off by many is being developed by a group of academic experts, with new data showing large LDL reductions on top of high-intensity statins.

Obicetrapib is a member of the cholesteryl ester transfer protein (CETP) inhibitor class, which had fallen out of favor after several disappointments with previous drugs in this class.

These agents were initially developed for their ability to raise HDL cholesterol, which was thought to be beneficial. But that approach has now been virtually abandoned after several studies failed to show a link between raising HDL and a reduction in subsequent cardiovascular events.

However, obicetrapib, which is said to be the most potent CETP inhibitor to date, has been shown to produce impressive LDL reductions, and it’s this important data that has caused several lipid experts to want to continue its development.

New data, presented at the recent American Heart Association scientific sessions, show that obicetrapib reduces LDL by 50% when given in addition to high-intensity statins, which could place it as competition for PCSK9 inhibitors or the new agent, inclisiran, but with the advantage of oral dosing.

The drug was in development by Amgen, but the company decided to discontinue its development in 2017 after disappointing results had been seen with several other CETP inhibitors and interest in this class of agent was waning.

But academic experts in the lipid field, led by John Kastelein, MD, PhD, professor of medicine at the Academic Medical Center, University of Amsterdam, and Michael Davidson, MD, clinical professor of medicine at University of Chicago, believed the drug had potential and have acquired obicetrapib from Amgen.

Dr. Kastelein and Dr. Davidson have set up a new company – New Amsterdam Pharma – to further develop obicetrapib, and have raised $200 million from venture capital funding to complete phase 2 and phase 3 studies.

The company has a heavyweight academic advisory board including Stephen Nicholls, MD, Monash University, Clayton, Australia; Kausik Ray, MD, Imperial College London; and Christie Ballantyne, MD, Baylor College of Medicine, Houston.

“We wanted to develop obicetrapib further because of its amazing LDL-lowering properties,” Dr. Kastelein said in an interview.

“No one has paid much attention to CETP inhibitors after the HDL hypothesis was disregarded, as everyone thought these drugs were just about raising HDL. But actually, they can also lower LDL, and this particular agent reduces LDL very effectively,” Dr. Kastelein said.
 

ROSE study

Dr. Nicholls presented the latest data on obicetrapib at the AHA meeting.

“Despite the use of high-intensity statins, two-thirds of patients do not reach their target LDL level, so we have a need for new therapies that lower LDL and can be used in combination with high-intensity statins,” he explained.

He noted that earlier studies with obicetrapib showed a 45% lowering of LDL with monotherapy.

Dr. Nicholls reported that recent evidence has emerged that increases interest in inhibiting CETP to be potentially cardioprotective.

To begin, genetic studies have shown that genetic polymorphisms associated with lower levels of CETP appear to be cardioprotective, and this is associated with lower levels of LDL rather than higher levels of HDL. 

Furthermore, the REVEAL cardiovascular outcomes trial with anacetrapib (also a CETP inhibitor) in 2017 showed a significant 9% reduction in major adverse cardiac events (MACE) after 4 years of follow-up. “This was exactly predicted by the 11 mg/dL drop in absolute LDL cholesterol level. It was not predicted or associated with the increase in HDL level observed with that agent,” Dr. Nicholls said.

The objective of the current ROSE study was to evaluate the lipid-lowering ability, safety, and tolerability of obicetrapib in patients on high-intensity statins.

The study included 120 patients who had been treated on a stable dose of high-intensity statins (atorvastatin at a dose of at least 40 mg daily or rosuvastatin at a dose of 20 mg daily) for at least 8 weeks. All patients were required to have a fasting LDL of at least 70 mg/dL and the median baseline LDL was 90 mg/dL. They were randomly assigned to obicetrapib (5 mg or 10 mg daily) or placebo.

The primary endpoint was the difference between groups in percentage change in LDL from baseline to week 8, with LDL levels measured by two different techniques.

Results showed a “robust” 51% reduction in LDL with the 10-mg dose of obicetrapib, and a 42% reduction with the 5-mg dose, Dr. Nicholls reported.

These effects were comparable regardless of baseline LDL and were similar with both methods of LDL measurement. 

Almost all patients demonstrated some degree of LDL cholesterol lowering, with only three patients on the 5-mg dose and one patient on the 10-mg dose not showing any reduction in LDL.

Other results showed a dose-dependent lowering of Apo B of up to 30%, and a reduction of non-HDL cholesterol of up to 44%.

“Predictably, there were also increases of HDL cholesterol,” Dr. Nicholls said. “At the 10-mg dose, we see a 165% increase in HDL levels. That is associated with a 48% increase in Apo A1 levels. This is very consistent with findings from the previous monotherapy study.”  

There was a 56% reduction in Lp(a) levels, and a modest 11% reduction in triglycerides.

Both doses of obicetrapib were well tolerated, with no increase in the rate of adverse events. Only one patient discontinued the study drug because of an adverse event and that patient was in the placebo group, Dr. Nicholls noted.  

“Blood pressure is an important adverse event to look at in the CETP class given the challenges seen with the first CETP evaluated – torcetrapib,” Dr. Nicholls said. “But in the three clinical trials with obicetrapib conducted to date, reassuringly, we see no increase in either systolic or diastolic blood pressure with either the 5-mg or 10-mg dose.”

He concluded that obicetrapib “could be a valuable addition to high-risk patients with atherosclerotic cardiovascular disease who do not achieve their target LDL level despite use of high-intensity statin therapy.”
 

Differences from other CETP inhibitors

Asked how obicetrapib differs from other agents in the CETP inhibitor class, Dr. Nicholls replied that obicetrapib is much more potent, as shown by the large lipid changes seen with very small quantities of this drug, 5 mg or 10 mg, whereas prior CETP inhibitors showed smaller changes with much higher doses.

“We are giving very small amounts of obicetrapib and seeing very robust effects on both atherogenic and lipid parameters,” he said.  

“The other major point with this class of agent is that the first drug, torcetrapib, had toxicity, which resulted in increased cardiovascular events. But it has now been established that torcetrapib had a number of off-target effects that have not been seen with subsequent agents in this class,” he said.

Studies so far show that obicetrapib does not have torcetrapib-like effects. “That is encouraging. This, and the impressive LDL lowering effects, certainly lay the foundation for larger studies moving forward,” he added.

“This has been an intriguing field to many of us involved from the start. We started with a very disappointing result with torcetrapib. Then a couple of studies looked to be clinically futile, but we were encouraged by the REVEAL study which suggested that there might be benefit,” Dr. Nicholls said.

“If we combined the REVEAL results with the genetic data, it has actually flipped the whole CETP story upside down. We started thinking that inhibiting CETP was all about raising HDL, but it turns out that it is about LDL lowering,” he said. “And that is not only important in terms of the lipid effects but also the trials and the way they are designed.

“I think you’ll find that the future trials in this class and with this agent will have LDL very much in mind and that will very much influence the study design,” he said, adding that a larger cardiovascular outcome trial is now being planned. 

“The regulatory perspective is that LDL is a pretty trusted surrogate ... but I think an outcomes trial will be important to reinforce and reassure on safety and outline cost-effectiveness, which will help us understand where the sweet spot for using this agent in the clinic will be,” Dr. Nicholls noted.  

Dr. Kastelein explained that it has taken some time to realize that CETP inhibitors may be valuable for reducing LDL.   

“The first agent, torcetrapib, had an off-target toxicity that led to increased blood pressure but a specific part of the torcetrapib molecule was subsequently identified that was responsible for that, and subsequent agents in the CETP inhibitor class did not have such adverse effects,” he said.  

“The next agent, dalcetrapib (Roche), raised HDL but didn’t move LDL, and an outcomes trial with evacetrapib (Lilly) was stopped after 2 years because of futility, but we now believe that lipid lowering trials need longer term follow-up – up to 5 years – to see a benefit,” he noted.  

Dr. Kastelein reports that anacetrapib (Merck) has been the most powerful CETP inhibitor until now, giving an LDL reduction of about 20%, which was associated with a 10% reduction in cardiovascular events in first 4 years of follow-up. 

“Oxford academic researchers decided to continue follow-up in this trial without Merck and showed a 20% reduction in cardiovascular events by 6 years. This has been the strongest rationale for our investors,” Dr. Kastelein said.   

He pointed out that obicetrapib is much more potent than anacetrapib. “Obicetrapib reduces LDL by 50% at just a 10-mg dose, whereas anacetrapib was used at a dose of 100 mg to give a 17%-20% LDL reduction.”
 

Could HDL increase be beneficial after all?

Although increasing HDL is currently not thought to bring about a direct reduction in cardiovascular events, there is new evidence emerging that increasing HDL may confer some benefit in protecting against the development of type 2 diabetes, Dr. Kastelein noted.

“We know that statins can increase risk of developing type 2 diabetes, and post hoc analyses of previous trials with CETP inhibitors suggest that these drugs have the opposite effect,” he said. “We will investigate this protectively in our phase 3 outcomes trial. If this is a true effect, it should eventually translate into a reduction in cardiovascular outcomes, but this could take a longer time to see than the benefits of lowering LDL.”

Commenting on the current data, Steven Nissen, MD, of Cleveland Clinic, said: “The results are truly impressive – a nearly 50% LDL reduction on a background of statins with a once-daily oral agent. While PCSK9 inhibitors can achieve similar results, they are injectable and costly.

“Since anacetrapib, a much weaker CETP inhibitor, was successful at reducing major adverse cardiac events, the likelihood that obicetrapib would reduce MACE even more substantially is very high,” he added.

Dr. Nissen said he has been aware of this drug for some time and has advised the company about development options and regulatory strategy. “I have encouraged this company to develop this very promising drug,” he said.

The current study was funded by New Amsterdam Pharma. Dr. Nicholls reports grants from AstraZeneca, Amgen, Anthera, Eli Lilly, Esperion, Novartis, Cerenis, The Medicines Company, Resverlogix, Infraredx, Roche, Sanofi-Regeneron and LipoScience, and honoraria from New Amsterdam Pharma, AstraZeneca, Akcea, Eli Lilly, Anthera, Omthera, Merck, Takeda, Resverlogix, Sanofi-Regeneron, CSL Behring, Esperion, and Boehringer Ingelheim. Dr. Kastelein is chief scientific officer of New Amsterdam Pharma.  

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

A new lipid-lowering agent in a class that had been written off by many is being developed by a group of academic experts, with new data showing large LDL reductions on top of high-intensity statins.

Obicetrapib is a member of the cholesteryl ester transfer protein (CETP) inhibitor class, which had fallen out of favor after several disappointments with previous drugs in this class.

These agents were initially developed for their ability to raise HDL cholesterol, which was thought to be beneficial. But that approach has now been virtually abandoned after several studies failed to show a link between raising HDL and a reduction in subsequent cardiovascular events.

However, obicetrapib, which is said to be the most potent CETP inhibitor to date, has been shown to produce impressive LDL reductions, and it’s this important data that has caused several lipid experts to want to continue its development.

New data, presented at the recent American Heart Association scientific sessions, show that obicetrapib reduces LDL by 50% when given in addition to high-intensity statins, which could place it as competition for PCSK9 inhibitors or the new agent, inclisiran, but with the advantage of oral dosing.

The drug was in development by Amgen, but the company decided to discontinue its development in 2017 after disappointing results had been seen with several other CETP inhibitors and interest in this class of agent was waning.

But academic experts in the lipid field, led by John Kastelein, MD, PhD, professor of medicine at the Academic Medical Center, University of Amsterdam, and Michael Davidson, MD, clinical professor of medicine at University of Chicago, believed the drug had potential and have acquired obicetrapib from Amgen.

Dr. Kastelein and Dr. Davidson have set up a new company – New Amsterdam Pharma – to further develop obicetrapib, and have raised $200 million from venture capital funding to complete phase 2 and phase 3 studies.

The company has a heavyweight academic advisory board including Stephen Nicholls, MD, Monash University, Clayton, Australia; Kausik Ray, MD, Imperial College London; and Christie Ballantyne, MD, Baylor College of Medicine, Houston.

“We wanted to develop obicetrapib further because of its amazing LDL-lowering properties,” Dr. Kastelein said in an interview.

“No one has paid much attention to CETP inhibitors after the HDL hypothesis was disregarded, as everyone thought these drugs were just about raising HDL. But actually, they can also lower LDL, and this particular agent reduces LDL very effectively,” Dr. Kastelein said.
 

ROSE study

Dr. Nicholls presented the latest data on obicetrapib at the AHA meeting.

“Despite the use of high-intensity statins, two-thirds of patients do not reach their target LDL level, so we have a need for new therapies that lower LDL and can be used in combination with high-intensity statins,” he explained.

He noted that earlier studies with obicetrapib showed a 45% lowering of LDL with monotherapy.

Dr. Nicholls reported that recent evidence has emerged that increases interest in inhibiting CETP to be potentially cardioprotective.

To begin, genetic studies have shown that genetic polymorphisms associated with lower levels of CETP appear to be cardioprotective, and this is associated with lower levels of LDL rather than higher levels of HDL. 

Furthermore, the REVEAL cardiovascular outcomes trial with anacetrapib (also a CETP inhibitor) in 2017 showed a significant 9% reduction in major adverse cardiac events (MACE) after 4 years of follow-up. “This was exactly predicted by the 11 mg/dL drop in absolute LDL cholesterol level. It was not predicted or associated with the increase in HDL level observed with that agent,” Dr. Nicholls said.

The objective of the current ROSE study was to evaluate the lipid-lowering ability, safety, and tolerability of obicetrapib in patients on high-intensity statins.

The study included 120 patients who had been treated on a stable dose of high-intensity statins (atorvastatin at a dose of at least 40 mg daily or rosuvastatin at a dose of 20 mg daily) for at least 8 weeks. All patients were required to have a fasting LDL of at least 70 mg/dL and the median baseline LDL was 90 mg/dL. They were randomly assigned to obicetrapib (5 mg or 10 mg daily) or placebo.

The primary endpoint was the difference between groups in percentage change in LDL from baseline to week 8, with LDL levels measured by two different techniques.

Results showed a “robust” 51% reduction in LDL with the 10-mg dose of obicetrapib, and a 42% reduction with the 5-mg dose, Dr. Nicholls reported.

These effects were comparable regardless of baseline LDL and were similar with both methods of LDL measurement. 

Almost all patients demonstrated some degree of LDL cholesterol lowering, with only three patients on the 5-mg dose and one patient on the 10-mg dose not showing any reduction in LDL.

Other results showed a dose-dependent lowering of Apo B of up to 30%, and a reduction of non-HDL cholesterol of up to 44%.

“Predictably, there were also increases of HDL cholesterol,” Dr. Nicholls said. “At the 10-mg dose, we see a 165% increase in HDL levels. That is associated with a 48% increase in Apo A1 levels. This is very consistent with findings from the previous monotherapy study.”  

There was a 56% reduction in Lp(a) levels, and a modest 11% reduction in triglycerides.

Both doses of obicetrapib were well tolerated, with no increase in the rate of adverse events. Only one patient discontinued the study drug because of an adverse event and that patient was in the placebo group, Dr. Nicholls noted.  

“Blood pressure is an important adverse event to look at in the CETP class given the challenges seen with the first CETP evaluated – torcetrapib,” Dr. Nicholls said. “But in the three clinical trials with obicetrapib conducted to date, reassuringly, we see no increase in either systolic or diastolic blood pressure with either the 5-mg or 10-mg dose.”

He concluded that obicetrapib “could be a valuable addition to high-risk patients with atherosclerotic cardiovascular disease who do not achieve their target LDL level despite use of high-intensity statin therapy.”
 

Differences from other CETP inhibitors

Asked how obicetrapib differs from other agents in the CETP inhibitor class, Dr. Nicholls replied that obicetrapib is much more potent, as shown by the large lipid changes seen with very small quantities of this drug, 5 mg or 10 mg, whereas prior CETP inhibitors showed smaller changes with much higher doses.

“We are giving very small amounts of obicetrapib and seeing very robust effects on both atherogenic and lipid parameters,” he said.  

“The other major point with this class of agent is that the first drug, torcetrapib, had toxicity, which resulted in increased cardiovascular events. But it has now been established that torcetrapib had a number of off-target effects that have not been seen with subsequent agents in this class,” he said.

Studies so far show that obicetrapib does not have torcetrapib-like effects. “That is encouraging. This, and the impressive LDL lowering effects, certainly lay the foundation for larger studies moving forward,” he added.

“This has been an intriguing field to many of us involved from the start. We started with a very disappointing result with torcetrapib. Then a couple of studies looked to be clinically futile, but we were encouraged by the REVEAL study which suggested that there might be benefit,” Dr. Nicholls said.

“If we combined the REVEAL results with the genetic data, it has actually flipped the whole CETP story upside down. We started thinking that inhibiting CETP was all about raising HDL, but it turns out that it is about LDL lowering,” he said. “And that is not only important in terms of the lipid effects but also the trials and the way they are designed.

“I think you’ll find that the future trials in this class and with this agent will have LDL very much in mind and that will very much influence the study design,” he said, adding that a larger cardiovascular outcome trial is now being planned. 

“The regulatory perspective is that LDL is a pretty trusted surrogate ... but I think an outcomes trial will be important to reinforce and reassure on safety and outline cost-effectiveness, which will help us understand where the sweet spot for using this agent in the clinic will be,” Dr. Nicholls noted.  

Dr. Kastelein explained that it has taken some time to realize that CETP inhibitors may be valuable for reducing LDL.   

“The first agent, torcetrapib, had an off-target toxicity that led to increased blood pressure but a specific part of the torcetrapib molecule was subsequently identified that was responsible for that, and subsequent agents in the CETP inhibitor class did not have such adverse effects,” he said.  

“The next agent, dalcetrapib (Roche), raised HDL but didn’t move LDL, and an outcomes trial with evacetrapib (Lilly) was stopped after 2 years because of futility, but we now believe that lipid lowering trials need longer term follow-up – up to 5 years – to see a benefit,” he noted.  

Dr. Kastelein reports that anacetrapib (Merck) has been the most powerful CETP inhibitor until now, giving an LDL reduction of about 20%, which was associated with a 10% reduction in cardiovascular events in first 4 years of follow-up. 

“Oxford academic researchers decided to continue follow-up in this trial without Merck and showed a 20% reduction in cardiovascular events by 6 years. This has been the strongest rationale for our investors,” Dr. Kastelein said.   

He pointed out that obicetrapib is much more potent than anacetrapib. “Obicetrapib reduces LDL by 50% at just a 10-mg dose, whereas anacetrapib was used at a dose of 100 mg to give a 17%-20% LDL reduction.”
 

Could HDL increase be beneficial after all?

Although increasing HDL is currently not thought to bring about a direct reduction in cardiovascular events, there is new evidence emerging that increasing HDL may confer some benefit in protecting against the development of type 2 diabetes, Dr. Kastelein noted.

“We know that statins can increase risk of developing type 2 diabetes, and post hoc analyses of previous trials with CETP inhibitors suggest that these drugs have the opposite effect,” he said. “We will investigate this protectively in our phase 3 outcomes trial. If this is a true effect, it should eventually translate into a reduction in cardiovascular outcomes, but this could take a longer time to see than the benefits of lowering LDL.”

Commenting on the current data, Steven Nissen, MD, of Cleveland Clinic, said: “The results are truly impressive – a nearly 50% LDL reduction on a background of statins with a once-daily oral agent. While PCSK9 inhibitors can achieve similar results, they are injectable and costly.

“Since anacetrapib, a much weaker CETP inhibitor, was successful at reducing major adverse cardiac events, the likelihood that obicetrapib would reduce MACE even more substantially is very high,” he added.

Dr. Nissen said he has been aware of this drug for some time and has advised the company about development options and regulatory strategy. “I have encouraged this company to develop this very promising drug,” he said.

The current study was funded by New Amsterdam Pharma. Dr. Nicholls reports grants from AstraZeneca, Amgen, Anthera, Eli Lilly, Esperion, Novartis, Cerenis, The Medicines Company, Resverlogix, Infraredx, Roche, Sanofi-Regeneron and LipoScience, and honoraria from New Amsterdam Pharma, AstraZeneca, Akcea, Eli Lilly, Anthera, Omthera, Merck, Takeda, Resverlogix, Sanofi-Regeneron, CSL Behring, Esperion, and Boehringer Ingelheim. Dr. Kastelein is chief scientific officer of New Amsterdam Pharma.  

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

Going to bed later than usual and/or getting a poor night’s sleep are both associated with impaired glycemic response to breakfast the following morning in healthy adults, according to a multiple test-meal challenge study conducted over 14 days.

“Our data suggest that sleep duration, efficiency, and midpoint are important determinants of postprandial glycemic control at a population level,” Neil Tsereteli, MD, Lund University Diabetes Centre, Malmo, Sweden, and colleagues wrote in their article, published online Nov. 30, 2021, in Diabetologia.

“And [the results] suggest that one-size-fits-all sleep recommendations are suboptimal, particularly in the context of postprandial glycemic control, a key component of diabetes prevention,” they added.
 

Prior research on sleep quality and control of glucose lacking

Diet, exercise, and sleep are fundamental components of a healthy lifestyle; however, the role that sleep plays in affecting blood glucose control in generally healthy people has been studied little so far, the researchers wrote.

Sleep disorders can act as a measure of general health as they often occur alongside other health problems. Sleep quality also has a direct causal effect on many conditions such as cardiovascular disease, obesity, and type 2 diabetes. And disturbed sleep caused by conditions such as obstructive sleep apnea is associated with the prevalence of type 2 diabetes and risk of associated complications.

This and other evidence suggest a strong link between glucose regulation and the quality and duration of sleep.

Dr. Tsereteli and colleagues set out to examine this further in the Personalized Responses to Dietary Composition Trial 1, which involved 953 healthy adults who consumed standardized meals over 2 weeks in a clinic setting and at home.

“The meals were consumed either for breakfast or lunch in a randomized meal order and consisted of eight different standardized meals,”  the researchers wrote.

Activity and sleep were monitored using a wearable device with an accelerometer. Postprandial blood glucose levels were measured using a continuous glucose monitor.

Sleep variables including quality, duration, and timing and their impact on glycemic response to breakfast the following morning, and were compared between participants and within each individual.
 

Better sleep efficiency, better glucose control

The study found that, although there was no significant association between length of sleep period and postmeal glycemic response, there was a significant interaction when the nutritional content of the breakfast meal was also considered.

Longer sleep periods were associated with lower blood glucose following high-carbohydrate and high-fat breakfasts, indicating better blood glucose control.

Additionally, the researchers observed a within-person effect in which a study participant who slept for longer than they typically would was likely to have reduced postprandial blood glucose following a high-carbohydrate or high-fat breakfast the next day.

The authors also found a significant link between sleep efficiency (ratio of time asleep to total length of sleep period) and glycemic control. When a participant slept more efficiently than usual, their postprandial blood glucose also tended to be lower than usual.

“This effect was largely driven by sleep onset (going to bed later) rather than sleep offset (waking up later),” Dr. Tsereteli and colleagues noted.
 

Sleep a key pillar of health

Asked whether these particular sleep effects might be exacerbated in patients with diabetes, senior author Paul Franks, MD, also from the Lund University Diabetes Centre, felt they could not meaningfully extrapolate results to people with diabetes, given that many take glucose-lowering medications.

“However, it is likely that these results would be similar or exacerbated in people with prediabetes, as glucose fluctuations in this subgroup of patients are generally greater than in people with normoglycemia,” he noted in an interview.

“Sleep is a key pillar of health, and focusing on both sleep and diet is key for healthy blood glucose control,” he added.

“Compensating for a bad night’s sleep by consuming a very sugary breakfast or energy drinks is likely to be especially detrimental for blood glucose control,” Dr. Franks said.

The study was funded by Lund University. Dr. Tsereteli and Dr. Franks reported no relevant financial relationships.

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

Going to bed later than usual and/or getting a poor night’s sleep are both associated with impaired glycemic response to breakfast the following morning in healthy adults, according to a multiple test-meal challenge study conducted over 14 days.

“Our data suggest that sleep duration, efficiency, and midpoint are important determinants of postprandial glycemic control at a population level,” Neil Tsereteli, MD, Lund University Diabetes Centre, Malmo, Sweden, and colleagues wrote in their article, published online Nov. 30, 2021, in Diabetologia.

“And [the results] suggest that one-size-fits-all sleep recommendations are suboptimal, particularly in the context of postprandial glycemic control, a key component of diabetes prevention,” they added.
 

Prior research on sleep quality and control of glucose lacking

Diet, exercise, and sleep are fundamental components of a healthy lifestyle; however, the role that sleep plays in affecting blood glucose control in generally healthy people has been studied little so far, the researchers wrote.

Sleep disorders can act as a measure of general health as they often occur alongside other health problems. Sleep quality also has a direct causal effect on many conditions such as cardiovascular disease, obesity, and type 2 diabetes. And disturbed sleep caused by conditions such as obstructive sleep apnea is associated with the prevalence of type 2 diabetes and risk of associated complications.

This and other evidence suggest a strong link between glucose regulation and the quality and duration of sleep.

Dr. Tsereteli and colleagues set out to examine this further in the Personalized Responses to Dietary Composition Trial 1, which involved 953 healthy adults who consumed standardized meals over 2 weeks in a clinic setting and at home.

“The meals were consumed either for breakfast or lunch in a randomized meal order and consisted of eight different standardized meals,”  the researchers wrote.

Activity and sleep were monitored using a wearable device with an accelerometer. Postprandial blood glucose levels were measured using a continuous glucose monitor.

Sleep variables including quality, duration, and timing and their impact on glycemic response to breakfast the following morning, and were compared between participants and within each individual.
 

Better sleep efficiency, better glucose control

The study found that, although there was no significant association between length of sleep period and postmeal glycemic response, there was a significant interaction when the nutritional content of the breakfast meal was also considered.

Longer sleep periods were associated with lower blood glucose following high-carbohydrate and high-fat breakfasts, indicating better blood glucose control.

Additionally, the researchers observed a within-person effect in which a study participant who slept for longer than they typically would was likely to have reduced postprandial blood glucose following a high-carbohydrate or high-fat breakfast the next day.

The authors also found a significant link between sleep efficiency (ratio of time asleep to total length of sleep period) and glycemic control. When a participant slept more efficiently than usual, their postprandial blood glucose also tended to be lower than usual.

“This effect was largely driven by sleep onset (going to bed later) rather than sleep offset (waking up later),” Dr. Tsereteli and colleagues noted.
 

Sleep a key pillar of health

Asked whether these particular sleep effects might be exacerbated in patients with diabetes, senior author Paul Franks, MD, also from the Lund University Diabetes Centre, felt they could not meaningfully extrapolate results to people with diabetes, given that many take glucose-lowering medications.

“However, it is likely that these results would be similar or exacerbated in people with prediabetes, as glucose fluctuations in this subgroup of patients are generally greater than in people with normoglycemia,” he noted in an interview.

“Sleep is a key pillar of health, and focusing on both sleep and diet is key for healthy blood glucose control,” he added.

“Compensating for a bad night’s sleep by consuming a very sugary breakfast or energy drinks is likely to be especially detrimental for blood glucose control,” Dr. Franks said.

The study was funded by Lund University. Dr. Tsereteli and Dr. Franks reported no relevant financial relationships.

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

Going to bed later than usual and/or getting a poor night’s sleep are both associated with impaired glycemic response to breakfast the following morning in healthy adults, according to a multiple test-meal challenge study conducted over 14 days.

“Our data suggest that sleep duration, efficiency, and midpoint are important determinants of postprandial glycemic control at a population level,” Neil Tsereteli, MD, Lund University Diabetes Centre, Malmo, Sweden, and colleagues wrote in their article, published online Nov. 30, 2021, in Diabetologia.

“And [the results] suggest that one-size-fits-all sleep recommendations are suboptimal, particularly in the context of postprandial glycemic control, a key component of diabetes prevention,” they added.
 

Prior research on sleep quality and control of glucose lacking

Diet, exercise, and sleep are fundamental components of a healthy lifestyle; however, the role that sleep plays in affecting blood glucose control in generally healthy people has been studied little so far, the researchers wrote.

Sleep disorders can act as a measure of general health as they often occur alongside other health problems. Sleep quality also has a direct causal effect on many conditions such as cardiovascular disease, obesity, and type 2 diabetes. And disturbed sleep caused by conditions such as obstructive sleep apnea is associated with the prevalence of type 2 diabetes and risk of associated complications.

This and other evidence suggest a strong link between glucose regulation and the quality and duration of sleep.

Dr. Tsereteli and colleagues set out to examine this further in the Personalized Responses to Dietary Composition Trial 1, which involved 953 healthy adults who consumed standardized meals over 2 weeks in a clinic setting and at home.

“The meals were consumed either for breakfast or lunch in a randomized meal order and consisted of eight different standardized meals,”  the researchers wrote.

Activity and sleep were monitored using a wearable device with an accelerometer. Postprandial blood glucose levels were measured using a continuous glucose monitor.

Sleep variables including quality, duration, and timing and their impact on glycemic response to breakfast the following morning, and were compared between participants and within each individual.
 

Better sleep efficiency, better glucose control

The study found that, although there was no significant association between length of sleep period and postmeal glycemic response, there was a significant interaction when the nutritional content of the breakfast meal was also considered.

Longer sleep periods were associated with lower blood glucose following high-carbohydrate and high-fat breakfasts, indicating better blood glucose control.

Additionally, the researchers observed a within-person effect in which a study participant who slept for longer than they typically would was likely to have reduced postprandial blood glucose following a high-carbohydrate or high-fat breakfast the next day.

The authors also found a significant link between sleep efficiency (ratio of time asleep to total length of sleep period) and glycemic control. When a participant slept more efficiently than usual, their postprandial blood glucose also tended to be lower than usual.

“This effect was largely driven by sleep onset (going to bed later) rather than sleep offset (waking up later),” Dr. Tsereteli and colleagues noted.
 

Sleep a key pillar of health

Asked whether these particular sleep effects might be exacerbated in patients with diabetes, senior author Paul Franks, MD, also from the Lund University Diabetes Centre, felt they could not meaningfully extrapolate results to people with diabetes, given that many take glucose-lowering medications.

“However, it is likely that these results would be similar or exacerbated in people with prediabetes, as glucose fluctuations in this subgroup of patients are generally greater than in people with normoglycemia,” he noted in an interview.

“Sleep is a key pillar of health, and focusing on both sleep and diet is key for healthy blood glucose control,” he added.

“Compensating for a bad night’s sleep by consuming a very sugary breakfast or energy drinks is likely to be especially detrimental for blood glucose control,” Dr. Franks said.

The study was funded by Lund University. Dr. Tsereteli and Dr. Franks reported no relevant financial relationships.

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

Like so many of you, I have weathered COVID-19 for the last almost 2 years. We’ve dealt with anxiety in our patients and ourselves, ever conflicting directives over masks, and uncertainty and hope over vaccinations.

In the beginning, it seemed elsewhere. Wuhan, China, the state of Washington, New York City.

In the beginning, I awoke with rising anxiety every morning at 4 a.m.

Now, it is part of life. We know how to do this.

I work in a D.C. hospital that takes care of COVID-19 patients. I don’t intubate or come into direct contact with patients’ secretions.

I felt lucky.

Last summer, I felt relief, after being fully vaccinated. We thought we were almost over it. But the numbers abroad and in the United States keep rising.

We have developed protocols. We test every patient for COVID-19 before admitting them to psychiatry, which is now routine. COVID-19–positive patients with suicidal ideation go to our medicine-psychiatric unit. We are single-room occupancy. No visitors.

Now, it feels like COVID is closing in. Lots of my patients on consultation-liaison psychiatry had COVID-19 or do now. The number of patients with long COVID is increasing. My elderly mother-in-law picked it up from a hospital. My young, healthy adult son got it but is now doing relatively OK. We will see if his ADHD worsens.

I received contact tracing recently for going into a patient room with contact precautions. I had put on the gown and gloves, but did I wear my goggles? I keep them on my forehead but could not remember if I had slipped them over my eyes.

I get tested weekly. My nose runs inside my mask. I sneeze. Is this COVID?

Of course, I am vaccinated with a booster shot. But breakthrough infections occur.

I am lucky, I keep reminding myself. I have a job and income and good PPE.

So, we are learning how to manage this disease. But it still closes in. My brain screams: “I do not want to catch this disease. I do not want to get sick. I do not want to get long COVID.”

“Calm down, Cam,” I tell myself. “You can do this!” I have learned how to do all the PPE, including tying the plastic ties along the backs of the plastic gowns.

All psychiatry meetings are virtual now. I cannot do virtual with enthusiasm. I say I will, but then do not log on. I miss the camaraderie.

All appointments are mainly telehealth. That has its pros and cons.

So bottom line – I will keep keeping on.

But I really want others to get vaccinated and wear masks. More than that, how can we as a psychiatric community get us through this pandemic? How can we support each other and our patients?

Here are a few suggestions, some of which I have made before:

• Focus on what we can control, especially exercise and sleep. Walk during times when the sun is shining. Rake the gorgeous autumn yellow and orange leaves.
• Give small (or large) gifts of kindness to others. Give to food banks, provide large tips to those who bring you takeout, help out at an animal shelter.
• Talk through established media about self-care and therapy for anxiety and depression.
• Clean out your closets. Give clothes to Afghan refugees.
• Read good books about trying times – such as World War II and the long wars in Afghanistan and Iraq.
• Take care of veterans and the elderly and homeless.
• Take care of yourself and your family.

Dr. Ritchie is chair of psychiatry at Medstar Washington Hospital Center. She has no conflicts of interest.

Like so many of you, I have weathered COVID-19 for the last almost 2 years. We’ve dealt with anxiety in our patients and ourselves, ever conflicting directives over masks, and uncertainty and hope over vaccinations.

In the beginning, it seemed elsewhere. Wuhan, China, the state of Washington, New York City.

In the beginning, I awoke with rising anxiety every morning at 4 a.m.

Now, it is part of life. We know how to do this.

I work in a D.C. hospital that takes care of COVID-19 patients. I don’t intubate or come into direct contact with patients’ secretions.

I felt lucky.

Last summer, I felt relief, after being fully vaccinated. We thought we were almost over it. But the numbers abroad and in the United States keep rising.

We have developed protocols. We test every patient for COVID-19 before admitting them to psychiatry, which is now routine. COVID-19–positive patients with suicidal ideation go to our medicine-psychiatric unit. We are single-room occupancy. No visitors.

Now, it feels like COVID is closing in. Lots of my patients on consultation-liaison psychiatry had COVID-19 or do now. The number of patients with long COVID is increasing. My elderly mother-in-law picked it up from a hospital. My young, healthy adult son got it but is now doing relatively OK. We will see if his ADHD worsens.

I received contact tracing recently for going into a patient room with contact precautions. I had put on the gown and gloves, but did I wear my goggles? I keep them on my forehead but could not remember if I had slipped them over my eyes.

I get tested weekly. My nose runs inside my mask. I sneeze. Is this COVID?

Of course, I am vaccinated with a booster shot. But breakthrough infections occur.

I am lucky, I keep reminding myself. I have a job and income and good PPE.

So, we are learning how to manage this disease. But it still closes in. My brain screams: “I do not want to catch this disease. I do not want to get sick. I do not want to get long COVID.”

“Calm down, Cam,” I tell myself. “You can do this!” I have learned how to do all the PPE, including tying the plastic ties along the backs of the plastic gowns.

All psychiatry meetings are virtual now. I cannot do virtual with enthusiasm. I say I will, but then do not log on. I miss the camaraderie.

All appointments are mainly telehealth. That has its pros and cons.

So bottom line – I will keep keeping on.

But I really want others to get vaccinated and wear masks. More than that, how can we as a psychiatric community get us through this pandemic? How can we support each other and our patients?

Here are a few suggestions, some of which I have made before:

• Focus on what we can control, especially exercise and sleep. Walk during times when the sun is shining. Rake the gorgeous autumn yellow and orange leaves.
• Give small (or large) gifts of kindness to others. Give to food banks, provide large tips to those who bring you takeout, help out at an animal shelter.
• Talk through established media about self-care and therapy for anxiety and depression.
• Clean out your closets. Give clothes to Afghan refugees.
• Read good books about trying times – such as World War II and the long wars in Afghanistan and Iraq.
• Take care of veterans and the elderly and homeless.
• Take care of yourself and your family.

Dr. Ritchie is chair of psychiatry at Medstar Washington Hospital Center. She has no conflicts of interest.

Like so many of you, I have weathered COVID-19 for the last almost 2 years. We’ve dealt with anxiety in our patients and ourselves, ever conflicting directives over masks, and uncertainty and hope over vaccinations.

In the beginning, it seemed elsewhere. Wuhan, China, the state of Washington, New York City.

In the beginning, I awoke with rising anxiety every morning at 4 a.m.

Now, it is part of life. We know how to do this.

I work in a D.C. hospital that takes care of COVID-19 patients. I don’t intubate or come into direct contact with patients’ secretions.

I felt lucky.

Last summer, I felt relief, after being fully vaccinated. We thought we were almost over it. But the numbers abroad and in the United States keep rising.

We have developed protocols. We test every patient for COVID-19 before admitting them to psychiatry, which is now routine. COVID-19–positive patients with suicidal ideation go to our medicine-psychiatric unit. We are single-room occupancy. No visitors.

Now, it feels like COVID is closing in. Lots of my patients on consultation-liaison psychiatry had COVID-19 or do now. The number of patients with long COVID is increasing. My elderly mother-in-law picked it up from a hospital. My young, healthy adult son got it but is now doing relatively OK. We will see if his ADHD worsens.

I received contact tracing recently for going into a patient room with contact precautions. I had put on the gown and gloves, but did I wear my goggles? I keep them on my forehead but could not remember if I had slipped them over my eyes.

I get tested weekly. My nose runs inside my mask. I sneeze. Is this COVID?

Of course, I am vaccinated with a booster shot. But breakthrough infections occur.

I am lucky, I keep reminding myself. I have a job and income and good PPE.

So, we are learning how to manage this disease. But it still closes in. My brain screams: “I do not want to catch this disease. I do not want to get sick. I do not want to get long COVID.”

“Calm down, Cam,” I tell myself. “You can do this!” I have learned how to do all the PPE, including tying the plastic ties along the backs of the plastic gowns.

All psychiatry meetings are virtual now. I cannot do virtual with enthusiasm. I say I will, but then do not log on. I miss the camaraderie.

All appointments are mainly telehealth. That has its pros and cons.

So bottom line – I will keep keeping on.

But I really want others to get vaccinated and wear masks. More than that, how can we as a psychiatric community get us through this pandemic? How can we support each other and our patients?

Here are a few suggestions, some of which I have made before:

• Focus on what we can control, especially exercise and sleep. Walk during times when the sun is shining. Rake the gorgeous autumn yellow and orange leaves.
• Give small (or large) gifts of kindness to others. Give to food banks, provide large tips to those who bring you takeout, help out at an animal shelter.
• Talk through established media about self-care and therapy for anxiety and depression.
• Clean out your closets. Give clothes to Afghan refugees.
• Read good books about trying times – such as World War II and the long wars in Afghanistan and Iraq.
• Take care of veterans and the elderly and homeless.
• Take care of yourself and your family.

Dr. Ritchie is chair of psychiatry at Medstar Washington Hospital Center. She has no conflicts of interest.

Working feverishly to complete the myriad patient notes accumulated throughout a hectic day, my phone vibrated – alerting me to a number that, over the past several years, has wrought uncertainty, grief, and overwhelming relief. Answering hesitantly, I listened to my physician’s pharmacist inform me of unexpected and alarming news.

Since COVID-19 was first identified more than 1 year ago, more than 770,000 people have died in the United States. In the wake of those losses, countless grieve while attempting to navigate a future without their loved ones. Meanwhile, scientists worked feverishly to combat a pandemic relentless in contagion. As health care professionals, we work tirelessly against the sharpened scythe of death, toiling day after day without an identifiable end. All the while, advocacy has prevailed as the need for personal protective equipment, improved ventilation systems, sanitization measures, and other mitigation measures, such as mask wearing and social distancing, echoed swiftly across the nation and around the world.

But, as the months have progressed, and life has seemingly transitioned toward a parallel version of reality, subsections of communities have grown restless. Several nontherapeutic, ineffective, and falsely touted regimens have been promoted. Amid the chaos of misinformation, most medical professionals have sought support from respected journals and infectious disease experts to filter out jargon and piece together scientifically sound protocols. Although many lives have prevailed by way of those advancements, mixed messages about interventions have emerged – and in many quarters across the country, anger, resistance, and outright refusal have prevailed.

Yet, we – the medical community – have forged ever onward as the cases continued and the death toll steadily climbed. In many cases, physicians who are years removed from critical care training have been thrust into COVID units, while residents have shifted toward working outside of their chosen specialty. Outpatient offices have closed, salaries have been cut, and furloughs have loomed as days fade into months. Beset with exhaustion and uncertainty, sacrifice has become a common thread that intrinsically united us against an unrelenting foe.

Most people continued navigating the many changes and made concerted efforts to mimic our prepandemic lives. Working from home in makeshift offices, dusting off math skills to assist children through the doldrums of distance learning, and mastering various audiovisual platforms, we reinforced social bonds and forged new connections echoing the hallmark resilience reminiscent of our shared distant ancestry.

As of this writing, thanks to our work – and that of scientists and policy makers – about 69% of Americans have received at least one dose of vaccine, and vaccines are widely available to children 5 and older. But it has been disheartening to watch misinformation about vaccine research and development propagated by political figures, social media, and lay people.
 

Processing the phone call

While listening to my physician’s pharmacist, I slowed my breaths in an effort to find calm. Years of navigating the American health care industry had left me both equipped and ill-prepared for the unexpected. I listened intently to the pharmacist’s words while staring blankly at a computer screen – uncertain of what had felt so assured not 10 minutes earlier.

That’s when I got the news. The intravenous medication that aided in my stabilization had suffered a critical shortage because of its successful use in the treatment of patients with COVID-19 pneumonia – patients who, in a majority of cases, had likely refused the vaccines. As result, the medication that had enabled my return to work, active engagement in nonwork pursuits, and most importantly, equipped my body to thrive despite the damage it had suffered, suddenly vanished.

Gently placing my phone on the desk, my heart beat rapidly as tears steadily streamed down my face. Staring blankly ahead, my hands gradually balled into fists as I let out a sound of fear, agony, and uncertainty. Screaming at everything and nothing, nausea swelled as panic flooded my body. In that moment, I ruminated on the conversation with the pharmacist. There had been no discussion, no option for me to maintain accessibility to this valuable medicine. Consequently, I felt helpless. Although the same medication, albeit a different mechanism of delivery, was promptly chosen as an adequate substitute, there was no guarantee of it bestowing the same degree of efficacy. So I was terrified, envisioning the progress made over several years as plummeting into an abyss of pain and despair. What are those of us who have chosen medicine as our profession but are immunocompromised expected to make of this?

Over the next several weeks, I diligently adhered to the new regimen and focused on positive mentation. Nevertheless, day by day, the symptoms worsened; eventually, I became bed ridden. I tried to gather what little composure remained to reschedule patients and justify the resounding guilt of perceived failure. I remember the sweet and gentle look of my child as I once again could not summon the strength to play pretend. This felt overwhelming. Would I ever go back to work? Would I see my child grow? No amount of pleading or screaming would change the fact that a medical system chose to roll the dice on my health. In a haze of discomfort and betrayal, I wondered how a physician or medical facility could justify removing medication from someone reliant upon it. How do we choose the appropriate allocation of resources when the consequences are potentially catastrophic?
 

Searching for context

When a country is founded on the mission of rising as a leading world power built upon the concepts of freedom, basic human rights, and individuality while supporting an infrastructure of capitalism, power, and control, crises – particularly those related to public health – can fan deep divisions. Here in the United States, we have seen misinterpretation, misunderstanding, and bitter indignation fuel the flames of provocation as protests of mask mandates, distance learning, and social distancing were touted as violating the very core upon which the country was established. Frustration, palpable among health care professionals, grew ever greater as the importance of vaccination in quelling virus mutations and decreasing morbidity and mortality were openly disparaged and ignored.

Not only have we watched people refuse the vaccines, but some are ignoring other mitigation measures. So the question becomes: How are we, as health care professionals trying to maintain a therapeutic alliance with those who reject lifesaving practices, expected to process this? Sitting in appointments and attempting interventions without judgment feels impractical and nearly impossible – particularly when the behaviors of these patients have the potential of violating our own health and well-being. How do we remain altruistic in our endeavors when those who seek our care seem callously indifferent to our lives – and to those of our families?
 

Measuring the value of life

Within the fevered haze of this past year, many stories highlighting grim realities have captured the media spotlight. From individuals unable to have emergency evaluations because of facilities being inundated by COVID-19 patients to individuals prematurely discharged, hospital bed shortages, and financial pressures from insurance companies. In reciting the phrase “Primum non noncere,” we physicians are committing to providing fair and competent medical treatment. At times, urgent decisions are necessary but are always made in the best interest of the patient(s). Ultimately, I am left debating how these agonizing weeks served any meaningful purpose. Moreover, when choosing the many over the few, what are the determinant factors? I am left asking: What is the value of a life?

Philosophically, this ethical dilemma is captured succinctly via the “trolley problem,” formulated in 1967 by Philippa Foot, MD. This is how Dr. Foot’s formulation unfolds: Close your eyes, and imagine you are inside a trolley careening unhindered down the rumbling tracks. Straight ahead you see five people bound to the tracks in imminent danger of being struck, and on the other side, one person is tied to the tracks. Do you continue the same course – thereby condemning five innocent people to death – or do you make the active decision to switch tracks, therefore consigning the one to their fate? Envision the people what do they look like? How old are they? If the one were a small child or a close friend, would that alter your decision? How does one make such a harrowing choice knowing the irreversible consequences? Depending on your action, this quandary falls within two primary schools of thought: Utilitarianism, which posits that the best action is the greatest good for the greatest number of people, and deontologicalism, which suggests that action is inherently right or wrong regardless of the consequences. Therefore, the decision to save the five is not favored.

However simplistic those scenarios may read, such principles when viewed through different lenses, they form the basis of medical ethics. In effect, every acute decision, every aspect of treatment is predicated upon the principles of nonmaleficence, beneficence, utility, distributive justice, and autonomy. Yet, the manner in which they are applied is highly contingent upon myriad variables. For example, sociopolitical factors, including population size (rural versus urban), economics (impoverished versus wealthy), as well as demographic factors (age, ethnicity, gender, sexuality) can highly influence and sometimes unknowingly influence interpretation and allocation of health care resources. This dilemma does not yield easily applicable and universal solutions. Nevertheless, it is paramount to evaluate policies effectively and tediously, particularly those with detrimental ramifications. Likewise, remaining flexible in our willingness to explore alternative solutions and encourage open discord among those with opposing viewpoints is key to instituting individual or institutional change that values the one as it values the many.

After several weeks of acute illness and a variety of short-acting interventions, I received approval to resume intravenous therapy. While the saga has ultimately reached a satisfactory conclusion, I am left with stupefied disbelief toward the people who took a gamble on my health. I am facing a battle between understanding the obligation of medicine to provide ethical and reasonable care without hesitation or judgment versus embittered resentment when faced with those who openly campaign against lifesaving interventions, such as the COVID-19 vaccine. For me, each day and the one that follows is riddled with complicated emotion. Every time I prematurely cease activity out of discomfort and weariness, I worry about my increasingly foreboding workload. In those moments, in that place of questions without answers, I remember that someone somewhere ultimately decided to switch the trolley’s track.

Dr. Thomas is a board-certified adult psychiatrist with interests in chronic illness, women’s behavioral health, and minority mental health. She currently practices in North Kingstown and East Providence, R.I. Dr. Thomas has no conflicts of interest.

Working feverishly to complete the myriad patient notes accumulated throughout a hectic day, my phone vibrated – alerting me to a number that, over the past several years, has wrought uncertainty, grief, and overwhelming relief. Answering hesitantly, I listened to my physician’s pharmacist inform me of unexpected and alarming news.

Since COVID-19 was first identified more than 1 year ago, more than 770,000 people have died in the United States. In the wake of those losses, countless grieve while attempting to navigate a future without their loved ones. Meanwhile, scientists worked feverishly to combat a pandemic relentless in contagion. As health care professionals, we work tirelessly against the sharpened scythe of death, toiling day after day without an identifiable end. All the while, advocacy has prevailed as the need for personal protective equipment, improved ventilation systems, sanitization measures, and other mitigation measures, such as mask wearing and social distancing, echoed swiftly across the nation and around the world.

But, as the months have progressed, and life has seemingly transitioned toward a parallel version of reality, subsections of communities have grown restless. Several nontherapeutic, ineffective, and falsely touted regimens have been promoted. Amid the chaos of misinformation, most medical professionals have sought support from respected journals and infectious disease experts to filter out jargon and piece together scientifically sound protocols. Although many lives have prevailed by way of those advancements, mixed messages about interventions have emerged – and in many quarters across the country, anger, resistance, and outright refusal have prevailed.

Yet, we – the medical community – have forged ever onward as the cases continued and the death toll steadily climbed. In many cases, physicians who are years removed from critical care training have been thrust into COVID units, while residents have shifted toward working outside of their chosen specialty. Outpatient offices have closed, salaries have been cut, and furloughs have loomed as days fade into months. Beset with exhaustion and uncertainty, sacrifice has become a common thread that intrinsically united us against an unrelenting foe.

Most people continued navigating the many changes and made concerted efforts to mimic our prepandemic lives. Working from home in makeshift offices, dusting off math skills to assist children through the doldrums of distance learning, and mastering various audiovisual platforms, we reinforced social bonds and forged new connections echoing the hallmark resilience reminiscent of our shared distant ancestry.

As of this writing, thanks to our work – and that of scientists and policy makers – about 69% of Americans have received at least one dose of vaccine, and vaccines are widely available to children 5 and older. But it has been disheartening to watch misinformation about vaccine research and development propagated by political figures, social media, and lay people.
 

Processing the phone call

While listening to my physician’s pharmacist, I slowed my breaths in an effort to find calm. Years of navigating the American health care industry had left me both equipped and ill-prepared for the unexpected. I listened intently to the pharmacist’s words while staring blankly at a computer screen – uncertain of what had felt so assured not 10 minutes earlier.

That’s when I got the news. The intravenous medication that aided in my stabilization had suffered a critical shortage because of its successful use in the treatment of patients with COVID-19 pneumonia – patients who, in a majority of cases, had likely refused the vaccines. As result, the medication that had enabled my return to work, active engagement in nonwork pursuits, and most importantly, equipped my body to thrive despite the damage it had suffered, suddenly vanished.

Gently placing my phone on the desk, my heart beat rapidly as tears steadily streamed down my face. Staring blankly ahead, my hands gradually balled into fists as I let out a sound of fear, agony, and uncertainty. Screaming at everything and nothing, nausea swelled as panic flooded my body. In that moment, I ruminated on the conversation with the pharmacist. There had been no discussion, no option for me to maintain accessibility to this valuable medicine. Consequently, I felt helpless. Although the same medication, albeit a different mechanism of delivery, was promptly chosen as an adequate substitute, there was no guarantee of it bestowing the same degree of efficacy. So I was terrified, envisioning the progress made over several years as plummeting into an abyss of pain and despair. What are those of us who have chosen medicine as our profession but are immunocompromised expected to make of this?

Over the next several weeks, I diligently adhered to the new regimen and focused on positive mentation. Nevertheless, day by day, the symptoms worsened; eventually, I became bed ridden. I tried to gather what little composure remained to reschedule patients and justify the resounding guilt of perceived failure. I remember the sweet and gentle look of my child as I once again could not summon the strength to play pretend. This felt overwhelming. Would I ever go back to work? Would I see my child grow? No amount of pleading or screaming would change the fact that a medical system chose to roll the dice on my health. In a haze of discomfort and betrayal, I wondered how a physician or medical facility could justify removing medication from someone reliant upon it. How do we choose the appropriate allocation of resources when the consequences are potentially catastrophic?
 

Searching for context

When a country is founded on the mission of rising as a leading world power built upon the concepts of freedom, basic human rights, and individuality while supporting an infrastructure of capitalism, power, and control, crises – particularly those related to public health – can fan deep divisions. Here in the United States, we have seen misinterpretation, misunderstanding, and bitter indignation fuel the flames of provocation as protests of mask mandates, distance learning, and social distancing were touted as violating the very core upon which the country was established. Frustration, palpable among health care professionals, grew ever greater as the importance of vaccination in quelling virus mutations and decreasing morbidity and mortality were openly disparaged and ignored.

Not only have we watched people refuse the vaccines, but some are ignoring other mitigation measures. So the question becomes: How are we, as health care professionals trying to maintain a therapeutic alliance with those who reject lifesaving practices, expected to process this? Sitting in appointments and attempting interventions without judgment feels impractical and nearly impossible – particularly when the behaviors of these patients have the potential of violating our own health and well-being. How do we remain altruistic in our endeavors when those who seek our care seem callously indifferent to our lives – and to those of our families?
 

Measuring the value of life

Within the fevered haze of this past year, many stories highlighting grim realities have captured the media spotlight. From individuals unable to have emergency evaluations because of facilities being inundated by COVID-19 patients to individuals prematurely discharged, hospital bed shortages, and financial pressures from insurance companies. In reciting the phrase “Primum non noncere,” we physicians are committing to providing fair and competent medical treatment. At times, urgent decisions are necessary but are always made in the best interest of the patient(s). Ultimately, I am left debating how these agonizing weeks served any meaningful purpose. Moreover, when choosing the many over the few, what are the determinant factors? I am left asking: What is the value of a life?

Philosophically, this ethical dilemma is captured succinctly via the “trolley problem,” formulated in 1967 by Philippa Foot, MD. This is how Dr. Foot’s formulation unfolds: Close your eyes, and imagine you are inside a trolley careening unhindered down the rumbling tracks. Straight ahead you see five people bound to the tracks in imminent danger of being struck, and on the other side, one person is tied to the tracks. Do you continue the same course – thereby condemning five innocent people to death – or do you make the active decision to switch tracks, therefore consigning the one to their fate? Envision the people what do they look like? How old are they? If the one were a small child or a close friend, would that alter your decision? How does one make such a harrowing choice knowing the irreversible consequences? Depending on your action, this quandary falls within two primary schools of thought: Utilitarianism, which posits that the best action is the greatest good for the greatest number of people, and deontologicalism, which suggests that action is inherently right or wrong regardless of the consequences. Therefore, the decision to save the five is not favored.

However simplistic those scenarios may read, such principles when viewed through different lenses, they form the basis of medical ethics. In effect, every acute decision, every aspect of treatment is predicated upon the principles of nonmaleficence, beneficence, utility, distributive justice, and autonomy. Yet, the manner in which they are applied is highly contingent upon myriad variables. For example, sociopolitical factors, including population size (rural versus urban), economics (impoverished versus wealthy), as well as demographic factors (age, ethnicity, gender, sexuality) can highly influence and sometimes unknowingly influence interpretation and allocation of health care resources. This dilemma does not yield easily applicable and universal solutions. Nevertheless, it is paramount to evaluate policies effectively and tediously, particularly those with detrimental ramifications. Likewise, remaining flexible in our willingness to explore alternative solutions and encourage open discord among those with opposing viewpoints is key to instituting individual or institutional change that values the one as it values the many.

After several weeks of acute illness and a variety of short-acting interventions, I received approval to resume intravenous therapy. While the saga has ultimately reached a satisfactory conclusion, I am left with stupefied disbelief toward the people who took a gamble on my health. I am facing a battle between understanding the obligation of medicine to provide ethical and reasonable care without hesitation or judgment versus embittered resentment when faced with those who openly campaign against lifesaving interventions, such as the COVID-19 vaccine. For me, each day and the one that follows is riddled with complicated emotion. Every time I prematurely cease activity out of discomfort and weariness, I worry about my increasingly foreboding workload. In those moments, in that place of questions without answers, I remember that someone somewhere ultimately decided to switch the trolley’s track.

Dr. Thomas is a board-certified adult psychiatrist with interests in chronic illness, women’s behavioral health, and minority mental health. She currently practices in North Kingstown and East Providence, R.I. Dr. Thomas has no conflicts of interest.

Working feverishly to complete the myriad patient notes accumulated throughout a hectic day, my phone vibrated – alerting me to a number that, over the past several years, has wrought uncertainty, grief, and overwhelming relief. Answering hesitantly, I listened to my physician’s pharmacist inform me of unexpected and alarming news.

Since COVID-19 was first identified more than 1 year ago, more than 770,000 people have died in the United States. In the wake of those losses, countless grieve while attempting to navigate a future without their loved ones. Meanwhile, scientists worked feverishly to combat a pandemic relentless in contagion. As health care professionals, we work tirelessly against the sharpened scythe of death, toiling day after day without an identifiable end. All the while, advocacy has prevailed as the need for personal protective equipment, improved ventilation systems, sanitization measures, and other mitigation measures, such as mask wearing and social distancing, echoed swiftly across the nation and around the world.

But, as the months have progressed, and life has seemingly transitioned toward a parallel version of reality, subsections of communities have grown restless. Several nontherapeutic, ineffective, and falsely touted regimens have been promoted. Amid the chaos of misinformation, most medical professionals have sought support from respected journals and infectious disease experts to filter out jargon and piece together scientifically sound protocols. Although many lives have prevailed by way of those advancements, mixed messages about interventions have emerged – and in many quarters across the country, anger, resistance, and outright refusal have prevailed.

Yet, we – the medical community – have forged ever onward as the cases continued and the death toll steadily climbed. In many cases, physicians who are years removed from critical care training have been thrust into COVID units, while residents have shifted toward working outside of their chosen specialty. Outpatient offices have closed, salaries have been cut, and furloughs have loomed as days fade into months. Beset with exhaustion and uncertainty, sacrifice has become a common thread that intrinsically united us against an unrelenting foe.

Most people continued navigating the many changes and made concerted efforts to mimic our prepandemic lives. Working from home in makeshift offices, dusting off math skills to assist children through the doldrums of distance learning, and mastering various audiovisual platforms, we reinforced social bonds and forged new connections echoing the hallmark resilience reminiscent of our shared distant ancestry.

As of this writing, thanks to our work – and that of scientists and policy makers – about 69% of Americans have received at least one dose of vaccine, and vaccines are widely available to children 5 and older. But it has been disheartening to watch misinformation about vaccine research and development propagated by political figures, social media, and lay people.
 

Processing the phone call

While listening to my physician’s pharmacist, I slowed my breaths in an effort to find calm. Years of navigating the American health care industry had left me both equipped and ill-prepared for the unexpected. I listened intently to the pharmacist’s words while staring blankly at a computer screen – uncertain of what had felt so assured not 10 minutes earlier.

That’s when I got the news. The intravenous medication that aided in my stabilization had suffered a critical shortage because of its successful use in the treatment of patients with COVID-19 pneumonia – patients who, in a majority of cases, had likely refused the vaccines. As result, the medication that had enabled my return to work, active engagement in nonwork pursuits, and most importantly, equipped my body to thrive despite the damage it had suffered, suddenly vanished.

Gently placing my phone on the desk, my heart beat rapidly as tears steadily streamed down my face. Staring blankly ahead, my hands gradually balled into fists as I let out a sound of fear, agony, and uncertainty. Screaming at everything and nothing, nausea swelled as panic flooded my body. In that moment, I ruminated on the conversation with the pharmacist. There had been no discussion, no option for me to maintain accessibility to this valuable medicine. Consequently, I felt helpless. Although the same medication, albeit a different mechanism of delivery, was promptly chosen as an adequate substitute, there was no guarantee of it bestowing the same degree of efficacy. So I was terrified, envisioning the progress made over several years as plummeting into an abyss of pain and despair. What are those of us who have chosen medicine as our profession but are immunocompromised expected to make of this?

Over the next several weeks, I diligently adhered to the new regimen and focused on positive mentation. Nevertheless, day by day, the symptoms worsened; eventually, I became bed ridden. I tried to gather what little composure remained to reschedule patients and justify the resounding guilt of perceived failure. I remember the sweet and gentle look of my child as I once again could not summon the strength to play pretend. This felt overwhelming. Would I ever go back to work? Would I see my child grow? No amount of pleading or screaming would change the fact that a medical system chose to roll the dice on my health. In a haze of discomfort and betrayal, I wondered how a physician or medical facility could justify removing medication from someone reliant upon it. How do we choose the appropriate allocation of resources when the consequences are potentially catastrophic?
 

Searching for context

When a country is founded on the mission of rising as a leading world power built upon the concepts of freedom, basic human rights, and individuality while supporting an infrastructure of capitalism, power, and control, crises – particularly those related to public health – can fan deep divisions. Here in the United States, we have seen misinterpretation, misunderstanding, and bitter indignation fuel the flames of provocation as protests of mask mandates, distance learning, and social distancing were touted as violating the very core upon which the country was established. Frustration, palpable among health care professionals, grew ever greater as the importance of vaccination in quelling virus mutations and decreasing morbidity and mortality were openly disparaged and ignored.

Not only have we watched people refuse the vaccines, but some are ignoring other mitigation measures. So the question becomes: How are we, as health care professionals trying to maintain a therapeutic alliance with those who reject lifesaving practices, expected to process this? Sitting in appointments and attempting interventions without judgment feels impractical and nearly impossible – particularly when the behaviors of these patients have the potential of violating our own health and well-being. How do we remain altruistic in our endeavors when those who seek our care seem callously indifferent to our lives – and to those of our families?
 

Measuring the value of life

Within the fevered haze of this past year, many stories highlighting grim realities have captured the media spotlight. From individuals unable to have emergency evaluations because of facilities being inundated by COVID-19 patients to individuals prematurely discharged, hospital bed shortages, and financial pressures from insurance companies. In reciting the phrase “Primum non noncere,” we physicians are committing to providing fair and competent medical treatment. At times, urgent decisions are necessary but are always made in the best interest of the patient(s). Ultimately, I am left debating how these agonizing weeks served any meaningful purpose. Moreover, when choosing the many over the few, what are the determinant factors? I am left asking: What is the value of a life?

Philosophically, this ethical dilemma is captured succinctly via the “trolley problem,” formulated in 1967 by Philippa Foot, MD. This is how Dr. Foot’s formulation unfolds: Close your eyes, and imagine you are inside a trolley careening unhindered down the rumbling tracks. Straight ahead you see five people bound to the tracks in imminent danger of being struck, and on the other side, one person is tied to the tracks. Do you continue the same course – thereby condemning five innocent people to death – or do you make the active decision to switch tracks, therefore consigning the one to their fate? Envision the people what do they look like? How old are they? If the one were a small child or a close friend, would that alter your decision? How does one make such a harrowing choice knowing the irreversible consequences? Depending on your action, this quandary falls within two primary schools of thought: Utilitarianism, which posits that the best action is the greatest good for the greatest number of people, and deontologicalism, which suggests that action is inherently right or wrong regardless of the consequences. Therefore, the decision to save the five is not favored.

However simplistic those scenarios may read, such principles when viewed through different lenses, they form the basis of medical ethics. In effect, every acute decision, every aspect of treatment is predicated upon the principles of nonmaleficence, beneficence, utility, distributive justice, and autonomy. Yet, the manner in which they are applied is highly contingent upon myriad variables. For example, sociopolitical factors, including population size (rural versus urban), economics (impoverished versus wealthy), as well as demographic factors (age, ethnicity, gender, sexuality) can highly influence and sometimes unknowingly influence interpretation and allocation of health care resources. This dilemma does not yield easily applicable and universal solutions. Nevertheless, it is paramount to evaluate policies effectively and tediously, particularly those with detrimental ramifications. Likewise, remaining flexible in our willingness to explore alternative solutions and encourage open discord among those with opposing viewpoints is key to instituting individual or institutional change that values the one as it values the many.

After several weeks of acute illness and a variety of short-acting interventions, I received approval to resume intravenous therapy. While the saga has ultimately reached a satisfactory conclusion, I am left with stupefied disbelief toward the people who took a gamble on my health. I am facing a battle between understanding the obligation of medicine to provide ethical and reasonable care without hesitation or judgment versus embittered resentment when faced with those who openly campaign against lifesaving interventions, such as the COVID-19 vaccine. For me, each day and the one that follows is riddled with complicated emotion. Every time I prematurely cease activity out of discomfort and weariness, I worry about my increasingly foreboding workload. In those moments, in that place of questions without answers, I remember that someone somewhere ultimately decided to switch the trolley’s track.

Dr. Thomas is a board-certified adult psychiatrist with interests in chronic illness, women’s behavioral health, and minority mental health. She currently practices in North Kingstown and East Providence, R.I. Dr. Thomas has no conflicts of interest.