In late June, Lisa Richardson, MD, emerged from Atlanta, Georgia’s initial COVID-19 lockdown, and “got back out there” for some overdue doctor’s appointments, including a mammogram.

The mammogram was a particular priority for her, since she is director of the CDC’s Division of Cancer Prevention and Control. But she knows that cancer screening is going to be a much tougher sell for the average person going forward in the pandemic era.

“It really is a challenge trying to get people to feel comfortable coming back in to be screened,” she said. Richardson was speaking recently at the AACR virtual meeting: COVID-19 and Cancer, a virtual symposium on cancer prevention and early detection in the COVID-19 pandemic organized by the American Association for Cancer Research.

While health service shutdowns and stay-at-home orders forced the country’s initial precipitous decline in cancer screening, fear of contracting COVID-19 is a big part of what is preventing patients from returning.

“We’ve known even pre-pandemic that people were hesitant to do cancer screening and in some ways this has really given them an out to say, ‘Well, I’m going to hold off on that colonoscopy,’ ” Amy Leader, MD, from Thomas Jefferson University’s Kimmel Cancer Center in Philadelphia, Pennsylvania, said during the symposium.
 

Estimating the pandemic’s impact on cancer care

While the impact of the pandemic on cancer can only be estimated at the moment, the prospects are already daunting, said Richardson, speculating that the hard-won 26% drop in cancer mortality over the past two decades “may be put on hold or reversed” by COVID-19.

There could be as many as 10,000 excess deaths in the US from colorectal and breast cancer alone because of COVID-19 delays, predicted Norman E. Sharpless, director of the US National Cancer Institute in Bethesda, Maryland.

But even Sharpless acknowledges that his modeling gives a conservative estimate, “as it does not consider other cancer types, it does not account for the additional nonlethal morbidity from upstaging, and it assumes a moderate disruption in care that completely resolves after 6 months.”

With still no end to the pandemic in sight, the true scope of cancer screening and treatment disruptions will take a long time to assess, but several studies presented during the symposium revealed some early indications.

A national survey launched in mid-May, which involved 534 women either diagnosed with breast cancer or undergoing screening or diagnostic evaluation for it, found that delays in screening were reported by 31.7% of those with breast cancer, and 26.7% of those without. Additionally, 21% of those on active treatment for breast cancer reported treatment delays.

“It’s going to be really important to implement strategies to help patients return to care ... creating a culture and a feeling of safety among patients and communicating through the uncertainty that exists in the pandemic,” said study investigator Erica T. Warner, ScD MPH, from Massachusetts General Hospital, Boston.

Screening for prostate cancer (via prostate-specific antigen testing) also declined, though not as dramatically as that for breast cancer, noted Mara Epstein, ScD, from The Meyers Primary Care Institute, University of Massachusetts Medical School, Worcester. Her study at a large healthcare provider group compared rates of both screening and diagnostic mammographies, and also PSA testing, as well as breast and prostate biopsies in the first five months of 2020 vs the same months in 2019.

While a decrease from 2019 to 2020 was seen in all procedures over the entire study period, the greatest decline was seen in April for screening mammography (down 98%), and tomosynthesis (down 96%), as well as PSA testing (down 83%), she said.

More recent figures are hard to come by, but a recent weekly survey from the Primary Care Collaborative shows 46% of practices are offering preventive and chronic care management visits, but patients are not scheduling them, and 44% report that in-person visit volume is between 30%-50% below normal over the last 4 weeks. 
 

Will COVID-19 exacerbate racial disparities in cancer?

Neither of the studies presented at the symposium analyzed cancer care disruptions by race, but there was concern among some panelists that cancer care disparities that existed before the pandemic will be magnified further.

“Over the next several months and into the next year there’s going to be some catch-up in screening and treatment, and one of my concerns is minority and underserved populations will not partake in that catch-up the way many middle-class Americans will,” said Otis Brawley, MD, from Johns Hopkins University, Baltimore, Maryland.

There is ample evidence that minority populations have been disproportionately hit by COVID-19, job losses, and lost health insurance, said the CDC’s Richardson, and all these factors could widen the cancer gap.

“It’s not a race thing, it’s a ‘what do you do thing,’ and an access to care thing, and what your socioeconomic status is,” Richardson said in an interview. “People who didn’t have sick leave before the pandemic still don’t have sick leave; if they didn’t have time to get their mammogram they still don’t have time.”

But she acknowledges that evidence is still lacking. Could some minority populations actually be less fearful of medical encounters because their work has already prevented them from sheltering in place? “It could go either way,” she said. “They might be less wary of venturing out into the clinic, but they also might reason that they’ve exposed themselves enough already at work and don’t want any additional exposure.”

In that regard, Richardson suggests population-specific messaging will be an important way of communicating with under-served populations to restart screening.

“We’re struggling at CDC with how to develop messages that resonate within different communities, because we’re missing the point of actually speaking to people within their culture and within the places that they live,” she said. “Just saying the same thing and putting a black face on it is not going to make a difference; you actually have to speak the language of the people you’re trying to reach — the same message in different packages.”

To that end, even before the pandemic, the CDC supported the development of Make It Your Own, a website that uses “evidence-based strategies” to assist healthcare organizations in customizing health information “by race, ethnicity, age, gender and location”, and target messages  to “specific populations, cultural groups and languages”.

But Mass General’s Warner says she’s not sure she would argue for messages to be tailored by race, “at least not without evidence that values and priorities regarding returning to care differ between racial/ethnic groups.”

“Tailoring in the absence of data requires assumptions that may or may not be correct and ignores within-group heterogeneity,” Warner told Medscape Medical News. “However, I do believe that messaging about return to cancer screening and care should be multifaceted and use diverse imagery. This recognizes that some messages will resonate more or less with individuals based on their own characteristics, of which race may be one.”

Warner does believe in the power of tailored messaging though. “Part of the onus for healthcare institutions and providers is to make some decisions about who it is really important to bring back in soonest,” she said.

“Those are the ones we want to prioritize, as opposed to those who we want to get back into care but we don’t need to get them in right now,” Warner emphasized. “As they are balancing all the needs of their family and their community and their other needs, messaging that adds additional stress, worry, anxiety and shame is not what we want to do. So really we need to distinguish between these populations, identify the priorities, hit the hard message to people who really need it now, and encourage others to come back in as they can.”
 

Building trust

All the panelists agreed that building trust with the public will be key to getting cancer care back on track.  

“I don’t think anyone trusts the healthcare community right now, but we already had this baseline distrust of healthcare among many minority communities, and now with COVID-19, the African American community in particular is seeing people go into the hospital and never come back,” said Richardson.

For Warner, the onus really falls on healthcare institutions. “We have to be proactive and not leave the burden of deciding when and how to return to care up to patients,” she said.

“What we need to focus on as much as possible is to get people to realize it is safe to come see the doctor,” said Johns Hopkins oncologist Brawley. “We have to make it safe for them to come see us, and then we have to convince them it is safe to come see us.”

Venturing out to her mammography appointment in early June, Richardson said she felt safe. “Everything was just the way it was supposed to be, everyone was masked, everyone was washing their hands,” she said.

Yet, by mid-June she had contracted COVID-19. “I don’t know where I got it,” she said. “No matter how careful you are, understand that if you’re in a total red spot, as I am, you can just get it.”

This article first appeared on Medscape.com.

In late June, Lisa Richardson, MD, emerged from Atlanta, Georgia’s initial COVID-19 lockdown, and “got back out there” for some overdue doctor’s appointments, including a mammogram.

The mammogram was a particular priority for her, since she is director of the CDC’s Division of Cancer Prevention and Control. But she knows that cancer screening is going to be a much tougher sell for the average person going forward in the pandemic era.

“It really is a challenge trying to get people to feel comfortable coming back in to be screened,” she said. Richardson was speaking recently at the AACR virtual meeting: COVID-19 and Cancer, a virtual symposium on cancer prevention and early detection in the COVID-19 pandemic organized by the American Association for Cancer Research.

While health service shutdowns and stay-at-home orders forced the country’s initial precipitous decline in cancer screening, fear of contracting COVID-19 is a big part of what is preventing patients from returning.

“We’ve known even pre-pandemic that people were hesitant to do cancer screening and in some ways this has really given them an out to say, ‘Well, I’m going to hold off on that colonoscopy,’ ” Amy Leader, MD, from Thomas Jefferson University’s Kimmel Cancer Center in Philadelphia, Pennsylvania, said during the symposium.
 

Estimating the pandemic’s impact on cancer care

While the impact of the pandemic on cancer can only be estimated at the moment, the prospects are already daunting, said Richardson, speculating that the hard-won 26% drop in cancer mortality over the past two decades “may be put on hold or reversed” by COVID-19.

There could be as many as 10,000 excess deaths in the US from colorectal and breast cancer alone because of COVID-19 delays, predicted Norman E. Sharpless, director of the US National Cancer Institute in Bethesda, Maryland.

But even Sharpless acknowledges that his modeling gives a conservative estimate, “as it does not consider other cancer types, it does not account for the additional nonlethal morbidity from upstaging, and it assumes a moderate disruption in care that completely resolves after 6 months.”

With still no end to the pandemic in sight, the true scope of cancer screening and treatment disruptions will take a long time to assess, but several studies presented during the symposium revealed some early indications.

A national survey launched in mid-May, which involved 534 women either diagnosed with breast cancer or undergoing screening or diagnostic evaluation for it, found that delays in screening were reported by 31.7% of those with breast cancer, and 26.7% of those without. Additionally, 21% of those on active treatment for breast cancer reported treatment delays.

“It’s going to be really important to implement strategies to help patients return to care ... creating a culture and a feeling of safety among patients and communicating through the uncertainty that exists in the pandemic,” said study investigator Erica T. Warner, ScD MPH, from Massachusetts General Hospital, Boston.

Screening for prostate cancer (via prostate-specific antigen testing) also declined, though not as dramatically as that for breast cancer, noted Mara Epstein, ScD, from The Meyers Primary Care Institute, University of Massachusetts Medical School, Worcester. Her study at a large healthcare provider group compared rates of both screening and diagnostic mammographies, and also PSA testing, as well as breast and prostate biopsies in the first five months of 2020 vs the same months in 2019.

While a decrease from 2019 to 2020 was seen in all procedures over the entire study period, the greatest decline was seen in April for screening mammography (down 98%), and tomosynthesis (down 96%), as well as PSA testing (down 83%), she said.

More recent figures are hard to come by, but a recent weekly survey from the Primary Care Collaborative shows 46% of practices are offering preventive and chronic care management visits, but patients are not scheduling them, and 44% report that in-person visit volume is between 30%-50% below normal over the last 4 weeks. 
 

Will COVID-19 exacerbate racial disparities in cancer?

Neither of the studies presented at the symposium analyzed cancer care disruptions by race, but there was concern among some panelists that cancer care disparities that existed before the pandemic will be magnified further.

“Over the next several months and into the next year there’s going to be some catch-up in screening and treatment, and one of my concerns is minority and underserved populations will not partake in that catch-up the way many middle-class Americans will,” said Otis Brawley, MD, from Johns Hopkins University, Baltimore, Maryland.

There is ample evidence that minority populations have been disproportionately hit by COVID-19, job losses, and lost health insurance, said the CDC’s Richardson, and all these factors could widen the cancer gap.

“It’s not a race thing, it’s a ‘what do you do thing,’ and an access to care thing, and what your socioeconomic status is,” Richardson said in an interview. “People who didn’t have sick leave before the pandemic still don’t have sick leave; if they didn’t have time to get their mammogram they still don’t have time.”

But she acknowledges that evidence is still lacking. Could some minority populations actually be less fearful of medical encounters because their work has already prevented them from sheltering in place? “It could go either way,” she said. “They might be less wary of venturing out into the clinic, but they also might reason that they’ve exposed themselves enough already at work and don’t want any additional exposure.”

In that regard, Richardson suggests population-specific messaging will be an important way of communicating with under-served populations to restart screening.

“We’re struggling at CDC with how to develop messages that resonate within different communities, because we’re missing the point of actually speaking to people within their culture and within the places that they live,” she said. “Just saying the same thing and putting a black face on it is not going to make a difference; you actually have to speak the language of the people you’re trying to reach — the same message in different packages.”

To that end, even before the pandemic, the CDC supported the development of Make It Your Own, a website that uses “evidence-based strategies” to assist healthcare organizations in customizing health information “by race, ethnicity, age, gender and location”, and target messages  to “specific populations, cultural groups and languages”.

But Mass General’s Warner says she’s not sure she would argue for messages to be tailored by race, “at least not without evidence that values and priorities regarding returning to care differ between racial/ethnic groups.”

“Tailoring in the absence of data requires assumptions that may or may not be correct and ignores within-group heterogeneity,” Warner told Medscape Medical News. “However, I do believe that messaging about return to cancer screening and care should be multifaceted and use diverse imagery. This recognizes that some messages will resonate more or less with individuals based on their own characteristics, of which race may be one.”

Warner does believe in the power of tailored messaging though. “Part of the onus for healthcare institutions and providers is to make some decisions about who it is really important to bring back in soonest,” she said.

“Those are the ones we want to prioritize, as opposed to those who we want to get back into care but we don’t need to get them in right now,” Warner emphasized. “As they are balancing all the needs of their family and their community and their other needs, messaging that adds additional stress, worry, anxiety and shame is not what we want to do. So really we need to distinguish between these populations, identify the priorities, hit the hard message to people who really need it now, and encourage others to come back in as they can.”
 

Building trust

All the panelists agreed that building trust with the public will be key to getting cancer care back on track.  

“I don’t think anyone trusts the healthcare community right now, but we already had this baseline distrust of healthcare among many minority communities, and now with COVID-19, the African American community in particular is seeing people go into the hospital and never come back,” said Richardson.

For Warner, the onus really falls on healthcare institutions. “We have to be proactive and not leave the burden of deciding when and how to return to care up to patients,” she said.

“What we need to focus on as much as possible is to get people to realize it is safe to come see the doctor,” said Johns Hopkins oncologist Brawley. “We have to make it safe for them to come see us, and then we have to convince them it is safe to come see us.”

Venturing out to her mammography appointment in early June, Richardson said she felt safe. “Everything was just the way it was supposed to be, everyone was masked, everyone was washing their hands,” she said.

Yet, by mid-June she had contracted COVID-19. “I don’t know where I got it,” she said. “No matter how careful you are, understand that if you’re in a total red spot, as I am, you can just get it.”

This article first appeared on Medscape.com.

In late June, Lisa Richardson, MD, emerged from Atlanta, Georgia’s initial COVID-19 lockdown, and “got back out there” for some overdue doctor’s appointments, including a mammogram.

The mammogram was a particular priority for her, since she is director of the CDC’s Division of Cancer Prevention and Control. But she knows that cancer screening is going to be a much tougher sell for the average person going forward in the pandemic era.

“It really is a challenge trying to get people to feel comfortable coming back in to be screened,” she said. Richardson was speaking recently at the AACR virtual meeting: COVID-19 and Cancer, a virtual symposium on cancer prevention and early detection in the COVID-19 pandemic organized by the American Association for Cancer Research.

While health service shutdowns and stay-at-home orders forced the country’s initial precipitous decline in cancer screening, fear of contracting COVID-19 is a big part of what is preventing patients from returning.

“We’ve known even pre-pandemic that people were hesitant to do cancer screening and in some ways this has really given them an out to say, ‘Well, I’m going to hold off on that colonoscopy,’ ” Amy Leader, MD, from Thomas Jefferson University’s Kimmel Cancer Center in Philadelphia, Pennsylvania, said during the symposium.
 

Estimating the pandemic’s impact on cancer care

While the impact of the pandemic on cancer can only be estimated at the moment, the prospects are already daunting, said Richardson, speculating that the hard-won 26% drop in cancer mortality over the past two decades “may be put on hold or reversed” by COVID-19.

There could be as many as 10,000 excess deaths in the US from colorectal and breast cancer alone because of COVID-19 delays, predicted Norman E. Sharpless, director of the US National Cancer Institute in Bethesda, Maryland.

But even Sharpless acknowledges that his modeling gives a conservative estimate, “as it does not consider other cancer types, it does not account for the additional nonlethal morbidity from upstaging, and it assumes a moderate disruption in care that completely resolves after 6 months.”

With still no end to the pandemic in sight, the true scope of cancer screening and treatment disruptions will take a long time to assess, but several studies presented during the symposium revealed some early indications.

A national survey launched in mid-May, which involved 534 women either diagnosed with breast cancer or undergoing screening or diagnostic evaluation for it, found that delays in screening were reported by 31.7% of those with breast cancer, and 26.7% of those without. Additionally, 21% of those on active treatment for breast cancer reported treatment delays.

“It’s going to be really important to implement strategies to help patients return to care ... creating a culture and a feeling of safety among patients and communicating through the uncertainty that exists in the pandemic,” said study investigator Erica T. Warner, ScD MPH, from Massachusetts General Hospital, Boston.

Screening for prostate cancer (via prostate-specific antigen testing) also declined, though not as dramatically as that for breast cancer, noted Mara Epstein, ScD, from The Meyers Primary Care Institute, University of Massachusetts Medical School, Worcester. Her study at a large healthcare provider group compared rates of both screening and diagnostic mammographies, and also PSA testing, as well as breast and prostate biopsies in the first five months of 2020 vs the same months in 2019.

While a decrease from 2019 to 2020 was seen in all procedures over the entire study period, the greatest decline was seen in April for screening mammography (down 98%), and tomosynthesis (down 96%), as well as PSA testing (down 83%), she said.

More recent figures are hard to come by, but a recent weekly survey from the Primary Care Collaborative shows 46% of practices are offering preventive and chronic care management visits, but patients are not scheduling them, and 44% report that in-person visit volume is between 30%-50% below normal over the last 4 weeks. 
 

Will COVID-19 exacerbate racial disparities in cancer?

Neither of the studies presented at the symposium analyzed cancer care disruptions by race, but there was concern among some panelists that cancer care disparities that existed before the pandemic will be magnified further.

“Over the next several months and into the next year there’s going to be some catch-up in screening and treatment, and one of my concerns is minority and underserved populations will not partake in that catch-up the way many middle-class Americans will,” said Otis Brawley, MD, from Johns Hopkins University, Baltimore, Maryland.

There is ample evidence that minority populations have been disproportionately hit by COVID-19, job losses, and lost health insurance, said the CDC’s Richardson, and all these factors could widen the cancer gap.

“It’s not a race thing, it’s a ‘what do you do thing,’ and an access to care thing, and what your socioeconomic status is,” Richardson said in an interview. “People who didn’t have sick leave before the pandemic still don’t have sick leave; if they didn’t have time to get their mammogram they still don’t have time.”

But she acknowledges that evidence is still lacking. Could some minority populations actually be less fearful of medical encounters because their work has already prevented them from sheltering in place? “It could go either way,” she said. “They might be less wary of venturing out into the clinic, but they also might reason that they’ve exposed themselves enough already at work and don’t want any additional exposure.”

In that regard, Richardson suggests population-specific messaging will be an important way of communicating with under-served populations to restart screening.

“We’re struggling at CDC with how to develop messages that resonate within different communities, because we’re missing the point of actually speaking to people within their culture and within the places that they live,” she said. “Just saying the same thing and putting a black face on it is not going to make a difference; you actually have to speak the language of the people you’re trying to reach — the same message in different packages.”

To that end, even before the pandemic, the CDC supported the development of Make It Your Own, a website that uses “evidence-based strategies” to assist healthcare organizations in customizing health information “by race, ethnicity, age, gender and location”, and target messages  to “specific populations, cultural groups and languages”.

But Mass General’s Warner says she’s not sure she would argue for messages to be tailored by race, “at least not without evidence that values and priorities regarding returning to care differ between racial/ethnic groups.”

“Tailoring in the absence of data requires assumptions that may or may not be correct and ignores within-group heterogeneity,” Warner told Medscape Medical News. “However, I do believe that messaging about return to cancer screening and care should be multifaceted and use diverse imagery. This recognizes that some messages will resonate more or less with individuals based on their own characteristics, of which race may be one.”

Warner does believe in the power of tailored messaging though. “Part of the onus for healthcare institutions and providers is to make some decisions about who it is really important to bring back in soonest,” she said.

“Those are the ones we want to prioritize, as opposed to those who we want to get back into care but we don’t need to get them in right now,” Warner emphasized. “As they are balancing all the needs of their family and their community and their other needs, messaging that adds additional stress, worry, anxiety and shame is not what we want to do. So really we need to distinguish between these populations, identify the priorities, hit the hard message to people who really need it now, and encourage others to come back in as they can.”
 

Building trust

All the panelists agreed that building trust with the public will be key to getting cancer care back on track.  

“I don’t think anyone trusts the healthcare community right now, but we already had this baseline distrust of healthcare among many minority communities, and now with COVID-19, the African American community in particular is seeing people go into the hospital and never come back,” said Richardson.

For Warner, the onus really falls on healthcare institutions. “We have to be proactive and not leave the burden of deciding when and how to return to care up to patients,” she said.

“What we need to focus on as much as possible is to get people to realize it is safe to come see the doctor,” said Johns Hopkins oncologist Brawley. “We have to make it safe for them to come see us, and then we have to convince them it is safe to come see us.”

Venturing out to her mammography appointment in early June, Richardson said she felt safe. “Everything was just the way it was supposed to be, everyone was masked, everyone was washing their hands,” she said.

Yet, by mid-June she had contracted COVID-19. “I don’t know where I got it,” she said. “No matter how careful you are, understand that if you’re in a total red spot, as I am, you can just get it.”

This article first appeared on Medscape.com.

A new Canadian clinical practice guideline for treating adults with obesity emphasizes improving health rather than simply losing weight, among other things.

A summary of the guideline, which was developed by Obesity Canada and the Canadian Association of Bariatric Physicians and Surgeons, was published online August 4 in the Canadian Medical Association Journal.

This patient-centered update to the 2006 guidelines is “provocative,” starting with its definition of obesity, co–lead author Sean Wharton, MD, adjunct professor at McMaster University, Hamilton, Ont., said in an interview.

The guideline was authored by more than 60 health care professionals and researchers who assessed more than 500,000 peer-reviewed articles and made 80 key recommendations.

These reflect substantial recent advances in the understanding of obesity. Individuals with obesity (from a patient committee of the Obesity Society) helped to shape the key messages.

“People who live with obesity have been shut out of receiving quality health care because of the biased, deeply flawed misconceptions about what drives obesity and how we can improve health,” Lisa Schaffer, chair of Obesity Canada’s Public Engagement Committee, said in a press release.

“Obesity is widely seen as the result of poor personal decisions, but research tells us it is far more complicated than that. Our hope with the [new] clinical practice guideline is that more health care professionals, health policy makers, benefits providers and people living with obesity will have a better understanding of it, so we can help more of those who need it.”

“Obesity management should be about compassion and empathy, and then everything falls into place,” Dr. Wharton said. “Think of obesity like breast cancer.”

Address the root causes of obesity

The guideline defines obesity as “a prevalent, complex, progressive and relapsing chronic disease, characterized by abnormal or excessive body fat (adiposity) that impairs health.”

Aimed at primary care providers, the document stresses that clinicians need to “move beyond simplistic approaches of ‘eat less, move more,’ and address the root drivers of obesity.”

As a first step, doctors should ask a patient for permission to discuss weight (e.g., they can ask: “Would it be all right if we discussed your weight?”) – which demonstrates empathy and can help build patient-provider trust.

Clinicians can still measure body mass index as part of a routine physical examination, but they should also obtain a comprehensive patient history to identify the root causes of any weight gain (which could include genetics or psychological factors such as depression and anxiety), as well as any barriers to managing obesity.

‘Eat less, move more’ is too simple: Employ three pillars

Advice to “eat less and move more is dangerously simplistic,” coauthor Arya M. Sharma, MD, from the University of Alberta, Edmonton, and scientific director of Obesity Canada, said in an interview that “the body fights to put back any lost weight.”

Patients with obesity need “medical nutrition therapy.” For patients at risk for heart disease, that may mean following a Mediterranean diet, Dr. Wharton said.

“Physical activity and medical nutrition therapy are absolutely necessary” to manage obesity, he clarified. As a person loses weight, their body “releases a cascade of neurochemicals and hormones that try to push the weight back up” to the original weight or even higher.

Therefore, to maintain weight loss, people need support from one or more of what he calls the “three pillars” of effective long-term weight loss – pharmacotherapy, bariatric surgery, and cognitive-behavioral therapy – which tempers this cascade of neurochemicals.

Cognitive-behavioral therapy could be given by various health care professionals, he noted. A behavioral strategy to stop snacking, for example, is to wait 5 minutes before eating a desired snack to make sure you still want it.

Similarly, Dr. Sharma noted, “the reason obesity is a chronic disease is that once you’ve gained the weight, your body is not going to want to lose it. That is what I tell all my patients: ‘Your body doesn’t care why you put on the weight, but it does care about keeping it there, and it’s going to fight you’ when you try to maintain weight loss.”

“Clinicians should feel very comfortable” treating obesity as a chronic disease, he added, because they are already treating chronic diseases such as heart, lung, and kidney disease.

Don’t play the blame game: ‘Think of obesity like breast cancer’

Clinicians also need to avoid “shaming and blaming patients with obesity,” said Dr. Sharma.

He noted that many patients have internalized weight bias and blame their excess weight on their lack of willpower. They may not want to talk about weight-loss medications or bariatric surgery because they feel that’s “cheating.”

By thinking of obesity in a similar way to cancer, doctors can help themselves respond to patients in a kinder way. “What would we do with somebody who has breast cancer? We would have compassion. We would talk about surgery to get the lump out and medication to keep the cancer from coming back, and we would engage them in psychological treatment or counseling for some of the challenges they have to face,” Dr. Wharton said.

“The right answer is to treat [obesity] like a disease – with surgery, medication, and psychological intervention,” depending on the individual patient, he added.

The complete guideline is available on the Obesity Canada website.

The study was funded by Obesity Canada, the Canadian Association of Bariatric Physicians and Surgeons, and the Canadian Institutes of Health Research. Dr. Wharton has received honoraria and travel expenses and has participated in academic advisory boards for Novo Nordisk, Bausch Health, Eli Lilly, and Janssen. He is the medical director of a medical clinic specializing in weight management and diabetes. Dr. Sharma has received speaker’s bureau and consulting fees from Novo Nordisk, Bausch Pharmaceuticals, and AstraZeneca.

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

A new Canadian clinical practice guideline for treating adults with obesity emphasizes improving health rather than simply losing weight, among other things.

A summary of the guideline, which was developed by Obesity Canada and the Canadian Association of Bariatric Physicians and Surgeons, was published online August 4 in the Canadian Medical Association Journal.

This patient-centered update to the 2006 guidelines is “provocative,” starting with its definition of obesity, co–lead author Sean Wharton, MD, adjunct professor at McMaster University, Hamilton, Ont., said in an interview.

The guideline was authored by more than 60 health care professionals and researchers who assessed more than 500,000 peer-reviewed articles and made 80 key recommendations.

These reflect substantial recent advances in the understanding of obesity. Individuals with obesity (from a patient committee of the Obesity Society) helped to shape the key messages.

“People who live with obesity have been shut out of receiving quality health care because of the biased, deeply flawed misconceptions about what drives obesity and how we can improve health,” Lisa Schaffer, chair of Obesity Canada’s Public Engagement Committee, said in a press release.

“Obesity is widely seen as the result of poor personal decisions, but research tells us it is far more complicated than that. Our hope with the [new] clinical practice guideline is that more health care professionals, health policy makers, benefits providers and people living with obesity will have a better understanding of it, so we can help more of those who need it.”

“Obesity management should be about compassion and empathy, and then everything falls into place,” Dr. Wharton said. “Think of obesity like breast cancer.”

Address the root causes of obesity

The guideline defines obesity as “a prevalent, complex, progressive and relapsing chronic disease, characterized by abnormal or excessive body fat (adiposity) that impairs health.”

Aimed at primary care providers, the document stresses that clinicians need to “move beyond simplistic approaches of ‘eat less, move more,’ and address the root drivers of obesity.”

As a first step, doctors should ask a patient for permission to discuss weight (e.g., they can ask: “Would it be all right if we discussed your weight?”) – which demonstrates empathy and can help build patient-provider trust.

Clinicians can still measure body mass index as part of a routine physical examination, but they should also obtain a comprehensive patient history to identify the root causes of any weight gain (which could include genetics or psychological factors such as depression and anxiety), as well as any barriers to managing obesity.

‘Eat less, move more’ is too simple: Employ three pillars

Advice to “eat less and move more is dangerously simplistic,” coauthor Arya M. Sharma, MD, from the University of Alberta, Edmonton, and scientific director of Obesity Canada, said in an interview that “the body fights to put back any lost weight.”

Patients with obesity need “medical nutrition therapy.” For patients at risk for heart disease, that may mean following a Mediterranean diet, Dr. Wharton said.

“Physical activity and medical nutrition therapy are absolutely necessary” to manage obesity, he clarified. As a person loses weight, their body “releases a cascade of neurochemicals and hormones that try to push the weight back up” to the original weight or even higher.

Therefore, to maintain weight loss, people need support from one or more of what he calls the “three pillars” of effective long-term weight loss – pharmacotherapy, bariatric surgery, and cognitive-behavioral therapy – which tempers this cascade of neurochemicals.

Cognitive-behavioral therapy could be given by various health care professionals, he noted. A behavioral strategy to stop snacking, for example, is to wait 5 minutes before eating a desired snack to make sure you still want it.

Similarly, Dr. Sharma noted, “the reason obesity is a chronic disease is that once you’ve gained the weight, your body is not going to want to lose it. That is what I tell all my patients: ‘Your body doesn’t care why you put on the weight, but it does care about keeping it there, and it’s going to fight you’ when you try to maintain weight loss.”

“Clinicians should feel very comfortable” treating obesity as a chronic disease, he added, because they are already treating chronic diseases such as heart, lung, and kidney disease.

Don’t play the blame game: ‘Think of obesity like breast cancer’

Clinicians also need to avoid “shaming and blaming patients with obesity,” said Dr. Sharma.

He noted that many patients have internalized weight bias and blame their excess weight on their lack of willpower. They may not want to talk about weight-loss medications or bariatric surgery because they feel that’s “cheating.”

By thinking of obesity in a similar way to cancer, doctors can help themselves respond to patients in a kinder way. “What would we do with somebody who has breast cancer? We would have compassion. We would talk about surgery to get the lump out and medication to keep the cancer from coming back, and we would engage them in psychological treatment or counseling for some of the challenges they have to face,” Dr. Wharton said.

“The right answer is to treat [obesity] like a disease – with surgery, medication, and psychological intervention,” depending on the individual patient, he added.

The complete guideline is available on the Obesity Canada website.

The study was funded by Obesity Canada, the Canadian Association of Bariatric Physicians and Surgeons, and the Canadian Institutes of Health Research. Dr. Wharton has received honoraria and travel expenses and has participated in academic advisory boards for Novo Nordisk, Bausch Health, Eli Lilly, and Janssen. He is the medical director of a medical clinic specializing in weight management and diabetes. Dr. Sharma has received speaker’s bureau and consulting fees from Novo Nordisk, Bausch Pharmaceuticals, and AstraZeneca.

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

A new Canadian clinical practice guideline for treating adults with obesity emphasizes improving health rather than simply losing weight, among other things.

A summary of the guideline, which was developed by Obesity Canada and the Canadian Association of Bariatric Physicians and Surgeons, was published online August 4 in the Canadian Medical Association Journal.

This patient-centered update to the 2006 guidelines is “provocative,” starting with its definition of obesity, co–lead author Sean Wharton, MD, adjunct professor at McMaster University, Hamilton, Ont., said in an interview.

The guideline was authored by more than 60 health care professionals and researchers who assessed more than 500,000 peer-reviewed articles and made 80 key recommendations.

These reflect substantial recent advances in the understanding of obesity. Individuals with obesity (from a patient committee of the Obesity Society) helped to shape the key messages.

“People who live with obesity have been shut out of receiving quality health care because of the biased, deeply flawed misconceptions about what drives obesity and how we can improve health,” Lisa Schaffer, chair of Obesity Canada’s Public Engagement Committee, said in a press release.

“Obesity is widely seen as the result of poor personal decisions, but research tells us it is far more complicated than that. Our hope with the [new] clinical practice guideline is that more health care professionals, health policy makers, benefits providers and people living with obesity will have a better understanding of it, so we can help more of those who need it.”

“Obesity management should be about compassion and empathy, and then everything falls into place,” Dr. Wharton said. “Think of obesity like breast cancer.”

Address the root causes of obesity

The guideline defines obesity as “a prevalent, complex, progressive and relapsing chronic disease, characterized by abnormal or excessive body fat (adiposity) that impairs health.”

Aimed at primary care providers, the document stresses that clinicians need to “move beyond simplistic approaches of ‘eat less, move more,’ and address the root drivers of obesity.”

As a first step, doctors should ask a patient for permission to discuss weight (e.g., they can ask: “Would it be all right if we discussed your weight?”) – which demonstrates empathy and can help build patient-provider trust.

Clinicians can still measure body mass index as part of a routine physical examination, but they should also obtain a comprehensive patient history to identify the root causes of any weight gain (which could include genetics or psychological factors such as depression and anxiety), as well as any barriers to managing obesity.

‘Eat less, move more’ is too simple: Employ three pillars

Advice to “eat less and move more is dangerously simplistic,” coauthor Arya M. Sharma, MD, from the University of Alberta, Edmonton, and scientific director of Obesity Canada, said in an interview that “the body fights to put back any lost weight.”

Patients with obesity need “medical nutrition therapy.” For patients at risk for heart disease, that may mean following a Mediterranean diet, Dr. Wharton said.

“Physical activity and medical nutrition therapy are absolutely necessary” to manage obesity, he clarified. As a person loses weight, their body “releases a cascade of neurochemicals and hormones that try to push the weight back up” to the original weight or even higher.

Therefore, to maintain weight loss, people need support from one or more of what he calls the “three pillars” of effective long-term weight loss – pharmacotherapy, bariatric surgery, and cognitive-behavioral therapy – which tempers this cascade of neurochemicals.

Cognitive-behavioral therapy could be given by various health care professionals, he noted. A behavioral strategy to stop snacking, for example, is to wait 5 minutes before eating a desired snack to make sure you still want it.

Similarly, Dr. Sharma noted, “the reason obesity is a chronic disease is that once you’ve gained the weight, your body is not going to want to lose it. That is what I tell all my patients: ‘Your body doesn’t care why you put on the weight, but it does care about keeping it there, and it’s going to fight you’ when you try to maintain weight loss.”

“Clinicians should feel very comfortable” treating obesity as a chronic disease, he added, because they are already treating chronic diseases such as heart, lung, and kidney disease.

Don’t play the blame game: ‘Think of obesity like breast cancer’

Clinicians also need to avoid “shaming and blaming patients with obesity,” said Dr. Sharma.

He noted that many patients have internalized weight bias and blame their excess weight on their lack of willpower. They may not want to talk about weight-loss medications or bariatric surgery because they feel that’s “cheating.”

By thinking of obesity in a similar way to cancer, doctors can help themselves respond to patients in a kinder way. “What would we do with somebody who has breast cancer? We would have compassion. We would talk about surgery to get the lump out and medication to keep the cancer from coming back, and we would engage them in psychological treatment or counseling for some of the challenges they have to face,” Dr. Wharton said.

“The right answer is to treat [obesity] like a disease – with surgery, medication, and psychological intervention,” depending on the individual patient, he added.

The complete guideline is available on the Obesity Canada website.

The study was funded by Obesity Canada, the Canadian Association of Bariatric Physicians and Surgeons, and the Canadian Institutes of Health Research. Dr. Wharton has received honoraria and travel expenses and has participated in academic advisory boards for Novo Nordisk, Bausch Health, Eli Lilly, and Janssen. He is the medical director of a medical clinic specializing in weight management and diabetes. Dr. Sharma has received speaker’s bureau and consulting fees from Novo Nordisk, Bausch Pharmaceuticals, and AstraZeneca.

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

The historically higher incidence rates of lung cancer among Black men, compared with White men, in the United States have all but been eliminated, at least among most men in the younger age groups, a new analysis from the American Cancer Society (ACS) indicates.

Among women, the trend is even more impressive, as the Black/White gap in lung cancer incidence rates has actually reversed in younger women. Black women in certain age groups are now less likely to develop lung cancer than White women, the same study indicates.

These trends reflect the steeper declines in smoking rates among Blacks in the US, compared with comparably-aged Whites, say the authors.

“This is the only cancer where this has happened,” lead author Ahmedin Jemal, DVM, PhD, senior vice president for Data Science at the American Cancer Society, told Medscape Medical News.

“If you look at cancers that are affected by access to screening and treatment, the disparity between the Blacks and the Whites has been increasing over the years because tests and treatment require access to insurance, so the Whites are getting more of them than the Blacks,” Jemal explained.

“But for smoking, all you have to do for prevention is just don’t smoke, so this is a success story that really should be highlighted,” he emphasized.

The study was published online Aug. 20 in JNCI Cancer: Spectrum.

Nationwide Incidence Data

For this study, Jemal and colleagues collected nationwide incidence data on individuals between ages 30 and 54 who had been diagnosed with lung cancer between 1997 and 2016.

“We categorized age at diagnosis by 5-year age intervals (from 30-34 to 50-54 years) and year of diagnosis by 5-year calendar period (from 1997-2001 to 2012-2016),” the investigators explain.

Analyses showed that lung cancer incidence rates generally decreased among both Black and White men during the study interval but the decline in incidence rates was steeper in Black men than in White men. As a consequence, the Black-to-White incidence rate ratios (IRRs) became similar in men born between 1967 and 1972 and reversed in women born since about 1967. For example, the Black-to-White IRRs in men between the ages of 40 and 44 who were born between 1957 and 1972 declined from 1.92 to 1.03.

Similarly, lung cancer incidence rates during the study interval declined among both Black and White women between the ages of 30 and 49 but, again, the decline was “considerably larger” among Black women. As a consequence, the Black-to-White IRR in women age 45 to 49 dropped from 1.25 during the period 1997-2001 down to 0.83 during the period 2012-2016.

This is in stark contrast to historical trends in lung cancer incidence rates, which were over 30% higher among similarly aged Black women born in the late 1950s. Now, lung cancer incidence rates are about 30% lower for similarly aged Black women born in 1972, compared with White women.

For Black and White women between age 50 and 54, lung cancer incidence rates either declined only slightly or remained stable during the study interval, the investigators reported.

The one exception to the diminishing gap in lung cancer incidence rates between Black and White men was an observed increase in IRRs in men born around the period 1977-1982

Among this group of men, who were between age 30 and 39 in the years 2012-2016, lung cancer incidence rates were higher in Black men than in White men.

As the authors point out, this increase in lung cancer rates among young Black men likely reflects a rapid rise in smoking seen among Black youth in the 1990s.

This trend coincided with an R.J. Reynolds tobacco ad campaign in which African Americans were targeted; between 1991 and 1997, the prevalence of smoking among Black high school students doubled from 14.1% to 28.2%, the investigators point out, citing a 2008 Centers for Disease Control and Prevention report on cigarette use among US high school students.

Smoking Prevalence Rates

Smoking prevalence rates were derived from National Health Interview Survey data from 1970 to 2016.

Mirroring findings in the racial patterns of lung cancer incidence rates, smoking prevalence rates declined in successive birth cohorts in both Black and White males and females, but the decline was again steeper in Black men and women than it was in White men and women.

As a result, the historically higher sex-specific smoking prevalence rates seen historically in Blacks disappeared in men born around 1960, and reversed in women born at the same time, Jemal and colleagues point out.

As the authors explain, the more rapid decline in smoking prevalence after 1960 is likely a reflection of the “precipitous” drop in smoking initiation rates among Black teenagers starting about the late 1970s through to the early 1990s.

For example, among 12th graders, smoking prevalence rates between 1977 and 1992 dropped from 36.7% to 8.1% among Black teens. In stark contrast, they hardly changed at all among White teens, dropping only from 38.3% in 1977 to 31.8% in 1992.

Jemal suggested that steeper decline in smoking initiation rates seen between the late 1970s and early 90s reflects the fact that Black teenagers were deterred from smoking because the cost of cigarettes kept going up.

He also suggested that smoking is less acceptable in the Black community than it is in the White community, especially among churchgoers, where smoking is severely frowned upon and nonsmoking is the community “norm.”

Additionally, Black youth may simply be heeding government antismoking messages to a greater extent than White youth, Jemal suggested.  

He wondered if there are parallels now in the current pandemic. “When I go to a store here in Georgia, I would say almost all Blacks are wearing a mask [even though masks are not mandatory in Georgia] whereas it’s amazing the number of Whites who don’t wear a mask,” he recounts.

“So it would seem that Whites feel that government is simply interfering with their lives, while Blacks have a better perspective of the harms of smoking, so they are listening to the government’s antismoking campaigns,” he speculated.

Some Isolated Areas

Asked to comment on the study’s findings, Otis Brawley, MD, Bloomberg, distinguished professor of oncology and epidemiology at Johns Hopkins University in Baltimore, said that, while overall Black smoking rates are declining, there are some isolated areas where they are still very high.

For example, in his hometown of Baltimore, recent prevalence rates indicate that over 30% of Blacks are still smoking, “so these areas with high usage are still areas to focus on,” he told Medscape Medical News.

On the other hand, the study also supports the benefits of local, state, and federal government efforts to promote antismoking messages and tobacco-control activities over the past number of years.

“It proves that tactics used to control tobacco use have had some effect [even though] the study also shows that the tobacco industry’s advertising tactics such as the R.J. Reynolds targeted ads in the 90s can have deleterious effects,” Brawley noted.

Lung cancer has traditionally been one of the biggest drivers in the Black/White cancer mortality gap, Brawley said, adding that steeper declines in smoking initiation rates among Blacks compared with Whites are the main reason why this disparity is decreasing.

The study was supported by the Intramural Research Department of the American Cancer Society. The study authors have disclosed no relevant financial relationships. Brawley declares he does some consulting work for pharmaceutical company Genentech.
 

This article first appeared on Medscape.com.

The historically higher incidence rates of lung cancer among Black men, compared with White men, in the United States have all but been eliminated, at least among most men in the younger age groups, a new analysis from the American Cancer Society (ACS) indicates.

Among women, the trend is even more impressive, as the Black/White gap in lung cancer incidence rates has actually reversed in younger women. Black women in certain age groups are now less likely to develop lung cancer than White women, the same study indicates.

These trends reflect the steeper declines in smoking rates among Blacks in the US, compared with comparably-aged Whites, say the authors.

“This is the only cancer where this has happened,” lead author Ahmedin Jemal, DVM, PhD, senior vice president for Data Science at the American Cancer Society, told Medscape Medical News.

“If you look at cancers that are affected by access to screening and treatment, the disparity between the Blacks and the Whites has been increasing over the years because tests and treatment require access to insurance, so the Whites are getting more of them than the Blacks,” Jemal explained.

“But for smoking, all you have to do for prevention is just don’t smoke, so this is a success story that really should be highlighted,” he emphasized.

The study was published online Aug. 20 in JNCI Cancer: Spectrum.

Nationwide Incidence Data

For this study, Jemal and colleagues collected nationwide incidence data on individuals between ages 30 and 54 who had been diagnosed with lung cancer between 1997 and 2016.

“We categorized age at diagnosis by 5-year age intervals (from 30-34 to 50-54 years) and year of diagnosis by 5-year calendar period (from 1997-2001 to 2012-2016),” the investigators explain.

Analyses showed that lung cancer incidence rates generally decreased among both Black and White men during the study interval but the decline in incidence rates was steeper in Black men than in White men. As a consequence, the Black-to-White incidence rate ratios (IRRs) became similar in men born between 1967 and 1972 and reversed in women born since about 1967. For example, the Black-to-White IRRs in men between the ages of 40 and 44 who were born between 1957 and 1972 declined from 1.92 to 1.03.

Similarly, lung cancer incidence rates during the study interval declined among both Black and White women between the ages of 30 and 49 but, again, the decline was “considerably larger” among Black women. As a consequence, the Black-to-White IRR in women age 45 to 49 dropped from 1.25 during the period 1997-2001 down to 0.83 during the period 2012-2016.

This is in stark contrast to historical trends in lung cancer incidence rates, which were over 30% higher among similarly aged Black women born in the late 1950s. Now, lung cancer incidence rates are about 30% lower for similarly aged Black women born in 1972, compared with White women.

For Black and White women between age 50 and 54, lung cancer incidence rates either declined only slightly or remained stable during the study interval, the investigators reported.

The one exception to the diminishing gap in lung cancer incidence rates between Black and White men was an observed increase in IRRs in men born around the period 1977-1982

Among this group of men, who were between age 30 and 39 in the years 2012-2016, lung cancer incidence rates were higher in Black men than in White men.

As the authors point out, this increase in lung cancer rates among young Black men likely reflects a rapid rise in smoking seen among Black youth in the 1990s.

This trend coincided with an R.J. Reynolds tobacco ad campaign in which African Americans were targeted; between 1991 and 1997, the prevalence of smoking among Black high school students doubled from 14.1% to 28.2%, the investigators point out, citing a 2008 Centers for Disease Control and Prevention report on cigarette use among US high school students.

Smoking Prevalence Rates

Smoking prevalence rates were derived from National Health Interview Survey data from 1970 to 2016.

Mirroring findings in the racial patterns of lung cancer incidence rates, smoking prevalence rates declined in successive birth cohorts in both Black and White males and females, but the decline was again steeper in Black men and women than it was in White men and women.

As a result, the historically higher sex-specific smoking prevalence rates seen historically in Blacks disappeared in men born around 1960, and reversed in women born at the same time, Jemal and colleagues point out.

As the authors explain, the more rapid decline in smoking prevalence after 1960 is likely a reflection of the “precipitous” drop in smoking initiation rates among Black teenagers starting about the late 1970s through to the early 1990s.

For example, among 12th graders, smoking prevalence rates between 1977 and 1992 dropped from 36.7% to 8.1% among Black teens. In stark contrast, they hardly changed at all among White teens, dropping only from 38.3% in 1977 to 31.8% in 1992.

Jemal suggested that steeper decline in smoking initiation rates seen between the late 1970s and early 90s reflects the fact that Black teenagers were deterred from smoking because the cost of cigarettes kept going up.

He also suggested that smoking is less acceptable in the Black community than it is in the White community, especially among churchgoers, where smoking is severely frowned upon and nonsmoking is the community “norm.”

Additionally, Black youth may simply be heeding government antismoking messages to a greater extent than White youth, Jemal suggested.  

He wondered if there are parallels now in the current pandemic. “When I go to a store here in Georgia, I would say almost all Blacks are wearing a mask [even though masks are not mandatory in Georgia] whereas it’s amazing the number of Whites who don’t wear a mask,” he recounts.

“So it would seem that Whites feel that government is simply interfering with their lives, while Blacks have a better perspective of the harms of smoking, so they are listening to the government’s antismoking campaigns,” he speculated.

Some Isolated Areas

Asked to comment on the study’s findings, Otis Brawley, MD, Bloomberg, distinguished professor of oncology and epidemiology at Johns Hopkins University in Baltimore, said that, while overall Black smoking rates are declining, there are some isolated areas where they are still very high.

For example, in his hometown of Baltimore, recent prevalence rates indicate that over 30% of Blacks are still smoking, “so these areas with high usage are still areas to focus on,” he told Medscape Medical News.

On the other hand, the study also supports the benefits of local, state, and federal government efforts to promote antismoking messages and tobacco-control activities over the past number of years.

“It proves that tactics used to control tobacco use have had some effect [even though] the study also shows that the tobacco industry’s advertising tactics such as the R.J. Reynolds targeted ads in the 90s can have deleterious effects,” Brawley noted.

Lung cancer has traditionally been one of the biggest drivers in the Black/White cancer mortality gap, Brawley said, adding that steeper declines in smoking initiation rates among Blacks compared with Whites are the main reason why this disparity is decreasing.

The study was supported by the Intramural Research Department of the American Cancer Society. The study authors have disclosed no relevant financial relationships. Brawley declares he does some consulting work for pharmaceutical company Genentech.
 

This article first appeared on Medscape.com.

The historically higher incidence rates of lung cancer among Black men, compared with White men, in the United States have all but been eliminated, at least among most men in the younger age groups, a new analysis from the American Cancer Society (ACS) indicates.

Among women, the trend is even more impressive, as the Black/White gap in lung cancer incidence rates has actually reversed in younger women. Black women in certain age groups are now less likely to develop lung cancer than White women, the same study indicates.

These trends reflect the steeper declines in smoking rates among Blacks in the US, compared with comparably-aged Whites, say the authors.

“This is the only cancer where this has happened,” lead author Ahmedin Jemal, DVM, PhD, senior vice president for Data Science at the American Cancer Society, told Medscape Medical News.

“If you look at cancers that are affected by access to screening and treatment, the disparity between the Blacks and the Whites has been increasing over the years because tests and treatment require access to insurance, so the Whites are getting more of them than the Blacks,” Jemal explained.

“But for smoking, all you have to do for prevention is just don’t smoke, so this is a success story that really should be highlighted,” he emphasized.

The study was published online Aug. 20 in JNCI Cancer: Spectrum.

Nationwide Incidence Data

For this study, Jemal and colleagues collected nationwide incidence data on individuals between ages 30 and 54 who had been diagnosed with lung cancer between 1997 and 2016.

“We categorized age at diagnosis by 5-year age intervals (from 30-34 to 50-54 years) and year of diagnosis by 5-year calendar period (from 1997-2001 to 2012-2016),” the investigators explain.

Analyses showed that lung cancer incidence rates generally decreased among both Black and White men during the study interval but the decline in incidence rates was steeper in Black men than in White men. As a consequence, the Black-to-White incidence rate ratios (IRRs) became similar in men born between 1967 and 1972 and reversed in women born since about 1967. For example, the Black-to-White IRRs in men between the ages of 40 and 44 who were born between 1957 and 1972 declined from 1.92 to 1.03.

Similarly, lung cancer incidence rates during the study interval declined among both Black and White women between the ages of 30 and 49 but, again, the decline was “considerably larger” among Black women. As a consequence, the Black-to-White IRR in women age 45 to 49 dropped from 1.25 during the period 1997-2001 down to 0.83 during the period 2012-2016.

This is in stark contrast to historical trends in lung cancer incidence rates, which were over 30% higher among similarly aged Black women born in the late 1950s. Now, lung cancer incidence rates are about 30% lower for similarly aged Black women born in 1972, compared with White women.

For Black and White women between age 50 and 54, lung cancer incidence rates either declined only slightly or remained stable during the study interval, the investigators reported.

The one exception to the diminishing gap in lung cancer incidence rates between Black and White men was an observed increase in IRRs in men born around the period 1977-1982

Among this group of men, who were between age 30 and 39 in the years 2012-2016, lung cancer incidence rates were higher in Black men than in White men.

As the authors point out, this increase in lung cancer rates among young Black men likely reflects a rapid rise in smoking seen among Black youth in the 1990s.

This trend coincided with an R.J. Reynolds tobacco ad campaign in which African Americans were targeted; between 1991 and 1997, the prevalence of smoking among Black high school students doubled from 14.1% to 28.2%, the investigators point out, citing a 2008 Centers for Disease Control and Prevention report on cigarette use among US high school students.

Smoking Prevalence Rates

Smoking prevalence rates were derived from National Health Interview Survey data from 1970 to 2016.

Mirroring findings in the racial patterns of lung cancer incidence rates, smoking prevalence rates declined in successive birth cohorts in both Black and White males and females, but the decline was again steeper in Black men and women than it was in White men and women.

As a result, the historically higher sex-specific smoking prevalence rates seen historically in Blacks disappeared in men born around 1960, and reversed in women born at the same time, Jemal and colleagues point out.

As the authors explain, the more rapid decline in smoking prevalence after 1960 is likely a reflection of the “precipitous” drop in smoking initiation rates among Black teenagers starting about the late 1970s through to the early 1990s.

For example, among 12th graders, smoking prevalence rates between 1977 and 1992 dropped from 36.7% to 8.1% among Black teens. In stark contrast, they hardly changed at all among White teens, dropping only from 38.3% in 1977 to 31.8% in 1992.

Jemal suggested that steeper decline in smoking initiation rates seen between the late 1970s and early 90s reflects the fact that Black teenagers were deterred from smoking because the cost of cigarettes kept going up.

He also suggested that smoking is less acceptable in the Black community than it is in the White community, especially among churchgoers, where smoking is severely frowned upon and nonsmoking is the community “norm.”

Additionally, Black youth may simply be heeding government antismoking messages to a greater extent than White youth, Jemal suggested.  

He wondered if there are parallels now in the current pandemic. “When I go to a store here in Georgia, I would say almost all Blacks are wearing a mask [even though masks are not mandatory in Georgia] whereas it’s amazing the number of Whites who don’t wear a mask,” he recounts.

“So it would seem that Whites feel that government is simply interfering with their lives, while Blacks have a better perspective of the harms of smoking, so they are listening to the government’s antismoking campaigns,” he speculated.

Some Isolated Areas

Asked to comment on the study’s findings, Otis Brawley, MD, Bloomberg, distinguished professor of oncology and epidemiology at Johns Hopkins University in Baltimore, said that, while overall Black smoking rates are declining, there are some isolated areas where they are still very high.

For example, in his hometown of Baltimore, recent prevalence rates indicate that over 30% of Blacks are still smoking, “so these areas with high usage are still areas to focus on,” he told Medscape Medical News.

On the other hand, the study also supports the benefits of local, state, and federal government efforts to promote antismoking messages and tobacco-control activities over the past number of years.

“It proves that tactics used to control tobacco use have had some effect [even though] the study also shows that the tobacco industry’s advertising tactics such as the R.J. Reynolds targeted ads in the 90s can have deleterious effects,” Brawley noted.

Lung cancer has traditionally been one of the biggest drivers in the Black/White cancer mortality gap, Brawley said, adding that steeper declines in smoking initiation rates among Blacks compared with Whites are the main reason why this disparity is decreasing.

The study was supported by the Intramural Research Department of the American Cancer Society. The study authors have disclosed no relevant financial relationships. Brawley declares he does some consulting work for pharmaceutical company Genentech.
 

This article first appeared on Medscape.com.

Spirituality and religion remain central to the worldview of millions of Americans. According to the Pew Research Center, almost 75% of Americans identify as Christian, Jewish, Muslim, Buddhist, or Hindu.¹ As is the case with many Americans,² the lens of spirituality³ and religion shaped my own worldview since childhood.

j-wildman/Getty Images

Growing up in a Christian household, many of my family’s discussions centered on bolstering our spiritual health. I grew to internalize the notion that spiritual health relates to a sense of self, a sense of purpose, and a connection to God, nature, and others. Religious texts such as the Bible, Quran, and Torah share principles aimed at developing believers’ spiritual health. However, the intricacies of mental health remain entirely foreign within many faith communities. In these communities, unfamiliarity with mental health topics seemingly leads to the conflation of spiritual health and mental health.⁴

Within faith communities, I often hear the phrase, “You can’t worry and pray at the same time.” This commonly used expression encourages people of faith to lean on their spiritual health in times of uncertainty. The perceived dichotomy between worry and prayer represents the theology of sole reliance on spiritual coping skills, such as prayer, when feelings of anxiety and other psychological stressors arise. Because of “pray it away” doctrines and ongoing stigma related to mental health, many of our spiritually minded patients are more likely to seek counsel from religious leaders than they are from mental health clinicians in times of psychological distress.^5,6

About 54% of U.S. adults identify as religious, and 75% think of themselves as spiritual.⁷ This intrapersonal conflict between religious/spiritual health and mental health raises an important question: How can psychiatrists more actively collaborate with religious communities to ease the perceived tensions between spiritual health and mental health for our patients?
 

Engaging with the community

In a recent virtual talk titled, “Dealing with Depression: Faith, Meds, and Therapy,” I openly discussed varying aspects of mental health and mental illness with approximately 70 women at my church in Philadelphia. Before this presentation, there had never been a leadership-sponsored conversation within the church to discuss spiritual health and mental health as separate but highly interconnected entities.

Throughout the nearly 2-hour session, I used biblical and biological principles to explain the differences between spiritual health and mental health, strategies to recognize signs and symptoms of depression, and treatment options for depression. After the formal presentation, a 45-minute question-and-answer session followed in which some members shared their own experiences with mental illness.

Two major themes emerged as central points of discussion during our time of open dialogue. First, several women shared the spiritual and clinical avenues they used to access support in times of psychological distress. There was a general tone of agreement among attendees that spiritual health and mental health are, in fact, different. Second, the presentation opened the door for attendees, previously unfamiliar with mental health services, to ask questions about connecting with the appropriate resources to receive mental health treatment. The subject of seeking psychiatric care for mental health challenges was, at least in part, demystified and brought to the forefront of the attendees’ minds.

Studies show that many faith-based communities are more likely to seek counsel for psychological distress from religious leaders than from mental health professionals. In this vein, my recent community engagement highlighted to me ways that we can readily reach spiritually and religiously minded patients who otherwise would not receive the psychiatric care that they need. Psychiatrists can play an integral role in bridging the gap in psychiatric care for faith-based persons through outreach to and collaboration with religious communities.
 

Opportunities for collaboration

In collaboration with religious leaders, psychiatrists can actively support the mental health of spiritually and religiously minded patients through several low-effort, but potentially high-yield, initiatives. Notably, many of my suggested interventions do not require significant, if any, infrastructural changes to the health care system or worship communities. As psychiatrists, we can collaborate with faith leaders as follows:

1. More regularly assess the role of religion and spirituality in our patients’ daily lives to better meet their spiritual and mental health needs.

2. Better use existing chaplain services to provide spiritual support for hospitalized patients.

3. Present information about mental health – in-person, virtually, or in written form – to religious communities through talks, discussions, popular religious publications, social media platforms, and webinars.

4. Amplify existing mental health guides for faith leaders (i.e., the American Psychiatric Association’s guidebook Mental Health: A Guide for Faith Leaders),⁸ thereby encouraging church leaders and staff to become better informed about common mental health conditions.

5. Collaborate with places of worship to offer psychiatric and psychological services to their members.

This sort of engagement with religious communities is the collective role of community-oriented psychiatrists, not just psychiatrists who ascribe to religious or spiritual beliefs. We ought to remain mindful of the spiritual distress that many spiritual and religious patients feel when they experience mental illness,⁹ particularly in light of the distress caused by the coronavirus pandemic.¹⁰ But first, we must become comfortable with asking our patients about their religious or spiritual affiliations using tools such as the Cultural Formulation Interview.¹¹ The more we recognize the role of spirituality in our patients’ lives, the better equipped we become to help patients identify and seek treatment for mental illness without the distress of their feeling spiritually deficient.
 

Dr. Jordan is a psychiatry resident physician in Philadelphia. She has no conflicts of interest.

References

1. Religious Landscape Study. pewforum.org.

2. U.S. Religion Census Census: Religious Congregations and Membership Study. Association of Religion Data Archives. 2010. doi: 10.17605/OSF.IO/9AMDJ.

3. J Med Ethics Hist Med. 2018 Apr 9;11:3.

4. The Dimensions of Health: Conceptual Models. Sudbury, Mass.: Jones & Bartlett, 2010.

5. J Res Christ Educ. 2014;23(2):176-86.

6. Health Serv Res. 2003 Apr;38(2):647-73.

7. “More Americans say they’re spiritual but not religious.” pewresearch.org. 2017 Sep 6.

8. Mental Health: A Guide for Faith Leaders. Washington: American Psychiatric Association Foundation, 2018.

9. Mental Health by the Numbers. NAMI: National Alliance on Mental Illness. 2019.

10. “Most Americans say coronavirus outbreak has impacted their lives. Pew Research Center. pewsocialtrends.org. 2020 Mar 30.

11. DSM-5 Handbook on the Cultural Formulation Interview. Washington: American Psychiatric Association Publishing, 2016.

Spirituality and religion remain central to the worldview of millions of Americans. According to the Pew Research Center, almost 75% of Americans identify as Christian, Jewish, Muslim, Buddhist, or Hindu.¹ As is the case with many Americans,² the lens of spirituality³ and religion shaped my own worldview since childhood.

j-wildman/Getty Images

Growing up in a Christian household, many of my family’s discussions centered on bolstering our spiritual health. I grew to internalize the notion that spiritual health relates to a sense of self, a sense of purpose, and a connection to God, nature, and others. Religious texts such as the Bible, Quran, and Torah share principles aimed at developing believers’ spiritual health. However, the intricacies of mental health remain entirely foreign within many faith communities. In these communities, unfamiliarity with mental health topics seemingly leads to the conflation of spiritual health and mental health.⁴

Within faith communities, I often hear the phrase, “You can’t worry and pray at the same time.” This commonly used expression encourages people of faith to lean on their spiritual health in times of uncertainty. The perceived dichotomy between worry and prayer represents the theology of sole reliance on spiritual coping skills, such as prayer, when feelings of anxiety and other psychological stressors arise. Because of “pray it away” doctrines and ongoing stigma related to mental health, many of our spiritually minded patients are more likely to seek counsel from religious leaders than they are from mental health clinicians in times of psychological distress.^5,6

About 54% of U.S. adults identify as religious, and 75% think of themselves as spiritual.⁷ This intrapersonal conflict between religious/spiritual health and mental health raises an important question: How can psychiatrists more actively collaborate with religious communities to ease the perceived tensions between spiritual health and mental health for our patients?
 

Engaging with the community

In a recent virtual talk titled, “Dealing with Depression: Faith, Meds, and Therapy,” I openly discussed varying aspects of mental health and mental illness with approximately 70 women at my church in Philadelphia. Before this presentation, there had never been a leadership-sponsored conversation within the church to discuss spiritual health and mental health as separate but highly interconnected entities.

Throughout the nearly 2-hour session, I used biblical and biological principles to explain the differences between spiritual health and mental health, strategies to recognize signs and symptoms of depression, and treatment options for depression. After the formal presentation, a 45-minute question-and-answer session followed in which some members shared their own experiences with mental illness.

Two major themes emerged as central points of discussion during our time of open dialogue. First, several women shared the spiritual and clinical avenues they used to access support in times of psychological distress. There was a general tone of agreement among attendees that spiritual health and mental health are, in fact, different. Second, the presentation opened the door for attendees, previously unfamiliar with mental health services, to ask questions about connecting with the appropriate resources to receive mental health treatment. The subject of seeking psychiatric care for mental health challenges was, at least in part, demystified and brought to the forefront of the attendees’ minds.

Studies show that many faith-based communities are more likely to seek counsel for psychological distress from religious leaders than from mental health professionals. In this vein, my recent community engagement highlighted to me ways that we can readily reach spiritually and religiously minded patients who otherwise would not receive the psychiatric care that they need. Psychiatrists can play an integral role in bridging the gap in psychiatric care for faith-based persons through outreach to and collaboration with religious communities.
 

Opportunities for collaboration

In collaboration with religious leaders, psychiatrists can actively support the mental health of spiritually and religiously minded patients through several low-effort, but potentially high-yield, initiatives. Notably, many of my suggested interventions do not require significant, if any, infrastructural changes to the health care system or worship communities. As psychiatrists, we can collaborate with faith leaders as follows:

1. More regularly assess the role of religion and spirituality in our patients’ daily lives to better meet their spiritual and mental health needs.

2. Better use existing chaplain services to provide spiritual support for hospitalized patients.

3. Present information about mental health – in-person, virtually, or in written form – to religious communities through talks, discussions, popular religious publications, social media platforms, and webinars.

4. Amplify existing mental health guides for faith leaders (i.e., the American Psychiatric Association’s guidebook Mental Health: A Guide for Faith Leaders),⁸ thereby encouraging church leaders and staff to become better informed about common mental health conditions.

5. Collaborate with places of worship to offer psychiatric and psychological services to their members.

This sort of engagement with religious communities is the collective role of community-oriented psychiatrists, not just psychiatrists who ascribe to religious or spiritual beliefs. We ought to remain mindful of the spiritual distress that many spiritual and religious patients feel when they experience mental illness,⁹ particularly in light of the distress caused by the coronavirus pandemic.¹⁰ But first, we must become comfortable with asking our patients about their religious or spiritual affiliations using tools such as the Cultural Formulation Interview.¹¹ The more we recognize the role of spirituality in our patients’ lives, the better equipped we become to help patients identify and seek treatment for mental illness without the distress of their feeling spiritually deficient.
 

Dr. Jordan is a psychiatry resident physician in Philadelphia. She has no conflicts of interest.

References

1. Religious Landscape Study. pewforum.org.

2. U.S. Religion Census Census: Religious Congregations and Membership Study. Association of Religion Data Archives. 2010. doi: 10.17605/OSF.IO/9AMDJ.

3. J Med Ethics Hist Med. 2018 Apr 9;11:3.

4. The Dimensions of Health: Conceptual Models. Sudbury, Mass.: Jones & Bartlett, 2010.

5. J Res Christ Educ. 2014;23(2):176-86.

6. Health Serv Res. 2003 Apr;38(2):647-73.

7. “More Americans say they’re spiritual but not religious.” pewresearch.org. 2017 Sep 6.

8. Mental Health: A Guide for Faith Leaders. Washington: American Psychiatric Association Foundation, 2018.

9. Mental Health by the Numbers. NAMI: National Alliance on Mental Illness. 2019.

10. “Most Americans say coronavirus outbreak has impacted their lives. Pew Research Center. pewsocialtrends.org. 2020 Mar 30.

11. DSM-5 Handbook on the Cultural Formulation Interview. Washington: American Psychiatric Association Publishing, 2016.

Spirituality and religion remain central to the worldview of millions of Americans. According to the Pew Research Center, almost 75% of Americans identify as Christian, Jewish, Muslim, Buddhist, or Hindu.¹ As is the case with many Americans,² the lens of spirituality³ and religion shaped my own worldview since childhood.

j-wildman/Getty Images

Growing up in a Christian household, many of my family’s discussions centered on bolstering our spiritual health. I grew to internalize the notion that spiritual health relates to a sense of self, a sense of purpose, and a connection to God, nature, and others. Religious texts such as the Bible, Quran, and Torah share principles aimed at developing believers’ spiritual health. However, the intricacies of mental health remain entirely foreign within many faith communities. In these communities, unfamiliarity with mental health topics seemingly leads to the conflation of spiritual health and mental health.⁴

Within faith communities, I often hear the phrase, “You can’t worry and pray at the same time.” This commonly used expression encourages people of faith to lean on their spiritual health in times of uncertainty. The perceived dichotomy between worry and prayer represents the theology of sole reliance on spiritual coping skills, such as prayer, when feelings of anxiety and other psychological stressors arise. Because of “pray it away” doctrines and ongoing stigma related to mental health, many of our spiritually minded patients are more likely to seek counsel from religious leaders than they are from mental health clinicians in times of psychological distress.^5,6

About 54% of U.S. adults identify as religious, and 75% think of themselves as spiritual.⁷ This intrapersonal conflict between religious/spiritual health and mental health raises an important question: How can psychiatrists more actively collaborate with religious communities to ease the perceived tensions between spiritual health and mental health for our patients?
 

Engaging with the community

In a recent virtual talk titled, “Dealing with Depression: Faith, Meds, and Therapy,” I openly discussed varying aspects of mental health and mental illness with approximately 70 women at my church in Philadelphia. Before this presentation, there had never been a leadership-sponsored conversation within the church to discuss spiritual health and mental health as separate but highly interconnected entities.

Throughout the nearly 2-hour session, I used biblical and biological principles to explain the differences between spiritual health and mental health, strategies to recognize signs and symptoms of depression, and treatment options for depression. After the formal presentation, a 45-minute question-and-answer session followed in which some members shared their own experiences with mental illness.

Two major themes emerged as central points of discussion during our time of open dialogue. First, several women shared the spiritual and clinical avenues they used to access support in times of psychological distress. There was a general tone of agreement among attendees that spiritual health and mental health are, in fact, different. Second, the presentation opened the door for attendees, previously unfamiliar with mental health services, to ask questions about connecting with the appropriate resources to receive mental health treatment. The subject of seeking psychiatric care for mental health challenges was, at least in part, demystified and brought to the forefront of the attendees’ minds.

Studies show that many faith-based communities are more likely to seek counsel for psychological distress from religious leaders than from mental health professionals. In this vein, my recent community engagement highlighted to me ways that we can readily reach spiritually and religiously minded patients who otherwise would not receive the psychiatric care that they need. Psychiatrists can play an integral role in bridging the gap in psychiatric care for faith-based persons through outreach to and collaboration with religious communities.
 

Opportunities for collaboration

In collaboration with religious leaders, psychiatrists can actively support the mental health of spiritually and religiously minded patients through several low-effort, but potentially high-yield, initiatives. Notably, many of my suggested interventions do not require significant, if any, infrastructural changes to the health care system or worship communities. As psychiatrists, we can collaborate with faith leaders as follows:

1. More regularly assess the role of religion and spirituality in our patients’ daily lives to better meet their spiritual and mental health needs.

2. Better use existing chaplain services to provide spiritual support for hospitalized patients.

3. Present information about mental health – in-person, virtually, or in written form – to religious communities through talks, discussions, popular religious publications, social media platforms, and webinars.

4. Amplify existing mental health guides for faith leaders (i.e., the American Psychiatric Association’s guidebook Mental Health: A Guide for Faith Leaders),⁸ thereby encouraging church leaders and staff to become better informed about common mental health conditions.

5. Collaborate with places of worship to offer psychiatric and psychological services to their members.

This sort of engagement with religious communities is the collective role of community-oriented psychiatrists, not just psychiatrists who ascribe to religious or spiritual beliefs. We ought to remain mindful of the spiritual distress that many spiritual and religious patients feel when they experience mental illness,⁹ particularly in light of the distress caused by the coronavirus pandemic.¹⁰ But first, we must become comfortable with asking our patients about their religious or spiritual affiliations using tools such as the Cultural Formulation Interview.¹¹ The more we recognize the role of spirituality in our patients’ lives, the better equipped we become to help patients identify and seek treatment for mental illness without the distress of their feeling spiritually deficient.
 

Dr. Jordan is a psychiatry resident physician in Philadelphia. She has no conflicts of interest.

References

1. Religious Landscape Study. pewforum.org.

2. U.S. Religion Census Census: Religious Congregations and Membership Study. Association of Religion Data Archives. 2010. doi: 10.17605/OSF.IO/9AMDJ.

3. J Med Ethics Hist Med. 2018 Apr 9;11:3.

4. The Dimensions of Health: Conceptual Models. Sudbury, Mass.: Jones & Bartlett, 2010.

5. J Res Christ Educ. 2014;23(2):176-86.

6. Health Serv Res. 2003 Apr;38(2):647-73.

7. “More Americans say they’re spiritual but not religious.” pewresearch.org. 2017 Sep 6.

8. Mental Health: A Guide for Faith Leaders. Washington: American Psychiatric Association Foundation, 2018.

9. Mental Health by the Numbers. NAMI: National Alliance on Mental Illness. 2019.

10. “Most Americans say coronavirus outbreak has impacted their lives. Pew Research Center. pewsocialtrends.org. 2020 Mar 30.

11. DSM-5 Handbook on the Cultural Formulation Interview. Washington: American Psychiatric Association Publishing, 2016.

The beneficial effect on all-cause mortality of coronary artery bypass grafting surgery observed at 4 and 5 years in women with complex coronary disease seen in the SYNTAX trial is gone at 10 years.

If anything, the results suggest a mortality benefit for coronary artery bypass grafting (CABG) over percutaneous coronary intervention (PCI) mainly for men (adjusted hazard ratio, 0.76; 95% confidence interval, 0.56-1.02) and not for women (adjusted HR, 0.90; 95% CI, 0.54-1.51) in the SYNTAX Extended Survival (SYNTAXES) study.

The sex-treatment interaction for all-cause mortality was significant at 5 years (P = .025) but not at 10 years (P = .952).

“I’m becoming very humble with trials because I’m not expecting the convergence of the curve. I was expecting like a surge, a further divergence,” senior author Patrick Serruys, MD, PhD, National University of Ireland, Galway, said in an interview. “You could say, at the end of the day, everybody dies. And that’s the life expectancy factor.”

Although female patients had slightly lower anatomic SYNTAX scores at randomization (27.0 vs. 29.2), they were on average 4 years older than men (mean age, 68 years) and had higher prevalence rates of diabetes, hypertension, and chronic kidney disease, he noted. “The other explanation is that we know that the bypass graft, the saphenous bypass graft, became vulnerable around 7 years; that’s probably the half-life.”

Overall, mortality in both men and women tended to be lower after CABG than after PCI, although the differences were not statistically significant, the authors reported August 17 in the Journal of the American College of Cardiology.

The 1,800-patient SYNTAX trial showed no difference in all-cause mortality at 5 years between CABG and PCI, although CABG was associated with fewer major adverse cardiac and cerebrovascular events (MACCE) and more favorable results among those with complex, three-vessel disease.

The findings were confirmed in 10-year follow-up reported last year from SYNTAXES, which analyzed only all-cause mortality.

Female sex, however, was an independent predictor of mortality with PCI at 4-years follow-up (HR, 2.87) in SYNTAX and led to sex being incorporated into the SYNTAX II score to help guide revascularization decisions. Notably, this interaction for all-cause mortality has not been seen in other studies.

Treatment effect by sex

In the new prespecified subgroup analysis, women had a higher crude rate of all-cause mortality at 10 years than men (32.8% vs. 24.7%; log-rank P = .002). This held true whether women were in the PCI group (33.0% vs. 27.0%; log-rank P = .053) or the CABG group (32.5% vs. 22.5%; log-rank P = .017).

In women, the mortality rate was significantly higher with PCI than with CABG at 5 years, but was no longer different at 10 years (33.0% vs. 32.5%; log-rank P = .601). This was largely caused by an uptick in deaths between 5 and 10 years in those treated with CABG, compared with PCI.

In men, the mortality rate was similar between PCI and CABG at 5 years, but tended to be higher with PCI at 10 years (27.0% vs. 22.5%; log-rank P = .082).

Asked about the possible late benefit for CABG in men, Dr. Serruys replied: “Of course, everyone had made a hypothesis – ‘let’s look at the use of internal mammary arteries in these patients, etc.’ – but I must be honest, we don’t have an explanation so far.”

Roxana Mehran, MD, Mount Sinai School of Medicine, New York City, said with just 402 women and using a no-longer-available, first-generation (Taxus) stent, the findings are, unfortunately, not informative.

“For me, it would be important for these investigators to share their data for women so we can do a patient-based analysis to better figure out the differential between first-generation stents and how well we’re doing,” Dr. Mehran said.

“What’s really important is to have a study where you actually collect female-specific risk factors that are never, ever looked at, [such as] age at menopause or having had pregnancy-related complications, that predispose these women to more of an atherosclerotic risk. And, even so, to better understand their anatomy and what suits them better,” she said. “I just don’t think we know enough or have put enough effort into understanding the biology that is sex specific and different for men and women.”
 

Revising SYNTAX II score

Given the lack of a sex-treatment interaction in the analysis, Dr. Serruys and colleagues suggest that the SYNTAX II score “should be reevaluated for the prediction of all-cause mortality at 10 years.”

Lending further support to this is the fact that SYNTAX II score was similar between women who died at 5-10 years and those who died in the first 5 years after CABG (31.8 vs. 31.6).

“The authors rightfully ask whether the SYNTAX II score should be revised to remove female sex, and given the current study result this appears warranted,” Arnold H. Seto, MD, MPA, Long Beach (Calif.) Veterans Administration Hospital, said in a related editorial.

He pointed out that women in SYNTAXES treated with CABG tended to have a survival time 0.51 years longer than women treated with PCI (P = .07). Nonetheless, the lack of confirmation for a sex-specific treatment interaction in any other study – EXCEL, FREEDOM, BEST, PRECOMBAT, BARI, or MASS – strongly suggests that the interaction seen in SYNTAX is likely a “type 1 error.”

Rather than focusing on early mortality, which may represent relatively rare events that are susceptible to chance, Dr. Seto suggested “other endpoints such years of life saved, quality adjusted life-years, and MACE may better capture the benefits of different revascularization decisions, even if they have a higher risk for bias.”

A new risk model, SYNTAX score 2020, has been developed and will be published imminently, Dr. Serruys said in an interview.

The SYNTAX Extended Survival study was supported by the German Foundation of Heart Research. The SYNTAX trial, during 0- to 5-years of follow-up, was funded by Boston Scientific. Both sponsors had no role in study design or data collection, analyses, and interpretation, nor were they involved in the decision to publish the final manuscript. Dr. Serruys has received personal fees from Biosensors, Micel Technologies, Sinomedical Sciences Technology, Philips/Volcano, Xeltis, and HeartFlow, outside the submitted work. Dr. Seto reported research grants from Philips and Acist, and honoraria from Terumo, Getinge, Boston Scientific, General Electric, and Janssen.

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

The beneficial effect on all-cause mortality of coronary artery bypass grafting surgery observed at 4 and 5 years in women with complex coronary disease seen in the SYNTAX trial is gone at 10 years.

If anything, the results suggest a mortality benefit for coronary artery bypass grafting (CABG) over percutaneous coronary intervention (PCI) mainly for men (adjusted hazard ratio, 0.76; 95% confidence interval, 0.56-1.02) and not for women (adjusted HR, 0.90; 95% CI, 0.54-1.51) in the SYNTAX Extended Survival (SYNTAXES) study.

The sex-treatment interaction for all-cause mortality was significant at 5 years (P = .025) but not at 10 years (P = .952).

“I’m becoming very humble with trials because I’m not expecting the convergence of the curve. I was expecting like a surge, a further divergence,” senior author Patrick Serruys, MD, PhD, National University of Ireland, Galway, said in an interview. “You could say, at the end of the day, everybody dies. And that’s the life expectancy factor.”

Although female patients had slightly lower anatomic SYNTAX scores at randomization (27.0 vs. 29.2), they were on average 4 years older than men (mean age, 68 years) and had higher prevalence rates of diabetes, hypertension, and chronic kidney disease, he noted. “The other explanation is that we know that the bypass graft, the saphenous bypass graft, became vulnerable around 7 years; that’s probably the half-life.”

Overall, mortality in both men and women tended to be lower after CABG than after PCI, although the differences were not statistically significant, the authors reported August 17 in the Journal of the American College of Cardiology.

The 1,800-patient SYNTAX trial showed no difference in all-cause mortality at 5 years between CABG and PCI, although CABG was associated with fewer major adverse cardiac and cerebrovascular events (MACCE) and more favorable results among those with complex, three-vessel disease.

The findings were confirmed in 10-year follow-up reported last year from SYNTAXES, which analyzed only all-cause mortality.

Female sex, however, was an independent predictor of mortality with PCI at 4-years follow-up (HR, 2.87) in SYNTAX and led to sex being incorporated into the SYNTAX II score to help guide revascularization decisions. Notably, this interaction for all-cause mortality has not been seen in other studies.

Treatment effect by sex

In the new prespecified subgroup analysis, women had a higher crude rate of all-cause mortality at 10 years than men (32.8% vs. 24.7%; log-rank P = .002). This held true whether women were in the PCI group (33.0% vs. 27.0%; log-rank P = .053) or the CABG group (32.5% vs. 22.5%; log-rank P = .017).

In women, the mortality rate was significantly higher with PCI than with CABG at 5 years, but was no longer different at 10 years (33.0% vs. 32.5%; log-rank P = .601). This was largely caused by an uptick in deaths between 5 and 10 years in those treated with CABG, compared with PCI.

In men, the mortality rate was similar between PCI and CABG at 5 years, but tended to be higher with PCI at 10 years (27.0% vs. 22.5%; log-rank P = .082).

Asked about the possible late benefit for CABG in men, Dr. Serruys replied: “Of course, everyone had made a hypothesis – ‘let’s look at the use of internal mammary arteries in these patients, etc.’ – but I must be honest, we don’t have an explanation so far.”

Roxana Mehran, MD, Mount Sinai School of Medicine, New York City, said with just 402 women and using a no-longer-available, first-generation (Taxus) stent, the findings are, unfortunately, not informative.

“For me, it would be important for these investigators to share their data for women so we can do a patient-based analysis to better figure out the differential between first-generation stents and how well we’re doing,” Dr. Mehran said.

“What’s really important is to have a study where you actually collect female-specific risk factors that are never, ever looked at, [such as] age at menopause or having had pregnancy-related complications, that predispose these women to more of an atherosclerotic risk. And, even so, to better understand their anatomy and what suits them better,” she said. “I just don’t think we know enough or have put enough effort into understanding the biology that is sex specific and different for men and women.”
 

Revising SYNTAX II score

Given the lack of a sex-treatment interaction in the analysis, Dr. Serruys and colleagues suggest that the SYNTAX II score “should be reevaluated for the prediction of all-cause mortality at 10 years.”

Lending further support to this is the fact that SYNTAX II score was similar between women who died at 5-10 years and those who died in the first 5 years after CABG (31.8 vs. 31.6).

“The authors rightfully ask whether the SYNTAX II score should be revised to remove female sex, and given the current study result this appears warranted,” Arnold H. Seto, MD, MPA, Long Beach (Calif.) Veterans Administration Hospital, said in a related editorial.

He pointed out that women in SYNTAXES treated with CABG tended to have a survival time 0.51 years longer than women treated with PCI (P = .07). Nonetheless, the lack of confirmation for a sex-specific treatment interaction in any other study – EXCEL, FREEDOM, BEST, PRECOMBAT, BARI, or MASS – strongly suggests that the interaction seen in SYNTAX is likely a “type 1 error.”

Rather than focusing on early mortality, which may represent relatively rare events that are susceptible to chance, Dr. Seto suggested “other endpoints such years of life saved, quality adjusted life-years, and MACE may better capture the benefits of different revascularization decisions, even if they have a higher risk for bias.”

A new risk model, SYNTAX score 2020, has been developed and will be published imminently, Dr. Serruys said in an interview.

The SYNTAX Extended Survival study was supported by the German Foundation of Heart Research. The SYNTAX trial, during 0- to 5-years of follow-up, was funded by Boston Scientific. Both sponsors had no role in study design or data collection, analyses, and interpretation, nor were they involved in the decision to publish the final manuscript. Dr. Serruys has received personal fees from Biosensors, Micel Technologies, Sinomedical Sciences Technology, Philips/Volcano, Xeltis, and HeartFlow, outside the submitted work. Dr. Seto reported research grants from Philips and Acist, and honoraria from Terumo, Getinge, Boston Scientific, General Electric, and Janssen.

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

The beneficial effect on all-cause mortality of coronary artery bypass grafting surgery observed at 4 and 5 years in women with complex coronary disease seen in the SYNTAX trial is gone at 10 years.

If anything, the results suggest a mortality benefit for coronary artery bypass grafting (CABG) over percutaneous coronary intervention (PCI) mainly for men (adjusted hazard ratio, 0.76; 95% confidence interval, 0.56-1.02) and not for women (adjusted HR, 0.90; 95% CI, 0.54-1.51) in the SYNTAX Extended Survival (SYNTAXES) study.

The sex-treatment interaction for all-cause mortality was significant at 5 years (P = .025) but not at 10 years (P = .952).

“I’m becoming very humble with trials because I’m not expecting the convergence of the curve. I was expecting like a surge, a further divergence,” senior author Patrick Serruys, MD, PhD, National University of Ireland, Galway, said in an interview. “You could say, at the end of the day, everybody dies. And that’s the life expectancy factor.”

Although female patients had slightly lower anatomic SYNTAX scores at randomization (27.0 vs. 29.2), they were on average 4 years older than men (mean age, 68 years) and had higher prevalence rates of diabetes, hypertension, and chronic kidney disease, he noted. “The other explanation is that we know that the bypass graft, the saphenous bypass graft, became vulnerable around 7 years; that’s probably the half-life.”

Overall, mortality in both men and women tended to be lower after CABG than after PCI, although the differences were not statistically significant, the authors reported August 17 in the Journal of the American College of Cardiology.

The 1,800-patient SYNTAX trial showed no difference in all-cause mortality at 5 years between CABG and PCI, although CABG was associated with fewer major adverse cardiac and cerebrovascular events (MACCE) and more favorable results among those with complex, three-vessel disease.

The findings were confirmed in 10-year follow-up reported last year from SYNTAXES, which analyzed only all-cause mortality.

Female sex, however, was an independent predictor of mortality with PCI at 4-years follow-up (HR, 2.87) in SYNTAX and led to sex being incorporated into the SYNTAX II score to help guide revascularization decisions. Notably, this interaction for all-cause mortality has not been seen in other studies.

Treatment effect by sex

In the new prespecified subgroup analysis, women had a higher crude rate of all-cause mortality at 10 years than men (32.8% vs. 24.7%; log-rank P = .002). This held true whether women were in the PCI group (33.0% vs. 27.0%; log-rank P = .053) or the CABG group (32.5% vs. 22.5%; log-rank P = .017).

In women, the mortality rate was significantly higher with PCI than with CABG at 5 years, but was no longer different at 10 years (33.0% vs. 32.5%; log-rank P = .601). This was largely caused by an uptick in deaths between 5 and 10 years in those treated with CABG, compared with PCI.

In men, the mortality rate was similar between PCI and CABG at 5 years, but tended to be higher with PCI at 10 years (27.0% vs. 22.5%; log-rank P = .082).

Asked about the possible late benefit for CABG in men, Dr. Serruys replied: “Of course, everyone had made a hypothesis – ‘let’s look at the use of internal mammary arteries in these patients, etc.’ – but I must be honest, we don’t have an explanation so far.”

Roxana Mehran, MD, Mount Sinai School of Medicine, New York City, said with just 402 women and using a no-longer-available, first-generation (Taxus) stent, the findings are, unfortunately, not informative.

“For me, it would be important for these investigators to share their data for women so we can do a patient-based analysis to better figure out the differential between first-generation stents and how well we’re doing,” Dr. Mehran said.

“What’s really important is to have a study where you actually collect female-specific risk factors that are never, ever looked at, [such as] age at menopause or having had pregnancy-related complications, that predispose these women to more of an atherosclerotic risk. And, even so, to better understand their anatomy and what suits them better,” she said. “I just don’t think we know enough or have put enough effort into understanding the biology that is sex specific and different for men and women.”
 

Revising SYNTAX II score

Given the lack of a sex-treatment interaction in the analysis, Dr. Serruys and colleagues suggest that the SYNTAX II score “should be reevaluated for the prediction of all-cause mortality at 10 years.”

Lending further support to this is the fact that SYNTAX II score was similar between women who died at 5-10 years and those who died in the first 5 years after CABG (31.8 vs. 31.6).

“The authors rightfully ask whether the SYNTAX II score should be revised to remove female sex, and given the current study result this appears warranted,” Arnold H. Seto, MD, MPA, Long Beach (Calif.) Veterans Administration Hospital, said in a related editorial.

He pointed out that women in SYNTAXES treated with CABG tended to have a survival time 0.51 years longer than women treated with PCI (P = .07). Nonetheless, the lack of confirmation for a sex-specific treatment interaction in any other study – EXCEL, FREEDOM, BEST, PRECOMBAT, BARI, or MASS – strongly suggests that the interaction seen in SYNTAX is likely a “type 1 error.”

Rather than focusing on early mortality, which may represent relatively rare events that are susceptible to chance, Dr. Seto suggested “other endpoints such years of life saved, quality adjusted life-years, and MACE may better capture the benefits of different revascularization decisions, even if they have a higher risk for bias.”

A new risk model, SYNTAX score 2020, has been developed and will be published imminently, Dr. Serruys said in an interview.

The SYNTAX Extended Survival study was supported by the German Foundation of Heart Research. The SYNTAX trial, during 0- to 5-years of follow-up, was funded by Boston Scientific. Both sponsors had no role in study design or data collection, analyses, and interpretation, nor were they involved in the decision to publish the final manuscript. Dr. Serruys has received personal fees from Biosensors, Micel Technologies, Sinomedical Sciences Technology, Philips/Volcano, Xeltis, and HeartFlow, outside the submitted work. Dr. Seto reported research grants from Philips and Acist, and honoraria from Terumo, Getinge, Boston Scientific, General Electric, and Janssen.

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

Key clinical point: The follow-up of patients with progressive multiple sclerosis (PMS) starting high-dose biotin (HDB) should include careful assessment of clinical and radiological activity to monitor the potential pro-inflammatory effect of biotin.

Major finding: In the crossover analysis among patients who received HDB (n=42), the number of relapses was statistically and clinically significantly higher after vs. before biotin initiation (incident rate ratio, 7.4; P less than .0001). With the propensity score matching method, relapse risk was significantly higher in the biotin vs. control group (hazard ratio [HR], 4.3; P = .01). The inverse probability of treatment weighting method with 440 control participants showed consistent results with higher risk in the biotin group (HR, 5.1; P less than .0001).

Study details: This study evaluated the association between exposure to HDB and the risk of relapse among 482 patients with PMS.

Disclosures: No study sponsor was identified. The authors declared no conflicts of interest.

Citation: Branger P et al. Neurotherapeutics. 2020 Jun 15. doi: 10.1007/s13311-020-00880-z.

Key clinical point: The follow-up of patients with progressive multiple sclerosis (PMS) starting high-dose biotin (HDB) should include careful assessment of clinical and radiological activity to monitor the potential pro-inflammatory effect of biotin.

Major finding: In the crossover analysis among patients who received HDB (n=42), the number of relapses was statistically and clinically significantly higher after vs. before biotin initiation (incident rate ratio, 7.4; P less than .0001). With the propensity score matching method, relapse risk was significantly higher in the biotin vs. control group (hazard ratio [HR], 4.3; P = .01). The inverse probability of treatment weighting method with 440 control participants showed consistent results with higher risk in the biotin group (HR, 5.1; P less than .0001).

Study details: This study evaluated the association between exposure to HDB and the risk of relapse among 482 patients with PMS.

Disclosures: No study sponsor was identified. The authors declared no conflicts of interest.

Citation: Branger P et al. Neurotherapeutics. 2020 Jun 15. doi: 10.1007/s13311-020-00880-z.

Key clinical point: The follow-up of patients with progressive multiple sclerosis (PMS) starting high-dose biotin (HDB) should include careful assessment of clinical and radiological activity to monitor the potential pro-inflammatory effect of biotin.

Major finding: In the crossover analysis among patients who received HDB (n=42), the number of relapses was statistically and clinically significantly higher after vs. before biotin initiation (incident rate ratio, 7.4; P less than .0001). With the propensity score matching method, relapse risk was significantly higher in the biotin vs. control group (hazard ratio [HR], 4.3; P = .01). The inverse probability of treatment weighting method with 440 control participants showed consistent results with higher risk in the biotin group (HR, 5.1; P less than .0001).

Study details: This study evaluated the association between exposure to HDB and the risk of relapse among 482 patients with PMS.

Disclosures: No study sponsor was identified. The authors declared no conflicts of interest.

Citation: Branger P et al. Neurotherapeutics. 2020 Jun 15. doi: 10.1007/s13311-020-00880-z.

Aggression in individuals is influenced by genetic and environmental factors, but can be reduced with treatment, according to Emil F. Coccaro, MD.

“It actually is a complex triad of emotion, cognition, and behavior. The emotion is anger, the cognition is hostility, and the behavior is aggression. And they sort of go in that order,” Dr. Coccaro said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

Although aggression can be thought of in a numerous ways, premeditated and impulsive aggression are most relevant to behavioral studies in psychiatry, Dr. Coccaro explained. Premeditated aggression is goal oriented, while impulsive aggression comes from frustration or a response to a threat. Impulsive aggression is “typically social or frustrative in nature, and studies that we’ve done that show that individuals move toward a threat while nonaggressives move away it,” he said. Both types of aggression can be seen in the same individuals at different times.

Aggression also can be considered using a threshold model. Calm individuals, for example, might have a low baseline of aggression and a high threshold before they act out. An aggressive person, on the other hand, has a lower threshold and a higher baseline level. “Their delta to get to the point where they’re going to explode is much shorter, much lower than it is in someone who is healthy,” Dr. Coccaro said.

“What we think is that the threshold to explode is probably regulated by various neurobiological features. The baseline state of aggression also may be related to baseline neurobiological features, but also what’s going on in the environment, because the neurobiological features that send someone to exploding aggression are there all the time,” he explained.

Individuals with secondary aggression are likely to have an underlying condition, such as a primary disease of the brain, systemic or metabolic disorder, or a psychiatric disorder such as schizophrenia. “If someone’s schizophrenic and they’ve got voices telling them to hurt somebody, or delusions that someone’s going to hurt them, that’s not primary aggression, that’s secondary to the psychosis,” Dr. Coccaro noted.

An individual with primary aggression is likely to have intermittent explosive disorder (IED). IED is not a new diagnosis and has been listed in the DSM since the DSM-I as “passive-aggressive personality.” It was relisted in the DSM-II as “explosive personality,” then changed to IED in the DSM-3 as a diagnosis of exclusion that was poorly operationalized, according to Dr. Coccaro. The criteria for IED under the DSM-III did not define the number of recurrent outbursts needed, what they looked like, the time frame, and excluded people who were generally impulsive.

“That’s not really what these people look like and it’s not what impulsive aggression looks like,” he said. Although the DSM-IV removed the exclusion criteria for general impulsivity and aggression, “it was still purely operational.”

The DSM-5 criteria define IED as “verbal and physical aggression without destruction or assault, twice equally on average for 3 months, or three or more episodes of physical destruction/assault over a 1-year period. These individuals have outbursts “grossly out of proportion to provocation,” the aggression is generally impulsive, and it causes stress and impairment with an age of onset at older than 6 years.

“It’s not better accounted for a whole variety of things, but we actually made some of those exclusion criteria a little less stringent,” compared with criteria in the DSM-IV, Dr. Coccaro said. “That’s because it turns out that it doesn’t really matter much of the time what the comorbidity is. If you have this aggressiveness in the absence of those other conditions, it’s IED.”

According to a reanalysis of the National Comorbidity Survey, 11.7% of adolescents displayed aggressiveness within the last year and 17.3% over a lifetime, compared with 5.1% of adults within the last year and 8.0% within a lifetime. Under DSM-5 criteria, 6.4% of adolescents within the last year and 8.9% over a lifetime currently have IED, compared with 2.6% of adults within the last year and 4.0% over a lifetime, but “could go as high” as the percentage of individuals diagnosed with aggressiveness, Dr. Coccaro noted.

“People who are not called IED many times are not called IED because we didn’t have all the information we needed to actually make the diagnosis,” he said.

Individuals with DSM-5 IED can have as many as 30 episodes in 1 year, compared with those who are nonaggressive and are also more likely to damage property. “These are the big episodes, not simply the episodes where people are getting irritable and snapping at people. These are the big ones, where they’re really destroying objects and pushing or hitting people,” Dr. Coccaro said. About one-fourth of individuals with IED hurt victims badly enough that they require medical attention, one-fifth exhibit aggression toward a partner, and one-fourth receive aggression from their own partner.

In terms of comorbidity with other psychiatric disorders, “IEDs don’t have more comorbidity in general than other disorders,” Dr. Coccaro noted. Personality disorders such as paranoid, antisocial, borderline narcissistic, and obsessive-compulsive disorders are more common in individuals with IED. Aggression in these people present differently depending on the personality disorder. “Someone who’s paranoid might blow up at you if you get in their face. For an antisocial, they’ll blow up at you if you’re preventing them from doing what they want to do. Borderlines, you reject them or you abandon them, they’re going to blow up. Narcissists will blow up when you reject. OCD will also blow up when you mess around with their sense of order,” Dr. Coccaro said.

Genetics also play a role in whether a person may have IED. There is a “clear signal” in families, with about one-fourth of individuals with IED having a relative with IED, compared with 8% of nonaggressive individuals. These percentages were consistent, regardless of whether the individual had a comorbid condition, history of alcohol or drug use, or history of suicide, he said. Other factors that influence likelihood of IED are environment, behaviors such as smoking, and conditions such as traumatic brain injury. Experiencing aggression as a child is another factor.

“IED is the categorical expression of impulsive aggression, and it’s far more common than once thought,” Dr. Coccaro said. “And IED is totally unrecognized in its role in societal violence.”
 

Treatment can suppress, but not cure aggression

Medications used to treat aggression and impulsive aggression include lithium, SSRIs, mood stabilizers, neuroleptics, and beta-blockers. However, the treatments are not a “magic bullet,” Dr. Coccaro noted. “The meds tend to suppress aggressiveness, but not cure it.”

Timing of treatment is also a factor for medication. In studies of patients taking lithium for aggression, for example, “when they gave the drug to people who liked being aggressive, they didn’t like being on these drugs because it made them feel unprotected. It just was at odds with who they thought they were,” Dr. Coccaro said. “The people who took the drug and did well and really liked being on the drug with people who didn’t like that they were aggressive.”

Neurorehabilitation and cognitive-behavioral therapy specific to aggression, called cognitive relaxation and coping skills therapy, are nonpsychotropic approaches to treating aggression. “These therapeutic approaches are working not only to reduce progression, but also to reduce the social information processing problems that aggressive individuals have,” Dr. Coccaro said.

Another approach, known as interpretation bias training, teaches individuals with aggression to judge slightly angry-looking photos of people as not being angry. After 7-14 days of training, aggressive behavior in adolescents has been shown to be reduced. The changes were also visible on functional MRI.

“What they found was that when you treated them, the change in the amygdala went down when you looked at the angry faces and in the left lateral, post training, they became happier,” Dr. Coccaro said.

Global Academy and this news organization are owned by the same parent company. Dr. Coccaro reported serving as a consultant for Avanir, Azevan, and Bracket. He also reported receiving research grants from the National Institute of Mental Health, the National Institute on Alcohol Abuse and Alcoholism, and the Pritzker Pucker Family Foundation.

Aggression in individuals is influenced by genetic and environmental factors, but can be reduced with treatment, according to Emil F. Coccaro, MD.

“It actually is a complex triad of emotion, cognition, and behavior. The emotion is anger, the cognition is hostility, and the behavior is aggression. And they sort of go in that order,” Dr. Coccaro said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

Although aggression can be thought of in a numerous ways, premeditated and impulsive aggression are most relevant to behavioral studies in psychiatry, Dr. Coccaro explained. Premeditated aggression is goal oriented, while impulsive aggression comes from frustration or a response to a threat. Impulsive aggression is “typically social or frustrative in nature, and studies that we’ve done that show that individuals move toward a threat while nonaggressives move away it,” he said. Both types of aggression can be seen in the same individuals at different times.

Aggression also can be considered using a threshold model. Calm individuals, for example, might have a low baseline of aggression and a high threshold before they act out. An aggressive person, on the other hand, has a lower threshold and a higher baseline level. “Their delta to get to the point where they’re going to explode is much shorter, much lower than it is in someone who is healthy,” Dr. Coccaro said.

“What we think is that the threshold to explode is probably regulated by various neurobiological features. The baseline state of aggression also may be related to baseline neurobiological features, but also what’s going on in the environment, because the neurobiological features that send someone to exploding aggression are there all the time,” he explained.

Individuals with secondary aggression are likely to have an underlying condition, such as a primary disease of the brain, systemic or metabolic disorder, or a psychiatric disorder such as schizophrenia. “If someone’s schizophrenic and they’ve got voices telling them to hurt somebody, or delusions that someone’s going to hurt them, that’s not primary aggression, that’s secondary to the psychosis,” Dr. Coccaro noted.

An individual with primary aggression is likely to have intermittent explosive disorder (IED). IED is not a new diagnosis and has been listed in the DSM since the DSM-I as “passive-aggressive personality.” It was relisted in the DSM-II as “explosive personality,” then changed to IED in the DSM-3 as a diagnosis of exclusion that was poorly operationalized, according to Dr. Coccaro. The criteria for IED under the DSM-III did not define the number of recurrent outbursts needed, what they looked like, the time frame, and excluded people who were generally impulsive.

“That’s not really what these people look like and it’s not what impulsive aggression looks like,” he said. Although the DSM-IV removed the exclusion criteria for general impulsivity and aggression, “it was still purely operational.”

The DSM-5 criteria define IED as “verbal and physical aggression without destruction or assault, twice equally on average for 3 months, or three or more episodes of physical destruction/assault over a 1-year period. These individuals have outbursts “grossly out of proportion to provocation,” the aggression is generally impulsive, and it causes stress and impairment with an age of onset at older than 6 years.

“It’s not better accounted for a whole variety of things, but we actually made some of those exclusion criteria a little less stringent,” compared with criteria in the DSM-IV, Dr. Coccaro said. “That’s because it turns out that it doesn’t really matter much of the time what the comorbidity is. If you have this aggressiveness in the absence of those other conditions, it’s IED.”

According to a reanalysis of the National Comorbidity Survey, 11.7% of adolescents displayed aggressiveness within the last year and 17.3% over a lifetime, compared with 5.1% of adults within the last year and 8.0% within a lifetime. Under DSM-5 criteria, 6.4% of adolescents within the last year and 8.9% over a lifetime currently have IED, compared with 2.6% of adults within the last year and 4.0% over a lifetime, but “could go as high” as the percentage of individuals diagnosed with aggressiveness, Dr. Coccaro noted.

“People who are not called IED many times are not called IED because we didn’t have all the information we needed to actually make the diagnosis,” he said.

Individuals with DSM-5 IED can have as many as 30 episodes in 1 year, compared with those who are nonaggressive and are also more likely to damage property. “These are the big episodes, not simply the episodes where people are getting irritable and snapping at people. These are the big ones, where they’re really destroying objects and pushing or hitting people,” Dr. Coccaro said. About one-fourth of individuals with IED hurt victims badly enough that they require medical attention, one-fifth exhibit aggression toward a partner, and one-fourth receive aggression from their own partner.

In terms of comorbidity with other psychiatric disorders, “IEDs don’t have more comorbidity in general than other disorders,” Dr. Coccaro noted. Personality disorders such as paranoid, antisocial, borderline narcissistic, and obsessive-compulsive disorders are more common in individuals with IED. Aggression in these people present differently depending on the personality disorder. “Someone who’s paranoid might blow up at you if you get in their face. For an antisocial, they’ll blow up at you if you’re preventing them from doing what they want to do. Borderlines, you reject them or you abandon them, they’re going to blow up. Narcissists will blow up when you reject. OCD will also blow up when you mess around with their sense of order,” Dr. Coccaro said.

Genetics also play a role in whether a person may have IED. There is a “clear signal” in families, with about one-fourth of individuals with IED having a relative with IED, compared with 8% of nonaggressive individuals. These percentages were consistent, regardless of whether the individual had a comorbid condition, history of alcohol or drug use, or history of suicide, he said. Other factors that influence likelihood of IED are environment, behaviors such as smoking, and conditions such as traumatic brain injury. Experiencing aggression as a child is another factor.

“IED is the categorical expression of impulsive aggression, and it’s far more common than once thought,” Dr. Coccaro said. “And IED is totally unrecognized in its role in societal violence.”
 

Treatment can suppress, but not cure aggression

Medications used to treat aggression and impulsive aggression include lithium, SSRIs, mood stabilizers, neuroleptics, and beta-blockers. However, the treatments are not a “magic bullet,” Dr. Coccaro noted. “The meds tend to suppress aggressiveness, but not cure it.”

Timing of treatment is also a factor for medication. In studies of patients taking lithium for aggression, for example, “when they gave the drug to people who liked being aggressive, they didn’t like being on these drugs because it made them feel unprotected. It just was at odds with who they thought they were,” Dr. Coccaro said. “The people who took the drug and did well and really liked being on the drug with people who didn’t like that they were aggressive.”

Neurorehabilitation and cognitive-behavioral therapy specific to aggression, called cognitive relaxation and coping skills therapy, are nonpsychotropic approaches to treating aggression. “These therapeutic approaches are working not only to reduce progression, but also to reduce the social information processing problems that aggressive individuals have,” Dr. Coccaro said.

Another approach, known as interpretation bias training, teaches individuals with aggression to judge slightly angry-looking photos of people as not being angry. After 7-14 days of training, aggressive behavior in adolescents has been shown to be reduced. The changes were also visible on functional MRI.

“What they found was that when you treated them, the change in the amygdala went down when you looked at the angry faces and in the left lateral, post training, they became happier,” Dr. Coccaro said.

Global Academy and this news organization are owned by the same parent company. Dr. Coccaro reported serving as a consultant for Avanir, Azevan, and Bracket. He also reported receiving research grants from the National Institute of Mental Health, the National Institute on Alcohol Abuse and Alcoholism, and the Pritzker Pucker Family Foundation.

Aggression in individuals is influenced by genetic and environmental factors, but can be reduced with treatment, according to Emil F. Coccaro, MD.

“It actually is a complex triad of emotion, cognition, and behavior. The emotion is anger, the cognition is hostility, and the behavior is aggression. And they sort of go in that order,” Dr. Coccaro said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

Although aggression can be thought of in a numerous ways, premeditated and impulsive aggression are most relevant to behavioral studies in psychiatry, Dr. Coccaro explained. Premeditated aggression is goal oriented, while impulsive aggression comes from frustration or a response to a threat. Impulsive aggression is “typically social or frustrative in nature, and studies that we’ve done that show that individuals move toward a threat while nonaggressives move away it,” he said. Both types of aggression can be seen in the same individuals at different times.

Aggression also can be considered using a threshold model. Calm individuals, for example, might have a low baseline of aggression and a high threshold before they act out. An aggressive person, on the other hand, has a lower threshold and a higher baseline level. “Their delta to get to the point where they’re going to explode is much shorter, much lower than it is in someone who is healthy,” Dr. Coccaro said.

“What we think is that the threshold to explode is probably regulated by various neurobiological features. The baseline state of aggression also may be related to baseline neurobiological features, but also what’s going on in the environment, because the neurobiological features that send someone to exploding aggression are there all the time,” he explained.

Individuals with secondary aggression are likely to have an underlying condition, such as a primary disease of the brain, systemic or metabolic disorder, or a psychiatric disorder such as schizophrenia. “If someone’s schizophrenic and they’ve got voices telling them to hurt somebody, or delusions that someone’s going to hurt them, that’s not primary aggression, that’s secondary to the psychosis,” Dr. Coccaro noted.

An individual with primary aggression is likely to have intermittent explosive disorder (IED). IED is not a new diagnosis and has been listed in the DSM since the DSM-I as “passive-aggressive personality.” It was relisted in the DSM-II as “explosive personality,” then changed to IED in the DSM-3 as a diagnosis of exclusion that was poorly operationalized, according to Dr. Coccaro. The criteria for IED under the DSM-III did not define the number of recurrent outbursts needed, what they looked like, the time frame, and excluded people who were generally impulsive.

“That’s not really what these people look like and it’s not what impulsive aggression looks like,” he said. Although the DSM-IV removed the exclusion criteria for general impulsivity and aggression, “it was still purely operational.”

The DSM-5 criteria define IED as “verbal and physical aggression without destruction or assault, twice equally on average for 3 months, or three or more episodes of physical destruction/assault over a 1-year period. These individuals have outbursts “grossly out of proportion to provocation,” the aggression is generally impulsive, and it causes stress and impairment with an age of onset at older than 6 years.

“It’s not better accounted for a whole variety of things, but we actually made some of those exclusion criteria a little less stringent,” compared with criteria in the DSM-IV, Dr. Coccaro said. “That’s because it turns out that it doesn’t really matter much of the time what the comorbidity is. If you have this aggressiveness in the absence of those other conditions, it’s IED.”

According to a reanalysis of the National Comorbidity Survey, 11.7% of adolescents displayed aggressiveness within the last year and 17.3% over a lifetime, compared with 5.1% of adults within the last year and 8.0% within a lifetime. Under DSM-5 criteria, 6.4% of adolescents within the last year and 8.9% over a lifetime currently have IED, compared with 2.6% of adults within the last year and 4.0% over a lifetime, but “could go as high” as the percentage of individuals diagnosed with aggressiveness, Dr. Coccaro noted.

“People who are not called IED many times are not called IED because we didn’t have all the information we needed to actually make the diagnosis,” he said.

Individuals with DSM-5 IED can have as many as 30 episodes in 1 year, compared with those who are nonaggressive and are also more likely to damage property. “These are the big episodes, not simply the episodes where people are getting irritable and snapping at people. These are the big ones, where they’re really destroying objects and pushing or hitting people,” Dr. Coccaro said. About one-fourth of individuals with IED hurt victims badly enough that they require medical attention, one-fifth exhibit aggression toward a partner, and one-fourth receive aggression from their own partner.

In terms of comorbidity with other psychiatric disorders, “IEDs don’t have more comorbidity in general than other disorders,” Dr. Coccaro noted. Personality disorders such as paranoid, antisocial, borderline narcissistic, and obsessive-compulsive disorders are more common in individuals with IED. Aggression in these people present differently depending on the personality disorder. “Someone who’s paranoid might blow up at you if you get in their face. For an antisocial, they’ll blow up at you if you’re preventing them from doing what they want to do. Borderlines, you reject them or you abandon them, they’re going to blow up. Narcissists will blow up when you reject. OCD will also blow up when you mess around with their sense of order,” Dr. Coccaro said.

Genetics also play a role in whether a person may have IED. There is a “clear signal” in families, with about one-fourth of individuals with IED having a relative with IED, compared with 8% of nonaggressive individuals. These percentages were consistent, regardless of whether the individual had a comorbid condition, history of alcohol or drug use, or history of suicide, he said. Other factors that influence likelihood of IED are environment, behaviors such as smoking, and conditions such as traumatic brain injury. Experiencing aggression as a child is another factor.

“IED is the categorical expression of impulsive aggression, and it’s far more common than once thought,” Dr. Coccaro said. “And IED is totally unrecognized in its role in societal violence.”
 

Treatment can suppress, but not cure aggression

Medications used to treat aggression and impulsive aggression include lithium, SSRIs, mood stabilizers, neuroleptics, and beta-blockers. However, the treatments are not a “magic bullet,” Dr. Coccaro noted. “The meds tend to suppress aggressiveness, but not cure it.”

Timing of treatment is also a factor for medication. In studies of patients taking lithium for aggression, for example, “when they gave the drug to people who liked being aggressive, they didn’t like being on these drugs because it made them feel unprotected. It just was at odds with who they thought they were,” Dr. Coccaro said. “The people who took the drug and did well and really liked being on the drug with people who didn’t like that they were aggressive.”

Neurorehabilitation and cognitive-behavioral therapy specific to aggression, called cognitive relaxation and coping skills therapy, are nonpsychotropic approaches to treating aggression. “These therapeutic approaches are working not only to reduce progression, but also to reduce the social information processing problems that aggressive individuals have,” Dr. Coccaro said.

Another approach, known as interpretation bias training, teaches individuals with aggression to judge slightly angry-looking photos of people as not being angry. After 7-14 days of training, aggressive behavior in adolescents has been shown to be reduced. The changes were also visible on functional MRI.

“What they found was that when you treated them, the change in the amygdala went down when you looked at the angry faces and in the left lateral, post training, they became happier,” Dr. Coccaro said.

Global Academy and this news organization are owned by the same parent company. Dr. Coccaro reported serving as a consultant for Avanir, Azevan, and Bracket. He also reported receiving research grants from the National Institute of Mental Health, the National Institute on Alcohol Abuse and Alcoholism, and the Pritzker Pucker Family Foundation.

Patients have often been labeled as “poor historians” if they are not able to recollect their own medical history, whether through illness or difficulties in communication. But Fred Ovsiew, MD, speaking at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists, sees that label as an excuse on the part of the clinician.

“I strongly advise you to drop that phrase from your vocabulary if you do use it, because the patient is not the historian. The doctor, the clinician is the historian,” Dr. Ovsiew said at the meeting, presented by Global Academy for Medical Education. “It is the clinician’s job to put the story together using the account by the patient as one source, but [also] interviewing a collateral informant and/or reviewing records, which is necessary in almost every case of a neuropsychiatric illness.”

Rather, clinicians taking history at the bedside should focus on why the patients cannot give a narrative account of their illness. Patients can have narrative incapacity on a psychogenic basis, such as in patients with conversion or somatoform disorder, he explained. “I think this is a result of the narrative incapacity that develops in people who have had trauma or adverse experiences in childhood and insecure attachment. This is shown on the adult attachment interview as a disorganized account of their childhoods.”

Other patients might not be able to recount their medical history because they are amnestic, which leaves their account vague because of a lack of access to information. “It may be frozen in time in the sense that, up to a certain point in their life, they can recount the history,” Dr. Ovsiew said. “But in recent years, their account becomes vague.”

Patients with right hemisphere lesions might not know that their account has incongruity and is implausible, while patients with dorsolateral prefrontal lesions might be aspontaneous, use few words to describe their situation, and have poor insight. Those with ventromedial prefrontal lesions can be impulsive and have poor insight, not considering alternative possibilities, Dr. Ovsiew noted.

Asking open-ended questions of the patient is the first step to identifying any potential narrative incapacity, followed by a detailed medical history by the clinician. When taking a medical history, try avoiding what Dr. Ovsiew calls the “anything like that?” problem, where a clinician asks a question about a cluster of symptoms that would make sense to a doctor, but not a patient. For example, a doctor might ask whether a patient is experiencing “chest pain or leg swelling – anything like that?” because he or she knows what those symptoms have in common, but the patient might not know the relationship between those symptoms. “You can’t count on the patient to tell you all the relevant information,” he said. “You have to know what to ask about.”

“Patients with brain disease have subtle personality changes, sometimes more obvious personality changes. These need to be inquired about,” Dr. Ovsiew said. He encouraged asking “non-DSM questions” to help identify specific symptoms of a neuropsychiatric illness. “The patient with apathy has reduced negative as well as positive emotions. The patient with depression has reduced positive emotions, but often tells you very clearly about the negative emotions of sadness, guilt. The patient with depression has diurnal variation in mood, a very telling symptom, especially when it’s disclosed spontaneously,” Dr. Ovsiew explained. “The point is, you need to know to ask about it.”

When taking a sleep history, clinicians should be aware of sleep disturbances apart from insomnia and early waking. REM sleep behavior disorder is a condition that should be inquired about. Obstructive sleep apnea is a condition that might not be immediately apparent to the patient, but a bed partner can identify whether a patient has problems breathing throughout the night.

“This is an important condition to uncover for the neuropsychiatrist because it contributes to treatment resistance and depression, and it contributes to cognitive impairment,” Dr. Ovsiew said. “These patients commonly have mild difficulties with attention and concentration.”

Always ask about head injury in every history, which can be relevant to later onset depression, PTSD, and cognitive impairment. Every head injury follows a trajectory of retrograde amnesia and altered state of consciousness (including coma), followed by a period of posttraumatic amnesia. Duration of these states can be used to assess the severity of brain injury, but the 15-point Glasgow Coma Scale is another way to assess injury severity, Dr. Ovsiew explained.

However, the two do not always overlap, he noted. “Someone may have a Glasgow Coma Scale score that is 9-12, predicting moderate brain injury, but they may have a short duration of amnesia. These don’t always follow the same path. There are many different ways of classifying how severe the brain injury is.”
 

Keep probes brief, straightforward

Cognitive exams of patients with suspected psychiatric disorders should be simple, easy to administer and focused on a single domain of cognition. “Probes should be brief. They should not require specialized equipment. The Purdue Pegboard Test might be a great neuropsychological instrument, but very few of us carry a pegboard around in our medical bags,” Dr. Ovsiew said.

The probe administered should also be accessible to the patient. The serial sevens clinical test, where a patient is asked to repeatedly subtract 7 from 100, is only effective at testing concentration if the patient is capable of completing the test. “There are going to be patients who can’t do the task, but it’s not because of concentration failure, it’s because of subtraction failure,” he said.

When assessing attention, effective tasks include having the patient perform the digit span test forward and backward, count backward from 20 to 1, listing the months of the year in reverse, and performing the Mental Alternation Test. However, Dr. Ovsiew explained there may be some barriers for patients in completing these tasks. “The person may be aphasic and not know the alphabet. The person may have English as a second language and not be skilled at giving the alphabet in English. In some cases, you may want to check and not assume that the patient can count and does know the alphabet.”

In assessing language, listen for aphasic abnormalities. “The patient, of course, is speaking throughout the interview, but you need to take a moment to listen for prosody, to listen to rate of speech, to listen for paraphasic errors or word-finding problems,” Dr. Ovsiew said. Any abnormalities should be probed further through confrontation naming tasks, which can be done in person and with some success through video, but not by phone. Naming to definition (“What do you call the part of a shirt that covers the arm?”) is one way of administering the test over the phone.

Visuospatial function can be assessed by clock drawing but also carries problems. Patients who do not plan their clock before beginning to draw, for example, may have an executive function problem instead of a visuospatial problem, Dr. Ovsiew noted. Patients in whom a clinician suspects hemineglect should be given a visual search task or line by section task. “I like doing clock drawing. It’s a nice screening test. It’s becoming, I think, less useful as people count on digital clocks and have trouble even imagining what an analog clock looks like.”

An approach that is better suited to in-person assessment, but also works by video, is the Poppelreuter figure visual perceptual function test, which is a prompt for the patient that involves common household items overlaying one another “in atypical positions and atypical configurations” where the patient is instructed to describe the items they see on the card. Another approach that works over video is the interlocking finger test, where the patient is asked to copy the hand positions made by the clinician.

Dr. Ovsiew admitted that visuospatial function is nearly impossible to assess over the phone. Asking topographical questions (“If you’re driving from Chicago to Los Angeles, is the Pacific Ocean in front of you, behind you, to your left, or to your right?”) may help judge visuospatial function, but this relies on the patient having the topographic knowledge to answer the questions. Some patients who are topographically disoriented can’t do them at all,” Dr. Ovsiew said.

Bedside neuropsychiatry assesses encoding of a memory, its retention and its retrieval as well as verbal and visual cues. Each one of these aspects of memory can be impaired on its own and should be explored separately, Dr. Ovsiew explained. “Neuropsychiatric clinicians have a rough-and-ready, seat-of-the-pants way of approaching this that wouldn’t pass muster if you’re a psychologist, but is the best we can do at the bedside.”

To test retrieval and retention, the Three Words–Three Shapes test works well in person, with some difficulty by video, and is not possible to administer over the phone. In lieu of that test, giving the patient a simple word list and asking them to repeat the list in order. Using the word list, “these different stages of memory function can be parsed out pretty well at the bedside or chairside, and even by the phone. Figuring out where the memory failure is diagnostically important,” Dr. Ovsiew said.

Executive function, which involves activation, planning, sequencing, maintaining, self-monitoring, and flexible employment of action and attention, is “complicated to evaluate because there are multiple aspects of executive function, multiple deficits that can be seen with executive dysfunction, and they don’t all correlate with each other.”

Within executive function evaluation, the Mental Alternation Test can assess working memory, motor sequencing can be assessed through the ring/fist, fist/edge/palm, alternating fist, and rampart tests. The Go/No-Go test can be used to assess response inhibition. For effortful retrieval evaluation, spontaneous word-list generation – such as thinking of all the items one can buy at a supermarket– can test category fluency, while a task to name all the words starting with a certain letter can assess letter stimulus.

Executive function “is of crucial importance in the neuropsychiatric evaluation because it’s strongly correlated with how well the person functions outside the office,” Dr. Ovsiew said.

Global Academy and this news organization are owned by the same parent company. Dr. Ovsiew reported relationships with Wolters Kluwer Health in the form of consulting, receiving royalty payments, and related activities.

Patients have often been labeled as “poor historians” if they are not able to recollect their own medical history, whether through illness or difficulties in communication. But Fred Ovsiew, MD, speaking at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists, sees that label as an excuse on the part of the clinician.

“I strongly advise you to drop that phrase from your vocabulary if you do use it, because the patient is not the historian. The doctor, the clinician is the historian,” Dr. Ovsiew said at the meeting, presented by Global Academy for Medical Education. “It is the clinician’s job to put the story together using the account by the patient as one source, but [also] interviewing a collateral informant and/or reviewing records, which is necessary in almost every case of a neuropsychiatric illness.”

Rather, clinicians taking history at the bedside should focus on why the patients cannot give a narrative account of their illness. Patients can have narrative incapacity on a psychogenic basis, such as in patients with conversion or somatoform disorder, he explained. “I think this is a result of the narrative incapacity that develops in people who have had trauma or adverse experiences in childhood and insecure attachment. This is shown on the adult attachment interview as a disorganized account of their childhoods.”

Other patients might not be able to recount their medical history because they are amnestic, which leaves their account vague because of a lack of access to information. “It may be frozen in time in the sense that, up to a certain point in their life, they can recount the history,” Dr. Ovsiew said. “But in recent years, their account becomes vague.”

Patients with right hemisphere lesions might not know that their account has incongruity and is implausible, while patients with dorsolateral prefrontal lesions might be aspontaneous, use few words to describe their situation, and have poor insight. Those with ventromedial prefrontal lesions can be impulsive and have poor insight, not considering alternative possibilities, Dr. Ovsiew noted.

Asking open-ended questions of the patient is the first step to identifying any potential narrative incapacity, followed by a detailed medical history by the clinician. When taking a medical history, try avoiding what Dr. Ovsiew calls the “anything like that?” problem, where a clinician asks a question about a cluster of symptoms that would make sense to a doctor, but not a patient. For example, a doctor might ask whether a patient is experiencing “chest pain or leg swelling – anything like that?” because he or she knows what those symptoms have in common, but the patient might not know the relationship between those symptoms. “You can’t count on the patient to tell you all the relevant information,” he said. “You have to know what to ask about.”

“Patients with brain disease have subtle personality changes, sometimes more obvious personality changes. These need to be inquired about,” Dr. Ovsiew said. He encouraged asking “non-DSM questions” to help identify specific symptoms of a neuropsychiatric illness. “The patient with apathy has reduced negative as well as positive emotions. The patient with depression has reduced positive emotions, but often tells you very clearly about the negative emotions of sadness, guilt. The patient with depression has diurnal variation in mood, a very telling symptom, especially when it’s disclosed spontaneously,” Dr. Ovsiew explained. “The point is, you need to know to ask about it.”

When taking a sleep history, clinicians should be aware of sleep disturbances apart from insomnia and early waking. REM sleep behavior disorder is a condition that should be inquired about. Obstructive sleep apnea is a condition that might not be immediately apparent to the patient, but a bed partner can identify whether a patient has problems breathing throughout the night.

“This is an important condition to uncover for the neuropsychiatrist because it contributes to treatment resistance and depression, and it contributes to cognitive impairment,” Dr. Ovsiew said. “These patients commonly have mild difficulties with attention and concentration.”

Always ask about head injury in every history, which can be relevant to later onset depression, PTSD, and cognitive impairment. Every head injury follows a trajectory of retrograde amnesia and altered state of consciousness (including coma), followed by a period of posttraumatic amnesia. Duration of these states can be used to assess the severity of brain injury, but the 15-point Glasgow Coma Scale is another way to assess injury severity, Dr. Ovsiew explained.

However, the two do not always overlap, he noted. “Someone may have a Glasgow Coma Scale score that is 9-12, predicting moderate brain injury, but they may have a short duration of amnesia. These don’t always follow the same path. There are many different ways of classifying how severe the brain injury is.”
 

Keep probes brief, straightforward

Cognitive exams of patients with suspected psychiatric disorders should be simple, easy to administer and focused on a single domain of cognition. “Probes should be brief. They should not require specialized equipment. The Purdue Pegboard Test might be a great neuropsychological instrument, but very few of us carry a pegboard around in our medical bags,” Dr. Ovsiew said.

The probe administered should also be accessible to the patient. The serial sevens clinical test, where a patient is asked to repeatedly subtract 7 from 100, is only effective at testing concentration if the patient is capable of completing the test. “There are going to be patients who can’t do the task, but it’s not because of concentration failure, it’s because of subtraction failure,” he said.

When assessing attention, effective tasks include having the patient perform the digit span test forward and backward, count backward from 20 to 1, listing the months of the year in reverse, and performing the Mental Alternation Test. However, Dr. Ovsiew explained there may be some barriers for patients in completing these tasks. “The person may be aphasic and not know the alphabet. The person may have English as a second language and not be skilled at giving the alphabet in English. In some cases, you may want to check and not assume that the patient can count and does know the alphabet.”

In assessing language, listen for aphasic abnormalities. “The patient, of course, is speaking throughout the interview, but you need to take a moment to listen for prosody, to listen to rate of speech, to listen for paraphasic errors or word-finding problems,” Dr. Ovsiew said. Any abnormalities should be probed further through confrontation naming tasks, which can be done in person and with some success through video, but not by phone. Naming to definition (“What do you call the part of a shirt that covers the arm?”) is one way of administering the test over the phone.

Visuospatial function can be assessed by clock drawing but also carries problems. Patients who do not plan their clock before beginning to draw, for example, may have an executive function problem instead of a visuospatial problem, Dr. Ovsiew noted. Patients in whom a clinician suspects hemineglect should be given a visual search task or line by section task. “I like doing clock drawing. It’s a nice screening test. It’s becoming, I think, less useful as people count on digital clocks and have trouble even imagining what an analog clock looks like.”

An approach that is better suited to in-person assessment, but also works by video, is the Poppelreuter figure visual perceptual function test, which is a prompt for the patient that involves common household items overlaying one another “in atypical positions and atypical configurations” where the patient is instructed to describe the items they see on the card. Another approach that works over video is the interlocking finger test, where the patient is asked to copy the hand positions made by the clinician.

Dr. Ovsiew admitted that visuospatial function is nearly impossible to assess over the phone. Asking topographical questions (“If you’re driving from Chicago to Los Angeles, is the Pacific Ocean in front of you, behind you, to your left, or to your right?”) may help judge visuospatial function, but this relies on the patient having the topographic knowledge to answer the questions. Some patients who are topographically disoriented can’t do them at all,” Dr. Ovsiew said.

Bedside neuropsychiatry assesses encoding of a memory, its retention and its retrieval as well as verbal and visual cues. Each one of these aspects of memory can be impaired on its own and should be explored separately, Dr. Ovsiew explained. “Neuropsychiatric clinicians have a rough-and-ready, seat-of-the-pants way of approaching this that wouldn’t pass muster if you’re a psychologist, but is the best we can do at the bedside.”

To test retrieval and retention, the Three Words–Three Shapes test works well in person, with some difficulty by video, and is not possible to administer over the phone. In lieu of that test, giving the patient a simple word list and asking them to repeat the list in order. Using the word list, “these different stages of memory function can be parsed out pretty well at the bedside or chairside, and even by the phone. Figuring out where the memory failure is diagnostically important,” Dr. Ovsiew said.

Executive function, which involves activation, planning, sequencing, maintaining, self-monitoring, and flexible employment of action and attention, is “complicated to evaluate because there are multiple aspects of executive function, multiple deficits that can be seen with executive dysfunction, and they don’t all correlate with each other.”

Within executive function evaluation, the Mental Alternation Test can assess working memory, motor sequencing can be assessed through the ring/fist, fist/edge/palm, alternating fist, and rampart tests. The Go/No-Go test can be used to assess response inhibition. For effortful retrieval evaluation, spontaneous word-list generation – such as thinking of all the items one can buy at a supermarket– can test category fluency, while a task to name all the words starting with a certain letter can assess letter stimulus.

Executive function “is of crucial importance in the neuropsychiatric evaluation because it’s strongly correlated with how well the person functions outside the office,” Dr. Ovsiew said.

Global Academy and this news organization are owned by the same parent company. Dr. Ovsiew reported relationships with Wolters Kluwer Health in the form of consulting, receiving royalty payments, and related activities.

Patients have often been labeled as “poor historians” if they are not able to recollect their own medical history, whether through illness or difficulties in communication. But Fred Ovsiew, MD, speaking at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists, sees that label as an excuse on the part of the clinician.

“I strongly advise you to drop that phrase from your vocabulary if you do use it, because the patient is not the historian. The doctor, the clinician is the historian,” Dr. Ovsiew said at the meeting, presented by Global Academy for Medical Education. “It is the clinician’s job to put the story together using the account by the patient as one source, but [also] interviewing a collateral informant and/or reviewing records, which is necessary in almost every case of a neuropsychiatric illness.”

Rather, clinicians taking history at the bedside should focus on why the patients cannot give a narrative account of their illness. Patients can have narrative incapacity on a psychogenic basis, such as in patients with conversion or somatoform disorder, he explained. “I think this is a result of the narrative incapacity that develops in people who have had trauma or adverse experiences in childhood and insecure attachment. This is shown on the adult attachment interview as a disorganized account of their childhoods.”

Other patients might not be able to recount their medical history because they are amnestic, which leaves their account vague because of a lack of access to information. “It may be frozen in time in the sense that, up to a certain point in their life, they can recount the history,” Dr. Ovsiew said. “But in recent years, their account becomes vague.”

Patients with right hemisphere lesions might not know that their account has incongruity and is implausible, while patients with dorsolateral prefrontal lesions might be aspontaneous, use few words to describe their situation, and have poor insight. Those with ventromedial prefrontal lesions can be impulsive and have poor insight, not considering alternative possibilities, Dr. Ovsiew noted.

Asking open-ended questions of the patient is the first step to identifying any potential narrative incapacity, followed by a detailed medical history by the clinician. When taking a medical history, try avoiding what Dr. Ovsiew calls the “anything like that?” problem, where a clinician asks a question about a cluster of symptoms that would make sense to a doctor, but not a patient. For example, a doctor might ask whether a patient is experiencing “chest pain or leg swelling – anything like that?” because he or she knows what those symptoms have in common, but the patient might not know the relationship between those symptoms. “You can’t count on the patient to tell you all the relevant information,” he said. “You have to know what to ask about.”

“Patients with brain disease have subtle personality changes, sometimes more obvious personality changes. These need to be inquired about,” Dr. Ovsiew said. He encouraged asking “non-DSM questions” to help identify specific symptoms of a neuropsychiatric illness. “The patient with apathy has reduced negative as well as positive emotions. The patient with depression has reduced positive emotions, but often tells you very clearly about the negative emotions of sadness, guilt. The patient with depression has diurnal variation in mood, a very telling symptom, especially when it’s disclosed spontaneously,” Dr. Ovsiew explained. “The point is, you need to know to ask about it.”

When taking a sleep history, clinicians should be aware of sleep disturbances apart from insomnia and early waking. REM sleep behavior disorder is a condition that should be inquired about. Obstructive sleep apnea is a condition that might not be immediately apparent to the patient, but a bed partner can identify whether a patient has problems breathing throughout the night.

“This is an important condition to uncover for the neuropsychiatrist because it contributes to treatment resistance and depression, and it contributes to cognitive impairment,” Dr. Ovsiew said. “These patients commonly have mild difficulties with attention and concentration.”

Always ask about head injury in every history, which can be relevant to later onset depression, PTSD, and cognitive impairment. Every head injury follows a trajectory of retrograde amnesia and altered state of consciousness (including coma), followed by a period of posttraumatic amnesia. Duration of these states can be used to assess the severity of brain injury, but the 15-point Glasgow Coma Scale is another way to assess injury severity, Dr. Ovsiew explained.

However, the two do not always overlap, he noted. “Someone may have a Glasgow Coma Scale score that is 9-12, predicting moderate brain injury, but they may have a short duration of amnesia. These don’t always follow the same path. There are many different ways of classifying how severe the brain injury is.”
 

Keep probes brief, straightforward

Cognitive exams of patients with suspected psychiatric disorders should be simple, easy to administer and focused on a single domain of cognition. “Probes should be brief. They should not require specialized equipment. The Purdue Pegboard Test might be a great neuropsychological instrument, but very few of us carry a pegboard around in our medical bags,” Dr. Ovsiew said.

The probe administered should also be accessible to the patient. The serial sevens clinical test, where a patient is asked to repeatedly subtract 7 from 100, is only effective at testing concentration if the patient is capable of completing the test. “There are going to be patients who can’t do the task, but it’s not because of concentration failure, it’s because of subtraction failure,” he said.

When assessing attention, effective tasks include having the patient perform the digit span test forward and backward, count backward from 20 to 1, listing the months of the year in reverse, and performing the Mental Alternation Test. However, Dr. Ovsiew explained there may be some barriers for patients in completing these tasks. “The person may be aphasic and not know the alphabet. The person may have English as a second language and not be skilled at giving the alphabet in English. In some cases, you may want to check and not assume that the patient can count and does know the alphabet.”

In assessing language, listen for aphasic abnormalities. “The patient, of course, is speaking throughout the interview, but you need to take a moment to listen for prosody, to listen to rate of speech, to listen for paraphasic errors or word-finding problems,” Dr. Ovsiew said. Any abnormalities should be probed further through confrontation naming tasks, which can be done in person and with some success through video, but not by phone. Naming to definition (“What do you call the part of a shirt that covers the arm?”) is one way of administering the test over the phone.

Visuospatial function can be assessed by clock drawing but also carries problems. Patients who do not plan their clock before beginning to draw, for example, may have an executive function problem instead of a visuospatial problem, Dr. Ovsiew noted. Patients in whom a clinician suspects hemineglect should be given a visual search task or line by section task. “I like doing clock drawing. It’s a nice screening test. It’s becoming, I think, less useful as people count on digital clocks and have trouble even imagining what an analog clock looks like.”

An approach that is better suited to in-person assessment, but also works by video, is the Poppelreuter figure visual perceptual function test, which is a prompt for the patient that involves common household items overlaying one another “in atypical positions and atypical configurations” where the patient is instructed to describe the items they see on the card. Another approach that works over video is the interlocking finger test, where the patient is asked to copy the hand positions made by the clinician.

Dr. Ovsiew admitted that visuospatial function is nearly impossible to assess over the phone. Asking topographical questions (“If you’re driving from Chicago to Los Angeles, is the Pacific Ocean in front of you, behind you, to your left, or to your right?”) may help judge visuospatial function, but this relies on the patient having the topographic knowledge to answer the questions. Some patients who are topographically disoriented can’t do them at all,” Dr. Ovsiew said.

Bedside neuropsychiatry assesses encoding of a memory, its retention and its retrieval as well as verbal and visual cues. Each one of these aspects of memory can be impaired on its own and should be explored separately, Dr. Ovsiew explained. “Neuropsychiatric clinicians have a rough-and-ready, seat-of-the-pants way of approaching this that wouldn’t pass muster if you’re a psychologist, but is the best we can do at the bedside.”

To test retrieval and retention, the Three Words–Three Shapes test works well in person, with some difficulty by video, and is not possible to administer over the phone. In lieu of that test, giving the patient a simple word list and asking them to repeat the list in order. Using the word list, “these different stages of memory function can be parsed out pretty well at the bedside or chairside, and even by the phone. Figuring out where the memory failure is diagnostically important,” Dr. Ovsiew said.

Executive function, which involves activation, planning, sequencing, maintaining, self-monitoring, and flexible employment of action and attention, is “complicated to evaluate because there are multiple aspects of executive function, multiple deficits that can be seen with executive dysfunction, and they don’t all correlate with each other.”

Within executive function evaluation, the Mental Alternation Test can assess working memory, motor sequencing can be assessed through the ring/fist, fist/edge/palm, alternating fist, and rampart tests. The Go/No-Go test can be used to assess response inhibition. For effortful retrieval evaluation, spontaneous word-list generation – such as thinking of all the items one can buy at a supermarket– can test category fluency, while a task to name all the words starting with a certain letter can assess letter stimulus.

Executive function “is of crucial importance in the neuropsychiatric evaluation because it’s strongly correlated with how well the person functions outside the office,” Dr. Ovsiew said.

Global Academy and this news organization are owned by the same parent company. Dr. Ovsiew reported relationships with Wolters Kluwer Health in the form of consulting, receiving royalty payments, and related activities.

Among migraine sufferers, levels of soluble vascular cell adhesion molecule 1 (sVCAM1) in cerebrospinal fluid (CSF) are higher in those who experience more frequent attacks, according to a new study. The molecule could be a novel biomarker for the study of the mechanisms that underlie migraine. The work also suggests that the barrier between blood and CSF, sometimes described as leaky, is in fact selectively permeable.

The findings complement recent PET and dynamic contrast-enhanced MRI studies that have shown no sign of damage to the blood brain barrier (BBB) in migraine. Instead, there may be heightened transport of some molecules from blood to the CSF, evidenced by greater increases in fibrinogen levels in CSF than albumin. sVCAM1 might influence BBB or blood-CSF barrier permeability, possibly as a protective measure against fibrinogen, according to Michael Harrington, MD, scientific director of neuroscience at the Huntington Medical Research Institutes, Pasadena, Calif., who presented the findings in a poster at the virtual annual meeting of the American Headache Society.
 

BBB disruption?

The BBB is a well-known structure that regulates what molecules enter the brain, but the blood-CSF barrier, while lesser known, is also important. It comprises choroid plexus epithelial cells that oversee selective exchange of waste products, ions, and nutrients. Acute inflammation or chronic effects from conditions like stroke, multiple sclerosis, and Alzheimer’s disease can alter the function of this barrier.

No other capillary biomarkers were different between controls and patients with migraine – only sVCAM1. “My data supports a highly selective transport change from blood to CSF, which I propose is less likely to come from brain capillaries than choroid plexuses, especially since choroid plexuses produce the bulk of the CSF. It’s a work in progress, but based on this likelihood of choroid plexus involvement, I am accumulating more data that support the choroid plexuses as the primary source of change in migraine,” said Dr. Harrington in an interview.

“The most important finding of the study is that the blood brain barrier is not compromised in people with migraine,” said Rami Burstein, PhD, professor of neuroscience at Harvard Medical School, Boston, who was asked to comment on the findings. “Most unwanted adverse events are caused by drug action inside the brain, and thus, peripherally acting drugs become more favorable as they usually have fewer side effects. Given that the headache aspect of migraine could be intercepted outside the brain, the fact that the BBB is not compromised is a very good news,” Dr. Burstein added.

Dr. Harrington’s team recruited 74 subjects: 14 nonmigraine controls, 16 who were experiencing migraine illness (ictal), 27 not experiencing migraine illness (interictal), and 17 with chronic migraine. The CSF/serum quotient for albumen was higher in the 60 migraineurs than in the 14 controls (5.6 g/L vs. 4.1 g/L; P = .04), as was the CSF/serum quotient for fibrinogen (161.5 g/L vs. 86.1 g/L; P = .007). CSF levels of plasminogen were also higher in patients with migraine (240.7 ng/mL vs. 186.2 ng/mL; P = .03).

When the researchers compared ictal to interictal subjects, they found no difference in fibrinogen or albumen. That suggested that these values are generally increased in migraine patients compared with controls, rather than spiking during attacks. They also divided subjects by annual frequency, including groups experiencing fewer than 24 migraines per year, 24-180 attacks per year, and more than 180 attacks per year. The quotient for fibrinogen increased in migraineurs in general, compared with controls, but then decreased as the frequency of migraine went up (198.6 g/L, 167.0 g/L, and 121.6 g/L, respectively; P = .004).

CSF levels of sVCAM1 were 4.7 ng/mL in controls, 4.5 in the group with fewer than 24 migraines per year, 5.5 in the 24-180 group, and 7.1 in the group with more than 180 (P = .004).
 

Implications for therapy

The research, though at a very early stage, could have implications for therapies. Most drugs that treat migraine remain something of a mystery because researchers don’t know for sure where they act. In the brain? Systemically? The question of permeability of various molecules through both barriers could lend insight into what’s happening. “That’s why there is interest in barrier transport, and we’re showing there is a selective change of transport in migraineurs,” said Dr. Harrington.

As for more general therapeutic implications, “I can only speculate, but clearly there is baseline altered transport, probably in the choroid plexuses of these people,” said Dr. Harrington. He added that in time researchers might test drugs to see if they alter sVCAM1 levels or even develop novel drug candidates to act directly on it.

But he also sounded a note of caution because of the exploratory nature of the study. “These are all really early speculations.”

The study was funded by NIH, the Sunstar Foundation, Wyngs Foundation, and the Higgins Family. Dr. Harrington has no relevant disclosures.

SOURCE: Harrington M et al. AHS 2020, Abstract 842752.

Among migraine sufferers, levels of soluble vascular cell adhesion molecule 1 (sVCAM1) in cerebrospinal fluid (CSF) are higher in those who experience more frequent attacks, according to a new study. The molecule could be a novel biomarker for the study of the mechanisms that underlie migraine. The work also suggests that the barrier between blood and CSF, sometimes described as leaky, is in fact selectively permeable.

The findings complement recent PET and dynamic contrast-enhanced MRI studies that have shown no sign of damage to the blood brain barrier (BBB) in migraine. Instead, there may be heightened transport of some molecules from blood to the CSF, evidenced by greater increases in fibrinogen levels in CSF than albumin. sVCAM1 might influence BBB or blood-CSF barrier permeability, possibly as a protective measure against fibrinogen, according to Michael Harrington, MD, scientific director of neuroscience at the Huntington Medical Research Institutes, Pasadena, Calif., who presented the findings in a poster at the virtual annual meeting of the American Headache Society.
 

BBB disruption?

The BBB is a well-known structure that regulates what molecules enter the brain, but the blood-CSF barrier, while lesser known, is also important. It comprises choroid plexus epithelial cells that oversee selective exchange of waste products, ions, and nutrients. Acute inflammation or chronic effects from conditions like stroke, multiple sclerosis, and Alzheimer’s disease can alter the function of this barrier.

No other capillary biomarkers were different between controls and patients with migraine – only sVCAM1. “My data supports a highly selective transport change from blood to CSF, which I propose is less likely to come from brain capillaries than choroid plexuses, especially since choroid plexuses produce the bulk of the CSF. It’s a work in progress, but based on this likelihood of choroid plexus involvement, I am accumulating more data that support the choroid plexuses as the primary source of change in migraine,” said Dr. Harrington in an interview.

“The most important finding of the study is that the blood brain barrier is not compromised in people with migraine,” said Rami Burstein, PhD, professor of neuroscience at Harvard Medical School, Boston, who was asked to comment on the findings. “Most unwanted adverse events are caused by drug action inside the brain, and thus, peripherally acting drugs become more favorable as they usually have fewer side effects. Given that the headache aspect of migraine could be intercepted outside the brain, the fact that the BBB is not compromised is a very good news,” Dr. Burstein added.

Dr. Harrington’s team recruited 74 subjects: 14 nonmigraine controls, 16 who were experiencing migraine illness (ictal), 27 not experiencing migraine illness (interictal), and 17 with chronic migraine. The CSF/serum quotient for albumen was higher in the 60 migraineurs than in the 14 controls (5.6 g/L vs. 4.1 g/L; P = .04), as was the CSF/serum quotient for fibrinogen (161.5 g/L vs. 86.1 g/L; P = .007). CSF levels of plasminogen were also higher in patients with migraine (240.7 ng/mL vs. 186.2 ng/mL; P = .03).

When the researchers compared ictal to interictal subjects, they found no difference in fibrinogen or albumen. That suggested that these values are generally increased in migraine patients compared with controls, rather than spiking during attacks. They also divided subjects by annual frequency, including groups experiencing fewer than 24 migraines per year, 24-180 attacks per year, and more than 180 attacks per year. The quotient for fibrinogen increased in migraineurs in general, compared with controls, but then decreased as the frequency of migraine went up (198.6 g/L, 167.0 g/L, and 121.6 g/L, respectively; P = .004).

CSF levels of sVCAM1 were 4.7 ng/mL in controls, 4.5 in the group with fewer than 24 migraines per year, 5.5 in the 24-180 group, and 7.1 in the group with more than 180 (P = .004).
 

Implications for therapy

The research, though at a very early stage, could have implications for therapies. Most drugs that treat migraine remain something of a mystery because researchers don’t know for sure where they act. In the brain? Systemically? The question of permeability of various molecules through both barriers could lend insight into what’s happening. “That’s why there is interest in barrier transport, and we’re showing there is a selective change of transport in migraineurs,” said Dr. Harrington.

As for more general therapeutic implications, “I can only speculate, but clearly there is baseline altered transport, probably in the choroid plexuses of these people,” said Dr. Harrington. He added that in time researchers might test drugs to see if they alter sVCAM1 levels or even develop novel drug candidates to act directly on it.

But he also sounded a note of caution because of the exploratory nature of the study. “These are all really early speculations.”

The study was funded by NIH, the Sunstar Foundation, Wyngs Foundation, and the Higgins Family. Dr. Harrington has no relevant disclosures.

SOURCE: Harrington M et al. AHS 2020, Abstract 842752.

Among migraine sufferers, levels of soluble vascular cell adhesion molecule 1 (sVCAM1) in cerebrospinal fluid (CSF) are higher in those who experience more frequent attacks, according to a new study. The molecule could be a novel biomarker for the study of the mechanisms that underlie migraine. The work also suggests that the barrier between blood and CSF, sometimes described as leaky, is in fact selectively permeable.

The findings complement recent PET and dynamic contrast-enhanced MRI studies that have shown no sign of damage to the blood brain barrier (BBB) in migraine. Instead, there may be heightened transport of some molecules from blood to the CSF, evidenced by greater increases in fibrinogen levels in CSF than albumin. sVCAM1 might influence BBB or blood-CSF barrier permeability, possibly as a protective measure against fibrinogen, according to Michael Harrington, MD, scientific director of neuroscience at the Huntington Medical Research Institutes, Pasadena, Calif., who presented the findings in a poster at the virtual annual meeting of the American Headache Society.
 

BBB disruption?

The BBB is a well-known structure that regulates what molecules enter the brain, but the blood-CSF barrier, while lesser known, is also important. It comprises choroid plexus epithelial cells that oversee selective exchange of waste products, ions, and nutrients. Acute inflammation or chronic effects from conditions like stroke, multiple sclerosis, and Alzheimer’s disease can alter the function of this barrier.

No other capillary biomarkers were different between controls and patients with migraine – only sVCAM1. “My data supports a highly selective transport change from blood to CSF, which I propose is less likely to come from brain capillaries than choroid plexuses, especially since choroid plexuses produce the bulk of the CSF. It’s a work in progress, but based on this likelihood of choroid plexus involvement, I am accumulating more data that support the choroid plexuses as the primary source of change in migraine,” said Dr. Harrington in an interview.

“The most important finding of the study is that the blood brain barrier is not compromised in people with migraine,” said Rami Burstein, PhD, professor of neuroscience at Harvard Medical School, Boston, who was asked to comment on the findings. “Most unwanted adverse events are caused by drug action inside the brain, and thus, peripherally acting drugs become more favorable as they usually have fewer side effects. Given that the headache aspect of migraine could be intercepted outside the brain, the fact that the BBB is not compromised is a very good news,” Dr. Burstein added.

Dr. Harrington’s team recruited 74 subjects: 14 nonmigraine controls, 16 who were experiencing migraine illness (ictal), 27 not experiencing migraine illness (interictal), and 17 with chronic migraine. The CSF/serum quotient for albumen was higher in the 60 migraineurs than in the 14 controls (5.6 g/L vs. 4.1 g/L; P = .04), as was the CSF/serum quotient for fibrinogen (161.5 g/L vs. 86.1 g/L; P = .007). CSF levels of plasminogen were also higher in patients with migraine (240.7 ng/mL vs. 186.2 ng/mL; P = .03).

When the researchers compared ictal to interictal subjects, they found no difference in fibrinogen or albumen. That suggested that these values are generally increased in migraine patients compared with controls, rather than spiking during attacks. They also divided subjects by annual frequency, including groups experiencing fewer than 24 migraines per year, 24-180 attacks per year, and more than 180 attacks per year. The quotient for fibrinogen increased in migraineurs in general, compared with controls, but then decreased as the frequency of migraine went up (198.6 g/L, 167.0 g/L, and 121.6 g/L, respectively; P = .004).

CSF levels of sVCAM1 were 4.7 ng/mL in controls, 4.5 in the group with fewer than 24 migraines per year, 5.5 in the 24-180 group, and 7.1 in the group with more than 180 (P = .004).
 

Implications for therapy

The research, though at a very early stage, could have implications for therapies. Most drugs that treat migraine remain something of a mystery because researchers don’t know for sure where they act. In the brain? Systemically? The question of permeability of various molecules through both barriers could lend insight into what’s happening. “That’s why there is interest in barrier transport, and we’re showing there is a selective change of transport in migraineurs,” said Dr. Harrington.

As for more general therapeutic implications, “I can only speculate, but clearly there is baseline altered transport, probably in the choroid plexuses of these people,” said Dr. Harrington. He added that in time researchers might test drugs to see if they alter sVCAM1 levels or even develop novel drug candidates to act directly on it.

But he also sounded a note of caution because of the exploratory nature of the study. “These are all really early speculations.”

The study was funded by NIH, the Sunstar Foundation, Wyngs Foundation, and the Higgins Family. Dr. Harrington has no relevant disclosures.

SOURCE: Harrington M et al. AHS 2020, Abstract 842752.

Hydrochlorothiazide (HCTZ) is associated with an increased risk of nonmelanoma skin cancer, and patients who take the drug should limit sun exposure and undergo regular skin cancer screening, according to updates to the medication’s label.

The skin cancer risk is small, however, and patients should continue taking HCTZ, a commonly used diuretic and antihypertensive drug, unless their doctor says otherwise, according to a U.S. Food and Drug Administration announcement about the labeling changes, which the agency approved on Aug. 20.

HCTZ, first approved in 1959, is associated with photosensitivity. Researchers identified a relationship between HCTZ and nonmelanoma skin cancer in postmarketing studies. Investigators have described dose-response patterns for basal cell carcinoma and squamous cell carcinoma (SCC).

An FDA analysis found that the risk mostly was increased for SCC. The drug was associated with approximately one additional case of SCC per 16,000 patients per year. For white patients who received a cumulative dose of 50,000 mg or more, the risk was greater. In this patient population, HCTZ was associated with about one additional case of SCC per 6,700 patients per year, according to the label.

Reliably estimating the frequency of nonmelanoma skin cancer and establishing a causal relationship to drug exposure is not possible with the available postmarketing data, the label notes

“Treatment for nonmelanoma skin cancer is typically local and successful, with very low rates of death,” the FDA said. “Meanwhile, the risks of uncontrolled blood pressure can be severe and include life-threatening heart attacks or stroke. Given this information, patients should continue to use HCTZ and take protective skin care measures to reduce their risk of nonmelanoma skin cancer, unless directed otherwise from their health care provider.”

Patients can reduce sun exposure by using broad-spectrum sunscreens with a sun protection factor value of at least 15, limiting time in the sun, and wearing protective clothing, the agency advised.

[email protected]

Hydrochlorothiazide (HCTZ) is associated with an increased risk of nonmelanoma skin cancer, and patients who take the drug should limit sun exposure and undergo regular skin cancer screening, according to updates to the medication’s label.

The skin cancer risk is small, however, and patients should continue taking HCTZ, a commonly used diuretic and antihypertensive drug, unless their doctor says otherwise, according to a U.S. Food and Drug Administration announcement about the labeling changes, which the agency approved on Aug. 20.

HCTZ, first approved in 1959, is associated with photosensitivity. Researchers identified a relationship between HCTZ and nonmelanoma skin cancer in postmarketing studies. Investigators have described dose-response patterns for basal cell carcinoma and squamous cell carcinoma (SCC).

An FDA analysis found that the risk mostly was increased for SCC. The drug was associated with approximately one additional case of SCC per 16,000 patients per year. For white patients who received a cumulative dose of 50,000 mg or more, the risk was greater. In this patient population, HCTZ was associated with about one additional case of SCC per 6,700 patients per year, according to the label.

Reliably estimating the frequency of nonmelanoma skin cancer and establishing a causal relationship to drug exposure is not possible with the available postmarketing data, the label notes

“Treatment for nonmelanoma skin cancer is typically local and successful, with very low rates of death,” the FDA said. “Meanwhile, the risks of uncontrolled blood pressure can be severe and include life-threatening heart attacks or stroke. Given this information, patients should continue to use HCTZ and take protective skin care measures to reduce their risk of nonmelanoma skin cancer, unless directed otherwise from their health care provider.”

Patients can reduce sun exposure by using broad-spectrum sunscreens with a sun protection factor value of at least 15, limiting time in the sun, and wearing protective clothing, the agency advised.

[email protected]

Hydrochlorothiazide (HCTZ) is associated with an increased risk of nonmelanoma skin cancer, and patients who take the drug should limit sun exposure and undergo regular skin cancer screening, according to updates to the medication’s label.

The skin cancer risk is small, however, and patients should continue taking HCTZ, a commonly used diuretic and antihypertensive drug, unless their doctor says otherwise, according to a U.S. Food and Drug Administration announcement about the labeling changes, which the agency approved on Aug. 20.

HCTZ, first approved in 1959, is associated with photosensitivity. Researchers identified a relationship between HCTZ and nonmelanoma skin cancer in postmarketing studies. Investigators have described dose-response patterns for basal cell carcinoma and squamous cell carcinoma (SCC).

An FDA analysis found that the risk mostly was increased for SCC. The drug was associated with approximately one additional case of SCC per 16,000 patients per year. For white patients who received a cumulative dose of 50,000 mg or more, the risk was greater. In this patient population, HCTZ was associated with about one additional case of SCC per 6,700 patients per year, according to the label.

Reliably estimating the frequency of nonmelanoma skin cancer and establishing a causal relationship to drug exposure is not possible with the available postmarketing data, the label notes

“Treatment for nonmelanoma skin cancer is typically local and successful, with very low rates of death,” the FDA said. “Meanwhile, the risks of uncontrolled blood pressure can be severe and include life-threatening heart attacks or stroke. Given this information, patients should continue to use HCTZ and take protective skin care measures to reduce their risk of nonmelanoma skin cancer, unless directed otherwise from their health care provider.”

Patients can reduce sun exposure by using broad-spectrum sunscreens with a sun protection factor value of at least 15, limiting time in the sun, and wearing protective clothing, the agency advised.

[email protected]