Clinical Psychiatry News

Most patients will not make a full recovery from attention-deficit/hyperactivity disorder in adulthood. This late-breaking finding headlined the World Congress on ADHD – Virtual Event. Held under the specter of SARS-CoV-2, the virtual program delved into the latest research on ADHD pathophysiology, imaging, genetics, and issues on medical and psychiatric comorbidities.

However, one of the conference’s highlights was a piece of unpublished work on remission patterns by Margaret Sibley, PhD, associate professor of psychiatry and behavioral sciences at the University of Washington, Seattle.

Anywhere from 65% to 67% of young adults have desistant ADHD – meaning that they no longer meet criteria. Only up to 23% experience full remission, said Dr. Sibley during a special late-breaking session. All research on remission and most on persistence consider just one endpoint – nothing is known about longitudinal fluctuations in remission status over time.

Her research sought to answer a key question: Do people fully recover from ADHD?

Using data from the Multimodal Treatment of Attention Deficit Hyperactivity Disorder (MTA) Study, Dr. Sibley prospectively followed over 550 children aged 7-9.9 years with DSM-IV combined-type ADHD over 14 years, until 16 years after baseline, using interviews, questionnaires, and rating scales to track symptoms, impairment, and treatment history.

The researchers also came up with a “winning” definition for full remission, which included three or fewer symptoms of inattention and hyperactive impulsivity from all available reporters, negligible ADHD-related impairment based on preestablished impairment rating thresholds, and discontinuation of medication and behavioral treatments for at least a month prior to assessment.

In the longitudinal results, Dr. Sibley and colleagues reported that the majority (63.8%) demonstrated fluctuations between full or partial remission and ADHD recurrence. Only 9.1% sustained full remission over the course of the study. From these findings, ADHD appears to be a fluctuating disorder. While it continues into adulthood for most people, there may also be periods of remission or “good functioning.”

Most desistance from ADHD represents partial, not full remission, said Dr. Sibley. The results also show that recovery by young adulthood is very rare – most patients with remitted ADHD have recurrences.

These are important findings, said Luis Augusto Rohde, MD, PhD, who co-organized the congress’ scientific program committee with Manfred Gerlach, PhD. It shows that a patient’s ADHD may sometimes be more definitive and at other times, no clear phenotype expression emerges.

COVID’s influence

COVID-19 greatly influenced this year’s program’s agenda, said Dr. Rohde. “There’s a lot of evidence that ADHD patients are at greater risk for COVID-19, which is not a surprise,” said Dr. Rohde, professor of child and adolescent psychiatry at the Federal University of Rio Grande do Sul’s department of psychiatry in Porto Alegre, Brazil.

ADHD is a combination of genetic liability and the demands of the environment. “In times like we are living in right now, if you have increasing demands and stress from the environment, you trigger symptoms in those even with lower genetic liability,” he said. ADHD’s pathophysiology involves attention and executive deficit disorder, which means these patients may not follow strategies to avoid infection.

This shows why COVID was so important to the discussion of program topics, he said.

Two experts addressed this subject head on in a point-counterpoint debate, “Residual effects of the 2019 pandemic will mirror the 1918 pandemic: Will we have lots of new ADHD cases?” James Swanson, PhD, professor of pediatrics at the University of California, Irvine, projected that biological coeffects of COVID-19 will lead to ADHD symptoms, generating potentially 5 million new ADHD cases.

David Coghill, MBChB, MD, a professor of child adolescent mental health at the University of Melbourne, countered that not enough data are available yet to back this hypothesis. “Researchers are asking this question, but clinically we don’t know enough.”

While the COVID virus might not directly lead to more cases of ADHD, this could potentially happen indirectly through environmental agents of the pandemic, offered Dr. Rohde. “We’ve clearly seen in our appointments with families and children that they can’t face the amount of schooling and working from home,” he said.

 

Novel treatments

The conference also addressed new treatments and nonpharmacologic interventions in the pipeline for ADHD. “We had a chance to discuss the possibilities about new medications that address the problems in the current market and to show the potential usefulness of nonpharma interventions such as neuromodulations in ADHD,” said Dr. Rohde. Speakers discussed strategies ranging from family-based mindfulness interventions to oligoantigenic diets in children with ADHD.

Other researchers are looking at novel digital tools to help patients manage and treat ADHD. Adherence is a major problem in chronic disorders like hypertension, diabetes, epilepsy, and ADHD, said Dr. Rohde. “Due to ADHD symptomatology including inattention, novelty-seeking, executive deficits, and difficulties in persistence, it is an even bigger problem in this disorder.”

Speakers at the “ADHD in the digital age – From pitfalls to challenges” session discussed video game strategies to reduce ADHD impairment, and a texting app to improve adherence. Dr. Rohde talked about the FOCUS app, which fosters collaboration between patients, families, and caregivers to efficiently track ADHD symptoms and help customize treatments.

Studies suggest these tools can significantly improve adherence. They’re also well accepted by patients, said Dr. Rohde. While the expectations are high, digital interventions are not a substitute for medication. “More data is needed to include them as part of the clinical interventions for ADHD.”

Dr. Sibley received book royalties from Guilford Press. Dr. Rohde has received grant or research support from, served as a consultant to, and served on the speakers’ bureau of Bial, Medice, Novartis/Sandoz, Pfizer, and Shire/Takeda in the last 3 years. The ADHD and Juvenile Bipolar Disorder Outpatient Programs chaired by Dr. Rohde have received unrestricted educational and research support from the following pharmaceutical companies in the last 3 years: Novartis/Sandoz and Shire/Takeda. Dr. Rohde has received authorship royalties from Oxford Press and ArtMed and travel grants from Shire to take part in the 2018 APA annual meeting. Dr. Swanson has two patents: (PIXA4), which uses a “time-of-flight” camera to measure growth of infants, and a provisional patent on the mechanism of tolerance to stimulant medication (PATSMTA). He has received travel support from Medice and has done legal review for NLS. Dr. Coghill worked for several pharmaceutical companies but had no disclosures relevant to the session debate on the pandemic.

Most patients will not make a full recovery from attention-deficit/hyperactivity disorder in adulthood. This late-breaking finding headlined the World Congress on ADHD – Virtual Event. Held under the specter of SARS-CoV-2, the virtual program delved into the latest research on ADHD pathophysiology, imaging, genetics, and issues on medical and psychiatric comorbidities.

However, one of the conference’s highlights was a piece of unpublished work on remission patterns by Margaret Sibley, PhD, associate professor of psychiatry and behavioral sciences at the University of Washington, Seattle.

Anywhere from 65% to 67% of young adults have desistant ADHD – meaning that they no longer meet criteria. Only up to 23% experience full remission, said Dr. Sibley during a special late-breaking session. All research on remission and most on persistence consider just one endpoint – nothing is known about longitudinal fluctuations in remission status over time.

Her research sought to answer a key question: Do people fully recover from ADHD?

Using data from the Multimodal Treatment of Attention Deficit Hyperactivity Disorder (MTA) Study, Dr. Sibley prospectively followed over 550 children aged 7-9.9 years with DSM-IV combined-type ADHD over 14 years, until 16 years after baseline, using interviews, questionnaires, and rating scales to track symptoms, impairment, and treatment history.

The researchers also came up with a “winning” definition for full remission, which included three or fewer symptoms of inattention and hyperactive impulsivity from all available reporters, negligible ADHD-related impairment based on preestablished impairment rating thresholds, and discontinuation of medication and behavioral treatments for at least a month prior to assessment.

In the longitudinal results, Dr. Sibley and colleagues reported that the majority (63.8%) demonstrated fluctuations between full or partial remission and ADHD recurrence. Only 9.1% sustained full remission over the course of the study. From these findings, ADHD appears to be a fluctuating disorder. While it continues into adulthood for most people, there may also be periods of remission or “good functioning.”

Most desistance from ADHD represents partial, not full remission, said Dr. Sibley. The results also show that recovery by young adulthood is very rare – most patients with remitted ADHD have recurrences.

These are important findings, said Luis Augusto Rohde, MD, PhD, who co-organized the congress’ scientific program committee with Manfred Gerlach, PhD. It shows that a patient’s ADHD may sometimes be more definitive and at other times, no clear phenotype expression emerges.

COVID’s influence

COVID-19 greatly influenced this year’s program’s agenda, said Dr. Rohde. “There’s a lot of evidence that ADHD patients are at greater risk for COVID-19, which is not a surprise,” said Dr. Rohde, professor of child and adolescent psychiatry at the Federal University of Rio Grande do Sul’s department of psychiatry in Porto Alegre, Brazil.

ADHD is a combination of genetic liability and the demands of the environment. “In times like we are living in right now, if you have increasing demands and stress from the environment, you trigger symptoms in those even with lower genetic liability,” he said. ADHD’s pathophysiology involves attention and executive deficit disorder, which means these patients may not follow strategies to avoid infection.

This shows why COVID was so important to the discussion of program topics, he said.

Two experts addressed this subject head on in a point-counterpoint debate, “Residual effects of the 2019 pandemic will mirror the 1918 pandemic: Will we have lots of new ADHD cases?” James Swanson, PhD, professor of pediatrics at the University of California, Irvine, projected that biological coeffects of COVID-19 will lead to ADHD symptoms, generating potentially 5 million new ADHD cases.

David Coghill, MBChB, MD, a professor of child adolescent mental health at the University of Melbourne, countered that not enough data are available yet to back this hypothesis. “Researchers are asking this question, but clinically we don’t know enough.”

While the COVID virus might not directly lead to more cases of ADHD, this could potentially happen indirectly through environmental agents of the pandemic, offered Dr. Rohde. “We’ve clearly seen in our appointments with families and children that they can’t face the amount of schooling and working from home,” he said.

 

Novel treatments

The conference also addressed new treatments and nonpharmacologic interventions in the pipeline for ADHD. “We had a chance to discuss the possibilities about new medications that address the problems in the current market and to show the potential usefulness of nonpharma interventions such as neuromodulations in ADHD,” said Dr. Rohde. Speakers discussed strategies ranging from family-based mindfulness interventions to oligoantigenic diets in children with ADHD.

Other researchers are looking at novel digital tools to help patients manage and treat ADHD. Adherence is a major problem in chronic disorders like hypertension, diabetes, epilepsy, and ADHD, said Dr. Rohde. “Due to ADHD symptomatology including inattention, novelty-seeking, executive deficits, and difficulties in persistence, it is an even bigger problem in this disorder.”

Speakers at the “ADHD in the digital age – From pitfalls to challenges” session discussed video game strategies to reduce ADHD impairment, and a texting app to improve adherence. Dr. Rohde talked about the FOCUS app, which fosters collaboration between patients, families, and caregivers to efficiently track ADHD symptoms and help customize treatments.

Studies suggest these tools can significantly improve adherence. They’re also well accepted by patients, said Dr. Rohde. While the expectations are high, digital interventions are not a substitute for medication. “More data is needed to include them as part of the clinical interventions for ADHD.”

Dr. Sibley received book royalties from Guilford Press. Dr. Rohde has received grant or research support from, served as a consultant to, and served on the speakers’ bureau of Bial, Medice, Novartis/Sandoz, Pfizer, and Shire/Takeda in the last 3 years. The ADHD and Juvenile Bipolar Disorder Outpatient Programs chaired by Dr. Rohde have received unrestricted educational and research support from the following pharmaceutical companies in the last 3 years: Novartis/Sandoz and Shire/Takeda. Dr. Rohde has received authorship royalties from Oxford Press and ArtMed and travel grants from Shire to take part in the 2018 APA annual meeting. Dr. Swanson has two patents: (PIXA4), which uses a “time-of-flight” camera to measure growth of infants, and a provisional patent on the mechanism of tolerance to stimulant medication (PATSMTA). He has received travel support from Medice and has done legal review for NLS. Dr. Coghill worked for several pharmaceutical companies but had no disclosures relevant to the session debate on the pandemic.

Most patients will not make a full recovery from attention-deficit/hyperactivity disorder in adulthood. This late-breaking finding headlined the World Congress on ADHD – Virtual Event. Held under the specter of SARS-CoV-2, the virtual program delved into the latest research on ADHD pathophysiology, imaging, genetics, and issues on medical and psychiatric comorbidities.

However, one of the conference’s highlights was a piece of unpublished work on remission patterns by Margaret Sibley, PhD, associate professor of psychiatry and behavioral sciences at the University of Washington, Seattle.

Anywhere from 65% to 67% of young adults have desistant ADHD – meaning that they no longer meet criteria. Only up to 23% experience full remission, said Dr. Sibley during a special late-breaking session. All research on remission and most on persistence consider just one endpoint – nothing is known about longitudinal fluctuations in remission status over time.

Her research sought to answer a key question: Do people fully recover from ADHD?

Using data from the Multimodal Treatment of Attention Deficit Hyperactivity Disorder (MTA) Study, Dr. Sibley prospectively followed over 550 children aged 7-9.9 years with DSM-IV combined-type ADHD over 14 years, until 16 years after baseline, using interviews, questionnaires, and rating scales to track symptoms, impairment, and treatment history.

The researchers also came up with a “winning” definition for full remission, which included three or fewer symptoms of inattention and hyperactive impulsivity from all available reporters, negligible ADHD-related impairment based on preestablished impairment rating thresholds, and discontinuation of medication and behavioral treatments for at least a month prior to assessment.

In the longitudinal results, Dr. Sibley and colleagues reported that the majority (63.8%) demonstrated fluctuations between full or partial remission and ADHD recurrence. Only 9.1% sustained full remission over the course of the study. From these findings, ADHD appears to be a fluctuating disorder. While it continues into adulthood for most people, there may also be periods of remission or “good functioning.”

Most desistance from ADHD represents partial, not full remission, said Dr. Sibley. The results also show that recovery by young adulthood is very rare – most patients with remitted ADHD have recurrences.

These are important findings, said Luis Augusto Rohde, MD, PhD, who co-organized the congress’ scientific program committee with Manfred Gerlach, PhD. It shows that a patient’s ADHD may sometimes be more definitive and at other times, no clear phenotype expression emerges.

COVID’s influence

COVID-19 greatly influenced this year’s program’s agenda, said Dr. Rohde. “There’s a lot of evidence that ADHD patients are at greater risk for COVID-19, which is not a surprise,” said Dr. Rohde, professor of child and adolescent psychiatry at the Federal University of Rio Grande do Sul’s department of psychiatry in Porto Alegre, Brazil.

ADHD is a combination of genetic liability and the demands of the environment. “In times like we are living in right now, if you have increasing demands and stress from the environment, you trigger symptoms in those even with lower genetic liability,” he said. ADHD’s pathophysiology involves attention and executive deficit disorder, which means these patients may not follow strategies to avoid infection.

This shows why COVID was so important to the discussion of program topics, he said.

Two experts addressed this subject head on in a point-counterpoint debate, “Residual effects of the 2019 pandemic will mirror the 1918 pandemic: Will we have lots of new ADHD cases?” James Swanson, PhD, professor of pediatrics at the University of California, Irvine, projected that biological coeffects of COVID-19 will lead to ADHD symptoms, generating potentially 5 million new ADHD cases.

David Coghill, MBChB, MD, a professor of child adolescent mental health at the University of Melbourne, countered that not enough data are available yet to back this hypothesis. “Researchers are asking this question, but clinically we don’t know enough.”

While the COVID virus might not directly lead to more cases of ADHD, this could potentially happen indirectly through environmental agents of the pandemic, offered Dr. Rohde. “We’ve clearly seen in our appointments with families and children that they can’t face the amount of schooling and working from home,” he said.

 

Novel treatments

The conference also addressed new treatments and nonpharmacologic interventions in the pipeline for ADHD. “We had a chance to discuss the possibilities about new medications that address the problems in the current market and to show the potential usefulness of nonpharma interventions such as neuromodulations in ADHD,” said Dr. Rohde. Speakers discussed strategies ranging from family-based mindfulness interventions to oligoantigenic diets in children with ADHD.

Other researchers are looking at novel digital tools to help patients manage and treat ADHD. Adherence is a major problem in chronic disorders like hypertension, diabetes, epilepsy, and ADHD, said Dr. Rohde. “Due to ADHD symptomatology including inattention, novelty-seeking, executive deficits, and difficulties in persistence, it is an even bigger problem in this disorder.”

Speakers at the “ADHD in the digital age – From pitfalls to challenges” session discussed video game strategies to reduce ADHD impairment, and a texting app to improve adherence. Dr. Rohde talked about the FOCUS app, which fosters collaboration between patients, families, and caregivers to efficiently track ADHD symptoms and help customize treatments.

Studies suggest these tools can significantly improve adherence. They’re also well accepted by patients, said Dr. Rohde. While the expectations are high, digital interventions are not a substitute for medication. “More data is needed to include them as part of the clinical interventions for ADHD.”

Dr. Sibley received book royalties from Guilford Press. Dr. Rohde has received grant or research support from, served as a consultant to, and served on the speakers’ bureau of Bial, Medice, Novartis/Sandoz, Pfizer, and Shire/Takeda in the last 3 years. The ADHD and Juvenile Bipolar Disorder Outpatient Programs chaired by Dr. Rohde have received unrestricted educational and research support from the following pharmaceutical companies in the last 3 years: Novartis/Sandoz and Shire/Takeda. Dr. Rohde has received authorship royalties from Oxford Press and ArtMed and travel grants from Shire to take part in the 2018 APA annual meeting. Dr. Swanson has two patents: (PIXA4), which uses a “time-of-flight” camera to measure growth of infants, and a provisional patent on the mechanism of tolerance to stimulant medication (PATSMTA). He has received travel support from Medice and has done legal review for NLS. Dr. Coghill worked for several pharmaceutical companies but had no disclosures relevant to the session debate on the pandemic.

The Biden administration is reversing a Trump-era policy that allowed health care providers to bar services to lesbian, gay, bisexual, transgender, or queer (LGBTQ) patients.

The U.S. Department of Health and Human Services gave notice on Monday that it would interpret the Affordable Care Act’s Section 1557 – which bars discrimination on the basis of sex – to include discrimination on the basis of sexual orientation or gender identity. The department said its position is consistent with a June 2020 U.S. Supreme Court ruling in Bostock v. Clayton County, GA. The ruling determined that the Civil Rights Act’s prohibition of employment discrimination on the basis of sex includes sexual orientation and gender identity.

“The mission of our Department is to enhance the health and well-being of all Americans, no matter their gender identity or sexual orientation,” said HHS Assistant Secretary for Health Rachel Levine, MD, in a statement released Monday.

“All people need access to health care services to fix a broken bone, protect their heart health, and screen for cancer risk,” she said. “No one should be discriminated against when seeking medical services because of who they are.”

Many physician organizations applauded the decision.

“The Biden administration did the right thing by terminating a short-lived effort to allow discrimination based on gender or sexual orientation when seeking health care,” said Susan R. Bailey, MD, president of the American Medical Association, in a statement.

When, in 2019, the Trump administration proposed to allow providers to deny care to LGBTQ people, the AMA said in a letter to the HHS that its interpretation “was contrary to the intent and the plain language of the law.”

Now, said Bailey, the AMA welcomes the Biden administration’s interpretation. It “is a victory for health equity and ends a dismal chapter in which a federal agency sought to remove civil rights protections,” she said.

An alliance of patient groups – including the American Cancer Society, the American Cancer Society Cancer Action Network, the American Heart Association, the American Lung Association, the Epilepsy Foundation, the National Multiple Sclerosis Society, and the National Organization for Rare Disorders – also applauded the new policy. “This community already faces significant health disparities,” the groups noted in a statement. People with chronic illness such as HIV and cancer “need to be able to access care quickly and without fear of discrimination,” they said.

The groups had filed a friend of the court brief in a case against the Trump administration rule.

“We welcome this positive step to ensure access is preserved without hindrance, as intended by the health care law,” they said.

Twenty-two states and Washington, D.C. – led by former California Attorney General Xavier Becerra, who is now HHS secretary – sued the Trump administration in July 2020, aiming to overturn the rule.

Chase Strangio, deputy director for Trans Justice with the American Civil Liberties Union LGBTQ & HIV Project, noted that the HHS announcement was crucial in the face of efforts in multiple states to bar health care for transgender youth. “The Biden administration has affirmed what courts have said for decades: Discrimination against LGBTQ people is against the law. It also affirms what transgender people have long said: Gender-affirming care is life-saving care,” he said in a statement.

Lambda Legal, which led another lawsuit against the Trump administration rule, said it welcomed the HHS action but noted in a statement by the organization’s senior attorney, Omar Gonzalez-Pagan, that it “does not address significant aspects of the Trump-era rule that we and others have challenged in court.”

The Trump rule also “limited the remedies available to people who face health disparities, limited access to health care for people with Limited English Proficiency, unlawfully incorporated religious exemptions, and dramatically reduced the number of health care entities and insurance subject to the rule, all of which today’s action does not address,” said Gonzalez-Pagan.

“We encourage Secretary Xavier Becerra and the Biden administration to take additional steps to ensure that all LGBTQ people are completely covered wherever and whenever they may encounter discrimination during some of the most delicate and precarious moments of their lives: When seeking health care,” he said.

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

The Biden administration is reversing a Trump-era policy that allowed health care providers to bar services to lesbian, gay, bisexual, transgender, or queer (LGBTQ) patients.

The U.S. Department of Health and Human Services gave notice on Monday that it would interpret the Affordable Care Act’s Section 1557 – which bars discrimination on the basis of sex – to include discrimination on the basis of sexual orientation or gender identity. The department said its position is consistent with a June 2020 U.S. Supreme Court ruling in Bostock v. Clayton County, GA. The ruling determined that the Civil Rights Act’s prohibition of employment discrimination on the basis of sex includes sexual orientation and gender identity.

“The mission of our Department is to enhance the health and well-being of all Americans, no matter their gender identity or sexual orientation,” said HHS Assistant Secretary for Health Rachel Levine, MD, in a statement released Monday.

“All people need access to health care services to fix a broken bone, protect their heart health, and screen for cancer risk,” she said. “No one should be discriminated against when seeking medical services because of who they are.”

Many physician organizations applauded the decision.

“The Biden administration did the right thing by terminating a short-lived effort to allow discrimination based on gender or sexual orientation when seeking health care,” said Susan R. Bailey, MD, president of the American Medical Association, in a statement.

When, in 2019, the Trump administration proposed to allow providers to deny care to LGBTQ people, the AMA said in a letter to the HHS that its interpretation “was contrary to the intent and the plain language of the law.”

Now, said Bailey, the AMA welcomes the Biden administration’s interpretation. It “is a victory for health equity and ends a dismal chapter in which a federal agency sought to remove civil rights protections,” she said.

An alliance of patient groups – including the American Cancer Society, the American Cancer Society Cancer Action Network, the American Heart Association, the American Lung Association, the Epilepsy Foundation, the National Multiple Sclerosis Society, and the National Organization for Rare Disorders – also applauded the new policy. “This community already faces significant health disparities,” the groups noted in a statement. People with chronic illness such as HIV and cancer “need to be able to access care quickly and without fear of discrimination,” they said.

The groups had filed a friend of the court brief in a case against the Trump administration rule.

“We welcome this positive step to ensure access is preserved without hindrance, as intended by the health care law,” they said.

Twenty-two states and Washington, D.C. – led by former California Attorney General Xavier Becerra, who is now HHS secretary – sued the Trump administration in July 2020, aiming to overturn the rule.

Chase Strangio, deputy director for Trans Justice with the American Civil Liberties Union LGBTQ & HIV Project, noted that the HHS announcement was crucial in the face of efforts in multiple states to bar health care for transgender youth. “The Biden administration has affirmed what courts have said for decades: Discrimination against LGBTQ people is against the law. It also affirms what transgender people have long said: Gender-affirming care is life-saving care,” he said in a statement.

Lambda Legal, which led another lawsuit against the Trump administration rule, said it welcomed the HHS action but noted in a statement by the organization’s senior attorney, Omar Gonzalez-Pagan, that it “does not address significant aspects of the Trump-era rule that we and others have challenged in court.”

The Trump rule also “limited the remedies available to people who face health disparities, limited access to health care for people with Limited English Proficiency, unlawfully incorporated religious exemptions, and dramatically reduced the number of health care entities and insurance subject to the rule, all of which today’s action does not address,” said Gonzalez-Pagan.

“We encourage Secretary Xavier Becerra and the Biden administration to take additional steps to ensure that all LGBTQ people are completely covered wherever and whenever they may encounter discrimination during some of the most delicate and precarious moments of their lives: When seeking health care,” he said.

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

The Biden administration is reversing a Trump-era policy that allowed health care providers to bar services to lesbian, gay, bisexual, transgender, or queer (LGBTQ) patients.

The U.S. Department of Health and Human Services gave notice on Monday that it would interpret the Affordable Care Act’s Section 1557 – which bars discrimination on the basis of sex – to include discrimination on the basis of sexual orientation or gender identity. The department said its position is consistent with a June 2020 U.S. Supreme Court ruling in Bostock v. Clayton County, GA. The ruling determined that the Civil Rights Act’s prohibition of employment discrimination on the basis of sex includes sexual orientation and gender identity.

“The mission of our Department is to enhance the health and well-being of all Americans, no matter their gender identity or sexual orientation,” said HHS Assistant Secretary for Health Rachel Levine, MD, in a statement released Monday.

“All people need access to health care services to fix a broken bone, protect their heart health, and screen for cancer risk,” she said. “No one should be discriminated against when seeking medical services because of who they are.”

Many physician organizations applauded the decision.

“The Biden administration did the right thing by terminating a short-lived effort to allow discrimination based on gender or sexual orientation when seeking health care,” said Susan R. Bailey, MD, president of the American Medical Association, in a statement.

When, in 2019, the Trump administration proposed to allow providers to deny care to LGBTQ people, the AMA said in a letter to the HHS that its interpretation “was contrary to the intent and the plain language of the law.”

Now, said Bailey, the AMA welcomes the Biden administration’s interpretation. It “is a victory for health equity and ends a dismal chapter in which a federal agency sought to remove civil rights protections,” she said.

An alliance of patient groups – including the American Cancer Society, the American Cancer Society Cancer Action Network, the American Heart Association, the American Lung Association, the Epilepsy Foundation, the National Multiple Sclerosis Society, and the National Organization for Rare Disorders – also applauded the new policy. “This community already faces significant health disparities,” the groups noted in a statement. People with chronic illness such as HIV and cancer “need to be able to access care quickly and without fear of discrimination,” they said.

The groups had filed a friend of the court brief in a case against the Trump administration rule.

“We welcome this positive step to ensure access is preserved without hindrance, as intended by the health care law,” they said.

Twenty-two states and Washington, D.C. – led by former California Attorney General Xavier Becerra, who is now HHS secretary – sued the Trump administration in July 2020, aiming to overturn the rule.

Chase Strangio, deputy director for Trans Justice with the American Civil Liberties Union LGBTQ & HIV Project, noted that the HHS announcement was crucial in the face of efforts in multiple states to bar health care for transgender youth. “The Biden administration has affirmed what courts have said for decades: Discrimination against LGBTQ people is against the law. It also affirms what transgender people have long said: Gender-affirming care is life-saving care,” he said in a statement.

Lambda Legal, which led another lawsuit against the Trump administration rule, said it welcomed the HHS action but noted in a statement by the organization’s senior attorney, Omar Gonzalez-Pagan, that it “does not address significant aspects of the Trump-era rule that we and others have challenged in court.”

The Trump rule also “limited the remedies available to people who face health disparities, limited access to health care for people with Limited English Proficiency, unlawfully incorporated religious exemptions, and dramatically reduced the number of health care entities and insurance subject to the rule, all of which today’s action does not address,” said Gonzalez-Pagan.

“We encourage Secretary Xavier Becerra and the Biden administration to take additional steps to ensure that all LGBTQ people are completely covered wherever and whenever they may encounter discrimination during some of the most delicate and precarious moments of their lives: When seeking health care,” he said.

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

Attention-deficit/hyperactivity disorder and autism spectrum disorder (ASD) often coexist in children and adults, but the range of cognitive abilities can vary widely in these patients. Researchers from around the world are leveraging symptom, cognitive assessment, and neurobiological measures to gain insights on how individuals with ADHD/ASD approach and solve problems.

Several experts discussed the progress of their research during the session, “Overlap and differences of ADHD and autism – new findings of functional imaging and cognition studies” at the World Congress on ADHD – Virtual Event.

“The overlap of these two disorders is a critical issue for our field,” said Sarah Karalunas, PhD, assistant professor of clinical psychology at Purdue University, West Lafayette, Ind., who moderated the session. Clinicians are often asked to make differential diagnoses between these two disorders. Only recently has the DSM-5 allowed their codiagnosis. “There’s increasing recognition that there may be shared cognitive and physiological features that reflect their shared risk and account for the high levels of symptom overlap,” said Dr. Karalunas.
 

Shared cognitive markers

Under the DSM’s change, “it’s now recognized that an estimated 20%-60% of children with ASD have comorbidities with ADHD, and around 20%-40% of children with ADHD have ASD symptoms,” said Beth Johnson, PhD, a research fellow with the Turner Institute for Brain and Mental Health at Monash University, Melbourne.

The shared overlap on genetic traits and comorbidities such as intellectual disability, anxiety, depression, and oppositional defiant disorder, make it difficult for clinicians to predict clinical outcomes, noted Dr. Johnson.

“We’re now understanding that they’re likely to be multiple autisms and ADHDs, that these symptoms exist on a spectrum of severity or ability,” she said. Dr. Johnson discussed a data-driven subtyping approach based on neurocognitive and symptom profiles in children with ADHD. The aim was to better understand how symptoms are managed across ADHD, ASD and comorbid ASD-ADHD.

As part of this research, her team recruited 295 controls and 117 children with ADHD who underwent clinical phenotyping and also completed working memory tasks, stop signal, and sustained attention tasks.

The researchers divided the children into four stable clusters based on the ADHD rating scale and autism questionnaire data: high ASD/ADHD traits, high ADHD/low ASD, low ADHD/moderate ASD, and low ADHD/ASD. Approximately half of the children with ADHD showed moderate to high ASD symptoms. Looking at neurocognition across the tasks, unsurprisingly, performance was lowest among the high-ASD/ADHD children, with performance on the stop signal being the most pronounced. “Notably, performance on the working memory task worsened with increasing ADHD symptoms,” she reported.
 

Drift model identifies information processing

Dr. Karalunas has also compared subgroups of ADHD and ASD children. “Our analysis examined whether cognitive impairments in ASD reflect a shared risk mechanism or co-occurring ADHD symptoms and why we see an overlap in these types of impairments,” she said.

Her study included 509 children with ADHD, 97 with ASD, and 301 controls (typical development). All three groups underwent a full cognitive assessment battery that measured attention arousal, basic processing speed, and working memory. Those tasks were collapsed into a series of variables as well as a set of tasks measuring response inhibition, switching, interference control, reward discounting, and measure of reaction time variability.

Four cognitive profiles emerged: a typically developing group, an ADHD group, an ASD group with low levels of ADHD symptoms and an ASD group with high levels of ADHD symptoms.

The ADHD group did worse on many of the tasks than the control group, and the ASD group with low ADHD levels also did poorly relative to the typically developing sample. This shows that autism – even in absence of co-occurring ADHD – demonstrates more cognitive impairment than typically developing kids. The ADHD group with high levels of autism did the most poorly across all of the tasks.

The findings also revealed a symptom severity pattern: the group with fewer symptoms did the best and the group with the most symptoms did the worst. “Overall, this reflects severity of impairment,” said Dr. Karalunas.

To identify measures more specific to either ADHD or autism, Dr. Karalunas and colleagues did a follow-up analysis to characterize cognitive performance. To accomplish this, they applied a drift-diffusion model to the same four cognitive profiles. The model assessed three parameters: drift rate, which relates to the speed or efficiency of information processing, boundary separation or speed accuracy trade-offs (impulsivity), and nondecision time such as motor preparation.

Using the same four cognitive profiles, they found that the ADHD group had slower drift rate relative to the control, although the two groups did not differ on boundary separation, which meant there were no differences on waiting to need to respond. The ADHD group had faster nondecision times. “This is a classic pattern, shown in the literature,” said Dr. Karalunas.
 

In other results, an interesting pattern began to evolve

Both ASD groups, for example, had much wider boundary separations, which meant they were waiting to be sure before they responded than the ADHD or typically developing groups. In contrast, the two ADHD groups had much faster non-decision times, whereas the two non-ADHD groups had similar nondecisions times.

Unlike the previous analysis, which saw a symptom severity pattern develop, “we’re getting two parameters that seem to track much more specifically to specific symptom domains,” observed Dr. Karalunas.

The results suggest there’s a substantial overlap in cognitive impairments in ADHD/ASD. “But we have pretty strong evidence at this point that these similarities are not accounted for by symptom overlap, especially for things like response and inhibition, working memory and processing speed. These seem to be independently related to ADHD and autism, regardless of the level of comorbid ADHD symptoms in the autism group,” said Dr. Karalunas.

The hope is to expand on these types of analyses to address the interaction of cognition-emotion and social cognition, and empirically define groups based on cognitive performance, she said.
 

Neurocognitive studies

Researchers have also been studying neural networks to assess ASD and ADHD. Roselyne Chauvin, PhD, a postdoctoral associate at Washington University, St. Louis, discussed the concept of “a task generic connectome,” in which researchers look for a common network between targeted task paradigms to get closer to a common alteration across impairments.

In her research, Dr. Chauvin and colleagues looked at connectivity modulations across three tasks: working memory, reward processing tasks, and stop signal tasks, comparing ADHD patients to siblings and controls. The ADHD group showed reduced sensitivity or a smaller number of connections modulated in the tasks compared with the other groups. Researchers wondered where those missed connections were located.

Dividing the cohorts into task generic and task specific groups, Dr. Chauvin and colleagues found that the ADHD group lacked common processing skills. They were also able to identify reproducible missing circuits in the ADHD participants. Among the cohorts, there was a higher modulation of task-specific edges in the ADHD group.

The ADHD patients seemed to be using more task-tailored alternative strategies that were more challenging and suboptimal.

She also previewed her ongoing work with the EU-AIMS Longitudinal European Autism Project (LEAP) database to study ASD-ADHD comorbidity. In this project, she and her colleagues looked at several tasks: probing emotion processing, inhibitory control, theory of mind, and reward anticipation. Comparing ASD groups with or without ADHD comorbidity or a shared connection, she and her team were able to devise a functional profile predictive of ADHD severity. As an example, “for the connection only used by the ASD with ADHD comorbidity, the more they were using those connections of higher amplitude in the modulation, inside this subset of connection, the higher they would have ADHD severity,” said Dr. Chauvin.

Neural correlates of different behavioral and cognitive profiles haven’t been widely studied, according to Charlotte Tye, PhD, who’s based at the Institute of Psychiatry, Psychology & Neuroscience, King’s College, London. Electroencephalography is a useful technique for understanding the neural correlates of cognitive impairments and teasing apart different models of co-occurrence in ASD and ADHD. 

Dr. Tye and colleagues tested this approach in a cohort of boys aged 8-13 years diagnosed with ASD and/or ADHD, measuring EEG while the children did various continuous performance tasks to assess changes in brain activity. Examining P3 amplitude (event-related potential components) they found that children with ADHD or ADHD+ASD showed an attenuated amplitude of the P3, compared with typically developing children and those with ASD.

“This suggests children with an ADHD diagnosis exhibited reduced inhibitory control,” said Dr. Tye. In contrast, children with ASD showed reduced conflict monitoring as indexed by altered N2 amplitude across task conditions.

These, and other studies conducted by Dr. Tye and colleagues indicate that children with ADHD show reduced neural responses during attentional processing, whereas autistic children show typical neural responses, supporting specific profiles.

“Autistic children with a diagnosis of ADHD appear to show the unique patterns of neural responses of autism and ADHD, supporting an additive co-occurrence rather than a distinct condition. This contributes to identification of transdiagnostic subgroups within neurodevelopmental conditions for targeting of personalized intervention, and suggests that children with co-occurring autism and ADHD require support for both conditions,” said Dr. Tye.

An important takeaway from all of these findings is “we can’t look just at how someone does overall on a single test,” said Dr. Karalunas in an interview. “There is a tremendous amount of variability between people who have the same diagnosis, and our research really needs to account for this.”

Attention-deficit/hyperactivity disorder and autism spectrum disorder (ASD) often coexist in children and adults, but the range of cognitive abilities can vary widely in these patients. Researchers from around the world are leveraging symptom, cognitive assessment, and neurobiological measures to gain insights on how individuals with ADHD/ASD approach and solve problems.

Several experts discussed the progress of their research during the session, “Overlap and differences of ADHD and autism – new findings of functional imaging and cognition studies” at the World Congress on ADHD – Virtual Event.

“The overlap of these two disorders is a critical issue for our field,” said Sarah Karalunas, PhD, assistant professor of clinical psychology at Purdue University, West Lafayette, Ind., who moderated the session. Clinicians are often asked to make differential diagnoses between these two disorders. Only recently has the DSM-5 allowed their codiagnosis. “There’s increasing recognition that there may be shared cognitive and physiological features that reflect their shared risk and account for the high levels of symptom overlap,” said Dr. Karalunas.
 

Shared cognitive markers

Under the DSM’s change, “it’s now recognized that an estimated 20%-60% of children with ASD have comorbidities with ADHD, and around 20%-40% of children with ADHD have ASD symptoms,” said Beth Johnson, PhD, a research fellow with the Turner Institute for Brain and Mental Health at Monash University, Melbourne.

The shared overlap on genetic traits and comorbidities such as intellectual disability, anxiety, depression, and oppositional defiant disorder, make it difficult for clinicians to predict clinical outcomes, noted Dr. Johnson.

“We’re now understanding that they’re likely to be multiple autisms and ADHDs, that these symptoms exist on a spectrum of severity or ability,” she said. Dr. Johnson discussed a data-driven subtyping approach based on neurocognitive and symptom profiles in children with ADHD. The aim was to better understand how symptoms are managed across ADHD, ASD and comorbid ASD-ADHD.

As part of this research, her team recruited 295 controls and 117 children with ADHD who underwent clinical phenotyping and also completed working memory tasks, stop signal, and sustained attention tasks.

The researchers divided the children into four stable clusters based on the ADHD rating scale and autism questionnaire data: high ASD/ADHD traits, high ADHD/low ASD, low ADHD/moderate ASD, and low ADHD/ASD. Approximately half of the children with ADHD showed moderate to high ASD symptoms. Looking at neurocognition across the tasks, unsurprisingly, performance was lowest among the high-ASD/ADHD children, with performance on the stop signal being the most pronounced. “Notably, performance on the working memory task worsened with increasing ADHD symptoms,” she reported.
 

Drift model identifies information processing

Dr. Karalunas has also compared subgroups of ADHD and ASD children. “Our analysis examined whether cognitive impairments in ASD reflect a shared risk mechanism or co-occurring ADHD symptoms and why we see an overlap in these types of impairments,” she said.

Her study included 509 children with ADHD, 97 with ASD, and 301 controls (typical development). All three groups underwent a full cognitive assessment battery that measured attention arousal, basic processing speed, and working memory. Those tasks were collapsed into a series of variables as well as a set of tasks measuring response inhibition, switching, interference control, reward discounting, and measure of reaction time variability.

Four cognitive profiles emerged: a typically developing group, an ADHD group, an ASD group with low levels of ADHD symptoms and an ASD group with high levels of ADHD symptoms.

The ADHD group did worse on many of the tasks than the control group, and the ASD group with low ADHD levels also did poorly relative to the typically developing sample. This shows that autism – even in absence of co-occurring ADHD – demonstrates more cognitive impairment than typically developing kids. The ADHD group with high levels of autism did the most poorly across all of the tasks.

The findings also revealed a symptom severity pattern: the group with fewer symptoms did the best and the group with the most symptoms did the worst. “Overall, this reflects severity of impairment,” said Dr. Karalunas.

To identify measures more specific to either ADHD or autism, Dr. Karalunas and colleagues did a follow-up analysis to characterize cognitive performance. To accomplish this, they applied a drift-diffusion model to the same four cognitive profiles. The model assessed three parameters: drift rate, which relates to the speed or efficiency of information processing, boundary separation or speed accuracy trade-offs (impulsivity), and nondecision time such as motor preparation.

Using the same four cognitive profiles, they found that the ADHD group had slower drift rate relative to the control, although the two groups did not differ on boundary separation, which meant there were no differences on waiting to need to respond. The ADHD group had faster nondecision times. “This is a classic pattern, shown in the literature,” said Dr. Karalunas.
 

In other results, an interesting pattern began to evolve

Both ASD groups, for example, had much wider boundary separations, which meant they were waiting to be sure before they responded than the ADHD or typically developing groups. In contrast, the two ADHD groups had much faster non-decision times, whereas the two non-ADHD groups had similar nondecisions times.

Unlike the previous analysis, which saw a symptom severity pattern develop, “we’re getting two parameters that seem to track much more specifically to specific symptom domains,” observed Dr. Karalunas.

The results suggest there’s a substantial overlap in cognitive impairments in ADHD/ASD. “But we have pretty strong evidence at this point that these similarities are not accounted for by symptom overlap, especially for things like response and inhibition, working memory and processing speed. These seem to be independently related to ADHD and autism, regardless of the level of comorbid ADHD symptoms in the autism group,” said Dr. Karalunas.

The hope is to expand on these types of analyses to address the interaction of cognition-emotion and social cognition, and empirically define groups based on cognitive performance, she said.
 

Neurocognitive studies

Researchers have also been studying neural networks to assess ASD and ADHD. Roselyne Chauvin, PhD, a postdoctoral associate at Washington University, St. Louis, discussed the concept of “a task generic connectome,” in which researchers look for a common network between targeted task paradigms to get closer to a common alteration across impairments.

In her research, Dr. Chauvin and colleagues looked at connectivity modulations across three tasks: working memory, reward processing tasks, and stop signal tasks, comparing ADHD patients to siblings and controls. The ADHD group showed reduced sensitivity or a smaller number of connections modulated in the tasks compared with the other groups. Researchers wondered where those missed connections were located.

Dividing the cohorts into task generic and task specific groups, Dr. Chauvin and colleagues found that the ADHD group lacked common processing skills. They were also able to identify reproducible missing circuits in the ADHD participants. Among the cohorts, there was a higher modulation of task-specific edges in the ADHD group.

The ADHD patients seemed to be using more task-tailored alternative strategies that were more challenging and suboptimal.

She also previewed her ongoing work with the EU-AIMS Longitudinal European Autism Project (LEAP) database to study ASD-ADHD comorbidity. In this project, she and her colleagues looked at several tasks: probing emotion processing, inhibitory control, theory of mind, and reward anticipation. Comparing ASD groups with or without ADHD comorbidity or a shared connection, she and her team were able to devise a functional profile predictive of ADHD severity. As an example, “for the connection only used by the ASD with ADHD comorbidity, the more they were using those connections of higher amplitude in the modulation, inside this subset of connection, the higher they would have ADHD severity,” said Dr. Chauvin.

Neural correlates of different behavioral and cognitive profiles haven’t been widely studied, according to Charlotte Tye, PhD, who’s based at the Institute of Psychiatry, Psychology & Neuroscience, King’s College, London. Electroencephalography is a useful technique for understanding the neural correlates of cognitive impairments and teasing apart different models of co-occurrence in ASD and ADHD. 

Dr. Tye and colleagues tested this approach in a cohort of boys aged 8-13 years diagnosed with ASD and/or ADHD, measuring EEG while the children did various continuous performance tasks to assess changes in brain activity. Examining P3 amplitude (event-related potential components) they found that children with ADHD or ADHD+ASD showed an attenuated amplitude of the P3, compared with typically developing children and those with ASD.

“This suggests children with an ADHD diagnosis exhibited reduced inhibitory control,” said Dr. Tye. In contrast, children with ASD showed reduced conflict monitoring as indexed by altered N2 amplitude across task conditions.

These, and other studies conducted by Dr. Tye and colleagues indicate that children with ADHD show reduced neural responses during attentional processing, whereas autistic children show typical neural responses, supporting specific profiles.

“Autistic children with a diagnosis of ADHD appear to show the unique patterns of neural responses of autism and ADHD, supporting an additive co-occurrence rather than a distinct condition. This contributes to identification of transdiagnostic subgroups within neurodevelopmental conditions for targeting of personalized intervention, and suggests that children with co-occurring autism and ADHD require support for both conditions,” said Dr. Tye.

An important takeaway from all of these findings is “we can’t look just at how someone does overall on a single test,” said Dr. Karalunas in an interview. “There is a tremendous amount of variability between people who have the same diagnosis, and our research really needs to account for this.”

Attention-deficit/hyperactivity disorder and autism spectrum disorder (ASD) often coexist in children and adults, but the range of cognitive abilities can vary widely in these patients. Researchers from around the world are leveraging symptom, cognitive assessment, and neurobiological measures to gain insights on how individuals with ADHD/ASD approach and solve problems.

Several experts discussed the progress of their research during the session, “Overlap and differences of ADHD and autism – new findings of functional imaging and cognition studies” at the World Congress on ADHD – Virtual Event.

“The overlap of these two disorders is a critical issue for our field,” said Sarah Karalunas, PhD, assistant professor of clinical psychology at Purdue University, West Lafayette, Ind., who moderated the session. Clinicians are often asked to make differential diagnoses between these two disorders. Only recently has the DSM-5 allowed their codiagnosis. “There’s increasing recognition that there may be shared cognitive and physiological features that reflect their shared risk and account for the high levels of symptom overlap,” said Dr. Karalunas.
 

Shared cognitive markers

Under the DSM’s change, “it’s now recognized that an estimated 20%-60% of children with ASD have comorbidities with ADHD, and around 20%-40% of children with ADHD have ASD symptoms,” said Beth Johnson, PhD, a research fellow with the Turner Institute for Brain and Mental Health at Monash University, Melbourne.

The shared overlap on genetic traits and comorbidities such as intellectual disability, anxiety, depression, and oppositional defiant disorder, make it difficult for clinicians to predict clinical outcomes, noted Dr. Johnson.

“We’re now understanding that they’re likely to be multiple autisms and ADHDs, that these symptoms exist on a spectrum of severity or ability,” she said. Dr. Johnson discussed a data-driven subtyping approach based on neurocognitive and symptom profiles in children with ADHD. The aim was to better understand how symptoms are managed across ADHD, ASD and comorbid ASD-ADHD.

As part of this research, her team recruited 295 controls and 117 children with ADHD who underwent clinical phenotyping and also completed working memory tasks, stop signal, and sustained attention tasks.

The researchers divided the children into four stable clusters based on the ADHD rating scale and autism questionnaire data: high ASD/ADHD traits, high ADHD/low ASD, low ADHD/moderate ASD, and low ADHD/ASD. Approximately half of the children with ADHD showed moderate to high ASD symptoms. Looking at neurocognition across the tasks, unsurprisingly, performance was lowest among the high-ASD/ADHD children, with performance on the stop signal being the most pronounced. “Notably, performance on the working memory task worsened with increasing ADHD symptoms,” she reported.
 

Drift model identifies information processing

Dr. Karalunas has also compared subgroups of ADHD and ASD children. “Our analysis examined whether cognitive impairments in ASD reflect a shared risk mechanism or co-occurring ADHD symptoms and why we see an overlap in these types of impairments,” she said.

Her study included 509 children with ADHD, 97 with ASD, and 301 controls (typical development). All three groups underwent a full cognitive assessment battery that measured attention arousal, basic processing speed, and working memory. Those tasks were collapsed into a series of variables as well as a set of tasks measuring response inhibition, switching, interference control, reward discounting, and measure of reaction time variability.

Four cognitive profiles emerged: a typically developing group, an ADHD group, an ASD group with low levels of ADHD symptoms and an ASD group with high levels of ADHD symptoms.

The ADHD group did worse on many of the tasks than the control group, and the ASD group with low ADHD levels also did poorly relative to the typically developing sample. This shows that autism – even in absence of co-occurring ADHD – demonstrates more cognitive impairment than typically developing kids. The ADHD group with high levels of autism did the most poorly across all of the tasks.

The findings also revealed a symptom severity pattern: the group with fewer symptoms did the best and the group with the most symptoms did the worst. “Overall, this reflects severity of impairment,” said Dr. Karalunas.

To identify measures more specific to either ADHD or autism, Dr. Karalunas and colleagues did a follow-up analysis to characterize cognitive performance. To accomplish this, they applied a drift-diffusion model to the same four cognitive profiles. The model assessed three parameters: drift rate, which relates to the speed or efficiency of information processing, boundary separation or speed accuracy trade-offs (impulsivity), and nondecision time such as motor preparation.

Using the same four cognitive profiles, they found that the ADHD group had slower drift rate relative to the control, although the two groups did not differ on boundary separation, which meant there were no differences on waiting to need to respond. The ADHD group had faster nondecision times. “This is a classic pattern, shown in the literature,” said Dr. Karalunas.
 

In other results, an interesting pattern began to evolve

Both ASD groups, for example, had much wider boundary separations, which meant they were waiting to be sure before they responded than the ADHD or typically developing groups. In contrast, the two ADHD groups had much faster non-decision times, whereas the two non-ADHD groups had similar nondecisions times.

Unlike the previous analysis, which saw a symptom severity pattern develop, “we’re getting two parameters that seem to track much more specifically to specific symptom domains,” observed Dr. Karalunas.

The results suggest there’s a substantial overlap in cognitive impairments in ADHD/ASD. “But we have pretty strong evidence at this point that these similarities are not accounted for by symptom overlap, especially for things like response and inhibition, working memory and processing speed. These seem to be independently related to ADHD and autism, regardless of the level of comorbid ADHD symptoms in the autism group,” said Dr. Karalunas.

The hope is to expand on these types of analyses to address the interaction of cognition-emotion and social cognition, and empirically define groups based on cognitive performance, she said.
 

Neurocognitive studies

Researchers have also been studying neural networks to assess ASD and ADHD. Roselyne Chauvin, PhD, a postdoctoral associate at Washington University, St. Louis, discussed the concept of “a task generic connectome,” in which researchers look for a common network between targeted task paradigms to get closer to a common alteration across impairments.

In her research, Dr. Chauvin and colleagues looked at connectivity modulations across three tasks: working memory, reward processing tasks, and stop signal tasks, comparing ADHD patients to siblings and controls. The ADHD group showed reduced sensitivity or a smaller number of connections modulated in the tasks compared with the other groups. Researchers wondered where those missed connections were located.

Dividing the cohorts into task generic and task specific groups, Dr. Chauvin and colleagues found that the ADHD group lacked common processing skills. They were also able to identify reproducible missing circuits in the ADHD participants. Among the cohorts, there was a higher modulation of task-specific edges in the ADHD group.

The ADHD patients seemed to be using more task-tailored alternative strategies that were more challenging and suboptimal.

She also previewed her ongoing work with the EU-AIMS Longitudinal European Autism Project (LEAP) database to study ASD-ADHD comorbidity. In this project, she and her colleagues looked at several tasks: probing emotion processing, inhibitory control, theory of mind, and reward anticipation. Comparing ASD groups with or without ADHD comorbidity or a shared connection, she and her team were able to devise a functional profile predictive of ADHD severity. As an example, “for the connection only used by the ASD with ADHD comorbidity, the more they were using those connections of higher amplitude in the modulation, inside this subset of connection, the higher they would have ADHD severity,” said Dr. Chauvin.

Neural correlates of different behavioral and cognitive profiles haven’t been widely studied, according to Charlotte Tye, PhD, who’s based at the Institute of Psychiatry, Psychology & Neuroscience, King’s College, London. Electroencephalography is a useful technique for understanding the neural correlates of cognitive impairments and teasing apart different models of co-occurrence in ASD and ADHD. 

Dr. Tye and colleagues tested this approach in a cohort of boys aged 8-13 years diagnosed with ASD and/or ADHD, measuring EEG while the children did various continuous performance tasks to assess changes in brain activity. Examining P3 amplitude (event-related potential components) they found that children with ADHD or ADHD+ASD showed an attenuated amplitude of the P3, compared with typically developing children and those with ASD.

“This suggests children with an ADHD diagnosis exhibited reduced inhibitory control,” said Dr. Tye. In contrast, children with ASD showed reduced conflict monitoring as indexed by altered N2 amplitude across task conditions.

These, and other studies conducted by Dr. Tye and colleagues indicate that children with ADHD show reduced neural responses during attentional processing, whereas autistic children show typical neural responses, supporting specific profiles.

“Autistic children with a diagnosis of ADHD appear to show the unique patterns of neural responses of autism and ADHD, supporting an additive co-occurrence rather than a distinct condition. This contributes to identification of transdiagnostic subgroups within neurodevelopmental conditions for targeting of personalized intervention, and suggests that children with co-occurring autism and ADHD require support for both conditions,” said Dr. Tye.

An important takeaway from all of these findings is “we can’t look just at how someone does overall on a single test,” said Dr. Karalunas in an interview. “There is a tremendous amount of variability between people who have the same diagnosis, and our research really needs to account for this.”

While it’s possible that residual effects of SARS-CoV-2 could lead to an eruption of attention-deficit/hyperactivity disorder (ADHD) cases, a debate at the World Congress on ADHD – Virtual Event underscored the fact that this is still a hypothesis. The bottom line is there needs to be more data, said Luis Augusto Rohde, MD, PhD, cochair of the congress’ scientific program committee and moderator of the session, “Residual effects of the 2019 pandemic will mirror the 1918 pandemic: Will we have lots of new ADHD cases?”

Considering the current pattern of the pandemic, there is not enough evidence for this to be a concern, Dr. Rohde said in an interview.

James Swanson, PhD, professor of pediatrics at the University of California, Irvine, opined that biological co-effects of COVID-19 are likely to have selective effects in children that may produce symptoms representative of ADHD. Using the 1918 Spanish flu pandemic as a historical reference, he estimated that COVID-19 would produce 5 million individuals with new-onset symptoms related to ADHD. “If these cases meet DSM-5 or ICD-11 criteria, there will be lots of new ADHD cases,” he predicted.

David Coghill, MD, a professor of child adolescent mental health at the University of Melbourne, observed that the sums Dr. Swanson presented “are based on maxing out the potential rather than looking at the sums more realistically.”
 

Could the 1918 pandemic offer clues?

In a commentary, Dr. Swanson and Nora D. Volkow, MD, wrote about “lessons learned” from the 1918 pandemic, and how residual sequelae in that era led to a condition labeled hyperkinetic syndrome in children. “It may be worthwhile to consider the hypothesis that the COVID-19 pandemic may result in a novel etiologic subtype of ADHD that clinicians may recognize in patients in the future,” wrote the commentators. 

In survivors of the 1918 pandemic, brain inflammation or encephalitis sometimes emerged as residual sequelae, said Dr. Swanson. In some adult cases, these symptoms were diagnosed as “encephalitis lethargica” (EL) and were associated with Parkinson’s disease. In 1930, based on patients evaluated after 1918, researchers Franz Kramer and Hans Pollnow at Charité Hospital in Berlin described the behavioral manifestation of EL in children as hyperkinetic syndrome, a condition that was characterized by symptoms similar to the properties of ADHD: lack of concentration, insufficient goal orientation, and increased distractibility. “They even reported on autopsy cases that described brain regions that we now know are associated with ADHD from decades of brain imaging studies,” said Dr. Swanson.

COVID-19 rarely results in severe respiratory problems in children but the absolute number requiring hospitalization has accumulated and is now relatively large, said Dr. Swanson. One study of 1,695 severe COVID-19 cases in children and adolescents used MRI and detected neural effects in specific brain regions such as basal ganglia and frontal lobes that previous research had associated with ADHD. Approximately 22% of these rare but severe cases had documented neurologic involvement, and studies of affected children with mild or none of the initial respiratory symptoms of COVID-19 also detected similar selective effects in these brain regions.

A recent survey of medical records of 80 million people that identified 240,000 COVID cases (mostly adults) revealed that a third had neurological and psychiatric sequelae. Dr. Swanson also mentioned an article he wrote more than a decade ago on environmental as well as genetic factors that resulted in etiologic subtypes of ADHD, which provided a model for the impact of COVID-19 on specific brain regions that are associated with ADHD.

So far, the COVID-19 pandemic has produced 150 million cases worldwide and there are about 100 million survivors, setting an estimate of a maximum number of cases with residual sequelae. “I think that severe COVID-19 will probably be related to severe residual sequelae, and that mild or asymptomatic COVID-19 may be associated with less severe residual sequelae, which may resemble ADHD” said Dr. Swanson. If one-third of the cases manifest in some neurologic or psychiatric systems, this means 27 million would have residual sequelae. If 20% have impaired concentration or brain fog, this could result in about 5 million ADHD cases, he said. 
 

Estimates aren’t evidence

The Swanson/Volkow commentary contains a lot of references to “might, could, and may,” said Dr. Coghill. While it’s true that COVID-19 could produce a novel etiologic subtype of ADHD, “the point here is at the moment, all of this is based on hypotheses,” he said.

The Spanish flu did produce mental health consequences – survivors reported depression, sleep disturbances, mental distraction, dizziness, and difficulties coping at work. In the United States, flu death rates from 1918 to 1920 were directly attributed to suicide rates. Unfortunately, these impacts weren’t widely researched, said Dr. Coghill.

It also seems clear that the 1918 Spanish flu outbreak was associated with significant neurological consequences, said Dr. Coghill. By 1919 and 1920, physicians and researchers in the United Kingdom were reporting increases in a variety of symptoms among some patients recovering from flu, such as neuropathy, neurasthenia, meningitis, degenerative changes in nerve cells, and a decline in visual acuity.

The EL cases Dr. Swanson mentioned did coincide with and reach epidemic proportions alongside the Spanish flu. “But still, a causal relationship is far from proven,” said Dr. Coghill.

Sol Levy, MD, described a “disease of criminals” following the 1918 pandemic, in which patients exhibited a high degree of general hyperkinesis, a difficulty in maintaining quiet attitudes, abruptness and clumsiness, and “explosive motor release of all voluntarily inhibited activities.”

However, these impairments suggest a much broader presentation typically seen in ADHD, noted Dr. Coghill.

Neurological complications occur more commonly than initially thought in severe COVID-19, with estimates ranging from 36% to 84%. But in a systematic review of neuropsychiatric complications of severe coronavirus infection, researchers found few psychiatric sequelae of these infections. While they did mention impaired concentration and difficulties with emotional ability, it’s very important to remember that these conditions “are cardinal symptoms of a wide range of psychiatric disorders,” said Dr. Coghill.

Overall, more neurological and neuropsychiatric symptoms largely confine to those with severe COVID-19, meaning they’re much less likely to occur in children and young adults, he said.

If there are severe effects of COVID-19, Dr. Swanson countered that “they might have more ADHD than the complex residual effects [Dr. Coghill] described. I hope that he’s right, but I do think there will be biological co-effects of COVID-19 that will produce symptoms that are more ADHD than other neurological disorders.”
 

Epigenetic effects

Researchers are now seeing transgenerational and intergenerational effects of potential infection. “So I certainly back high-quality studies looking at the effects of maternal and paternal infection on offspring,” said Dr. Coghill. Establishing clinical cohort studies to follow up on this population would be essential in understanding the risks of SARS-CoV-2. “That might be one way we’ll see an increase in ADHD,” said Dr. Coghill.

The reality is COVID-19 hasn’t been around for that long, and current knowledge about it is limited, he said. Rapid publications, cross-sectional or retrospective data, and poor methodological quality and rigor make generalizability difficult. In addition, limited testing and detection probably underestimate prevalence of neurological and neuropsychiatric complications.

“If history teaches us anything, it is that we should always be measured in how we glean lessons from the past. So let’s not get ahead of ourselves,” he cautioned.

An informal, post-discussion survey of session participants revealed that a slight majority – 55%-60% – expected residual effects of COVID-19 to lead to more ADHD, compared to 40%-45% who didn’t think this would happen.

Dr. Swanson has two patents: (PIXA4), which uses a “time-of-flight” camera to measure growth on infants, and a provisional patent on the mechanism of tolerance to stimulant medication (PATSMTA). Dr. Coghill worked for several pharmaceutical companies but had no disclosures relevant to this debate.

While it’s possible that residual effects of SARS-CoV-2 could lead to an eruption of attention-deficit/hyperactivity disorder (ADHD) cases, a debate at the World Congress on ADHD – Virtual Event underscored the fact that this is still a hypothesis. The bottom line is there needs to be more data, said Luis Augusto Rohde, MD, PhD, cochair of the congress’ scientific program committee and moderator of the session, “Residual effects of the 2019 pandemic will mirror the 1918 pandemic: Will we have lots of new ADHD cases?”

Considering the current pattern of the pandemic, there is not enough evidence for this to be a concern, Dr. Rohde said in an interview.

James Swanson, PhD, professor of pediatrics at the University of California, Irvine, opined that biological co-effects of COVID-19 are likely to have selective effects in children that may produce symptoms representative of ADHD. Using the 1918 Spanish flu pandemic as a historical reference, he estimated that COVID-19 would produce 5 million individuals with new-onset symptoms related to ADHD. “If these cases meet DSM-5 or ICD-11 criteria, there will be lots of new ADHD cases,” he predicted.

David Coghill, MD, a professor of child adolescent mental health at the University of Melbourne, observed that the sums Dr. Swanson presented “are based on maxing out the potential rather than looking at the sums more realistically.”
 

Could the 1918 pandemic offer clues?

In a commentary, Dr. Swanson and Nora D. Volkow, MD, wrote about “lessons learned” from the 1918 pandemic, and how residual sequelae in that era led to a condition labeled hyperkinetic syndrome in children. “It may be worthwhile to consider the hypothesis that the COVID-19 pandemic may result in a novel etiologic subtype of ADHD that clinicians may recognize in patients in the future,” wrote the commentators. 

In survivors of the 1918 pandemic, brain inflammation or encephalitis sometimes emerged as residual sequelae, said Dr. Swanson. In some adult cases, these symptoms were diagnosed as “encephalitis lethargica” (EL) and were associated with Parkinson’s disease. In 1930, based on patients evaluated after 1918, researchers Franz Kramer and Hans Pollnow at Charité Hospital in Berlin described the behavioral manifestation of EL in children as hyperkinetic syndrome, a condition that was characterized by symptoms similar to the properties of ADHD: lack of concentration, insufficient goal orientation, and increased distractibility. “They even reported on autopsy cases that described brain regions that we now know are associated with ADHD from decades of brain imaging studies,” said Dr. Swanson.

COVID-19 rarely results in severe respiratory problems in children but the absolute number requiring hospitalization has accumulated and is now relatively large, said Dr. Swanson. One study of 1,695 severe COVID-19 cases in children and adolescents used MRI and detected neural effects in specific brain regions such as basal ganglia and frontal lobes that previous research had associated with ADHD. Approximately 22% of these rare but severe cases had documented neurologic involvement, and studies of affected children with mild or none of the initial respiratory symptoms of COVID-19 also detected similar selective effects in these brain regions.

A recent survey of medical records of 80 million people that identified 240,000 COVID cases (mostly adults) revealed that a third had neurological and psychiatric sequelae. Dr. Swanson also mentioned an article he wrote more than a decade ago on environmental as well as genetic factors that resulted in etiologic subtypes of ADHD, which provided a model for the impact of COVID-19 on specific brain regions that are associated with ADHD.

So far, the COVID-19 pandemic has produced 150 million cases worldwide and there are about 100 million survivors, setting an estimate of a maximum number of cases with residual sequelae. “I think that severe COVID-19 will probably be related to severe residual sequelae, and that mild or asymptomatic COVID-19 may be associated with less severe residual sequelae, which may resemble ADHD” said Dr. Swanson. If one-third of the cases manifest in some neurologic or psychiatric systems, this means 27 million would have residual sequelae. If 20% have impaired concentration or brain fog, this could result in about 5 million ADHD cases, he said. 
 

Estimates aren’t evidence

The Swanson/Volkow commentary contains a lot of references to “might, could, and may,” said Dr. Coghill. While it’s true that COVID-19 could produce a novel etiologic subtype of ADHD, “the point here is at the moment, all of this is based on hypotheses,” he said.

The Spanish flu did produce mental health consequences – survivors reported depression, sleep disturbances, mental distraction, dizziness, and difficulties coping at work. In the United States, flu death rates from 1918 to 1920 were directly attributed to suicide rates. Unfortunately, these impacts weren’t widely researched, said Dr. Coghill.

It also seems clear that the 1918 Spanish flu outbreak was associated with significant neurological consequences, said Dr. Coghill. By 1919 and 1920, physicians and researchers in the United Kingdom were reporting increases in a variety of symptoms among some patients recovering from flu, such as neuropathy, neurasthenia, meningitis, degenerative changes in nerve cells, and a decline in visual acuity.

The EL cases Dr. Swanson mentioned did coincide with and reach epidemic proportions alongside the Spanish flu. “But still, a causal relationship is far from proven,” said Dr. Coghill.

Sol Levy, MD, described a “disease of criminals” following the 1918 pandemic, in which patients exhibited a high degree of general hyperkinesis, a difficulty in maintaining quiet attitudes, abruptness and clumsiness, and “explosive motor release of all voluntarily inhibited activities.”

However, these impairments suggest a much broader presentation typically seen in ADHD, noted Dr. Coghill.

Neurological complications occur more commonly than initially thought in severe COVID-19, with estimates ranging from 36% to 84%. But in a systematic review of neuropsychiatric complications of severe coronavirus infection, researchers found few psychiatric sequelae of these infections. While they did mention impaired concentration and difficulties with emotional ability, it’s very important to remember that these conditions “are cardinal symptoms of a wide range of psychiatric disorders,” said Dr. Coghill.

Overall, more neurological and neuropsychiatric symptoms largely confine to those with severe COVID-19, meaning they’re much less likely to occur in children and young adults, he said.

If there are severe effects of COVID-19, Dr. Swanson countered that “they might have more ADHD than the complex residual effects [Dr. Coghill] described. I hope that he’s right, but I do think there will be biological co-effects of COVID-19 that will produce symptoms that are more ADHD than other neurological disorders.”
 

Epigenetic effects

Researchers are now seeing transgenerational and intergenerational effects of potential infection. “So I certainly back high-quality studies looking at the effects of maternal and paternal infection on offspring,” said Dr. Coghill. Establishing clinical cohort studies to follow up on this population would be essential in understanding the risks of SARS-CoV-2. “That might be one way we’ll see an increase in ADHD,” said Dr. Coghill.

The reality is COVID-19 hasn’t been around for that long, and current knowledge about it is limited, he said. Rapid publications, cross-sectional or retrospective data, and poor methodological quality and rigor make generalizability difficult. In addition, limited testing and detection probably underestimate prevalence of neurological and neuropsychiatric complications.

“If history teaches us anything, it is that we should always be measured in how we glean lessons from the past. So let’s not get ahead of ourselves,” he cautioned.

An informal, post-discussion survey of session participants revealed that a slight majority – 55%-60% – expected residual effects of COVID-19 to lead to more ADHD, compared to 40%-45% who didn’t think this would happen.

Dr. Swanson has two patents: (PIXA4), which uses a “time-of-flight” camera to measure growth on infants, and a provisional patent on the mechanism of tolerance to stimulant medication (PATSMTA). Dr. Coghill worked for several pharmaceutical companies but had no disclosures relevant to this debate.

While it’s possible that residual effects of SARS-CoV-2 could lead to an eruption of attention-deficit/hyperactivity disorder (ADHD) cases, a debate at the World Congress on ADHD – Virtual Event underscored the fact that this is still a hypothesis. The bottom line is there needs to be more data, said Luis Augusto Rohde, MD, PhD, cochair of the congress’ scientific program committee and moderator of the session, “Residual effects of the 2019 pandemic will mirror the 1918 pandemic: Will we have lots of new ADHD cases?”

Considering the current pattern of the pandemic, there is not enough evidence for this to be a concern, Dr. Rohde said in an interview.

James Swanson, PhD, professor of pediatrics at the University of California, Irvine, opined that biological co-effects of COVID-19 are likely to have selective effects in children that may produce symptoms representative of ADHD. Using the 1918 Spanish flu pandemic as a historical reference, he estimated that COVID-19 would produce 5 million individuals with new-onset symptoms related to ADHD. “If these cases meet DSM-5 or ICD-11 criteria, there will be lots of new ADHD cases,” he predicted.

David Coghill, MD, a professor of child adolescent mental health at the University of Melbourne, observed that the sums Dr. Swanson presented “are based on maxing out the potential rather than looking at the sums more realistically.”
 

Could the 1918 pandemic offer clues?

In a commentary, Dr. Swanson and Nora D. Volkow, MD, wrote about “lessons learned” from the 1918 pandemic, and how residual sequelae in that era led to a condition labeled hyperkinetic syndrome in children. “It may be worthwhile to consider the hypothesis that the COVID-19 pandemic may result in a novel etiologic subtype of ADHD that clinicians may recognize in patients in the future,” wrote the commentators. 

In survivors of the 1918 pandemic, brain inflammation or encephalitis sometimes emerged as residual sequelae, said Dr. Swanson. In some adult cases, these symptoms were diagnosed as “encephalitis lethargica” (EL) and were associated with Parkinson’s disease. In 1930, based on patients evaluated after 1918, researchers Franz Kramer and Hans Pollnow at Charité Hospital in Berlin described the behavioral manifestation of EL in children as hyperkinetic syndrome, a condition that was characterized by symptoms similar to the properties of ADHD: lack of concentration, insufficient goal orientation, and increased distractibility. “They even reported on autopsy cases that described brain regions that we now know are associated with ADHD from decades of brain imaging studies,” said Dr. Swanson.

COVID-19 rarely results in severe respiratory problems in children but the absolute number requiring hospitalization has accumulated and is now relatively large, said Dr. Swanson. One study of 1,695 severe COVID-19 cases in children and adolescents used MRI and detected neural effects in specific brain regions such as basal ganglia and frontal lobes that previous research had associated with ADHD. Approximately 22% of these rare but severe cases had documented neurologic involvement, and studies of affected children with mild or none of the initial respiratory symptoms of COVID-19 also detected similar selective effects in these brain regions.

A recent survey of medical records of 80 million people that identified 240,000 COVID cases (mostly adults) revealed that a third had neurological and psychiatric sequelae. Dr. Swanson also mentioned an article he wrote more than a decade ago on environmental as well as genetic factors that resulted in etiologic subtypes of ADHD, which provided a model for the impact of COVID-19 on specific brain regions that are associated with ADHD.

So far, the COVID-19 pandemic has produced 150 million cases worldwide and there are about 100 million survivors, setting an estimate of a maximum number of cases with residual sequelae. “I think that severe COVID-19 will probably be related to severe residual sequelae, and that mild or asymptomatic COVID-19 may be associated with less severe residual sequelae, which may resemble ADHD” said Dr. Swanson. If one-third of the cases manifest in some neurologic or psychiatric systems, this means 27 million would have residual sequelae. If 20% have impaired concentration or brain fog, this could result in about 5 million ADHD cases, he said. 
 

Estimates aren’t evidence

The Swanson/Volkow commentary contains a lot of references to “might, could, and may,” said Dr. Coghill. While it’s true that COVID-19 could produce a novel etiologic subtype of ADHD, “the point here is at the moment, all of this is based on hypotheses,” he said.

The Spanish flu did produce mental health consequences – survivors reported depression, sleep disturbances, mental distraction, dizziness, and difficulties coping at work. In the United States, flu death rates from 1918 to 1920 were directly attributed to suicide rates. Unfortunately, these impacts weren’t widely researched, said Dr. Coghill.

It also seems clear that the 1918 Spanish flu outbreak was associated with significant neurological consequences, said Dr. Coghill. By 1919 and 1920, physicians and researchers in the United Kingdom were reporting increases in a variety of symptoms among some patients recovering from flu, such as neuropathy, neurasthenia, meningitis, degenerative changes in nerve cells, and a decline in visual acuity.

The EL cases Dr. Swanson mentioned did coincide with and reach epidemic proportions alongside the Spanish flu. “But still, a causal relationship is far from proven,” said Dr. Coghill.

Sol Levy, MD, described a “disease of criminals” following the 1918 pandemic, in which patients exhibited a high degree of general hyperkinesis, a difficulty in maintaining quiet attitudes, abruptness and clumsiness, and “explosive motor release of all voluntarily inhibited activities.”

However, these impairments suggest a much broader presentation typically seen in ADHD, noted Dr. Coghill.

Neurological complications occur more commonly than initially thought in severe COVID-19, with estimates ranging from 36% to 84%. But in a systematic review of neuropsychiatric complications of severe coronavirus infection, researchers found few psychiatric sequelae of these infections. While they did mention impaired concentration and difficulties with emotional ability, it’s very important to remember that these conditions “are cardinal symptoms of a wide range of psychiatric disorders,” said Dr. Coghill.

Overall, more neurological and neuropsychiatric symptoms largely confine to those with severe COVID-19, meaning they’re much less likely to occur in children and young adults, he said.

If there are severe effects of COVID-19, Dr. Swanson countered that “they might have more ADHD than the complex residual effects [Dr. Coghill] described. I hope that he’s right, but I do think there will be biological co-effects of COVID-19 that will produce symptoms that are more ADHD than other neurological disorders.”
 

Epigenetic effects

Researchers are now seeing transgenerational and intergenerational effects of potential infection. “So I certainly back high-quality studies looking at the effects of maternal and paternal infection on offspring,” said Dr. Coghill. Establishing clinical cohort studies to follow up on this population would be essential in understanding the risks of SARS-CoV-2. “That might be one way we’ll see an increase in ADHD,” said Dr. Coghill.

The reality is COVID-19 hasn’t been around for that long, and current knowledge about it is limited, he said. Rapid publications, cross-sectional or retrospective data, and poor methodological quality and rigor make generalizability difficult. In addition, limited testing and detection probably underestimate prevalence of neurological and neuropsychiatric complications.

“If history teaches us anything, it is that we should always be measured in how we glean lessons from the past. So let’s not get ahead of ourselves,” he cautioned.

An informal, post-discussion survey of session participants revealed that a slight majority – 55%-60% – expected residual effects of COVID-19 to lead to more ADHD, compared to 40%-45% who didn’t think this would happen.

Dr. Swanson has two patents: (PIXA4), which uses a “time-of-flight” camera to measure growth on infants, and a provisional patent on the mechanism of tolerance to stimulant medication (PATSMTA). Dr. Coghill worked for several pharmaceutical companies but had no disclosures relevant to this debate.

An examination of coffee consumption habits of almost 400,000 people suggests that those habits are largely driven by a person’s cardiovascular health.

©Elena Moiseeva/fotolia.com

Data from a large population database showed that people with essential hypertension, angina, or cardiac arrhythmias drank less coffee than people who had none of these conditions. When they did drink coffee, it tended to be decaffeinated.

The investigators, led by Elina Hyppönen, PhD, director of the Australian Centre for Precision Health at the University of South Australia, Adelaide, say that this predilection for avoiding coffee, which is known to produce jitteriness and heart palpitations, is based on genetics.

“If your body is telling you not to drink that extra cup of coffee, there’s likely a reason why,” Dr. Hyppönen said in an interview.

The study was published online in the American Journal of Clinical Nutrition.

“People drink coffee as a pick-me-up when they’re feeling tired, or because it tastes good, or simply because it’s part of their daily routine, but what we don’t recognize is that people subconsciously self-regulate safe levels of caffeine based on how high their blood pressure is, and this is likely a result of a protective genetic mechanism, [meaning] that someone who drinks a lot of coffee is likely more genetically tolerant of caffeine, as compared to someone who drinks very little,” Dr. Hyppönen said.

“In addition, we’ve known from past research that when people feel unwell, they tend to drink less coffee. This type of phenomenon, where disease drives behavior, is called reverse causality,” Dr. Hyppönen said.

For this analysis, she and her team used information on 390,435 individuals of European ancestry from the UK Biobank, a large epidemiologic database. Habitual coffee consumption was self-reported, and systolic and diastolic blood pressure and heart rate were measured at baseline. Cardiovascular symptoms at baseline were gleaned from hospital diagnoses, primary care records, and/or self report, the authors note.

To look at the relationship of systolic BP, diastolic BP, and heart rate with coffee consumption, they used a strategy called Mendelian randomization, which allows genetic information such as variants reflecting higher blood pressures and heart rate to be used to provide evidence for a causal association.

Results showed that participants with essential hypertension, angina, or arrhythmia were “all more likely to drink less caffeinated coffee and to be nonhabitual or decaffeinated coffee drinkers compared with those who did not report related symptoms,” the authors write.

Those with higher systolic and diastolic BP based on their genetics tended to drink less caffeinated coffee at baseline, “with consistent genetic evidence to support a causal explanation across all methods,” they noted.

They also found that those people who have a higher resting heart rate due to their genes were more likely to choose decaffeinated coffee.

“These results have two major implications,” Dr. Hyppönen said. “Firstly, they show that our bodies can regulate behavior in ways that we may not realize, and that if something does not feel good to us, there is a likely to be a reason why.”

“Second, our results show that our health status in part regulates the amount of coffee we drink. This is important, because when disease drives behavior, it can lead to misleading health associations in observational studies, and indeed, create a false impression for health benefits if the group of people who do not drink coffee also includes more people who are unwell,” she said.

For now, doctors can tell their patients that this study provides an explanation as to why research on the health effects of habitual coffee consumption has been conflicting, Dr. Hyppönen said.

“Our study also highlights the uncertainty that underlies the claimed health benefits of coffee, but at the same time, it gives a positive message about the ability of our body to regulate our level of coffee consumption in a way that helps us avoid adverse effects.”

“The most common symptoms of excessive coffee consumption are palpitations and rapid heartbeat, also known as tachycardia,” Nieca Goldberg, MD, medical director of the NYU Women’s Heart Program at NYU Langone Health, said in an interview.

“This study was designed to see if cardiac symptoms affect coffee consumption, and it showed that people with hypertension, angina, history of arrhythmias, and poor health tend to be decaffeinated coffee drinkers or no coffee drinkers,” Dr. Goldberg said.

“People naturally alter their coffee intake base on their blood pressure and symptoms of palpitations and/or rapid heart rate,” she said.

The results also suggest that, “we cannot infer health benefit or harm based on the available coffee studies,” Dr. Goldberg added.

The study was funded by the National Health and Medical Research Council, Australia. Dr. Hyppönen and Dr. Goldberg have disclosed no relevant financial relationships.

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

An examination of coffee consumption habits of almost 400,000 people suggests that those habits are largely driven by a person’s cardiovascular health.

©Elena Moiseeva/fotolia.com

Data from a large population database showed that people with essential hypertension, angina, or cardiac arrhythmias drank less coffee than people who had none of these conditions. When they did drink coffee, it tended to be decaffeinated.

The investigators, led by Elina Hyppönen, PhD, director of the Australian Centre for Precision Health at the University of South Australia, Adelaide, say that this predilection for avoiding coffee, which is known to produce jitteriness and heart palpitations, is based on genetics.

“If your body is telling you not to drink that extra cup of coffee, there’s likely a reason why,” Dr. Hyppönen said in an interview.

The study was published online in the American Journal of Clinical Nutrition.

“People drink coffee as a pick-me-up when they’re feeling tired, or because it tastes good, or simply because it’s part of their daily routine, but what we don’t recognize is that people subconsciously self-regulate safe levels of caffeine based on how high their blood pressure is, and this is likely a result of a protective genetic mechanism, [meaning] that someone who drinks a lot of coffee is likely more genetically tolerant of caffeine, as compared to someone who drinks very little,” Dr. Hyppönen said.

“In addition, we’ve known from past research that when people feel unwell, they tend to drink less coffee. This type of phenomenon, where disease drives behavior, is called reverse causality,” Dr. Hyppönen said.

For this analysis, she and her team used information on 390,435 individuals of European ancestry from the UK Biobank, a large epidemiologic database. Habitual coffee consumption was self-reported, and systolic and diastolic blood pressure and heart rate were measured at baseline. Cardiovascular symptoms at baseline were gleaned from hospital diagnoses, primary care records, and/or self report, the authors note.

To look at the relationship of systolic BP, diastolic BP, and heart rate with coffee consumption, they used a strategy called Mendelian randomization, which allows genetic information such as variants reflecting higher blood pressures and heart rate to be used to provide evidence for a causal association.

Results showed that participants with essential hypertension, angina, or arrhythmia were “all more likely to drink less caffeinated coffee and to be nonhabitual or decaffeinated coffee drinkers compared with those who did not report related symptoms,” the authors write.

Those with higher systolic and diastolic BP based on their genetics tended to drink less caffeinated coffee at baseline, “with consistent genetic evidence to support a causal explanation across all methods,” they noted.

They also found that those people who have a higher resting heart rate due to their genes were more likely to choose decaffeinated coffee.

“These results have two major implications,” Dr. Hyppönen said. “Firstly, they show that our bodies can regulate behavior in ways that we may not realize, and that if something does not feel good to us, there is a likely to be a reason why.”

“Second, our results show that our health status in part regulates the amount of coffee we drink. This is important, because when disease drives behavior, it can lead to misleading health associations in observational studies, and indeed, create a false impression for health benefits if the group of people who do not drink coffee also includes more people who are unwell,” she said.

For now, doctors can tell their patients that this study provides an explanation as to why research on the health effects of habitual coffee consumption has been conflicting, Dr. Hyppönen said.

“Our study also highlights the uncertainty that underlies the claimed health benefits of coffee, but at the same time, it gives a positive message about the ability of our body to regulate our level of coffee consumption in a way that helps us avoid adverse effects.”

“The most common symptoms of excessive coffee consumption are palpitations and rapid heartbeat, also known as tachycardia,” Nieca Goldberg, MD, medical director of the NYU Women’s Heart Program at NYU Langone Health, said in an interview.

“This study was designed to see if cardiac symptoms affect coffee consumption, and it showed that people with hypertension, angina, history of arrhythmias, and poor health tend to be decaffeinated coffee drinkers or no coffee drinkers,” Dr. Goldberg said.

“People naturally alter their coffee intake base on their blood pressure and symptoms of palpitations and/or rapid heart rate,” she said.

The results also suggest that, “we cannot infer health benefit or harm based on the available coffee studies,” Dr. Goldberg added.

The study was funded by the National Health and Medical Research Council, Australia. Dr. Hyppönen and Dr. Goldberg have disclosed no relevant financial relationships.

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

An examination of coffee consumption habits of almost 400,000 people suggests that those habits are largely driven by a person’s cardiovascular health.

©Elena Moiseeva/fotolia.com

Data from a large population database showed that people with essential hypertension, angina, or cardiac arrhythmias drank less coffee than people who had none of these conditions. When they did drink coffee, it tended to be decaffeinated.

The investigators, led by Elina Hyppönen, PhD, director of the Australian Centre for Precision Health at the University of South Australia, Adelaide, say that this predilection for avoiding coffee, which is known to produce jitteriness and heart palpitations, is based on genetics.

“If your body is telling you not to drink that extra cup of coffee, there’s likely a reason why,” Dr. Hyppönen said in an interview.

The study was published online in the American Journal of Clinical Nutrition.

“People drink coffee as a pick-me-up when they’re feeling tired, or because it tastes good, or simply because it’s part of their daily routine, but what we don’t recognize is that people subconsciously self-regulate safe levels of caffeine based on how high their blood pressure is, and this is likely a result of a protective genetic mechanism, [meaning] that someone who drinks a lot of coffee is likely more genetically tolerant of caffeine, as compared to someone who drinks very little,” Dr. Hyppönen said.

“In addition, we’ve known from past research that when people feel unwell, they tend to drink less coffee. This type of phenomenon, where disease drives behavior, is called reverse causality,” Dr. Hyppönen said.

For this analysis, she and her team used information on 390,435 individuals of European ancestry from the UK Biobank, a large epidemiologic database. Habitual coffee consumption was self-reported, and systolic and diastolic blood pressure and heart rate were measured at baseline. Cardiovascular symptoms at baseline were gleaned from hospital diagnoses, primary care records, and/or self report, the authors note.

To look at the relationship of systolic BP, diastolic BP, and heart rate with coffee consumption, they used a strategy called Mendelian randomization, which allows genetic information such as variants reflecting higher blood pressures and heart rate to be used to provide evidence for a causal association.

Results showed that participants with essential hypertension, angina, or arrhythmia were “all more likely to drink less caffeinated coffee and to be nonhabitual or decaffeinated coffee drinkers compared with those who did not report related symptoms,” the authors write.

Those with higher systolic and diastolic BP based on their genetics tended to drink less caffeinated coffee at baseline, “with consistent genetic evidence to support a causal explanation across all methods,” they noted.

They also found that those people who have a higher resting heart rate due to their genes were more likely to choose decaffeinated coffee.

“These results have two major implications,” Dr. Hyppönen said. “Firstly, they show that our bodies can regulate behavior in ways that we may not realize, and that if something does not feel good to us, there is a likely to be a reason why.”

“Second, our results show that our health status in part regulates the amount of coffee we drink. This is important, because when disease drives behavior, it can lead to misleading health associations in observational studies, and indeed, create a false impression for health benefits if the group of people who do not drink coffee also includes more people who are unwell,” she said.

For now, doctors can tell their patients that this study provides an explanation as to why research on the health effects of habitual coffee consumption has been conflicting, Dr. Hyppönen said.

“Our study also highlights the uncertainty that underlies the claimed health benefits of coffee, but at the same time, it gives a positive message about the ability of our body to regulate our level of coffee consumption in a way that helps us avoid adverse effects.”

“The most common symptoms of excessive coffee consumption are palpitations and rapid heartbeat, also known as tachycardia,” Nieca Goldberg, MD, medical director of the NYU Women’s Heart Program at NYU Langone Health, said in an interview.

“This study was designed to see if cardiac symptoms affect coffee consumption, and it showed that people with hypertension, angina, history of arrhythmias, and poor health tend to be decaffeinated coffee drinkers or no coffee drinkers,” Dr. Goldberg said.

“People naturally alter their coffee intake base on their blood pressure and symptoms of palpitations and/or rapid heart rate,” she said.

The results also suggest that, “we cannot infer health benefit or harm based on the available coffee studies,” Dr. Goldberg added.

The study was funded by the National Health and Medical Research Council, Australia. Dr. Hyppönen and Dr. Goldberg have disclosed no relevant financial relationships.

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

For children with attention-deficit/hyperactivity disorder, taking a weekend or summer break from methylphenidate may have some benefits. A drug “holiday” can help assess whether a drug is still useful and possibly help with drug tolerance, weight gain, and growth suppression. But drug holidays are not without their problems, Lily Hechtman, MD, FRCP, professor at the department of psychiatry, McGill University, Montreal, said during a session at the World Congress on ADHD – Virtual Event.

Ceasing a medication can have repercussions from a health and social standpoint, cautioned Dr. Hechtman, a presenter and moderator of the session, “Unsolved mysteries in the treatment of ADHD with psychostimulants.”

The rate of drug holidays is somewhere between 30% and 40% in ADHD patients. Patients have multiple reasons for taking them, said Dr. Hechtman. The American Academy of Child & Adolescent Psychology as well as the National Institute for Health and Clinical Excellence recommend this method to assess whether a medication is still necessary. Parents may opt for a drug holiday because most would prefer their children to take less medication.

A drug holiday can counteract some of the key side effects of stimulant medication such as decreased appetite and weight loss, and the moodiness and irritability that accompanies the medication, as well as sleep problems.

It may also be used to avoid drug tolerance, the need to increase dosage as medication continues. A 2002 study of 166 children and adolescents treated with methylphenidate revealed that 60% had developed drug tolerance. Drug tolerance increases with duration. “So, the longer the child is on medication, the more likely he or she will develop some drug tolerance,” said Dr. Hechtman.

It is hypothesized that a drug holiday results in the resensitization of the neurons in the brain because they aren’t exposed to the stimulation of dopamine release and dopamine exposure.

The minimum time a patient needs a drug holiday to deal with some drug tolerance is about a month. “Even if you have a drug holiday and your drug tolerance has been decreased, it can reoccur with increasing dosages, once medication resumes” after the holiday, said Dr. Hechtman.
 

The growth factor

A drug holiday can also address concerns about growth suppression. “Some studies show that drug holidays help with growth suppression and others do not,” said Dr. Hechtman.

The Multimodal Treatment of ADHD (MTA) study, which followed children with ADHD from childhood to adolescence into adulthood, offers some key insights on the effects of treatment on growth.

Over a 10-year period, “you could see that the rate of medication use decreased significantly with time” among participants, said Dr. Hechtman, a coauthor of the MTA research. Only 10% who began the study aged 7-9 years were still using stimulants 10 years later. Looking at short-term effects on growth among these children, those who never went on stimulants to begin with had no growth suppression at all, whereas those who underwent early and consistent treatment experienced the greatest growth suppression.

Comparatively, inconsistently medicated participants had less growth suppression than those who remained on medication. “They were pretty close to the controls,” said Dr. Hechtman.

These patterns continued in a 16-year follow-up, as these patients became adults. Based on the results in the inconsistently treated group, this suggests that drug holidays can limit the effects of growth suppression, at least to a certain extent, said Dr. Hechtman.

Other studies have yielded varying results on the impact of drug holidays on height and weight. “The evidence for the utility of drug holidays for medication side effects is there for decreased appetite and weight, but not so much for decreased height,” summarized Dr. Hechtman.

One recent study of 230 children by James Waxmonsky and colleagues that examined drug holidays on weekends and summers showed that drug holidays did increase weight but interestingly, not height. Older studies Dr. Hechtman cited had inconsistent results on height and weight gain and loss. A 2012 study suggested that drug holidays resulted in a slight improvement in appetite for both weekend and school holidays. But only 9% of the children in the sample (n = 51) saw their appetite return to normal levels.
 

‘Negative things can happen’

The downside of drug holidays is parents may rationalize that their child is doing fine without the medication, and discontinue it. The process of stopping and starting medication can lead to other problems. “Negative things can happen during drug holidays,” said Dr. Hechtman.

The large variability of doses over the weekend can result in rebound and side effects.

A child may go from a full dose, which could be 50-60 mg of stimulant to zero from Friday to Saturday. As a result they have a lot of rebound on that Saturday. Similarly, they go from zero on Sunday to full dose on the Monday, causing lots of side effects. “Also, they will never have a stable effective dose because of the roller-coaster effect of being on and off the drugs,” she noted.

The lack of consistency and accommodation to the side effects can lead to discontinuation of the medication.

Off medication, the child may be more accident prone or have more injuries. “Their behavior off the medication may be such that it leads to social problems,” Dr. Hechtman continued. Weekend activities that require medication such as homework or school projects, family or religious gatherings, or sports and social activities with family and peers may be affected. If the child is behaving poorly off the medication, they may be expelled from such activities. If it’s a summer drug holiday, they may get kicked out of camp or the swimming pool.

If the child’s condition is already worsening, and a drug holiday takes place on top of this, the child may experience a rebound or relapse, in which the condition looks a lot worse than it did with the drugs.
 

Do drug holidays matter?

Another session speaker, James Swanson, PhD, who noted that the “emergence of tolerance may limit and eventually undermine initial relative benefit” of stimulants, said there may be instances in which drug holidays may be impractical.

Given the poor adherence to ADHD medication, “most treated ADHD cases stop medication anyway and these patients do not have an opportunity for drug holidays,” he said in an interview.

“If tolerance does emerge, then for long-term treatment the concept of drug holiday seems difficult to evaluate to me,” said Dr. Swanson, director of the Child Development Center at the University of California, Irvine.

Planned medication breaks may not be a good way to evaluate efficacy unless it is performed under “double-blind” conditions, he offered. The MTA used an approach of switching between short periods of time, with and without medication. “We did this to compare medication to placebo and to compare doses of medication to optimize the short-term benefit,” said Dr. Swanson, a coauthor of the MTA study.

Dr. Hechtman receives funding from The Canadian Institutes of Health Research. Dr. Swanson has two patents: (PIXA4), which uses a “time-of-flight” camera to measure growth on infants, and a provisional patent on the mechanism of tolerance to stimulant medication (PATSMTA).

For children with attention-deficit/hyperactivity disorder, taking a weekend or summer break from methylphenidate may have some benefits. A drug “holiday” can help assess whether a drug is still useful and possibly help with drug tolerance, weight gain, and growth suppression. But drug holidays are not without their problems, Lily Hechtman, MD, FRCP, professor at the department of psychiatry, McGill University, Montreal, said during a session at the World Congress on ADHD – Virtual Event.

Ceasing a medication can have repercussions from a health and social standpoint, cautioned Dr. Hechtman, a presenter and moderator of the session, “Unsolved mysteries in the treatment of ADHD with psychostimulants.”

The rate of drug holidays is somewhere between 30% and 40% in ADHD patients. Patients have multiple reasons for taking them, said Dr. Hechtman. The American Academy of Child & Adolescent Psychology as well as the National Institute for Health and Clinical Excellence recommend this method to assess whether a medication is still necessary. Parents may opt for a drug holiday because most would prefer their children to take less medication.

A drug holiday can counteract some of the key side effects of stimulant medication such as decreased appetite and weight loss, and the moodiness and irritability that accompanies the medication, as well as sleep problems.

It may also be used to avoid drug tolerance, the need to increase dosage as medication continues. A 2002 study of 166 children and adolescents treated with methylphenidate revealed that 60% had developed drug tolerance. Drug tolerance increases with duration. “So, the longer the child is on medication, the more likely he or she will develop some drug tolerance,” said Dr. Hechtman.

It is hypothesized that a drug holiday results in the resensitization of the neurons in the brain because they aren’t exposed to the stimulation of dopamine release and dopamine exposure.

The minimum time a patient needs a drug holiday to deal with some drug tolerance is about a month. “Even if you have a drug holiday and your drug tolerance has been decreased, it can reoccur with increasing dosages, once medication resumes” after the holiday, said Dr. Hechtman.
 

The growth factor

A drug holiday can also address concerns about growth suppression. “Some studies show that drug holidays help with growth suppression and others do not,” said Dr. Hechtman.

The Multimodal Treatment of ADHD (MTA) study, which followed children with ADHD from childhood to adolescence into adulthood, offers some key insights on the effects of treatment on growth.

Over a 10-year period, “you could see that the rate of medication use decreased significantly with time” among participants, said Dr. Hechtman, a coauthor of the MTA research. Only 10% who began the study aged 7-9 years were still using stimulants 10 years later. Looking at short-term effects on growth among these children, those who never went on stimulants to begin with had no growth suppression at all, whereas those who underwent early and consistent treatment experienced the greatest growth suppression.

Comparatively, inconsistently medicated participants had less growth suppression than those who remained on medication. “They were pretty close to the controls,” said Dr. Hechtman.

These patterns continued in a 16-year follow-up, as these patients became adults. Based on the results in the inconsistently treated group, this suggests that drug holidays can limit the effects of growth suppression, at least to a certain extent, said Dr. Hechtman.

Other studies have yielded varying results on the impact of drug holidays on height and weight. “The evidence for the utility of drug holidays for medication side effects is there for decreased appetite and weight, but not so much for decreased height,” summarized Dr. Hechtman.

One recent study of 230 children by James Waxmonsky and colleagues that examined drug holidays on weekends and summers showed that drug holidays did increase weight but interestingly, not height. Older studies Dr. Hechtman cited had inconsistent results on height and weight gain and loss. A 2012 study suggested that drug holidays resulted in a slight improvement in appetite for both weekend and school holidays. But only 9% of the children in the sample (n = 51) saw their appetite return to normal levels.
 

‘Negative things can happen’

The downside of drug holidays is parents may rationalize that their child is doing fine without the medication, and discontinue it. The process of stopping and starting medication can lead to other problems. “Negative things can happen during drug holidays,” said Dr. Hechtman.

The large variability of doses over the weekend can result in rebound and side effects.

A child may go from a full dose, which could be 50-60 mg of stimulant to zero from Friday to Saturday. As a result they have a lot of rebound on that Saturday. Similarly, they go from zero on Sunday to full dose on the Monday, causing lots of side effects. “Also, they will never have a stable effective dose because of the roller-coaster effect of being on and off the drugs,” she noted.

The lack of consistency and accommodation to the side effects can lead to discontinuation of the medication.

Off medication, the child may be more accident prone or have more injuries. “Their behavior off the medication may be such that it leads to social problems,” Dr. Hechtman continued. Weekend activities that require medication such as homework or school projects, family or religious gatherings, or sports and social activities with family and peers may be affected. If the child is behaving poorly off the medication, they may be expelled from such activities. If it’s a summer drug holiday, they may get kicked out of camp or the swimming pool.

If the child’s condition is already worsening, and a drug holiday takes place on top of this, the child may experience a rebound or relapse, in which the condition looks a lot worse than it did with the drugs.
 

Do drug holidays matter?

Another session speaker, James Swanson, PhD, who noted that the “emergence of tolerance may limit and eventually undermine initial relative benefit” of stimulants, said there may be instances in which drug holidays may be impractical.

Given the poor adherence to ADHD medication, “most treated ADHD cases stop medication anyway and these patients do not have an opportunity for drug holidays,” he said in an interview.

“If tolerance does emerge, then for long-term treatment the concept of drug holiday seems difficult to evaluate to me,” said Dr. Swanson, director of the Child Development Center at the University of California, Irvine.

Planned medication breaks may not be a good way to evaluate efficacy unless it is performed under “double-blind” conditions, he offered. The MTA used an approach of switching between short periods of time, with and without medication. “We did this to compare medication to placebo and to compare doses of medication to optimize the short-term benefit,” said Dr. Swanson, a coauthor of the MTA study.

Dr. Hechtman receives funding from The Canadian Institutes of Health Research. Dr. Swanson has two patents: (PIXA4), which uses a “time-of-flight” camera to measure growth on infants, and a provisional patent on the mechanism of tolerance to stimulant medication (PATSMTA).

For children with attention-deficit/hyperactivity disorder, taking a weekend or summer break from methylphenidate may have some benefits. A drug “holiday” can help assess whether a drug is still useful and possibly help with drug tolerance, weight gain, and growth suppression. But drug holidays are not without their problems, Lily Hechtman, MD, FRCP, professor at the department of psychiatry, McGill University, Montreal, said during a session at the World Congress on ADHD – Virtual Event.

Ceasing a medication can have repercussions from a health and social standpoint, cautioned Dr. Hechtman, a presenter and moderator of the session, “Unsolved mysteries in the treatment of ADHD with psychostimulants.”

The rate of drug holidays is somewhere between 30% and 40% in ADHD patients. Patients have multiple reasons for taking them, said Dr. Hechtman. The American Academy of Child & Adolescent Psychology as well as the National Institute for Health and Clinical Excellence recommend this method to assess whether a medication is still necessary. Parents may opt for a drug holiday because most would prefer their children to take less medication.

A drug holiday can counteract some of the key side effects of stimulant medication such as decreased appetite and weight loss, and the moodiness and irritability that accompanies the medication, as well as sleep problems.

It may also be used to avoid drug tolerance, the need to increase dosage as medication continues. A 2002 study of 166 children and adolescents treated with methylphenidate revealed that 60% had developed drug tolerance. Drug tolerance increases with duration. “So, the longer the child is on medication, the more likely he or she will develop some drug tolerance,” said Dr. Hechtman.

It is hypothesized that a drug holiday results in the resensitization of the neurons in the brain because they aren’t exposed to the stimulation of dopamine release and dopamine exposure.

The minimum time a patient needs a drug holiday to deal with some drug tolerance is about a month. “Even if you have a drug holiday and your drug tolerance has been decreased, it can reoccur with increasing dosages, once medication resumes” after the holiday, said Dr. Hechtman.
 

The growth factor

A drug holiday can also address concerns about growth suppression. “Some studies show that drug holidays help with growth suppression and others do not,” said Dr. Hechtman.

The Multimodal Treatment of ADHD (MTA) study, which followed children with ADHD from childhood to adolescence into adulthood, offers some key insights on the effects of treatment on growth.

Over a 10-year period, “you could see that the rate of medication use decreased significantly with time” among participants, said Dr. Hechtman, a coauthor of the MTA research. Only 10% who began the study aged 7-9 years were still using stimulants 10 years later. Looking at short-term effects on growth among these children, those who never went on stimulants to begin with had no growth suppression at all, whereas those who underwent early and consistent treatment experienced the greatest growth suppression.

Comparatively, inconsistently medicated participants had less growth suppression than those who remained on medication. “They were pretty close to the controls,” said Dr. Hechtman.

These patterns continued in a 16-year follow-up, as these patients became adults. Based on the results in the inconsistently treated group, this suggests that drug holidays can limit the effects of growth suppression, at least to a certain extent, said Dr. Hechtman.

Other studies have yielded varying results on the impact of drug holidays on height and weight. “The evidence for the utility of drug holidays for medication side effects is there for decreased appetite and weight, but not so much for decreased height,” summarized Dr. Hechtman.

One recent study of 230 children by James Waxmonsky and colleagues that examined drug holidays on weekends and summers showed that drug holidays did increase weight but interestingly, not height. Older studies Dr. Hechtman cited had inconsistent results on height and weight gain and loss. A 2012 study suggested that drug holidays resulted in a slight improvement in appetite for both weekend and school holidays. But only 9% of the children in the sample (n = 51) saw their appetite return to normal levels.
 

‘Negative things can happen’

The downside of drug holidays is parents may rationalize that their child is doing fine without the medication, and discontinue it. The process of stopping and starting medication can lead to other problems. “Negative things can happen during drug holidays,” said Dr. Hechtman.

The large variability of doses over the weekend can result in rebound and side effects.

A child may go from a full dose, which could be 50-60 mg of stimulant to zero from Friday to Saturday. As a result they have a lot of rebound on that Saturday. Similarly, they go from zero on Sunday to full dose on the Monday, causing lots of side effects. “Also, they will never have a stable effective dose because of the roller-coaster effect of being on and off the drugs,” she noted.

The lack of consistency and accommodation to the side effects can lead to discontinuation of the medication.

Off medication, the child may be more accident prone or have more injuries. “Their behavior off the medication may be such that it leads to social problems,” Dr. Hechtman continued. Weekend activities that require medication such as homework or school projects, family or religious gatherings, or sports and social activities with family and peers may be affected. If the child is behaving poorly off the medication, they may be expelled from such activities. If it’s a summer drug holiday, they may get kicked out of camp or the swimming pool.

If the child’s condition is already worsening, and a drug holiday takes place on top of this, the child may experience a rebound or relapse, in which the condition looks a lot worse than it did with the drugs.
 

Do drug holidays matter?

Another session speaker, James Swanson, PhD, who noted that the “emergence of tolerance may limit and eventually undermine initial relative benefit” of stimulants, said there may be instances in which drug holidays may be impractical.

Given the poor adherence to ADHD medication, “most treated ADHD cases stop medication anyway and these patients do not have an opportunity for drug holidays,” he said in an interview.

“If tolerance does emerge, then for long-term treatment the concept of drug holiday seems difficult to evaluate to me,” said Dr. Swanson, director of the Child Development Center at the University of California, Irvine.

Planned medication breaks may not be a good way to evaluate efficacy unless it is performed under “double-blind” conditions, he offered. The MTA used an approach of switching between short periods of time, with and without medication. “We did this to compare medication to placebo and to compare doses of medication to optimize the short-term benefit,” said Dr. Swanson, a coauthor of the MTA study.

Dr. Hechtman receives funding from The Canadian Institutes of Health Research. Dr. Swanson has two patents: (PIXA4), which uses a “time-of-flight” camera to measure growth on infants, and a provisional patent on the mechanism of tolerance to stimulant medication (PATSMTA).

Six months after mild SARS-CoV-2 infection in a representative health care workforce, no long-term cardiovascular sequelae were detected, compared with a matched SARS-CoV-2 seronegative group.

“Mild COVID-19 left no measurable cardiovascular impact on LV structure, function, scar burden, aortic stiffness, or serum biomarkers,” the researchers reported in an article published online May 8 in JACC: Cardiovascular Imaging.

“We provide societal reassurance and support for the position that screening in asymptomatic individuals following mild disease is not indicated,” first author George Joy, MBBS, University College London, said in presenting the results at EuroCMR, the annual CMR congress of the European Association of Cardiovascular Imaging (EACVI).

Briefing comoderator Leyla Elif Sade, MD, University of Baskent, Ankara, Turkey, said, “This is the hot topic of our time because of obvious reasons and I think [this] study is quite important to avoid unnecessary further testing, surveillance testing, and to avoid a significant burden of health care costs.”
 

‘Alarming’ early data

Early cardiac magnetic resonance (CMR) studies in patients recovered from mild COVID-19 were “alarming,” Dr. Joy said.

As previously reported, one study showed cardiac abnormalities after mild COVID-19 in up to 78% of patients, with evidence of ongoing myocardial inflammation in 60%. The CMR findings correlated with elevations in troponin T by high-sensitivity assay (hs-TnT).

To investigate further, Dr. Joy and colleagues did a nested case-control study within the COVIDsortium, a prospective study of 731 health care workers from three London hospitals who underwent weekly symptom, polymerase chain reaction, and serology assessment over 4 months during the first wave of the pandemic.

A total of 157 (21.5%) participants seroconverted during the study period.

Six months after infection, 74 seropositive (median age, 39; 62% women) and 75 age-, sex-, and ethnicity-matched seronegative controls underwent cardiovascular phenotyping (comprehensive phantom-calibrated CMR and blood biomarkers). The analysis was blinded, using objective artificial intelligence analytics when available.

The results showed no statistically significant differences between seropositive and seronegative participants in cardiac structure (left ventricular volumes, mass, atrial area), function (ejection fraction, global longitudinal shortening, aortic distensibility), tissue characterization (T1, T2, extracellular volume fraction mapping, late gadolinium enhancement) or biomarkers (troponin, N-terminal pro–B-type natriuretic peptide).

Cardiovascular abnormalities were no more common in seropositive than seronegative otherwise healthy health care workers 6 months post mild SARS-CoV-2 infection. Measured abnormalities were “evenly distributed between both groups,” Dr. Joy said.

Therefore, it’s “important to reassure patients with mild SARS-CoV-2 infection regarding its cardiovascular effects,” Dr. Joy and colleagues concluded.
 

Limitations and caveats

They caution, however, that the study provides insight only into the short- to medium-term sequelae of patients aged 18-69 with mild COVID-19 who did not require hospitalization and had low numbers of comorbidities.

The study does not address the cardiovascular effects after severe COVID-19 infection requiring hospitalization or in those with multiple comorbid conditions, they noted. It also does not prove that apparently mild SARS-CoV-2 never causes chronic myocarditis.

“The study design would not distinguish between people who had sustained completely healed myocarditis and pericarditis and those in whom the heart had never been affected,” the researchers noted.

They pointed to a recent cross-sectional study of athletes 1-month post mild COVID-19 that found significant pericardial involvement (late enhancement and/or pericardial effusion), although no baseline pre-COVID-19 imaging was performed. In the current study at 6 months post infection the pericardium was normal.

The coauthors of a linked editorial say this study provides “welcome, reassuring information that in healthy individuals who experience mild infection with COVID-19, persisting evidence of cardiovascular complications is very uncommon. The results do not support cardiovascular screening in individuals with mild or asymptomatic infection with COVID-19.”  

Colin Berry, PhD, and Kenneth Mangion, PhD, both from University of Glasgow, cautioned that the population is restricted to health care workers; therefore, the findings may not necessarily be generalized to a community population .

“Healthcare workers do not reflect the population of individuals most clinically affected by COVID-19 illness. The severity of acute COVID-19 infection is greatest in older individuals and those with preexisting health problems. Healthcare workers are not representative of the wider, unselected, at-risk, community population,” they pointed out.

Cardiovascular risk factors and concomitant health problems (heart and respiratory disease) may be more common in the community than in health care workers, and prior studies have highlighted their potential impact for disease pathogenesis in COVID-19.

Dr. Berry and Dr. Mangion also noted that women made up nearly two-thirds of the seropositive group. This may reflect a selection bias or may naturally reflect the fact that proportionately more women are asymptomatic or have milder forms of illness, whereas severe SARS-CoV-2 infection requiring hospitalization affects men to a greater degree.

COVIDsortium funding was donated by individuals, charitable trusts, and corporations including Goldman Sachs, Citadel and Citadel Securities, The Guy Foundation, GW Pharmaceuticals, Kusuma Trust, and Jagclif Charitable Trust, and enabled by Barts Charity with support from UCLH Charity. The authors have disclosed no relevant financial relationships.

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

Six months after mild SARS-CoV-2 infection in a representative health care workforce, no long-term cardiovascular sequelae were detected, compared with a matched SARS-CoV-2 seronegative group.

“Mild COVID-19 left no measurable cardiovascular impact on LV structure, function, scar burden, aortic stiffness, or serum biomarkers,” the researchers reported in an article published online May 8 in JACC: Cardiovascular Imaging.

“We provide societal reassurance and support for the position that screening in asymptomatic individuals following mild disease is not indicated,” first author George Joy, MBBS, University College London, said in presenting the results at EuroCMR, the annual CMR congress of the European Association of Cardiovascular Imaging (EACVI).

Briefing comoderator Leyla Elif Sade, MD, University of Baskent, Ankara, Turkey, said, “This is the hot topic of our time because of obvious reasons and I think [this] study is quite important to avoid unnecessary further testing, surveillance testing, and to avoid a significant burden of health care costs.”
 

‘Alarming’ early data

Early cardiac magnetic resonance (CMR) studies in patients recovered from mild COVID-19 were “alarming,” Dr. Joy said.

As previously reported, one study showed cardiac abnormalities after mild COVID-19 in up to 78% of patients, with evidence of ongoing myocardial inflammation in 60%. The CMR findings correlated with elevations in troponin T by high-sensitivity assay (hs-TnT).

To investigate further, Dr. Joy and colleagues did a nested case-control study within the COVIDsortium, a prospective study of 731 health care workers from three London hospitals who underwent weekly symptom, polymerase chain reaction, and serology assessment over 4 months during the first wave of the pandemic.

A total of 157 (21.5%) participants seroconverted during the study period.

Six months after infection, 74 seropositive (median age, 39; 62% women) and 75 age-, sex-, and ethnicity-matched seronegative controls underwent cardiovascular phenotyping (comprehensive phantom-calibrated CMR and blood biomarkers). The analysis was blinded, using objective artificial intelligence analytics when available.

The results showed no statistically significant differences between seropositive and seronegative participants in cardiac structure (left ventricular volumes, mass, atrial area), function (ejection fraction, global longitudinal shortening, aortic distensibility), tissue characterization (T1, T2, extracellular volume fraction mapping, late gadolinium enhancement) or biomarkers (troponin, N-terminal pro–B-type natriuretic peptide).

Cardiovascular abnormalities were no more common in seropositive than seronegative otherwise healthy health care workers 6 months post mild SARS-CoV-2 infection. Measured abnormalities were “evenly distributed between both groups,” Dr. Joy said.

Therefore, it’s “important to reassure patients with mild SARS-CoV-2 infection regarding its cardiovascular effects,” Dr. Joy and colleagues concluded.
 

Limitations and caveats

They caution, however, that the study provides insight only into the short- to medium-term sequelae of patients aged 18-69 with mild COVID-19 who did not require hospitalization and had low numbers of comorbidities.

The study does not address the cardiovascular effects after severe COVID-19 infection requiring hospitalization or in those with multiple comorbid conditions, they noted. It also does not prove that apparently mild SARS-CoV-2 never causes chronic myocarditis.

“The study design would not distinguish between people who had sustained completely healed myocarditis and pericarditis and those in whom the heart had never been affected,” the researchers noted.

They pointed to a recent cross-sectional study of athletes 1-month post mild COVID-19 that found significant pericardial involvement (late enhancement and/or pericardial effusion), although no baseline pre-COVID-19 imaging was performed. In the current study at 6 months post infection the pericardium was normal.

The coauthors of a linked editorial say this study provides “welcome, reassuring information that in healthy individuals who experience mild infection with COVID-19, persisting evidence of cardiovascular complications is very uncommon. The results do not support cardiovascular screening in individuals with mild or asymptomatic infection with COVID-19.”  

Colin Berry, PhD, and Kenneth Mangion, PhD, both from University of Glasgow, cautioned that the population is restricted to health care workers; therefore, the findings may not necessarily be generalized to a community population .

“Healthcare workers do not reflect the population of individuals most clinically affected by COVID-19 illness. The severity of acute COVID-19 infection is greatest in older individuals and those with preexisting health problems. Healthcare workers are not representative of the wider, unselected, at-risk, community population,” they pointed out.

Cardiovascular risk factors and concomitant health problems (heart and respiratory disease) may be more common in the community than in health care workers, and prior studies have highlighted their potential impact for disease pathogenesis in COVID-19.

Dr. Berry and Dr. Mangion also noted that women made up nearly two-thirds of the seropositive group. This may reflect a selection bias or may naturally reflect the fact that proportionately more women are asymptomatic or have milder forms of illness, whereas severe SARS-CoV-2 infection requiring hospitalization affects men to a greater degree.

COVIDsortium funding was donated by individuals, charitable trusts, and corporations including Goldman Sachs, Citadel and Citadel Securities, The Guy Foundation, GW Pharmaceuticals, Kusuma Trust, and Jagclif Charitable Trust, and enabled by Barts Charity with support from UCLH Charity. The authors have disclosed no relevant financial relationships.

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

Six months after mild SARS-CoV-2 infection in a representative health care workforce, no long-term cardiovascular sequelae were detected, compared with a matched SARS-CoV-2 seronegative group.

“Mild COVID-19 left no measurable cardiovascular impact on LV structure, function, scar burden, aortic stiffness, or serum biomarkers,” the researchers reported in an article published online May 8 in JACC: Cardiovascular Imaging.

“We provide societal reassurance and support for the position that screening in asymptomatic individuals following mild disease is not indicated,” first author George Joy, MBBS, University College London, said in presenting the results at EuroCMR, the annual CMR congress of the European Association of Cardiovascular Imaging (EACVI).

Briefing comoderator Leyla Elif Sade, MD, University of Baskent, Ankara, Turkey, said, “This is the hot topic of our time because of obvious reasons and I think [this] study is quite important to avoid unnecessary further testing, surveillance testing, and to avoid a significant burden of health care costs.”
 

‘Alarming’ early data

Early cardiac magnetic resonance (CMR) studies in patients recovered from mild COVID-19 were “alarming,” Dr. Joy said.

As previously reported, one study showed cardiac abnormalities after mild COVID-19 in up to 78% of patients, with evidence of ongoing myocardial inflammation in 60%. The CMR findings correlated with elevations in troponin T by high-sensitivity assay (hs-TnT).

To investigate further, Dr. Joy and colleagues did a nested case-control study within the COVIDsortium, a prospective study of 731 health care workers from three London hospitals who underwent weekly symptom, polymerase chain reaction, and serology assessment over 4 months during the first wave of the pandemic.

A total of 157 (21.5%) participants seroconverted during the study period.

Six months after infection, 74 seropositive (median age, 39; 62% women) and 75 age-, sex-, and ethnicity-matched seronegative controls underwent cardiovascular phenotyping (comprehensive phantom-calibrated CMR and blood biomarkers). The analysis was blinded, using objective artificial intelligence analytics when available.

The results showed no statistically significant differences between seropositive and seronegative participants in cardiac structure (left ventricular volumes, mass, atrial area), function (ejection fraction, global longitudinal shortening, aortic distensibility), tissue characterization (T1, T2, extracellular volume fraction mapping, late gadolinium enhancement) or biomarkers (troponin, N-terminal pro–B-type natriuretic peptide).

Cardiovascular abnormalities were no more common in seropositive than seronegative otherwise healthy health care workers 6 months post mild SARS-CoV-2 infection. Measured abnormalities were “evenly distributed between both groups,” Dr. Joy said.

Therefore, it’s “important to reassure patients with mild SARS-CoV-2 infection regarding its cardiovascular effects,” Dr. Joy and colleagues concluded.
 

Limitations and caveats

They caution, however, that the study provides insight only into the short- to medium-term sequelae of patients aged 18-69 with mild COVID-19 who did not require hospitalization and had low numbers of comorbidities.

The study does not address the cardiovascular effects after severe COVID-19 infection requiring hospitalization or in those with multiple comorbid conditions, they noted. It also does not prove that apparently mild SARS-CoV-2 never causes chronic myocarditis.

“The study design would not distinguish between people who had sustained completely healed myocarditis and pericarditis and those in whom the heart had never been affected,” the researchers noted.

They pointed to a recent cross-sectional study of athletes 1-month post mild COVID-19 that found significant pericardial involvement (late enhancement and/or pericardial effusion), although no baseline pre-COVID-19 imaging was performed. In the current study at 6 months post infection the pericardium was normal.

The coauthors of a linked editorial say this study provides “welcome, reassuring information that in healthy individuals who experience mild infection with COVID-19, persisting evidence of cardiovascular complications is very uncommon. The results do not support cardiovascular screening in individuals with mild or asymptomatic infection with COVID-19.”  

Colin Berry, PhD, and Kenneth Mangion, PhD, both from University of Glasgow, cautioned that the population is restricted to health care workers; therefore, the findings may not necessarily be generalized to a community population .

“Healthcare workers do not reflect the population of individuals most clinically affected by COVID-19 illness. The severity of acute COVID-19 infection is greatest in older individuals and those with preexisting health problems. Healthcare workers are not representative of the wider, unselected, at-risk, community population,” they pointed out.

Cardiovascular risk factors and concomitant health problems (heart and respiratory disease) may be more common in the community than in health care workers, and prior studies have highlighted their potential impact for disease pathogenesis in COVID-19.

Dr. Berry and Dr. Mangion also noted that women made up nearly two-thirds of the seropositive group. This may reflect a selection bias or may naturally reflect the fact that proportionately more women are asymptomatic or have milder forms of illness, whereas severe SARS-CoV-2 infection requiring hospitalization affects men to a greater degree.

COVIDsortium funding was donated by individuals, charitable trusts, and corporations including Goldman Sachs, Citadel and Citadel Securities, The Guy Foundation, GW Pharmaceuticals, Kusuma Trust, and Jagclif Charitable Trust, and enabled by Barts Charity with support from UCLH Charity. The authors have disclosed no relevant financial relationships.

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

Patients who receive the mRNA COVID-19 vaccines are experiencing a variety of skin rashes, a dermatologist told colleagues, and some lesions don’t appear until several days after an injection. The good news is that these side effects tend to be minor and vanish within a few days, Esther Freeman, MD, PhD, said in a presentation at the American Academy of Dermatology Virtual Meeting Experience.

“The reality is actually very reassuring,” Dr. Freeman said, especially in light of what is currently known about when the rashes occur and how anaphylaxis is extremely uncommon. Now, she added, dermatologists can tell patients who had reactions to their initial vaccination that “we know you had this big reaction, and we know that it was upsetting and uncomfortable. But it may not happen the second time around. And if it does, [the reaction is] probably going to be smaller.”

Dr. Freeman, associate professor of dermatology at Harvard Medical School, Boston, highlighted a study published in the Journal of the American Academy of Dermatology that she coauthored with dermatologists across the United States. The researchers tracked 414 cutaneous reactions to the Moderna (83%) and Pfizer (17%) COVID-19 vaccines in a group of patients, which was 90% female, 78% White, and mostly from the United States. Their average age was 44 years. The cases were reported to the AAD–International League of Dermatological Societies registry of COVID-19 cutaneous manifestations.

While most were women, “it’s a little hard to know if this is really going to end up being a true finding,” said Dr. Freeman, the registry’s principal investigator and a member of the AAD’s COVID-19 Ad Hoc Task Force. “If you think about who got vaccinated early, it was health care providers, and the American health care workforce is over 70% female. So I think there’s a little bit of bias here. There may also be a bias because women may be slightly more likely to report or go to their health care provider for a rash.”

Delayed large local reactions were the most common, accounting for 66% (175 cases) of the 267 skin reactions reported after the first Moderna vaccine dose and 30% (31 cases) of the 102 reactions reported after the second dose. These reactions represented 15% (5 cases) of the 34 skin reactions reported after the first Pfizer vaccine dose and 18% (7 cases) of the 40 reactions after the second dose.

There are two peaks with that first dose, Dr. Freeman said. “There’s a peak around day 2 or 3. And there’s another peak around day 7 or 8 with some of these reactions. Only 27% who had a reaction with the first dose had the same reaction with the second.” She added that these reactions “are not cellulitis and don’t require antibiotics.”

Other more common reactions included local injection-site reactions (swelling, erythema, and pain), urticaria (after 24 hours in almost all cases, occurring at a higher rate in patients who received the Pfizer vaccine), and morbilliform eruptions.

Dr. Freeman said that patients may experience redness and swelling in the hands and feet that can be “very uncomfortable.” She described one patient “who was having a hard time actually closing his fist, just because of the amount of swelling and redness in his hand. It did resolve, and it’s important to reassure your patients it will go away.”

According to this study, less common reports of other cutaneous findings with both vaccines included 9 reports of swelling at the site of cosmetic fillers, 8 reports of pernio/chilblains, 10 reports of varicella zoster, 4 reports of herpes simplex flares, 4 pityriasis rosea–like reactions, and 4 rashes in infants of vaccinated breastfeeding mothers.

The study noted that “patients responded well to topical corticosteroids, oral antihistamines, and/or pain-relieving medications. These reactions resolved after a median of 3-4 days.”

It’s important to understand that none of the patients developed anaphylaxis after the second dose even if they’d had a reaction to the first dose, Dr. Freeman said. “But I should point out that we’re talking about reactions that have started more than 4 hours after the vaccine. If a rash such as a urticaria specifically starts within 4 hours of vaccination, that’s in a different category. Those are considered more immediate allergic reactions, and those patients need to be seen by allergy before a second dose.”

Dr. Freeman added that “it’s really interesting to think about how our bodies are really reacting to the vaccine in a way that’s mimicking our body’s reactions to COVID-19.” For example, some patients who got vaccinated developed chilblains similar to the “COVID toes” described in infected patients, apparently as part of the body’s immune response to the virus. “We’ve seen this in patients who actually had COVID and had prior COVID toes and then actually got a flare with their vaccine. And then we’ve also seen it in patients who never had COVID.”

In regard to general advice for patients, she said, “I do still encourage my patients who previously had COVID to go ahead and get the vaccine even if they had a skin manifestation with COVID.”

Shari Lipner, MD, PhD, associate professor of clinical dermatology, Weill Cornell Medicine, New York, said she has have seen only a handful of cases of delayed large local reactions and local injection site reactions after COVID-19 vaccination. “I have seen a significant number of cases of acute urticaria following the first and second doses,” she said in an interview. “However, it is important to keep in mind that we cannot determine cause and effect for the cases of acute urticaria. They may or may not be vaccine related.”

Fortunately, none of the adverse effects she’s seen have been severe. “It is important that dermatologists educate the public and their patients that most people do not develop any skin reaction in response to the vaccine,” she said. In the minority who do, “reactions tend to be mild and are not life-threatening. Many of these skin reactions resolve on their own without treatment.”

She added that “patients with pernio/chilblains or herpes zoster following vaccination should be referred by a board-certified dermatologist for prompt treatment and to avoid sequelae.”


 

‘COVID vaccine arm’

Delayed local reactions to the Moderna vaccine were also described in a report published online on May 12, 2021, in JAMA Dermatology, after the AAD meeting, in 16 patients referred to the Yale New Haven (Conn.) Hospital Dermatology service who experienced delayed localized cutaneous hypersensitivity reactions a median of 7 days after receiving the vaccine (range, 2-12 days), from Jan. 20 to Feb. 12, 2021. No such cases were reported in Pfizer vaccine recipients.

Of the 16 patients, whose median age was 38 years and who were mostly women, 15 developed the reaction after the first dose, described as “pruritic and variably painful erythematous reactions near the injection site,” which lasted a median of 5 days (range, 1-21 days). After the second dose, 12 of the 16 patients developed injection-site reactions (including one patient who had no reaction after dose 1), a median of 2 days after the vaccine was administered (range, 0-5 days). Histologic results of a biopsy in one patient with a reaction to the second dose “ demonstrated mild predominantly perivascular and focal interstitial mixed infiltrate with lymphocytes and eosinophils consistent with a dermal hypersensitivity reaction,” wrote Alicia J. Little, MD, PhD, of the department of dermatology, Yale University, New Haven, and coauthors.

Compared with immediate hypersensitivity reactions, occurring within 4 hours of vaccination, such as anaphylaxis and urticaria, they concluded that “these delayed localized hypersensitivity reactions are not a contraindication to subsequent vaccination,” and they proposed that they be named “COVID vaccine arm.”

Dr. Freeman reported no disclosures. Dr. Lipner also had no relevant disclosures. Dr. Little reported receiving a grant from the National Center for Advancing Translational Science and a Women’s Health Career Development Award from the Dermatology Foundation while the study was conducted; another author reported equity in Johnson & Johnson in his spouse’s retirement fund outside the submitted work.
 

Patients who receive the mRNA COVID-19 vaccines are experiencing a variety of skin rashes, a dermatologist told colleagues, and some lesions don’t appear until several days after an injection. The good news is that these side effects tend to be minor and vanish within a few days, Esther Freeman, MD, PhD, said in a presentation at the American Academy of Dermatology Virtual Meeting Experience.

“The reality is actually very reassuring,” Dr. Freeman said, especially in light of what is currently known about when the rashes occur and how anaphylaxis is extremely uncommon. Now, she added, dermatologists can tell patients who had reactions to their initial vaccination that “we know you had this big reaction, and we know that it was upsetting and uncomfortable. But it may not happen the second time around. And if it does, [the reaction is] probably going to be smaller.”

Dr. Freeman, associate professor of dermatology at Harvard Medical School, Boston, highlighted a study published in the Journal of the American Academy of Dermatology that she coauthored with dermatologists across the United States. The researchers tracked 414 cutaneous reactions to the Moderna (83%) and Pfizer (17%) COVID-19 vaccines in a group of patients, which was 90% female, 78% White, and mostly from the United States. Their average age was 44 years. The cases were reported to the AAD–International League of Dermatological Societies registry of COVID-19 cutaneous manifestations.

While most were women, “it’s a little hard to know if this is really going to end up being a true finding,” said Dr. Freeman, the registry’s principal investigator and a member of the AAD’s COVID-19 Ad Hoc Task Force. “If you think about who got vaccinated early, it was health care providers, and the American health care workforce is over 70% female. So I think there’s a little bit of bias here. There may also be a bias because women may be slightly more likely to report or go to their health care provider for a rash.”

Delayed large local reactions were the most common, accounting for 66% (175 cases) of the 267 skin reactions reported after the first Moderna vaccine dose and 30% (31 cases) of the 102 reactions reported after the second dose. These reactions represented 15% (5 cases) of the 34 skin reactions reported after the first Pfizer vaccine dose and 18% (7 cases) of the 40 reactions after the second dose.

There are two peaks with that first dose, Dr. Freeman said. “There’s a peak around day 2 or 3. And there’s another peak around day 7 or 8 with some of these reactions. Only 27% who had a reaction with the first dose had the same reaction with the second.” She added that these reactions “are not cellulitis and don’t require antibiotics.”

Other more common reactions included local injection-site reactions (swelling, erythema, and pain), urticaria (after 24 hours in almost all cases, occurring at a higher rate in patients who received the Pfizer vaccine), and morbilliform eruptions.

Dr. Freeman said that patients may experience redness and swelling in the hands and feet that can be “very uncomfortable.” She described one patient “who was having a hard time actually closing his fist, just because of the amount of swelling and redness in his hand. It did resolve, and it’s important to reassure your patients it will go away.”

According to this study, less common reports of other cutaneous findings with both vaccines included 9 reports of swelling at the site of cosmetic fillers, 8 reports of pernio/chilblains, 10 reports of varicella zoster, 4 reports of herpes simplex flares, 4 pityriasis rosea–like reactions, and 4 rashes in infants of vaccinated breastfeeding mothers.

The study noted that “patients responded well to topical corticosteroids, oral antihistamines, and/or pain-relieving medications. These reactions resolved after a median of 3-4 days.”

It’s important to understand that none of the patients developed anaphylaxis after the second dose even if they’d had a reaction to the first dose, Dr. Freeman said. “But I should point out that we’re talking about reactions that have started more than 4 hours after the vaccine. If a rash such as a urticaria specifically starts within 4 hours of vaccination, that’s in a different category. Those are considered more immediate allergic reactions, and those patients need to be seen by allergy before a second dose.”

Dr. Freeman added that “it’s really interesting to think about how our bodies are really reacting to the vaccine in a way that’s mimicking our body’s reactions to COVID-19.” For example, some patients who got vaccinated developed chilblains similar to the “COVID toes” described in infected patients, apparently as part of the body’s immune response to the virus. “We’ve seen this in patients who actually had COVID and had prior COVID toes and then actually got a flare with their vaccine. And then we’ve also seen it in patients who never had COVID.”

In regard to general advice for patients, she said, “I do still encourage my patients who previously had COVID to go ahead and get the vaccine even if they had a skin manifestation with COVID.”

Shari Lipner, MD, PhD, associate professor of clinical dermatology, Weill Cornell Medicine, New York, said she has have seen only a handful of cases of delayed large local reactions and local injection site reactions after COVID-19 vaccination. “I have seen a significant number of cases of acute urticaria following the first and second doses,” she said in an interview. “However, it is important to keep in mind that we cannot determine cause and effect for the cases of acute urticaria. They may or may not be vaccine related.”

Fortunately, none of the adverse effects she’s seen have been severe. “It is important that dermatologists educate the public and their patients that most people do not develop any skin reaction in response to the vaccine,” she said. In the minority who do, “reactions tend to be mild and are not life-threatening. Many of these skin reactions resolve on their own without treatment.”

She added that “patients with pernio/chilblains or herpes zoster following vaccination should be referred by a board-certified dermatologist for prompt treatment and to avoid sequelae.”


 

‘COVID vaccine arm’

Delayed local reactions to the Moderna vaccine were also described in a report published online on May 12, 2021, in JAMA Dermatology, after the AAD meeting, in 16 patients referred to the Yale New Haven (Conn.) Hospital Dermatology service who experienced delayed localized cutaneous hypersensitivity reactions a median of 7 days after receiving the vaccine (range, 2-12 days), from Jan. 20 to Feb. 12, 2021. No such cases were reported in Pfizer vaccine recipients.

Of the 16 patients, whose median age was 38 years and who were mostly women, 15 developed the reaction after the first dose, described as “pruritic and variably painful erythematous reactions near the injection site,” which lasted a median of 5 days (range, 1-21 days). After the second dose, 12 of the 16 patients developed injection-site reactions (including one patient who had no reaction after dose 1), a median of 2 days after the vaccine was administered (range, 0-5 days). Histologic results of a biopsy in one patient with a reaction to the second dose “ demonstrated mild predominantly perivascular and focal interstitial mixed infiltrate with lymphocytes and eosinophils consistent with a dermal hypersensitivity reaction,” wrote Alicia J. Little, MD, PhD, of the department of dermatology, Yale University, New Haven, and coauthors.

Compared with immediate hypersensitivity reactions, occurring within 4 hours of vaccination, such as anaphylaxis and urticaria, they concluded that “these delayed localized hypersensitivity reactions are not a contraindication to subsequent vaccination,” and they proposed that they be named “COVID vaccine arm.”

Dr. Freeman reported no disclosures. Dr. Lipner also had no relevant disclosures. Dr. Little reported receiving a grant from the National Center for Advancing Translational Science and a Women’s Health Career Development Award from the Dermatology Foundation while the study was conducted; another author reported equity in Johnson & Johnson in his spouse’s retirement fund outside the submitted work.
 

Patients who receive the mRNA COVID-19 vaccines are experiencing a variety of skin rashes, a dermatologist told colleagues, and some lesions don’t appear until several days after an injection. The good news is that these side effects tend to be minor and vanish within a few days, Esther Freeman, MD, PhD, said in a presentation at the American Academy of Dermatology Virtual Meeting Experience.

“The reality is actually very reassuring,” Dr. Freeman said, especially in light of what is currently known about when the rashes occur and how anaphylaxis is extremely uncommon. Now, she added, dermatologists can tell patients who had reactions to their initial vaccination that “we know you had this big reaction, and we know that it was upsetting and uncomfortable. But it may not happen the second time around. And if it does, [the reaction is] probably going to be smaller.”

Dr. Freeman, associate professor of dermatology at Harvard Medical School, Boston, highlighted a study published in the Journal of the American Academy of Dermatology that she coauthored with dermatologists across the United States. The researchers tracked 414 cutaneous reactions to the Moderna (83%) and Pfizer (17%) COVID-19 vaccines in a group of patients, which was 90% female, 78% White, and mostly from the United States. Their average age was 44 years. The cases were reported to the AAD–International League of Dermatological Societies registry of COVID-19 cutaneous manifestations.

While most were women, “it’s a little hard to know if this is really going to end up being a true finding,” said Dr. Freeman, the registry’s principal investigator and a member of the AAD’s COVID-19 Ad Hoc Task Force. “If you think about who got vaccinated early, it was health care providers, and the American health care workforce is over 70% female. So I think there’s a little bit of bias here. There may also be a bias because women may be slightly more likely to report or go to their health care provider for a rash.”

Delayed large local reactions were the most common, accounting for 66% (175 cases) of the 267 skin reactions reported after the first Moderna vaccine dose and 30% (31 cases) of the 102 reactions reported after the second dose. These reactions represented 15% (5 cases) of the 34 skin reactions reported after the first Pfizer vaccine dose and 18% (7 cases) of the 40 reactions after the second dose.

There are two peaks with that first dose, Dr. Freeman said. “There’s a peak around day 2 or 3. And there’s another peak around day 7 or 8 with some of these reactions. Only 27% who had a reaction with the first dose had the same reaction with the second.” She added that these reactions “are not cellulitis and don’t require antibiotics.”

Other more common reactions included local injection-site reactions (swelling, erythema, and pain), urticaria (after 24 hours in almost all cases, occurring at a higher rate in patients who received the Pfizer vaccine), and morbilliform eruptions.

Dr. Freeman said that patients may experience redness and swelling in the hands and feet that can be “very uncomfortable.” She described one patient “who was having a hard time actually closing his fist, just because of the amount of swelling and redness in his hand. It did resolve, and it’s important to reassure your patients it will go away.”

According to this study, less common reports of other cutaneous findings with both vaccines included 9 reports of swelling at the site of cosmetic fillers, 8 reports of pernio/chilblains, 10 reports of varicella zoster, 4 reports of herpes simplex flares, 4 pityriasis rosea–like reactions, and 4 rashes in infants of vaccinated breastfeeding mothers.

The study noted that “patients responded well to topical corticosteroids, oral antihistamines, and/or pain-relieving medications. These reactions resolved after a median of 3-4 days.”

It’s important to understand that none of the patients developed anaphylaxis after the second dose even if they’d had a reaction to the first dose, Dr. Freeman said. “But I should point out that we’re talking about reactions that have started more than 4 hours after the vaccine. If a rash such as a urticaria specifically starts within 4 hours of vaccination, that’s in a different category. Those are considered more immediate allergic reactions, and those patients need to be seen by allergy before a second dose.”

Dr. Freeman added that “it’s really interesting to think about how our bodies are really reacting to the vaccine in a way that’s mimicking our body’s reactions to COVID-19.” For example, some patients who got vaccinated developed chilblains similar to the “COVID toes” described in infected patients, apparently as part of the body’s immune response to the virus. “We’ve seen this in patients who actually had COVID and had prior COVID toes and then actually got a flare with their vaccine. And then we’ve also seen it in patients who never had COVID.”

In regard to general advice for patients, she said, “I do still encourage my patients who previously had COVID to go ahead and get the vaccine even if they had a skin manifestation with COVID.”

Shari Lipner, MD, PhD, associate professor of clinical dermatology, Weill Cornell Medicine, New York, said she has have seen only a handful of cases of delayed large local reactions and local injection site reactions after COVID-19 vaccination. “I have seen a significant number of cases of acute urticaria following the first and second doses,” she said in an interview. “However, it is important to keep in mind that we cannot determine cause and effect for the cases of acute urticaria. They may or may not be vaccine related.”

Fortunately, none of the adverse effects she’s seen have been severe. “It is important that dermatologists educate the public and their patients that most people do not develop any skin reaction in response to the vaccine,” she said. In the minority who do, “reactions tend to be mild and are not life-threatening. Many of these skin reactions resolve on their own without treatment.”

She added that “patients with pernio/chilblains or herpes zoster following vaccination should be referred by a board-certified dermatologist for prompt treatment and to avoid sequelae.”


 

‘COVID vaccine arm’

Delayed local reactions to the Moderna vaccine were also described in a report published online on May 12, 2021, in JAMA Dermatology, after the AAD meeting, in 16 patients referred to the Yale New Haven (Conn.) Hospital Dermatology service who experienced delayed localized cutaneous hypersensitivity reactions a median of 7 days after receiving the vaccine (range, 2-12 days), from Jan. 20 to Feb. 12, 2021. No such cases were reported in Pfizer vaccine recipients.

Of the 16 patients, whose median age was 38 years and who were mostly women, 15 developed the reaction after the first dose, described as “pruritic and variably painful erythematous reactions near the injection site,” which lasted a median of 5 days (range, 1-21 days). After the second dose, 12 of the 16 patients developed injection-site reactions (including one patient who had no reaction after dose 1), a median of 2 days after the vaccine was administered (range, 0-5 days). Histologic results of a biopsy in one patient with a reaction to the second dose “ demonstrated mild predominantly perivascular and focal interstitial mixed infiltrate with lymphocytes and eosinophils consistent with a dermal hypersensitivity reaction,” wrote Alicia J. Little, MD, PhD, of the department of dermatology, Yale University, New Haven, and coauthors.

Compared with immediate hypersensitivity reactions, occurring within 4 hours of vaccination, such as anaphylaxis and urticaria, they concluded that “these delayed localized hypersensitivity reactions are not a contraindication to subsequent vaccination,” and they proposed that they be named “COVID vaccine arm.”

Dr. Freeman reported no disclosures. Dr. Lipner also had no relevant disclosures. Dr. Little reported receiving a grant from the National Center for Advancing Translational Science and a Women’s Health Career Development Award from the Dermatology Foundation while the study was conducted; another author reported equity in Johnson & Johnson in his spouse’s retirement fund outside the submitted work.
 

Society is having a moment of reflection about the role of law enforcement and correctional facilities in addressing societal problems. During this moment, psychiatry is being asked by courts to arbitrate who qualifies and ultimately deserves certain judgments.

In particular, we are asked to assess how dangerous an individual may be using violent risk assessment tools and measures of antisocial disorders. As such, we are tasked with pointing out the negative factors of defendants. Alternatively, psychiatry is also asked to explain, using biopsychosocial determinants, what led an individual to act in a deviant manner. As such, we are tasked with pointing out mitigating factors of defendants. In this article, we attempt to look at limitations in both paradigms to encourage a more prudent forensic approach.
 

Negative factors

A conundrum for the forensic psychiatry evaluator is that diagnostic criteria are not designed for the rigors and needs of court. The criteria in the Diagnostic and Statistical Manual of Mental Disorders (DSM) are not composed of rigid rules with validity markers to measure their veracity but leave room for clinical judgment, variance across individuals, and future research and treatment needs.

There are some benefits to having room for clinical judgment, but it can also lead to overdiagnosis.¹ This problem is particularly reflected in the diagnosis of antisocial personality disorder (ASPD), the criteria of which includes failure to conform to social norms, deceitfulness, impulsivity, irritability, recklessness, irresponsibility, and lack of remorse. Each of these criteria is ripe for subjectivity by an inexperienced or biased reviewer.

Mitigating factors

On the other side, the defense expert also faces significant challenges, though the tools are different. Contrary to the prosecuting expert who loads an arsenal of subjective assessment tools, the defense expert will point to childhood trauma and mental illness as extenuating explanations for a crime. Having suffered abuse as a child is advanced to justify someone’s subsequent violence. This problem is reflected in the diagnosis of posttraumatic stress disorder (PTSD). An unscrupulous expert may simply allow an evaluee to endorse symptoms without clinical correlates or rigorous validation to advance this narrative.

For example, psychiatrists commonly ascribe the DSM criteria A for PTSD, “directly experiencing the traumatic event(s),” to a smaller slight in life. Some experts suggest that a medical diagnosis, even if not life-threatening but perceived as such, could warrant the diagnosis.¹⁰ This would expand our understanding of trauma and its consequences significantly. Yet already, a survey of Detroit area residents in 1998 found that 89.6% of the interviewees reported having experienced a significant trauma and that the average number of traumatic experiences was 4.8.¹¹ The meaning of a diagnosis that can be applied to almost 90% of a population has unclear usefulness, especially if meant to diminish guilt and responsibility.

More recently, citing Adverse Childhood Experiences (ACEs) has been a common method of supporting mitigating evaluations. Using the ACEs questionnaires, researchers have supported the idea that social programs are a key player in an improved criminal justice system. The ACEs study identified 10 forms of childhood trauma in 17,000 patients, including abuse, neglect, abandonment, household dysfunction, and exposure to violence, that were strongly associated with negative psychological outcomes, engagement in high-risk behaviors, significant medical consequences, and even early death.¹² However, similarly to past trauma, the prevalence of ACEs in the forensic population is the norm, not the exception.
 

Additional thoughts

Of particular concern is when diagnostic criteria intersect or seemingly contradict one another. For example, acts such as an outburst of anger may be interpreted by one evaluator as a sign of deviance, irritability, or recklessness – and meeting antisocial personality disorder criteria. Whereas another evaluator may interpret the same incident as hypervigilance, exaggerated startle response, or self-destructive behavior in PTSD.

An incident of not assisting someone in need may be interpreted as lack of remorse and glibness from antisocial characteristics or avoidance and detachment from others as a reaction to past trauma. Flashbacks from trauma can be interpreted by some as violent fantasies. Even the experience of trauma can be viewed as a risk factor for future violence. In some ways, our perspectives are influenced by our examination of someone’s history through the lens of sociopathy or empathy.
 

In summary

Psychiatry is entrusted by courts to comment on negative and mitigating factors. Negative factors hinge in part on our subjective impression of sociopathy, and mitigating factors hinge, in part, on our empathy for a defendant’s trauma. Psychiatry should recognize the limitations of both sides and humble itself in providing balanced evaluations to courts.

Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Amendolara is a first-year psychiatry resident at University of California, San Diego. He spent years advocating for survivors of rape and domestic violence at the Crime Victims Treatment Center in New York and conducted public health research at Lourdes Center for Public Health in Camden, N.J. Dr. Amendolara has no disclosures. Dr. Ngo is a second-year child neurology resident at University of California, Los Angeles. She received a master’s degree in narrative medicine from Columbia University, New York. She has no disclosures.

References

1. Frances A. Saving Normal: An Insider’s Revolt Against Out-of-Control Psychiatric Diagnosis, DSM-5, Big Pharma and the Medicalization of Ordinary Life. Harper Collins, 2013.

2. Key Substance Use and Mental Health Indicators in the United States. National Survey on Drug Use and Health. 2018.

3. Wong SCP and Gordon A. Psychol Public Policy Law. 2006;12(3):279-309.

4. Douglas KS et al. Mental Health Law & Policy Institute. About the Historical Clinical Risk Management-20, Version 3.

5. Angwin J et al. ProPublica. 2016 May 23.

6. Dressel J and Farid H. Sci Adv. 2018;4(1). doi: 10.1126/sciady.aao5580.

7. Freedman R et al. Am J Psychiatry. 2013 Jan;170(1):1-5.

8. Lillie B. The complexities of the psychopath test: A Q&A with Ron Jonson. TEDBlog. 2012 Aug 15.

9. Larsen RR et al. Psychol Public Policy Law. 2020;26(3):297-311.

10. Cordova MJ. Psychiatric Times. 2020 Jul 31;37(7).

11. Breslau N et al. Arch Gen Psychiatry. 1998;55(7):626-32.

12. Reavis JA et al. Perm J. 2013 Spring;17(2):44-8.

Society is having a moment of reflection about the role of law enforcement and correctional facilities in addressing societal problems. During this moment, psychiatry is being asked by courts to arbitrate who qualifies and ultimately deserves certain judgments.

In particular, we are asked to assess how dangerous an individual may be using violent risk assessment tools and measures of antisocial disorders. As such, we are tasked with pointing out the negative factors of defendants. Alternatively, psychiatry is also asked to explain, using biopsychosocial determinants, what led an individual to act in a deviant manner. As such, we are tasked with pointing out mitigating factors of defendants. In this article, we attempt to look at limitations in both paradigms to encourage a more prudent forensic approach.
 

Negative factors

A conundrum for the forensic psychiatry evaluator is that diagnostic criteria are not designed for the rigors and needs of court. The criteria in the Diagnostic and Statistical Manual of Mental Disorders (DSM) are not composed of rigid rules with validity markers to measure their veracity but leave room for clinical judgment, variance across individuals, and future research and treatment needs.

There are some benefits to having room for clinical judgment, but it can also lead to overdiagnosis.¹ This problem is particularly reflected in the diagnosis of antisocial personality disorder (ASPD), the criteria of which includes failure to conform to social norms, deceitfulness, impulsivity, irritability, recklessness, irresponsibility, and lack of remorse. Each of these criteria is ripe for subjectivity by an inexperienced or biased reviewer.

Mitigating factors

On the other side, the defense expert also faces significant challenges, though the tools are different. Contrary to the prosecuting expert who loads an arsenal of subjective assessment tools, the defense expert will point to childhood trauma and mental illness as extenuating explanations for a crime. Having suffered abuse as a child is advanced to justify someone’s subsequent violence. This problem is reflected in the diagnosis of posttraumatic stress disorder (PTSD). An unscrupulous expert may simply allow an evaluee to endorse symptoms without clinical correlates or rigorous validation to advance this narrative.

For example, psychiatrists commonly ascribe the DSM criteria A for PTSD, “directly experiencing the traumatic event(s),” to a smaller slight in life. Some experts suggest that a medical diagnosis, even if not life-threatening but perceived as such, could warrant the diagnosis.¹⁰ This would expand our understanding of trauma and its consequences significantly. Yet already, a survey of Detroit area residents in 1998 found that 89.6% of the interviewees reported having experienced a significant trauma and that the average number of traumatic experiences was 4.8.¹¹ The meaning of a diagnosis that can be applied to almost 90% of a population has unclear usefulness, especially if meant to diminish guilt and responsibility.

More recently, citing Adverse Childhood Experiences (ACEs) has been a common method of supporting mitigating evaluations. Using the ACEs questionnaires, researchers have supported the idea that social programs are a key player in an improved criminal justice system. The ACEs study identified 10 forms of childhood trauma in 17,000 patients, including abuse, neglect, abandonment, household dysfunction, and exposure to violence, that were strongly associated with negative psychological outcomes, engagement in high-risk behaviors, significant medical consequences, and even early death.¹² However, similarly to past trauma, the prevalence of ACEs in the forensic population is the norm, not the exception.
 

Additional thoughts

Of particular concern is when diagnostic criteria intersect or seemingly contradict one another. For example, acts such as an outburst of anger may be interpreted by one evaluator as a sign of deviance, irritability, or recklessness – and meeting antisocial personality disorder criteria. Whereas another evaluator may interpret the same incident as hypervigilance, exaggerated startle response, or self-destructive behavior in PTSD.

An incident of not assisting someone in need may be interpreted as lack of remorse and glibness from antisocial characteristics or avoidance and detachment from others as a reaction to past trauma. Flashbacks from trauma can be interpreted by some as violent fantasies. Even the experience of trauma can be viewed as a risk factor for future violence. In some ways, our perspectives are influenced by our examination of someone’s history through the lens of sociopathy or empathy.
 

In summary

Psychiatry is entrusted by courts to comment on negative and mitigating factors. Negative factors hinge in part on our subjective impression of sociopathy, and mitigating factors hinge, in part, on our empathy for a defendant’s trauma. Psychiatry should recognize the limitations of both sides and humble itself in providing balanced evaluations to courts.

Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Amendolara is a first-year psychiatry resident at University of California, San Diego. He spent years advocating for survivors of rape and domestic violence at the Crime Victims Treatment Center in New York and conducted public health research at Lourdes Center for Public Health in Camden, N.J. Dr. Amendolara has no disclosures. Dr. Ngo is a second-year child neurology resident at University of California, Los Angeles. She received a master’s degree in narrative medicine from Columbia University, New York. She has no disclosures.

References

1. Frances A. Saving Normal: An Insider’s Revolt Against Out-of-Control Psychiatric Diagnosis, DSM-5, Big Pharma and the Medicalization of Ordinary Life. Harper Collins, 2013.

2. Key Substance Use and Mental Health Indicators in the United States. National Survey on Drug Use and Health. 2018.

3. Wong SCP and Gordon A. Psychol Public Policy Law. 2006;12(3):279-309.

4. Douglas KS et al. Mental Health Law & Policy Institute. About the Historical Clinical Risk Management-20, Version 3.

5. Angwin J et al. ProPublica. 2016 May 23.

6. Dressel J and Farid H. Sci Adv. 2018;4(1). doi: 10.1126/sciady.aao5580.

7. Freedman R et al. Am J Psychiatry. 2013 Jan;170(1):1-5.

8. Lillie B. The complexities of the psychopath test: A Q&A with Ron Jonson. TEDBlog. 2012 Aug 15.

9. Larsen RR et al. Psychol Public Policy Law. 2020;26(3):297-311.

10. Cordova MJ. Psychiatric Times. 2020 Jul 31;37(7).

11. Breslau N et al. Arch Gen Psychiatry. 1998;55(7):626-32.

12. Reavis JA et al. Perm J. 2013 Spring;17(2):44-8.

Society is having a moment of reflection about the role of law enforcement and correctional facilities in addressing societal problems. During this moment, psychiatry is being asked by courts to arbitrate who qualifies and ultimately deserves certain judgments.

In particular, we are asked to assess how dangerous an individual may be using violent risk assessment tools and measures of antisocial disorders. As such, we are tasked with pointing out the negative factors of defendants. Alternatively, psychiatry is also asked to explain, using biopsychosocial determinants, what led an individual to act in a deviant manner. As such, we are tasked with pointing out mitigating factors of defendants. In this article, we attempt to look at limitations in both paradigms to encourage a more prudent forensic approach.
 

Negative factors

A conundrum for the forensic psychiatry evaluator is that diagnostic criteria are not designed for the rigors and needs of court. The criteria in the Diagnostic and Statistical Manual of Mental Disorders (DSM) are not composed of rigid rules with validity markers to measure their veracity but leave room for clinical judgment, variance across individuals, and future research and treatment needs.

There are some benefits to having room for clinical judgment, but it can also lead to overdiagnosis.¹ This problem is particularly reflected in the diagnosis of antisocial personality disorder (ASPD), the criteria of which includes failure to conform to social norms, deceitfulness, impulsivity, irritability, recklessness, irresponsibility, and lack of remorse. Each of these criteria is ripe for subjectivity by an inexperienced or biased reviewer.

Mitigating factors

On the other side, the defense expert also faces significant challenges, though the tools are different. Contrary to the prosecuting expert who loads an arsenal of subjective assessment tools, the defense expert will point to childhood trauma and mental illness as extenuating explanations for a crime. Having suffered abuse as a child is advanced to justify someone’s subsequent violence. This problem is reflected in the diagnosis of posttraumatic stress disorder (PTSD). An unscrupulous expert may simply allow an evaluee to endorse symptoms without clinical correlates or rigorous validation to advance this narrative.

For example, psychiatrists commonly ascribe the DSM criteria A for PTSD, “directly experiencing the traumatic event(s),” to a smaller slight in life. Some experts suggest that a medical diagnosis, even if not life-threatening but perceived as such, could warrant the diagnosis.¹⁰ This would expand our understanding of trauma and its consequences significantly. Yet already, a survey of Detroit area residents in 1998 found that 89.6% of the interviewees reported having experienced a significant trauma and that the average number of traumatic experiences was 4.8.¹¹ The meaning of a diagnosis that can be applied to almost 90% of a population has unclear usefulness, especially if meant to diminish guilt and responsibility.

More recently, citing Adverse Childhood Experiences (ACEs) has been a common method of supporting mitigating evaluations. Using the ACEs questionnaires, researchers have supported the idea that social programs are a key player in an improved criminal justice system. The ACEs study identified 10 forms of childhood trauma in 17,000 patients, including abuse, neglect, abandonment, household dysfunction, and exposure to violence, that were strongly associated with negative psychological outcomes, engagement in high-risk behaviors, significant medical consequences, and even early death.¹² However, similarly to past trauma, the prevalence of ACEs in the forensic population is the norm, not the exception.
 

Additional thoughts

Of particular concern is when diagnostic criteria intersect or seemingly contradict one another. For example, acts such as an outburst of anger may be interpreted by one evaluator as a sign of deviance, irritability, or recklessness – and meeting antisocial personality disorder criteria. Whereas another evaluator may interpret the same incident as hypervigilance, exaggerated startle response, or self-destructive behavior in PTSD.

An incident of not assisting someone in need may be interpreted as lack of remorse and glibness from antisocial characteristics or avoidance and detachment from others as a reaction to past trauma. Flashbacks from trauma can be interpreted by some as violent fantasies. Even the experience of trauma can be viewed as a risk factor for future violence. In some ways, our perspectives are influenced by our examination of someone’s history through the lens of sociopathy or empathy.
 

In summary

Psychiatry is entrusted by courts to comment on negative and mitigating factors. Negative factors hinge in part on our subjective impression of sociopathy, and mitigating factors hinge, in part, on our empathy for a defendant’s trauma. Psychiatry should recognize the limitations of both sides and humble itself in providing balanced evaluations to courts.

Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Amendolara is a first-year psychiatry resident at University of California, San Diego. He spent years advocating for survivors of rape and domestic violence at the Crime Victims Treatment Center in New York and conducted public health research at Lourdes Center for Public Health in Camden, N.J. Dr. Amendolara has no disclosures. Dr. Ngo is a second-year child neurology resident at University of California, Los Angeles. She received a master’s degree in narrative medicine from Columbia University, New York. She has no disclosures.

References

1. Frances A. Saving Normal: An Insider’s Revolt Against Out-of-Control Psychiatric Diagnosis, DSM-5, Big Pharma and the Medicalization of Ordinary Life. Harper Collins, 2013.

2. Key Substance Use and Mental Health Indicators in the United States. National Survey on Drug Use and Health. 2018.

3. Wong SCP and Gordon A. Psychol Public Policy Law. 2006;12(3):279-309.

4. Douglas KS et al. Mental Health Law & Policy Institute. About the Historical Clinical Risk Management-20, Version 3.

5. Angwin J et al. ProPublica. 2016 May 23.

6. Dressel J and Farid H. Sci Adv. 2018;4(1). doi: 10.1126/sciady.aao5580.

7. Freedman R et al. Am J Psychiatry. 2013 Jan;170(1):1-5.

8. Lillie B. The complexities of the psychopath test: A Q&A with Ron Jonson. TEDBlog. 2012 Aug 15.

9. Larsen RR et al. Psychol Public Policy Law. 2020;26(3):297-311.

10. Cordova MJ. Psychiatric Times. 2020 Jul 31;37(7).

11. Breslau N et al. Arch Gen Psychiatry. 1998;55(7):626-32.

12. Reavis JA et al. Perm J. 2013 Spring;17(2):44-8.

The composition of street drugs like heroin and cocaine are changing. According to a new analysis, almost all contain at least one toxic adulterant, and many contain a plethora. Most adulterants have pharmacologic activities and toxicities. Their presence has added impact in the context of the COVID-19 pandemic, since some may cause a drastic drop in white blood cells that could leave drug users more vulnerable to infection.

“It’s remarkable that we just forgot to notice, in the horrendous transition from prescription opioid epidemic to the illicit opioid and psychostimulant epidemics, that we would have to pay special attention to what the medications are in the drugs that the person was exposed to – and for how long,” said Mark S. Gold, MD, a coauthor of the review.

The analysis showed that adulterants include new psychoactive substances, industrial compounds, fungicides, veterinary medications, and various impurities. In addition, other various medications are being found in street drugs, such as antipsychotics, antidepressants, anxiolytics, antihistamines, anthelmintics, anesthetics, anti-inflammatory agents, antipyretics, analgesics, antispasmodics, antiarrhythmics, antimalarials, bronchodilators, decongestants, expectorants, muscle relaxers, natural/synthetic hallucinogens, and sedatives.

Illicit drugs are by nature manufactured without Food and Drug Administration oversight, and it is becoming increasingly common that substances like leftover medicines and other active drugs are added to illicit drug batches to add weight, said Dr. Gold, a professor at Washington University,St. Louis. The study appeared in Current Psychopharmacology.
 

Effects of adulterants ‘terrifying’

The findings of adulterants and their consequences are concerning, according to Jean Lud Cadet, MD, who was asked to comment on the findings. “The blood dysplasia, the pulmonary problems that some of those adulterants can cause – it’s actually terrifying, to put it bluntly,” said Dr. Cadet, who is a senior investigator and chief of the Molecular Neuropsychiatry Research Branch at the National Institute on Drug Abuse.

Before 2000, street drugs were generally diluted with comparatively benign substances such as caffeine, sugars, or lidocaine. Drugs like phenacetin, levamisole, acetaminophen, and diltiazem began to appear in heroin and cocaine in the late 1990s, and by 2010, more powerful adulterants like fentanyl, ketamine, and quetiapine became common. Adulterants can lead to a range of clinical effects, including renal and liver problems, blood disorders, infections, respiratory depression, and cardiac arrest.

In 2015, the U.S. Department of State partnered with the Colombo Plan, an international organization based in Sri Lanka, to use field spectroscopy to detect toxins directly in cocaine and heroin samples found in Argentina, Brazil, Ecuador, Peru, Sri Lanka, Thailand, Honduras, Guatemala, Mexico, Colombia, and South Africa. They found a range of adulterants such as aminopyrine, diltiazem, metamizole, levamisole, and phenacetin.

A similar project with 431 heroin and cocaine samples from Vermont and Kentucky found that 69% of samples had five or more controlled drugs, toxic adulterants, or impurities. About 15% had nine or more, and 95% of samples had at least one toxic adulterant.

In the midst of the COVID-19 pandemic, these adulterants take on even greater significance. Individuals with substance use disorders often have other health conditions that can make them more vulnerable to viral infections, and this could be exacerbated by the effects of adulterants on white blood cells or other systems. The pandemic has also had an indirect effect by causing a shortage of street drugs. During production shortages, traffickers might boost potency by adding more cutting agents and adulterants. As a result, COVID-19 and opioid addiction tend to reinforce each other.

“The clinical message would be that our [substance use] patients will contract infectious disease and need to be prioritized for [COVID-19] vaccination,” said Dr. Gold.

The findings came as a surprise to Dr. Cadet, and that illustrates a need to publicize the presence of adulterants in street drugs.

“If I wasn’t aware of many of these, then the general public is also not going to be aware of them,” Dr. Cadet said. “Scientists, including myself, and government agencies need to do a better job [of communicating this issue].”

The study references individuals with substance use disorder, but Dr. Cadet cautioned that anyone who uses street drugs, even once or twice, could be a victim of adulterants. “You don’t need to have met criteria for diagnosis in order to suffer the consequences.”

The study had no funding. Dr. Gold and Dr. Cadet have no relevant financial disclosures.

The composition of street drugs like heroin and cocaine are changing. According to a new analysis, almost all contain at least one toxic adulterant, and many contain a plethora. Most adulterants have pharmacologic activities and toxicities. Their presence has added impact in the context of the COVID-19 pandemic, since some may cause a drastic drop in white blood cells that could leave drug users more vulnerable to infection.

“It’s remarkable that we just forgot to notice, in the horrendous transition from prescription opioid epidemic to the illicit opioid and psychostimulant epidemics, that we would have to pay special attention to what the medications are in the drugs that the person was exposed to – and for how long,” said Mark S. Gold, MD, a coauthor of the review.

The analysis showed that adulterants include new psychoactive substances, industrial compounds, fungicides, veterinary medications, and various impurities. In addition, other various medications are being found in street drugs, such as antipsychotics, antidepressants, anxiolytics, antihistamines, anthelmintics, anesthetics, anti-inflammatory agents, antipyretics, analgesics, antispasmodics, antiarrhythmics, antimalarials, bronchodilators, decongestants, expectorants, muscle relaxers, natural/synthetic hallucinogens, and sedatives.

Illicit drugs are by nature manufactured without Food and Drug Administration oversight, and it is becoming increasingly common that substances like leftover medicines and other active drugs are added to illicit drug batches to add weight, said Dr. Gold, a professor at Washington University,St. Louis. The study appeared in Current Psychopharmacology.
 

Effects of adulterants ‘terrifying’

The findings of adulterants and their consequences are concerning, according to Jean Lud Cadet, MD, who was asked to comment on the findings. “The blood dysplasia, the pulmonary problems that some of those adulterants can cause – it’s actually terrifying, to put it bluntly,” said Dr. Cadet, who is a senior investigator and chief of the Molecular Neuropsychiatry Research Branch at the National Institute on Drug Abuse.

Before 2000, street drugs were generally diluted with comparatively benign substances such as caffeine, sugars, or lidocaine. Drugs like phenacetin, levamisole, acetaminophen, and diltiazem began to appear in heroin and cocaine in the late 1990s, and by 2010, more powerful adulterants like fentanyl, ketamine, and quetiapine became common. Adulterants can lead to a range of clinical effects, including renal and liver problems, blood disorders, infections, respiratory depression, and cardiac arrest.

In 2015, the U.S. Department of State partnered with the Colombo Plan, an international organization based in Sri Lanka, to use field spectroscopy to detect toxins directly in cocaine and heroin samples found in Argentina, Brazil, Ecuador, Peru, Sri Lanka, Thailand, Honduras, Guatemala, Mexico, Colombia, and South Africa. They found a range of adulterants such as aminopyrine, diltiazem, metamizole, levamisole, and phenacetin.

A similar project with 431 heroin and cocaine samples from Vermont and Kentucky found that 69% of samples had five or more controlled drugs, toxic adulterants, or impurities. About 15% had nine or more, and 95% of samples had at least one toxic adulterant.

In the midst of the COVID-19 pandemic, these adulterants take on even greater significance. Individuals with substance use disorders often have other health conditions that can make them more vulnerable to viral infections, and this could be exacerbated by the effects of adulterants on white blood cells or other systems. The pandemic has also had an indirect effect by causing a shortage of street drugs. During production shortages, traffickers might boost potency by adding more cutting agents and adulterants. As a result, COVID-19 and opioid addiction tend to reinforce each other.

“The clinical message would be that our [substance use] patients will contract infectious disease and need to be prioritized for [COVID-19] vaccination,” said Dr. Gold.

The findings came as a surprise to Dr. Cadet, and that illustrates a need to publicize the presence of adulterants in street drugs.

“If I wasn’t aware of many of these, then the general public is also not going to be aware of them,” Dr. Cadet said. “Scientists, including myself, and government agencies need to do a better job [of communicating this issue].”

The study references individuals with substance use disorder, but Dr. Cadet cautioned that anyone who uses street drugs, even once or twice, could be a victim of adulterants. “You don’t need to have met criteria for diagnosis in order to suffer the consequences.”

The study had no funding. Dr. Gold and Dr. Cadet have no relevant financial disclosures.

The composition of street drugs like heroin and cocaine are changing. According to a new analysis, almost all contain at least one toxic adulterant, and many contain a plethora. Most adulterants have pharmacologic activities and toxicities. Their presence has added impact in the context of the COVID-19 pandemic, since some may cause a drastic drop in white blood cells that could leave drug users more vulnerable to infection.

“It’s remarkable that we just forgot to notice, in the horrendous transition from prescription opioid epidemic to the illicit opioid and psychostimulant epidemics, that we would have to pay special attention to what the medications are in the drugs that the person was exposed to – and for how long,” said Mark S. Gold, MD, a coauthor of the review.

The analysis showed that adulterants include new psychoactive substances, industrial compounds, fungicides, veterinary medications, and various impurities. In addition, other various medications are being found in street drugs, such as antipsychotics, antidepressants, anxiolytics, antihistamines, anthelmintics, anesthetics, anti-inflammatory agents, antipyretics, analgesics, antispasmodics, antiarrhythmics, antimalarials, bronchodilators, decongestants, expectorants, muscle relaxers, natural/synthetic hallucinogens, and sedatives.

Illicit drugs are by nature manufactured without Food and Drug Administration oversight, and it is becoming increasingly common that substances like leftover medicines and other active drugs are added to illicit drug batches to add weight, said Dr. Gold, a professor at Washington University,St. Louis. The study appeared in Current Psychopharmacology.
 

Effects of adulterants ‘terrifying’

The findings of adulterants and their consequences are concerning, according to Jean Lud Cadet, MD, who was asked to comment on the findings. “The blood dysplasia, the pulmonary problems that some of those adulterants can cause – it’s actually terrifying, to put it bluntly,” said Dr. Cadet, who is a senior investigator and chief of the Molecular Neuropsychiatry Research Branch at the National Institute on Drug Abuse.

Before 2000, street drugs were generally diluted with comparatively benign substances such as caffeine, sugars, or lidocaine. Drugs like phenacetin, levamisole, acetaminophen, and diltiazem began to appear in heroin and cocaine in the late 1990s, and by 2010, more powerful adulterants like fentanyl, ketamine, and quetiapine became common. Adulterants can lead to a range of clinical effects, including renal and liver problems, blood disorders, infections, respiratory depression, and cardiac arrest.

In 2015, the U.S. Department of State partnered with the Colombo Plan, an international organization based in Sri Lanka, to use field spectroscopy to detect toxins directly in cocaine and heroin samples found in Argentina, Brazil, Ecuador, Peru, Sri Lanka, Thailand, Honduras, Guatemala, Mexico, Colombia, and South Africa. They found a range of adulterants such as aminopyrine, diltiazem, metamizole, levamisole, and phenacetin.

A similar project with 431 heroin and cocaine samples from Vermont and Kentucky found that 69% of samples had five or more controlled drugs, toxic adulterants, or impurities. About 15% had nine or more, and 95% of samples had at least one toxic adulterant.

In the midst of the COVID-19 pandemic, these adulterants take on even greater significance. Individuals with substance use disorders often have other health conditions that can make them more vulnerable to viral infections, and this could be exacerbated by the effects of adulterants on white blood cells or other systems. The pandemic has also had an indirect effect by causing a shortage of street drugs. During production shortages, traffickers might boost potency by adding more cutting agents and adulterants. As a result, COVID-19 and opioid addiction tend to reinforce each other.

“The clinical message would be that our [substance use] patients will contract infectious disease and need to be prioritized for [COVID-19] vaccination,” said Dr. Gold.

The findings came as a surprise to Dr. Cadet, and that illustrates a need to publicize the presence of adulterants in street drugs.

“If I wasn’t aware of many of these, then the general public is also not going to be aware of them,” Dr. Cadet said. “Scientists, including myself, and government agencies need to do a better job [of communicating this issue].”

The study references individuals with substance use disorder, but Dr. Cadet cautioned that anyone who uses street drugs, even once or twice, could be a victim of adulterants. “You don’t need to have met criteria for diagnosis in order to suffer the consequences.”

The study had no funding. Dr. Gold and Dr. Cadet have no relevant financial disclosures.