Kelli Whitlock Burton

BOSTON – Noninvasive tests performed in midlife may help identify people who are at risk of late-onset epilepsy, a new study suggests. New data from the Framingham Heart Study show those who scored better on a neurocognitive test that measures executive function were 75% less likely to develop late-onset epilepsy.

An analysis of MRI revealed that those with higher cortical volumes also had a lower risk of epilepsy later in life, while those with higher white matter hyperintensities had an increased risk.

The study could help identify at-risk individuals years before symptoms of epilepsy appear.

“We present possible markers that could potentially identify patients at risk for developing late-onset epilepsy, even in the preclinical phase and before the clinical manifestation of conditions like stroke and dementia that are known now to be linked with the condition,” said lead investigator Maria Stefanidou, MD, assistant professor of neurology at Boston University.

The findings were presented at the 2023 annual meeting of the American Academy of Neurology.
 

Protection against late-onset epilepsy?

Hypertension and stroke are known risk factors for late-onset epilepsy. Dementia is also a known risk factor. But in about 30% of cases, the cause of epilepsy in older individuals is unknown.

For this study, investigators analyzed data from the offspring cohort of the Framingham Heart Study. Participants were at least 45 years old; underwent neuropsychological evaluation and brain MRI; and had no prior history of stroke, dementia, or epilepsy. Cognitive measures included Visual Reproductions Delayed Recall, Logical Memory Delayed Recall, Similarities, Trail Making B-A (TrB-TrA), and the Hooper Visual Organization Test.

Participants also underwent an MRI to measure total cerebral brain volume, cortical gray matter volume, white matter hyperintensities, and hippocampal volume.

After a mean follow-up of 13.5 years, late-onset epilepsy was diagnosed in 31 of participants who underwent neuropsychological testing (n = 2,349) and in 27 of those who underwent MRI (n = 2,056).

Better performance on the TrB-TrA test (a measure of executive function, processing speed, and occult vascular injury) was associated with a reduced risk of late-onset epilepsy (adjusted hazard ratio, 0.25; P = .011).

The findings held even after adjusting for age, sex, educational level, and known risk factors for late-onset epilepsy, such as hypertension (aHR, 0.30; P = .0401).

Higher white matter hyperintensities, a measure of occult vascular injury, was associated with increased epilepsy risk (aHR, 1.5; P = .042) when adjusted only for age, sex, and education, but was no longer significant after adjusting for hypertension and other risk factors (aHR, 1.47; P = .065).

The analysis also revealed that participants with a higher cortical gray matter volume had a lower risk for late-onset epilepsy (aHR, 0.73; P = .001).

“There is increasing literature supporting that late-onset epilepsy may be secondary to accumulative occult cerebrovascular and neurodegenerative processes that occur during aging,” Dr. Stefanidou said. “Our findings likely reflect that a lesser degree of occult vascular brain injury in midlife may be protective against late-onset epilepsy.”

However, the epidemiological study points to association, not causation, Dr. Stefanidou cautions.

“Further studies will be needed to study our observations in the clinical setting,” she said.
 

‘Intriguing’ findings

Commenting on the findings, Joseph Sirven, MD, a neurologist at the Mayo Clinic in Jacksonville, Fla., said the findings are “intriguing,” but also raise some questions. “Late-onset epilepsy remains an issue for many and it’s common,” said Dr. Sirven, who has patients with late-onset epilepsy.

Dr. Sirven was particularly interested in the findings on white matter hyperintensities. “Hippocampal volumes have been used but not so much cortical volumes,” he said. “I would like to know more about how white matter changes suggest pathology that would explain epilepsy.”

Study funding was not disclosed. Dr. Stefanidou and Dr. Sirven report no relevant financial relationships.

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

BOSTON – Noninvasive tests performed in midlife may help identify people who are at risk of late-onset epilepsy, a new study suggests. New data from the Framingham Heart Study show those who scored better on a neurocognitive test that measures executive function were 75% less likely to develop late-onset epilepsy.

An analysis of MRI revealed that those with higher cortical volumes also had a lower risk of epilepsy later in life, while those with higher white matter hyperintensities had an increased risk.

The study could help identify at-risk individuals years before symptoms of epilepsy appear.

“We present possible markers that could potentially identify patients at risk for developing late-onset epilepsy, even in the preclinical phase and before the clinical manifestation of conditions like stroke and dementia that are known now to be linked with the condition,” said lead investigator Maria Stefanidou, MD, assistant professor of neurology at Boston University.

The findings were presented at the 2023 annual meeting of the American Academy of Neurology.
 

Protection against late-onset epilepsy?

Hypertension and stroke are known risk factors for late-onset epilepsy. Dementia is also a known risk factor. But in about 30% of cases, the cause of epilepsy in older individuals is unknown.

For this study, investigators analyzed data from the offspring cohort of the Framingham Heart Study. Participants were at least 45 years old; underwent neuropsychological evaluation and brain MRI; and had no prior history of stroke, dementia, or epilepsy. Cognitive measures included Visual Reproductions Delayed Recall, Logical Memory Delayed Recall, Similarities, Trail Making B-A (TrB-TrA), and the Hooper Visual Organization Test.

Participants also underwent an MRI to measure total cerebral brain volume, cortical gray matter volume, white matter hyperintensities, and hippocampal volume.

After a mean follow-up of 13.5 years, late-onset epilepsy was diagnosed in 31 of participants who underwent neuropsychological testing (n = 2,349) and in 27 of those who underwent MRI (n = 2,056).

Better performance on the TrB-TrA test (a measure of executive function, processing speed, and occult vascular injury) was associated with a reduced risk of late-onset epilepsy (adjusted hazard ratio, 0.25; P = .011).

The findings held even after adjusting for age, sex, educational level, and known risk factors for late-onset epilepsy, such as hypertension (aHR, 0.30; P = .0401).

Higher white matter hyperintensities, a measure of occult vascular injury, was associated with increased epilepsy risk (aHR, 1.5; P = .042) when adjusted only for age, sex, and education, but was no longer significant after adjusting for hypertension and other risk factors (aHR, 1.47; P = .065).

The analysis also revealed that participants with a higher cortical gray matter volume had a lower risk for late-onset epilepsy (aHR, 0.73; P = .001).

“There is increasing literature supporting that late-onset epilepsy may be secondary to accumulative occult cerebrovascular and neurodegenerative processes that occur during aging,” Dr. Stefanidou said. “Our findings likely reflect that a lesser degree of occult vascular brain injury in midlife may be protective against late-onset epilepsy.”

However, the epidemiological study points to association, not causation, Dr. Stefanidou cautions.

“Further studies will be needed to study our observations in the clinical setting,” she said.
 

‘Intriguing’ findings

Commenting on the findings, Joseph Sirven, MD, a neurologist at the Mayo Clinic in Jacksonville, Fla., said the findings are “intriguing,” but also raise some questions. “Late-onset epilepsy remains an issue for many and it’s common,” said Dr. Sirven, who has patients with late-onset epilepsy.

Dr. Sirven was particularly interested in the findings on white matter hyperintensities. “Hippocampal volumes have been used but not so much cortical volumes,” he said. “I would like to know more about how white matter changes suggest pathology that would explain epilepsy.”

Study funding was not disclosed. Dr. Stefanidou and Dr. Sirven report no relevant financial relationships.

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

BOSTON – Noninvasive tests performed in midlife may help identify people who are at risk of late-onset epilepsy, a new study suggests. New data from the Framingham Heart Study show those who scored better on a neurocognitive test that measures executive function were 75% less likely to develop late-onset epilepsy.

An analysis of MRI revealed that those with higher cortical volumes also had a lower risk of epilepsy later in life, while those with higher white matter hyperintensities had an increased risk.

The study could help identify at-risk individuals years before symptoms of epilepsy appear.

“We present possible markers that could potentially identify patients at risk for developing late-onset epilepsy, even in the preclinical phase and before the clinical manifestation of conditions like stroke and dementia that are known now to be linked with the condition,” said lead investigator Maria Stefanidou, MD, assistant professor of neurology at Boston University.

The findings were presented at the 2023 annual meeting of the American Academy of Neurology.
 

Protection against late-onset epilepsy?

Hypertension and stroke are known risk factors for late-onset epilepsy. Dementia is also a known risk factor. But in about 30% of cases, the cause of epilepsy in older individuals is unknown.

For this study, investigators analyzed data from the offspring cohort of the Framingham Heart Study. Participants were at least 45 years old; underwent neuropsychological evaluation and brain MRI; and had no prior history of stroke, dementia, or epilepsy. Cognitive measures included Visual Reproductions Delayed Recall, Logical Memory Delayed Recall, Similarities, Trail Making B-A (TrB-TrA), and the Hooper Visual Organization Test.

Participants also underwent an MRI to measure total cerebral brain volume, cortical gray matter volume, white matter hyperintensities, and hippocampal volume.

After a mean follow-up of 13.5 years, late-onset epilepsy was diagnosed in 31 of participants who underwent neuropsychological testing (n = 2,349) and in 27 of those who underwent MRI (n = 2,056).

Better performance on the TrB-TrA test (a measure of executive function, processing speed, and occult vascular injury) was associated with a reduced risk of late-onset epilepsy (adjusted hazard ratio, 0.25; P = .011).

The findings held even after adjusting for age, sex, educational level, and known risk factors for late-onset epilepsy, such as hypertension (aHR, 0.30; P = .0401).

Higher white matter hyperintensities, a measure of occult vascular injury, was associated with increased epilepsy risk (aHR, 1.5; P = .042) when adjusted only for age, sex, and education, but was no longer significant after adjusting for hypertension and other risk factors (aHR, 1.47; P = .065).

The analysis also revealed that participants with a higher cortical gray matter volume had a lower risk for late-onset epilepsy (aHR, 0.73; P = .001).

“There is increasing literature supporting that late-onset epilepsy may be secondary to accumulative occult cerebrovascular and neurodegenerative processes that occur during aging,” Dr. Stefanidou said. “Our findings likely reflect that a lesser degree of occult vascular brain injury in midlife may be protective against late-onset epilepsy.”

However, the epidemiological study points to association, not causation, Dr. Stefanidou cautions.

“Further studies will be needed to study our observations in the clinical setting,” she said.
 

‘Intriguing’ findings

Commenting on the findings, Joseph Sirven, MD, a neurologist at the Mayo Clinic in Jacksonville, Fla., said the findings are “intriguing,” but also raise some questions. “Late-onset epilepsy remains an issue for many and it’s common,” said Dr. Sirven, who has patients with late-onset epilepsy.

Dr. Sirven was particularly interested in the findings on white matter hyperintensities. “Hippocampal volumes have been used but not so much cortical volumes,” he said. “I would like to know more about how white matter changes suggest pathology that would explain epilepsy.”

Study funding was not disclosed. Dr. Stefanidou and Dr. Sirven report no relevant financial relationships.

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

Early menopause and delayed initiation of hormone therapy (HT) have been linked to an increase in Alzheimer’s disease (AD) pathology in women, a new imaging study shows.

Investigators found elevated levels of tau protein in the brains of women who initiated HT more than 5 years after menopause onset, while those who started the therapy earlier had normal levels.

Tau levels were also higher in women who started menopause before age 45, either naturally or following surgery, but only in those who already had high levels of beta-amyloid.

The findings were published online in JAMA Neurology.
 

Hotly debated

Previous research has suggested the timing of menopause and HT initiation may be associated with AD. However, the current research is the first to suggest tau deposition may explain that link.

“There have been a lot of conflicting findings around whether HT induces risk for Alzheimer’s disease dementia or not, and – at least in our hands – our observational evidence suggests that any risk is fairly limited to those rarer cases when women might delay their initiation of HT considerably,” senior investigator Rachel Buckley, PhD, assistant investigator in neurology at Massachusetts General Hospital and assistant professor of neurology at Harvard Medical School, Boston, told this news organization.

The link between HT, dementia, and cognitive decline has been hotly debated since the initial release of findings from the Women’s Health Initiative Memory Study, reported 20 years ago.

Since then, dozens of studies have yielded conflicting evidence about HT and AD risk, with some showing a protective effect and others showing the treatment may increase AD risk.

For this study, researchers analyzed data from 292 cognitively unimpaired participants (66.1% female) in the Wisconsin Registry for Alzheimer Prevention. About half of the women had received HT.

Women had higher levels of tau measured on PET imaging than age-matched males, even after adjustment for APOE status and other potential confounders.

Higher tau levels were found in those with an earlier age at menopause (P < .001) and HT use (P = .008) compared with male sex; later menopause onset; or HT nonuse – but only in patients who also had a higher beta-amyloid burden.

Late initiation of HT (> 5 years following age at menopause) was associated with higher tau compared with early initiation (P = .001), regardless of amyloid levels.
 

Surprising finding

Although researchers expected to find that surgical history (specifically oophorectomy) might have a greater impact on risk, that wasn’t the case.

“Given that bilateral oophorectomy involves the removal of both ovaries, and the immediate ceasing of estrogen production, I had expected this to be the primary driver of higher tau levels,” Dr. Buckley said. “But early age at menopause – regardless of whether the genesis was natural or surgical – seemed to have similar impacts.”

These findings are the latest from Dr. Buckley’s group that indicate that women tend to have higher levels of tau than men, regardless of preexisting amyloid burden in the brain.

“We see this in healthy older women, women with dementia, and even in postmortem cases,” Dr. Buckley said. “It really remains to be seen whether women tend to accumulate tau faster in the brain than men, or whether this is simply a one-shot phenomenon that we see in observational studies at the baseline.”

“One could really flip this finding on its head and suggest that women are truly resilient to the disease,” she continued. “That is, they can hold much more tau in their brain and remain well enough to be studied, unlike men.”

Among the study’s limitations is that the data were collected at a single time point and did not include information on subsequent Alzheimer’s diagnosis or cognitive decline.

“It is important to remember that the participants in this study were not as representative of the general population in the United States, so we cannot extrapolate our findings to women from a range of socioeconomic, racial and ethnic backgrounds or education levels,” she said.

The study’s observational design left researchers unable to demonstrate causation. What’s more, the findings don’t support the assertion that hormone therapy may protect against AD, Dr. Buckley added.

“I would more confidently say that evidence from our work, and that of many others, seems to suggest that HT initiated around the time of menopause may be benign – not providing benefit or risk, at least in the context of Alzheimer’s disease risk,” she said.

Another important takeaway from the study, Dr. Buckley said, is that not all women are at high risk for AD.

“Often the headlines might make you think that most women are destined to progress to dementia, but this simply is not the case,” Dr. Buckley said. “We are now starting to really drill down on what might elevate risk for AD in women and use this information to better inform clinical trials and doctors on how best to think about treating these higher-risk groups.”
 

New mechanism?

Commenting on the findings, Pauline Maki, PhD, professor of psychiatry, psychology and obstetrics & gynecology at the University of Illinois at Chicago, called the study “interesting.”

“It identifies a new mechanism in humans that could underlie a possible link between sex hormones and dementia,” Dr. Maki said.

However, Dr. Maki noted that the study wasn’t randomized and information about menopause onset was self-reported.

“We must remember that many of the hypotheses about hormone therapy and brain health that came from observational studies were not validated in randomized trials, including the hypothesis that hormone therapy prevents dementia,” she said.

The findings don’t resolve the debate over hormone therapy and AD risk and point to the need for randomized, prospective studies on the topic, Dr. Maki added. Still, she said, they underscore the gender disparity in AD risk.

“It’s a good reminder to clinicians that women have a higher lifetime risk of Alzheimer’s disease and should be advised on factors that might lower their risk,” she said.

The study was funded by the National Institutes of Health. Dr. Buckley reports no relevant financial conflicts. Dr. Maki serves on the advisory boards for Astellas, Bayer, Johnson & Johnson, consults for Pfizer and Mithra, and has equity in Estrigenix, Midi-Health, and Alloy.
 

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

Early menopause and delayed initiation of hormone therapy (HT) have been linked to an increase in Alzheimer’s disease (AD) pathology in women, a new imaging study shows.

Investigators found elevated levels of tau protein in the brains of women who initiated HT more than 5 years after menopause onset, while those who started the therapy earlier had normal levels.

Tau levels were also higher in women who started menopause before age 45, either naturally or following surgery, but only in those who already had high levels of beta-amyloid.

The findings were published online in JAMA Neurology.
 

Hotly debated

Previous research has suggested the timing of menopause and HT initiation may be associated with AD. However, the current research is the first to suggest tau deposition may explain that link.

“There have been a lot of conflicting findings around whether HT induces risk for Alzheimer’s disease dementia or not, and – at least in our hands – our observational evidence suggests that any risk is fairly limited to those rarer cases when women might delay their initiation of HT considerably,” senior investigator Rachel Buckley, PhD, assistant investigator in neurology at Massachusetts General Hospital and assistant professor of neurology at Harvard Medical School, Boston, told this news organization.

The link between HT, dementia, and cognitive decline has been hotly debated since the initial release of findings from the Women’s Health Initiative Memory Study, reported 20 years ago.

Since then, dozens of studies have yielded conflicting evidence about HT and AD risk, with some showing a protective effect and others showing the treatment may increase AD risk.

For this study, researchers analyzed data from 292 cognitively unimpaired participants (66.1% female) in the Wisconsin Registry for Alzheimer Prevention. About half of the women had received HT.

Women had higher levels of tau measured on PET imaging than age-matched males, even after adjustment for APOE status and other potential confounders.

Higher tau levels were found in those with an earlier age at menopause (P < .001) and HT use (P = .008) compared with male sex; later menopause onset; or HT nonuse – but only in patients who also had a higher beta-amyloid burden.

Late initiation of HT (> 5 years following age at menopause) was associated with higher tau compared with early initiation (P = .001), regardless of amyloid levels.
 

Surprising finding

Although researchers expected to find that surgical history (specifically oophorectomy) might have a greater impact on risk, that wasn’t the case.

“Given that bilateral oophorectomy involves the removal of both ovaries, and the immediate ceasing of estrogen production, I had expected this to be the primary driver of higher tau levels,” Dr. Buckley said. “But early age at menopause – regardless of whether the genesis was natural or surgical – seemed to have similar impacts.”

These findings are the latest from Dr. Buckley’s group that indicate that women tend to have higher levels of tau than men, regardless of preexisting amyloid burden in the brain.

“We see this in healthy older women, women with dementia, and even in postmortem cases,” Dr. Buckley said. “It really remains to be seen whether women tend to accumulate tau faster in the brain than men, or whether this is simply a one-shot phenomenon that we see in observational studies at the baseline.”

“One could really flip this finding on its head and suggest that women are truly resilient to the disease,” she continued. “That is, they can hold much more tau in their brain and remain well enough to be studied, unlike men.”

Among the study’s limitations is that the data were collected at a single time point and did not include information on subsequent Alzheimer’s diagnosis or cognitive decline.

“It is important to remember that the participants in this study were not as representative of the general population in the United States, so we cannot extrapolate our findings to women from a range of socioeconomic, racial and ethnic backgrounds or education levels,” she said.

The study’s observational design left researchers unable to demonstrate causation. What’s more, the findings don’t support the assertion that hormone therapy may protect against AD, Dr. Buckley added.

“I would more confidently say that evidence from our work, and that of many others, seems to suggest that HT initiated around the time of menopause may be benign – not providing benefit or risk, at least in the context of Alzheimer’s disease risk,” she said.

Another important takeaway from the study, Dr. Buckley said, is that not all women are at high risk for AD.

“Often the headlines might make you think that most women are destined to progress to dementia, but this simply is not the case,” Dr. Buckley said. “We are now starting to really drill down on what might elevate risk for AD in women and use this information to better inform clinical trials and doctors on how best to think about treating these higher-risk groups.”
 

New mechanism?

Commenting on the findings, Pauline Maki, PhD, professor of psychiatry, psychology and obstetrics & gynecology at the University of Illinois at Chicago, called the study “interesting.”

“It identifies a new mechanism in humans that could underlie a possible link between sex hormones and dementia,” Dr. Maki said.

However, Dr. Maki noted that the study wasn’t randomized and information about menopause onset was self-reported.

“We must remember that many of the hypotheses about hormone therapy and brain health that came from observational studies were not validated in randomized trials, including the hypothesis that hormone therapy prevents dementia,” she said.

The findings don’t resolve the debate over hormone therapy and AD risk and point to the need for randomized, prospective studies on the topic, Dr. Maki added. Still, she said, they underscore the gender disparity in AD risk.

“It’s a good reminder to clinicians that women have a higher lifetime risk of Alzheimer’s disease and should be advised on factors that might lower their risk,” she said.

The study was funded by the National Institutes of Health. Dr. Buckley reports no relevant financial conflicts. Dr. Maki serves on the advisory boards for Astellas, Bayer, Johnson & Johnson, consults for Pfizer and Mithra, and has equity in Estrigenix, Midi-Health, and Alloy.
 

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

Early menopause and delayed initiation of hormone therapy (HT) have been linked to an increase in Alzheimer’s disease (AD) pathology in women, a new imaging study shows.

Investigators found elevated levels of tau protein in the brains of women who initiated HT more than 5 years after menopause onset, while those who started the therapy earlier had normal levels.

Tau levels were also higher in women who started menopause before age 45, either naturally or following surgery, but only in those who already had high levels of beta-amyloid.

The findings were published online in JAMA Neurology.
 

Hotly debated

Previous research has suggested the timing of menopause and HT initiation may be associated with AD. However, the current research is the first to suggest tau deposition may explain that link.

“There have been a lot of conflicting findings around whether HT induces risk for Alzheimer’s disease dementia or not, and – at least in our hands – our observational evidence suggests that any risk is fairly limited to those rarer cases when women might delay their initiation of HT considerably,” senior investigator Rachel Buckley, PhD, assistant investigator in neurology at Massachusetts General Hospital and assistant professor of neurology at Harvard Medical School, Boston, told this news organization.

The link between HT, dementia, and cognitive decline has been hotly debated since the initial release of findings from the Women’s Health Initiative Memory Study, reported 20 years ago.

Since then, dozens of studies have yielded conflicting evidence about HT and AD risk, with some showing a protective effect and others showing the treatment may increase AD risk.

For this study, researchers analyzed data from 292 cognitively unimpaired participants (66.1% female) in the Wisconsin Registry for Alzheimer Prevention. About half of the women had received HT.

Women had higher levels of tau measured on PET imaging than age-matched males, even after adjustment for APOE status and other potential confounders.

Higher tau levels were found in those with an earlier age at menopause (P < .001) and HT use (P = .008) compared with male sex; later menopause onset; or HT nonuse – but only in patients who also had a higher beta-amyloid burden.

Late initiation of HT (> 5 years following age at menopause) was associated with higher tau compared with early initiation (P = .001), regardless of amyloid levels.
 

Surprising finding

Although researchers expected to find that surgical history (specifically oophorectomy) might have a greater impact on risk, that wasn’t the case.

“Given that bilateral oophorectomy involves the removal of both ovaries, and the immediate ceasing of estrogen production, I had expected this to be the primary driver of higher tau levels,” Dr. Buckley said. “But early age at menopause – regardless of whether the genesis was natural or surgical – seemed to have similar impacts.”

These findings are the latest from Dr. Buckley’s group that indicate that women tend to have higher levels of tau than men, regardless of preexisting amyloid burden in the brain.

“We see this in healthy older women, women with dementia, and even in postmortem cases,” Dr. Buckley said. “It really remains to be seen whether women tend to accumulate tau faster in the brain than men, or whether this is simply a one-shot phenomenon that we see in observational studies at the baseline.”

“One could really flip this finding on its head and suggest that women are truly resilient to the disease,” she continued. “That is, they can hold much more tau in their brain and remain well enough to be studied, unlike men.”

Among the study’s limitations is that the data were collected at a single time point and did not include information on subsequent Alzheimer’s diagnosis or cognitive decline.

“It is important to remember that the participants in this study were not as representative of the general population in the United States, so we cannot extrapolate our findings to women from a range of socioeconomic, racial and ethnic backgrounds or education levels,” she said.

The study’s observational design left researchers unable to demonstrate causation. What’s more, the findings don’t support the assertion that hormone therapy may protect against AD, Dr. Buckley added.

“I would more confidently say that evidence from our work, and that of many others, seems to suggest that HT initiated around the time of menopause may be benign – not providing benefit or risk, at least in the context of Alzheimer’s disease risk,” she said.

Another important takeaway from the study, Dr. Buckley said, is that not all women are at high risk for AD.

“Often the headlines might make you think that most women are destined to progress to dementia, but this simply is not the case,” Dr. Buckley said. “We are now starting to really drill down on what might elevate risk for AD in women and use this information to better inform clinical trials and doctors on how best to think about treating these higher-risk groups.”
 

New mechanism?

Commenting on the findings, Pauline Maki, PhD, professor of psychiatry, psychology and obstetrics & gynecology at the University of Illinois at Chicago, called the study “interesting.”

“It identifies a new mechanism in humans that could underlie a possible link between sex hormones and dementia,” Dr. Maki said.

However, Dr. Maki noted that the study wasn’t randomized and information about menopause onset was self-reported.

“We must remember that many of the hypotheses about hormone therapy and brain health that came from observational studies were not validated in randomized trials, including the hypothesis that hormone therapy prevents dementia,” she said.

The findings don’t resolve the debate over hormone therapy and AD risk and point to the need for randomized, prospective studies on the topic, Dr. Maki added. Still, she said, they underscore the gender disparity in AD risk.

“It’s a good reminder to clinicians that women have a higher lifetime risk of Alzheimer’s disease and should be advised on factors that might lower their risk,” she said.

The study was funded by the National Institutes of Health. Dr. Buckley reports no relevant financial conflicts. Dr. Maki serves on the advisory boards for Astellas, Bayer, Johnson & Johnson, consults for Pfizer and Mithra, and has equity in Estrigenix, Midi-Health, and Alloy.
 

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

Food insecurity is linked to a more rapid decline in executive function in older adults, a new study shows.

The findings were reported just weeks after a pandemic-era expansion in Supplemental Nutrition Assistance Program benefits ended, leading to less food assistance for about 5 million people over age 60 who participate in the program.

“Even though we found only a very small association between food insecurity and executive function, it’s still meaningful, because food insecurity is something we can prevent,” lead investigator Boeun Kim, PhD, MPH, RN, postdoctoral fellow at Johns Hopkins University School of Nursing, Baltimore, told this news organization.

The findings were published online  in JAMA Network Open.
 

National data

The number of Americans over 60 with food insecurity has more than doubled since 2007, with an estimated 5.2 million older adults reporting food insecurity in 2020.

Prior studies have linked malnutrition and food insecurity to a decline in cognitive function. Participating in food assistance programs such as SNAP is associated with slower memory decline in older adults.

However, to date, there has been no longitudinal study that has used data from a nationally representative sample of older Americans, which, Dr. Kim said, could limit generalizability of the findings.

To address that issue, investigators analyzed data from 3,037 participants in the National Health and Aging Trends Study, which includes community dwellers age 65 and older who receive Medicare.

Participants reported food insecurity over 7 years, from 2012 to 2019. Data on immediate memory, delayed memory, and executive function were from 2013 to 2020.

Food insecurity was defined as going without groceries due to limited ability or social support; a lack of hot meals related to functional limitation or no help; going without eating because of the inability to feed oneself or no available support; skipping meals due to insufficient food or money; or skipping meals for 5 days or more.

Immediate and delayed recall were assessed using a 10-item word-list memory task, and executive function was measured using a clock drawing test. Each year’s cognitive functions were linked to the prior year’s food insecurity data.

Over 7 years, 417 people, or 12.1%, experienced food insecurity at least once.

Those with food insecurity were more likely to be older, female, part of racial and ethnic minority groups, living alone, obese, and have a lower income and educational attainment, depressive symptoms, social isolation and disability, compared with those without food insecurity.

After adjusting for age, sex, race/ethnicity, educational level, income, marital status, body mass index, functional disability, social isolation, and other potential confounders, researchers found that food insecurity was associated with a more rapid decline in executive function (mean difference in annual change in executive function score, −0.04; 95% confidence interval, −0.09 to −0.003).

Food insecurity was not associated with baseline cognitive function scores or changes in immediate or delayed recall.

“Clinicians should be aware of the experience of food insecurity and the higher risk of cognitive decline so maybe they could do universal screening and refer people with food insecurity to programs that can help them access nutritious meals,” Dr. Kim said.
 

A sign of other problems?

Thomas Vidic, MD, said food insecurity often goes hand-in-hand with lack of medication adherence, lack of regular medical care, and a host of other issues. Dr. Vidic is a neurologist at the Elkhart Clinic, Ind., and an adjunct clinical professor of neurology at Indiana University.

“When a person has food insecurity, they likely have other problems, and they’re going to degenerate faster,” said Dr. Vidic, who was not part of the study. “This is one important component, and it’s one more way of getting a handle on people who are failing.”

Dr. Vidic, who has dealt with the issue of food insecurity with his own patients, said he suspects the self-report nature of the study may hide the true scale of the problem.

“I suspect the numbers might actually be higher,” he said, adding that the study fills a gap in the literature with a large, nationally representative sample.

“We’re looking for issues to help with the elderly as far as what can we do to keep dementia from progressing,” he said. “There are some things that make sense, but we’ve never had this kind of data before.”

The study was funded by the National Institute on Aging. Dr. Kim and Dr. Vidic have reported no relevant financial relationships.

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

Food insecurity is linked to a more rapid decline in executive function in older adults, a new study shows.

The findings were reported just weeks after a pandemic-era expansion in Supplemental Nutrition Assistance Program benefits ended, leading to less food assistance for about 5 million people over age 60 who participate in the program.

“Even though we found only a very small association between food insecurity and executive function, it’s still meaningful, because food insecurity is something we can prevent,” lead investigator Boeun Kim, PhD, MPH, RN, postdoctoral fellow at Johns Hopkins University School of Nursing, Baltimore, told this news organization.

The findings were published online  in JAMA Network Open.
 

National data

The number of Americans over 60 with food insecurity has more than doubled since 2007, with an estimated 5.2 million older adults reporting food insecurity in 2020.

Prior studies have linked malnutrition and food insecurity to a decline in cognitive function. Participating in food assistance programs such as SNAP is associated with slower memory decline in older adults.

However, to date, there has been no longitudinal study that has used data from a nationally representative sample of older Americans, which, Dr. Kim said, could limit generalizability of the findings.

To address that issue, investigators analyzed data from 3,037 participants in the National Health and Aging Trends Study, which includes community dwellers age 65 and older who receive Medicare.

Participants reported food insecurity over 7 years, from 2012 to 2019. Data on immediate memory, delayed memory, and executive function were from 2013 to 2020.

Food insecurity was defined as going without groceries due to limited ability or social support; a lack of hot meals related to functional limitation or no help; going without eating because of the inability to feed oneself or no available support; skipping meals due to insufficient food or money; or skipping meals for 5 days or more.

Immediate and delayed recall were assessed using a 10-item word-list memory task, and executive function was measured using a clock drawing test. Each year’s cognitive functions were linked to the prior year’s food insecurity data.

Over 7 years, 417 people, or 12.1%, experienced food insecurity at least once.

Those with food insecurity were more likely to be older, female, part of racial and ethnic minority groups, living alone, obese, and have a lower income and educational attainment, depressive symptoms, social isolation and disability, compared with those without food insecurity.

After adjusting for age, sex, race/ethnicity, educational level, income, marital status, body mass index, functional disability, social isolation, and other potential confounders, researchers found that food insecurity was associated with a more rapid decline in executive function (mean difference in annual change in executive function score, −0.04; 95% confidence interval, −0.09 to −0.003).

Food insecurity was not associated with baseline cognitive function scores or changes in immediate or delayed recall.

“Clinicians should be aware of the experience of food insecurity and the higher risk of cognitive decline so maybe they could do universal screening and refer people with food insecurity to programs that can help them access nutritious meals,” Dr. Kim said.
 

A sign of other problems?

Thomas Vidic, MD, said food insecurity often goes hand-in-hand with lack of medication adherence, lack of regular medical care, and a host of other issues. Dr. Vidic is a neurologist at the Elkhart Clinic, Ind., and an adjunct clinical professor of neurology at Indiana University.

“When a person has food insecurity, they likely have other problems, and they’re going to degenerate faster,” said Dr. Vidic, who was not part of the study. “This is one important component, and it’s one more way of getting a handle on people who are failing.”

Dr. Vidic, who has dealt with the issue of food insecurity with his own patients, said he suspects the self-report nature of the study may hide the true scale of the problem.

“I suspect the numbers might actually be higher,” he said, adding that the study fills a gap in the literature with a large, nationally representative sample.

“We’re looking for issues to help with the elderly as far as what can we do to keep dementia from progressing,” he said. “There are some things that make sense, but we’ve never had this kind of data before.”

The study was funded by the National Institute on Aging. Dr. Kim and Dr. Vidic have reported no relevant financial relationships.

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

Food insecurity is linked to a more rapid decline in executive function in older adults, a new study shows.

The findings were reported just weeks after a pandemic-era expansion in Supplemental Nutrition Assistance Program benefits ended, leading to less food assistance for about 5 million people over age 60 who participate in the program.

“Even though we found only a very small association between food insecurity and executive function, it’s still meaningful, because food insecurity is something we can prevent,” lead investigator Boeun Kim, PhD, MPH, RN, postdoctoral fellow at Johns Hopkins University School of Nursing, Baltimore, told this news organization.

The findings were published online  in JAMA Network Open.
 

National data

The number of Americans over 60 with food insecurity has more than doubled since 2007, with an estimated 5.2 million older adults reporting food insecurity in 2020.

Prior studies have linked malnutrition and food insecurity to a decline in cognitive function. Participating in food assistance programs such as SNAP is associated with slower memory decline in older adults.

However, to date, there has been no longitudinal study that has used data from a nationally representative sample of older Americans, which, Dr. Kim said, could limit generalizability of the findings.

To address that issue, investigators analyzed data from 3,037 participants in the National Health and Aging Trends Study, which includes community dwellers age 65 and older who receive Medicare.

Participants reported food insecurity over 7 years, from 2012 to 2019. Data on immediate memory, delayed memory, and executive function were from 2013 to 2020.

Food insecurity was defined as going without groceries due to limited ability or social support; a lack of hot meals related to functional limitation or no help; going without eating because of the inability to feed oneself or no available support; skipping meals due to insufficient food or money; or skipping meals for 5 days or more.

Immediate and delayed recall were assessed using a 10-item word-list memory task, and executive function was measured using a clock drawing test. Each year’s cognitive functions were linked to the prior year’s food insecurity data.

Over 7 years, 417 people, or 12.1%, experienced food insecurity at least once.

Those with food insecurity were more likely to be older, female, part of racial and ethnic minority groups, living alone, obese, and have a lower income and educational attainment, depressive symptoms, social isolation and disability, compared with those without food insecurity.

After adjusting for age, sex, race/ethnicity, educational level, income, marital status, body mass index, functional disability, social isolation, and other potential confounders, researchers found that food insecurity was associated with a more rapid decline in executive function (mean difference in annual change in executive function score, −0.04; 95% confidence interval, −0.09 to −0.003).

Food insecurity was not associated with baseline cognitive function scores or changes in immediate or delayed recall.

“Clinicians should be aware of the experience of food insecurity and the higher risk of cognitive decline so maybe they could do universal screening and refer people with food insecurity to programs that can help them access nutritious meals,” Dr. Kim said.
 

A sign of other problems?

Thomas Vidic, MD, said food insecurity often goes hand-in-hand with lack of medication adherence, lack of regular medical care, and a host of other issues. Dr. Vidic is a neurologist at the Elkhart Clinic, Ind., and an adjunct clinical professor of neurology at Indiana University.

“When a person has food insecurity, they likely have other problems, and they’re going to degenerate faster,” said Dr. Vidic, who was not part of the study. “This is one important component, and it’s one more way of getting a handle on people who are failing.”

Dr. Vidic, who has dealt with the issue of food insecurity with his own patients, said he suspects the self-report nature of the study may hide the true scale of the problem.

“I suspect the numbers might actually be higher,” he said, adding that the study fills a gap in the literature with a large, nationally representative sample.

“We’re looking for issues to help with the elderly as far as what can we do to keep dementia from progressing,” he said. “There are some things that make sense, but we’ve never had this kind of data before.”

The study was funded by the National Institute on Aging. Dr. Kim and Dr. Vidic have reported no relevant financial relationships.

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

Disordered sleep is associated with a significantly increased risk for stroke, new research shows.

Results of a large international study show stroke risk was more than three times higher in those who slept too little, more than twice as high in those who sleep too much, and two to three times higher in those with symptoms of severe obstructive sleep apnea.

The study also showed that the greater the number of sleep disorder symptoms, the greater the stroke risk. The 11% of study participants with five or more symptoms of disordered sleep had a fivefold increased risk for stroke.

Jupiterimages/Thinkstock

More symptoms, more risk

Previous research shows severe OSA doubles the risk of stroke and increases the chance of recurrent stroke. A 2019 study showed that people with insomnia had a small increased risk of stroke.

“Both snoring and extremes of sleep duration have been previously associated with an increased risk of stroke in observational research, but less is known about other symptoms of sleep impairment, with less consistent findings,” Dr. McCarthy said.

Prior studies have also generally come from a single geographic region, which Dr. McCarthy noted could limit their generalizability.

For this effort, investigators used data from 4,496 participants in INTERSTROKE, an international case-control study of risk factors for a first acute stroke. About half of the participants had a history of stroke.

Using information collected from a survey of sleep habits, researchers found an elevated stroke risk in those who received less than 5 hours of sleep per night (odds ratio, 3.15; 95% confidence interval, 2.09-4.76) or more than 9 hours of sleep per night (OR, 2.67; 95% CI, 1.89-3.78), compared with those who slept 7 hours a night.

Participants who took unplanned naps or naps lasting an hour or more (OR, 2.46; 95% CI, 1.69-3.57) and participants who reported poor quality sleep (OR,1.52; 95% CI, 1.32-1.75) were also at an increased risk for stroke.

Symptoms of OSA were also strongly associated with increased stroke risk, including snoring (OR, 1.91; 95% CI, 1.62-2.24), snorting (OR, 2.64; 95% CI, 2.17-3.20), and breathing cessation (OR, 2.87; 95% CI, 2.28-2.60).

Stroke risk increased as the number of sleep disturbance symptoms rose, with the greatest risk in the 11% of participants who had five or more symptoms (OR, 5.38; 95% CI, 4.03-7.18).

“This study finds an association between a broad range of sleep impairment symptoms and stroke, and a graded association with increasing symptoms, in an international setting,” Dr. McCarthy said.

Researchers aren’t sure what’s driving the higher stroke risk among people with sleep disturbances. Although the study did control for potential confounders, it wasn’t designed to get at what’s driving the association.

“Sleep disturbance may also have a bi-directional relationship with many stroke risk factors; for example, sleep disturbance may be a symptom of disease and exacerbate disease,” Dr. McCarthy said. “Future interventional studies are required to determine the true direction of the relationship.”
 

A marker of stroke risk

Daniel Lackland, DrPH, professor of neurology at the Medical University of South Carolina, Charleston, said the findings provide additional evidence of the link between sleep and stroke risk.

“The results confirm sleep disorders as a potential marker and part of the risk profile,” he said.

Collecting information about sleep using a validated assessment tool is an important piece of clinical care, Dr. Lackland said, especially among patients with other stroke risk factors.

One limitation of the study was that data on sleep was collected only at one point, and participants were not followed over time to see if changes in sleep affected stroke risk.

“This is an important point and should be a focus for future studies, as it is critical in the design of interventions,” Dr. Lackland said.

The INTERSTROKE study is funded by the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, Canadian Stroke Network, Swedish Research Council, Swedish Heart and Lung Foundation, The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, Astra Zeneca, Boehringer Ingelheim (Canada), Pfizer (Canada), MERCK, Sharp and Dohme, Swedish Heart and Lung Foundation, U.K. Chest, and U.K. Heart and Stroke. Dr. McCarthy and Lackland report no relevant financial relationships.

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

Disordered sleep is associated with a significantly increased risk for stroke, new research shows.

Results of a large international study show stroke risk was more than three times higher in those who slept too little, more than twice as high in those who sleep too much, and two to three times higher in those with symptoms of severe obstructive sleep apnea.

The study also showed that the greater the number of sleep disorder symptoms, the greater the stroke risk. The 11% of study participants with five or more symptoms of disordered sleep had a fivefold increased risk for stroke.

Jupiterimages/Thinkstock

More symptoms, more risk

Previous research shows severe OSA doubles the risk of stroke and increases the chance of recurrent stroke. A 2019 study showed that people with insomnia had a small increased risk of stroke.

“Both snoring and extremes of sleep duration have been previously associated with an increased risk of stroke in observational research, but less is known about other symptoms of sleep impairment, with less consistent findings,” Dr. McCarthy said.

Prior studies have also generally come from a single geographic region, which Dr. McCarthy noted could limit their generalizability.

For this effort, investigators used data from 4,496 participants in INTERSTROKE, an international case-control study of risk factors for a first acute stroke. About half of the participants had a history of stroke.

Using information collected from a survey of sleep habits, researchers found an elevated stroke risk in those who received less than 5 hours of sleep per night (odds ratio, 3.15; 95% confidence interval, 2.09-4.76) or more than 9 hours of sleep per night (OR, 2.67; 95% CI, 1.89-3.78), compared with those who slept 7 hours a night.

Participants who took unplanned naps or naps lasting an hour or more (OR, 2.46; 95% CI, 1.69-3.57) and participants who reported poor quality sleep (OR,1.52; 95% CI, 1.32-1.75) were also at an increased risk for stroke.

Symptoms of OSA were also strongly associated with increased stroke risk, including snoring (OR, 1.91; 95% CI, 1.62-2.24), snorting (OR, 2.64; 95% CI, 2.17-3.20), and breathing cessation (OR, 2.87; 95% CI, 2.28-2.60).

Stroke risk increased as the number of sleep disturbance symptoms rose, with the greatest risk in the 11% of participants who had five or more symptoms (OR, 5.38; 95% CI, 4.03-7.18).

“This study finds an association between a broad range of sleep impairment symptoms and stroke, and a graded association with increasing symptoms, in an international setting,” Dr. McCarthy said.

Researchers aren’t sure what’s driving the higher stroke risk among people with sleep disturbances. Although the study did control for potential confounders, it wasn’t designed to get at what’s driving the association.

“Sleep disturbance may also have a bi-directional relationship with many stroke risk factors; for example, sleep disturbance may be a symptom of disease and exacerbate disease,” Dr. McCarthy said. “Future interventional studies are required to determine the true direction of the relationship.”
 

A marker of stroke risk

Daniel Lackland, DrPH, professor of neurology at the Medical University of South Carolina, Charleston, said the findings provide additional evidence of the link between sleep and stroke risk.

“The results confirm sleep disorders as a potential marker and part of the risk profile,” he said.

Collecting information about sleep using a validated assessment tool is an important piece of clinical care, Dr. Lackland said, especially among patients with other stroke risk factors.

One limitation of the study was that data on sleep was collected only at one point, and participants were not followed over time to see if changes in sleep affected stroke risk.

“This is an important point and should be a focus for future studies, as it is critical in the design of interventions,” Dr. Lackland said.

The INTERSTROKE study is funded by the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, Canadian Stroke Network, Swedish Research Council, Swedish Heart and Lung Foundation, The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, Astra Zeneca, Boehringer Ingelheim (Canada), Pfizer (Canada), MERCK, Sharp and Dohme, Swedish Heart and Lung Foundation, U.K. Chest, and U.K. Heart and Stroke. Dr. McCarthy and Lackland report no relevant financial relationships.

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

Disordered sleep is associated with a significantly increased risk for stroke, new research shows.

Results of a large international study show stroke risk was more than three times higher in those who slept too little, more than twice as high in those who sleep too much, and two to three times higher in those with symptoms of severe obstructive sleep apnea.

The study also showed that the greater the number of sleep disorder symptoms, the greater the stroke risk. The 11% of study participants with five or more symptoms of disordered sleep had a fivefold increased risk for stroke.

Jupiterimages/Thinkstock

More symptoms, more risk

Previous research shows severe OSA doubles the risk of stroke and increases the chance of recurrent stroke. A 2019 study showed that people with insomnia had a small increased risk of stroke.

“Both snoring and extremes of sleep duration have been previously associated with an increased risk of stroke in observational research, but less is known about other symptoms of sleep impairment, with less consistent findings,” Dr. McCarthy said.

Prior studies have also generally come from a single geographic region, which Dr. McCarthy noted could limit their generalizability.

For this effort, investigators used data from 4,496 participants in INTERSTROKE, an international case-control study of risk factors for a first acute stroke. About half of the participants had a history of stroke.

Using information collected from a survey of sleep habits, researchers found an elevated stroke risk in those who received less than 5 hours of sleep per night (odds ratio, 3.15; 95% confidence interval, 2.09-4.76) or more than 9 hours of sleep per night (OR, 2.67; 95% CI, 1.89-3.78), compared with those who slept 7 hours a night.

Participants who took unplanned naps or naps lasting an hour or more (OR, 2.46; 95% CI, 1.69-3.57) and participants who reported poor quality sleep (OR,1.52; 95% CI, 1.32-1.75) were also at an increased risk for stroke.

Symptoms of OSA were also strongly associated with increased stroke risk, including snoring (OR, 1.91; 95% CI, 1.62-2.24), snorting (OR, 2.64; 95% CI, 2.17-3.20), and breathing cessation (OR, 2.87; 95% CI, 2.28-2.60).

Stroke risk increased as the number of sleep disturbance symptoms rose, with the greatest risk in the 11% of participants who had five or more symptoms (OR, 5.38; 95% CI, 4.03-7.18).

“This study finds an association between a broad range of sleep impairment symptoms and stroke, and a graded association with increasing symptoms, in an international setting,” Dr. McCarthy said.

Researchers aren’t sure what’s driving the higher stroke risk among people with sleep disturbances. Although the study did control for potential confounders, it wasn’t designed to get at what’s driving the association.

“Sleep disturbance may also have a bi-directional relationship with many stroke risk factors; for example, sleep disturbance may be a symptom of disease and exacerbate disease,” Dr. McCarthy said. “Future interventional studies are required to determine the true direction of the relationship.”
 

A marker of stroke risk

Daniel Lackland, DrPH, professor of neurology at the Medical University of South Carolina, Charleston, said the findings provide additional evidence of the link between sleep and stroke risk.

“The results confirm sleep disorders as a potential marker and part of the risk profile,” he said.

Collecting information about sleep using a validated assessment tool is an important piece of clinical care, Dr. Lackland said, especially among patients with other stroke risk factors.

One limitation of the study was that data on sleep was collected only at one point, and participants were not followed over time to see if changes in sleep affected stroke risk.

“This is an important point and should be a focus for future studies, as it is critical in the design of interventions,” Dr. Lackland said.

The INTERSTROKE study is funded by the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, Canadian Stroke Network, Swedish Research Council, Swedish Heart and Lung Foundation, The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, Astra Zeneca, Boehringer Ingelheim (Canada), Pfizer (Canada), MERCK, Sharp and Dohme, Swedish Heart and Lung Foundation, U.K. Chest, and U.K. Heart and Stroke. Dr. McCarthy and Lackland report no relevant financial relationships.

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

Increasing intake of folate and vitamin B6 beyond recommended daily levels offers no protective benefit against Parkinson’s disease (PD), a new study shows.

Though there was some evidence that vitamin B12 early in life was associated with decreased PD risk, the findings were inconsistent and were observed only in people whose daily intake was 10 times the recommended level.

“The results of this large prospective study do not support the hypothesis that increasing folate or vitamin B6 intakes above the current levels would reduce PD risk in this population of mostly White U.S. health professionals,” lead investigator Mario H. Flores-Torres, MD, PhD, a research scientist in the department of nutrition at the Harvard T.H. Chan School of Public Health, Boston, said in an interview.

However, he added, the study “leaves open the possibility that in some individuals the intake of vitamin B12 contributes to PD risk – a finding that warrants further research.”

The findings were published online  in Movement Disorders.
 

Mixed findings

Previous studies have suggested B vitamins – including folate, B6 and B12 – might affect PD risk, but results have been mixed.

The new study included 80,965 women from the Nurses’ Health Study (1984-2016) and 48,837 men from the Health Professionals Follow-up Study (1986-2016). The average age at baseline was 50 years in women and 54 years in men, and participants were followed for about 30 years.

Participants completed questionnaires about diet at the beginning of the study and again every 4 years.

To account for the possibility of reverse causation due to the long prodromal phase of PD, investigators conducted lagged analyses at 8, 12, 16, and 20 years.

During the follow-up period, 1,426 incident cases of PD were diagnosed (687 in women and 739 in men).

Researchers found no link between reduced PD risk and intake of vitamin B6 or folate.

Though the total cumulative average intake of vitamin B12 was not associated with PD risk, investigators noted a modest decrease in risk between those with highest baseline of B12 and participants with the lowest baseline levels (hazard ratio, 0.80; P = .01).

Individuals in the highest quintile of B12 intake at baseline had an average intake of 21-22 mcg/d, close to 10 times the recommended daily intake of 2.4 mcg/d.

“Although some of our results suggest that a higher intake of vitamin B12 may decrease the risk of PD in a population of U.S. health professionals, the associations we observed were modest and not entirely consistent,” Dr. Flores-Torres said.

“Additional studies need to confirm our findings to better understand whether people who take higher amounts of B12 younger in life may have a protective benefit against PD,” he added.
 

The whole picture?

Commenting on the findings for this article, Rebecca Gilbert, MD, PhD, chief scientific officer of the American Parkinson Disease Association, New York, noted that checking B vitamin levels is a fairly standard practice for most clinicians. In that regard, this study highlights why this is important.

“Neurologists will often test B12 levels and recommend a supplement if your level is below the normal range,” she said. “No one is questioning the value of B12 for nerves and recommend that B12 is in the normal to high normal range.”

But understanding how B vitamins may or may not affect PD risk might require a different kind of study.

“This analysis, much like many others, is trying so hard to figure out what is it in diets that affects Parkinson’s disease risk,” Dr. Gilbert said. “But we have yet to say these are the nutrients that prevent Parkinson’s or increase the risk.”

One reason for the conflicting results in studies such as this could be that the explanation for the link between diet and PD risk may not be in specific minerals consumed but rather in the diet as a whole.

“Focusing on specific elements of a diet may not give us the answer,” Dr. Gilbert said. “We should be analyzing diet as a complete holistic picture because it’s not just the elements but how everything in what we eat works together.”

The study was funded by the National Institutes of Health and the Parkinson’s Foundation. Dr. Flores-Torres and Dr. Gilbert report no relevant conflicts.
 

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

Increasing intake of folate and vitamin B6 beyond recommended daily levels offers no protective benefit against Parkinson’s disease (PD), a new study shows.

Though there was some evidence that vitamin B12 early in life was associated with decreased PD risk, the findings were inconsistent and were observed only in people whose daily intake was 10 times the recommended level.

“The results of this large prospective study do not support the hypothesis that increasing folate or vitamin B6 intakes above the current levels would reduce PD risk in this population of mostly White U.S. health professionals,” lead investigator Mario H. Flores-Torres, MD, PhD, a research scientist in the department of nutrition at the Harvard T.H. Chan School of Public Health, Boston, said in an interview.

However, he added, the study “leaves open the possibility that in some individuals the intake of vitamin B12 contributes to PD risk – a finding that warrants further research.”

The findings were published online  in Movement Disorders.
 

Mixed findings

Previous studies have suggested B vitamins – including folate, B6 and B12 – might affect PD risk, but results have been mixed.

The new study included 80,965 women from the Nurses’ Health Study (1984-2016) and 48,837 men from the Health Professionals Follow-up Study (1986-2016). The average age at baseline was 50 years in women and 54 years in men, and participants were followed for about 30 years.

Participants completed questionnaires about diet at the beginning of the study and again every 4 years.

To account for the possibility of reverse causation due to the long prodromal phase of PD, investigators conducted lagged analyses at 8, 12, 16, and 20 years.

During the follow-up period, 1,426 incident cases of PD were diagnosed (687 in women and 739 in men).

Researchers found no link between reduced PD risk and intake of vitamin B6 or folate.

Though the total cumulative average intake of vitamin B12 was not associated with PD risk, investigators noted a modest decrease in risk between those with highest baseline of B12 and participants with the lowest baseline levels (hazard ratio, 0.80; P = .01).

Individuals in the highest quintile of B12 intake at baseline had an average intake of 21-22 mcg/d, close to 10 times the recommended daily intake of 2.4 mcg/d.

“Although some of our results suggest that a higher intake of vitamin B12 may decrease the risk of PD in a population of U.S. health professionals, the associations we observed were modest and not entirely consistent,” Dr. Flores-Torres said.

“Additional studies need to confirm our findings to better understand whether people who take higher amounts of B12 younger in life may have a protective benefit against PD,” he added.
 

The whole picture?

Commenting on the findings for this article, Rebecca Gilbert, MD, PhD, chief scientific officer of the American Parkinson Disease Association, New York, noted that checking B vitamin levels is a fairly standard practice for most clinicians. In that regard, this study highlights why this is important.

“Neurologists will often test B12 levels and recommend a supplement if your level is below the normal range,” she said. “No one is questioning the value of B12 for nerves and recommend that B12 is in the normal to high normal range.”

But understanding how B vitamins may or may not affect PD risk might require a different kind of study.

“This analysis, much like many others, is trying so hard to figure out what is it in diets that affects Parkinson’s disease risk,” Dr. Gilbert said. “But we have yet to say these are the nutrients that prevent Parkinson’s or increase the risk.”

One reason for the conflicting results in studies such as this could be that the explanation for the link between diet and PD risk may not be in specific minerals consumed but rather in the diet as a whole.

“Focusing on specific elements of a diet may not give us the answer,” Dr. Gilbert said. “We should be analyzing diet as a complete holistic picture because it’s not just the elements but how everything in what we eat works together.”

The study was funded by the National Institutes of Health and the Parkinson’s Foundation. Dr. Flores-Torres and Dr. Gilbert report no relevant conflicts.
 

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

Increasing intake of folate and vitamin B6 beyond recommended daily levels offers no protective benefit against Parkinson’s disease (PD), a new study shows.

Though there was some evidence that vitamin B12 early in life was associated with decreased PD risk, the findings were inconsistent and were observed only in people whose daily intake was 10 times the recommended level.

“The results of this large prospective study do not support the hypothesis that increasing folate or vitamin B6 intakes above the current levels would reduce PD risk in this population of mostly White U.S. health professionals,” lead investigator Mario H. Flores-Torres, MD, PhD, a research scientist in the department of nutrition at the Harvard T.H. Chan School of Public Health, Boston, said in an interview.

However, he added, the study “leaves open the possibility that in some individuals the intake of vitamin B12 contributes to PD risk – a finding that warrants further research.”

The findings were published online  in Movement Disorders.
 

Mixed findings

Previous studies have suggested B vitamins – including folate, B6 and B12 – might affect PD risk, but results have been mixed.

The new study included 80,965 women from the Nurses’ Health Study (1984-2016) and 48,837 men from the Health Professionals Follow-up Study (1986-2016). The average age at baseline was 50 years in women and 54 years in men, and participants were followed for about 30 years.

Participants completed questionnaires about diet at the beginning of the study and again every 4 years.

To account for the possibility of reverse causation due to the long prodromal phase of PD, investigators conducted lagged analyses at 8, 12, 16, and 20 years.

During the follow-up period, 1,426 incident cases of PD were diagnosed (687 in women and 739 in men).

Researchers found no link between reduced PD risk and intake of vitamin B6 or folate.

Though the total cumulative average intake of vitamin B12 was not associated with PD risk, investigators noted a modest decrease in risk between those with highest baseline of B12 and participants with the lowest baseline levels (hazard ratio, 0.80; P = .01).

Individuals in the highest quintile of B12 intake at baseline had an average intake of 21-22 mcg/d, close to 10 times the recommended daily intake of 2.4 mcg/d.

“Although some of our results suggest that a higher intake of vitamin B12 may decrease the risk of PD in a population of U.S. health professionals, the associations we observed were modest and not entirely consistent,” Dr. Flores-Torres said.

“Additional studies need to confirm our findings to better understand whether people who take higher amounts of B12 younger in life may have a protective benefit against PD,” he added.
 

The whole picture?

Commenting on the findings for this article, Rebecca Gilbert, MD, PhD, chief scientific officer of the American Parkinson Disease Association, New York, noted that checking B vitamin levels is a fairly standard practice for most clinicians. In that regard, this study highlights why this is important.

“Neurologists will often test B12 levels and recommend a supplement if your level is below the normal range,” she said. “No one is questioning the value of B12 for nerves and recommend that B12 is in the normal to high normal range.”

But understanding how B vitamins may or may not affect PD risk might require a different kind of study.

“This analysis, much like many others, is trying so hard to figure out what is it in diets that affects Parkinson’s disease risk,” Dr. Gilbert said. “But we have yet to say these are the nutrients that prevent Parkinson’s or increase the risk.”

One reason for the conflicting results in studies such as this could be that the explanation for the link between diet and PD risk may not be in specific minerals consumed but rather in the diet as a whole.

“Focusing on specific elements of a diet may not give us the answer,” Dr. Gilbert said. “We should be analyzing diet as a complete holistic picture because it’s not just the elements but how everything in what we eat works together.”

The study was funded by the National Institutes of Health and the Parkinson’s Foundation. Dr. Flores-Torres and Dr. Gilbert report no relevant conflicts.
 

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

Expansions in telehealth services and increased use of medications for opioid use disorder (MOUD) were associated with significant decreases in fatal drug overdoses during the pandemic, a new study of Medicare beneficiaries shows.

Telehealth services for opioid use disorder (OUD) were used far more often during the pandemic than before COVID-19, and those who used them were 33% less likely to die of a drug overdose.

Investigators also found a significant increase in MOUD use during the pandemic. Fatal drug overdoses were 59% less likely among individuals who received MOUD from an opioid treatment program and 38% less likely among those treated with buprenorphine in an office-based setting.

The results come as policymakers are preparing for the end of the public health emergency that prompted the expansion of OUD-related telehealth and MOUD prescribing and are deciding whether to make those expansions permanent.

“The expansion of telehealth during the COVID-19 pandemic appears to have had positive effects on patients receiving MOUD, improved retention among patients who received MOUD, and lowered risks for both nonfatal and fatal overdose,” lead investigator Christopher M. Jones, PharmD, DrPH, director of the National Center for Injury Prevention and Control at the Centers for Disease Control and Prevention, Atlanta, Georgia, told this news organization. “Our results suggest that telehealth is a valuable tool in the toolbox for expanding access to and improving retention on MOUD.”

The findings were published online in JAMA Psychiatry.
 

Increase in treatment

The study included 105,162 Medicare beneficiaries who began OUD treatment between March and August in 2019 (prepandemic cohort; 67.6%

aged 45-74 years), and 70,479 who began treatment between March and August of 2020 (pandemic cohort; 66.3% aged 45-74 years).

Participants had not received OUD treatment in the 6 months leading up to study enrollment and were followed for 6 months after treatment began.

Significantly more study participants received OUD-related telehealth services during the pandemic than prior to 2019 (19.6% vs. 0.6%; P < .001). Receipt of MOUD was also significantly higher in the pandemic cohort (12.6% vs. 10.8%; P < .001).

The rate of drug overdose deaths was higher in the pandemic cohort (5.1 deaths vs. 3.7 deaths per 1,000 beneficiaries; P < .001). But the percentage of deaths from drug overdoses did not differ between groups (4.8% in the prepandemic cohort vs. 5.1% in the pandemic cohort; P = .49).

In the pandemic cohort, fatal drug overdoses were 33% less likely among those who received OUD-related telehealth services (adjusted odds ratio, 0.67; 95% confidence interval, 0.48-0.92); 59% less likely among those who received MOUD from opioid treatment programs (aOR, 0.41; 95% CI, 0.25-0.68), and 38% less likely among those who received buprenorphine in office-based settings (aOR, 0.62; 95% CI, 0.43-0.91).

Risk of fatal overdose was significantly lower among women and those aged 65 years and older. There were no significant differences in risk based on urban or rural residency or on ethnicity.

“Against the backdrop of a highly potent illicit drug supply driven by illicit fentanyl and fentanyl analogues and historically large increases in overdose deaths during the COVID-19 pandemic, MOUD was still highly effective at reducing risk for fatal overdose,” Dr. Jones said.

While the use of buprenorphine in office-based settings was associated with a decreased risk of overdose death, use of extended-release naltrexone was not.

“Prior research has demonstrated the effectiveness of extended-release naltrexone in the treatment of opioid use disorder,” Dr. Jones said. “However, research has also shown that patients have challenges getting started, or inducted, on extended-release naltrexone.”

An earlier study by Dr. Jones and colleagues showed that rates of retention were lower with extended-release naltrexone, compared with buprenorphine in office-based settings or MOUD from opioid treatment programs.

The new study included only a small number of individuals who were receiving extended-release naltrexone, which may have influenced the findings. In addition, challenges with induction and retention may be driving the results, Dr. Jones noted.

“Efforts to improve induction and retention with extended-release naltrexone are important areas for future research and clinical practice,” he added.
 

An important engagement tool

A number of questions about telehealth care for OUD remain, including whether increased access to care accounts for the reduction in drug overdose risk that the investigators found or whether other factors are at play.

“There is still more we need to understand about telehealth, such as the quality of care provided and the particular aspects of care provided by telehealth and how this influences health outcomes,” Dr. Jones said.

The results also suggest treatments for OUD are still not finding their way to patients who might benefit, he added.

“Despite the positive findings and the prior research showing that MOUD is highly effective, we found that only one in five patients received telehealth services and only one in eight received any MOUD. This really underscores the need to expand these services across clinical settings,” he added.

These and earlier findings demonstrate the potential benefits of continuing pandemic-era expansion of OUD-related telehealth services and MOUD access, Dr. Jones said.

In preparation for the end of the public health emergency on May 1, the Drug Enforcement Agency recently released a proposal that would allow providers to prescribe a 30-day supply of buprenorphine, but for patients to receive additional prescriptions, a face-to-face meeting would be required. The proposal has drawn criticism from addiction medicine specialists.

The current study didn’t explore if or how the proposal might affect patients with OUD or whether it could blunt the positive effects of the findings.

“Prior research shows that keeping individuals engaged in treatment, including on medications, is a critical part of reducing the negative health and social impacts of opioid use disorder. Our results suggest that telehealth can be an important tool in helping patients engage in and stay connected in care,” said Dr. Jones.

The study was funded by the Centers for Disease Control and Prevention, the Centers for Medicare & Medicaid Services, and the National Institutes of Health. Dr. Johnson reports no relevant financial relationships.

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

Expansions in telehealth services and increased use of medications for opioid use disorder (MOUD) were associated with significant decreases in fatal drug overdoses during the pandemic, a new study of Medicare beneficiaries shows.

Telehealth services for opioid use disorder (OUD) were used far more often during the pandemic than before COVID-19, and those who used them were 33% less likely to die of a drug overdose.

Investigators also found a significant increase in MOUD use during the pandemic. Fatal drug overdoses were 59% less likely among individuals who received MOUD from an opioid treatment program and 38% less likely among those treated with buprenorphine in an office-based setting.

The results come as policymakers are preparing for the end of the public health emergency that prompted the expansion of OUD-related telehealth and MOUD prescribing and are deciding whether to make those expansions permanent.

“The expansion of telehealth during the COVID-19 pandemic appears to have had positive effects on patients receiving MOUD, improved retention among patients who received MOUD, and lowered risks for both nonfatal and fatal overdose,” lead investigator Christopher M. Jones, PharmD, DrPH, director of the National Center for Injury Prevention and Control at the Centers for Disease Control and Prevention, Atlanta, Georgia, told this news organization. “Our results suggest that telehealth is a valuable tool in the toolbox for expanding access to and improving retention on MOUD.”

The findings were published online in JAMA Psychiatry.
 

Increase in treatment

The study included 105,162 Medicare beneficiaries who began OUD treatment between March and August in 2019 (prepandemic cohort; 67.6%

aged 45-74 years), and 70,479 who began treatment between March and August of 2020 (pandemic cohort; 66.3% aged 45-74 years).

Participants had not received OUD treatment in the 6 months leading up to study enrollment and were followed for 6 months after treatment began.

Significantly more study participants received OUD-related telehealth services during the pandemic than prior to 2019 (19.6% vs. 0.6%; P < .001). Receipt of MOUD was also significantly higher in the pandemic cohort (12.6% vs. 10.8%; P < .001).

The rate of drug overdose deaths was higher in the pandemic cohort (5.1 deaths vs. 3.7 deaths per 1,000 beneficiaries; P < .001). But the percentage of deaths from drug overdoses did not differ between groups (4.8% in the prepandemic cohort vs. 5.1% in the pandemic cohort; P = .49).

In the pandemic cohort, fatal drug overdoses were 33% less likely among those who received OUD-related telehealth services (adjusted odds ratio, 0.67; 95% confidence interval, 0.48-0.92); 59% less likely among those who received MOUD from opioid treatment programs (aOR, 0.41; 95% CI, 0.25-0.68), and 38% less likely among those who received buprenorphine in office-based settings (aOR, 0.62; 95% CI, 0.43-0.91).

Risk of fatal overdose was significantly lower among women and those aged 65 years and older. There were no significant differences in risk based on urban or rural residency or on ethnicity.

“Against the backdrop of a highly potent illicit drug supply driven by illicit fentanyl and fentanyl analogues and historically large increases in overdose deaths during the COVID-19 pandemic, MOUD was still highly effective at reducing risk for fatal overdose,” Dr. Jones said.

While the use of buprenorphine in office-based settings was associated with a decreased risk of overdose death, use of extended-release naltrexone was not.

“Prior research has demonstrated the effectiveness of extended-release naltrexone in the treatment of opioid use disorder,” Dr. Jones said. “However, research has also shown that patients have challenges getting started, or inducted, on extended-release naltrexone.”

An earlier study by Dr. Jones and colleagues showed that rates of retention were lower with extended-release naltrexone, compared with buprenorphine in office-based settings or MOUD from opioid treatment programs.

The new study included only a small number of individuals who were receiving extended-release naltrexone, which may have influenced the findings. In addition, challenges with induction and retention may be driving the results, Dr. Jones noted.

“Efforts to improve induction and retention with extended-release naltrexone are important areas for future research and clinical practice,” he added.
 

An important engagement tool

A number of questions about telehealth care for OUD remain, including whether increased access to care accounts for the reduction in drug overdose risk that the investigators found or whether other factors are at play.

“There is still more we need to understand about telehealth, such as the quality of care provided and the particular aspects of care provided by telehealth and how this influences health outcomes,” Dr. Jones said.

The results also suggest treatments for OUD are still not finding their way to patients who might benefit, he added.

“Despite the positive findings and the prior research showing that MOUD is highly effective, we found that only one in five patients received telehealth services and only one in eight received any MOUD. This really underscores the need to expand these services across clinical settings,” he added.

These and earlier findings demonstrate the potential benefits of continuing pandemic-era expansion of OUD-related telehealth services and MOUD access, Dr. Jones said.

In preparation for the end of the public health emergency on May 1, the Drug Enforcement Agency recently released a proposal that would allow providers to prescribe a 30-day supply of buprenorphine, but for patients to receive additional prescriptions, a face-to-face meeting would be required. The proposal has drawn criticism from addiction medicine specialists.

The current study didn’t explore if or how the proposal might affect patients with OUD or whether it could blunt the positive effects of the findings.

“Prior research shows that keeping individuals engaged in treatment, including on medications, is a critical part of reducing the negative health and social impacts of opioid use disorder. Our results suggest that telehealth can be an important tool in helping patients engage in and stay connected in care,” said Dr. Jones.

The study was funded by the Centers for Disease Control and Prevention, the Centers for Medicare & Medicaid Services, and the National Institutes of Health. Dr. Johnson reports no relevant financial relationships.

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

Expansions in telehealth services and increased use of medications for opioid use disorder (MOUD) were associated with significant decreases in fatal drug overdoses during the pandemic, a new study of Medicare beneficiaries shows.

Telehealth services for opioid use disorder (OUD) were used far more often during the pandemic than before COVID-19, and those who used them were 33% less likely to die of a drug overdose.

Investigators also found a significant increase in MOUD use during the pandemic. Fatal drug overdoses were 59% less likely among individuals who received MOUD from an opioid treatment program and 38% less likely among those treated with buprenorphine in an office-based setting.

The results come as policymakers are preparing for the end of the public health emergency that prompted the expansion of OUD-related telehealth and MOUD prescribing and are deciding whether to make those expansions permanent.

“The expansion of telehealth during the COVID-19 pandemic appears to have had positive effects on patients receiving MOUD, improved retention among patients who received MOUD, and lowered risks for both nonfatal and fatal overdose,” lead investigator Christopher M. Jones, PharmD, DrPH, director of the National Center for Injury Prevention and Control at the Centers for Disease Control and Prevention, Atlanta, Georgia, told this news organization. “Our results suggest that telehealth is a valuable tool in the toolbox for expanding access to and improving retention on MOUD.”

The findings were published online in JAMA Psychiatry.
 

Increase in treatment

The study included 105,162 Medicare beneficiaries who began OUD treatment between March and August in 2019 (prepandemic cohort; 67.6%

aged 45-74 years), and 70,479 who began treatment between March and August of 2020 (pandemic cohort; 66.3% aged 45-74 years).

Participants had not received OUD treatment in the 6 months leading up to study enrollment and were followed for 6 months after treatment began.

Significantly more study participants received OUD-related telehealth services during the pandemic than prior to 2019 (19.6% vs. 0.6%; P < .001). Receipt of MOUD was also significantly higher in the pandemic cohort (12.6% vs. 10.8%; P < .001).

The rate of drug overdose deaths was higher in the pandemic cohort (5.1 deaths vs. 3.7 deaths per 1,000 beneficiaries; P < .001). But the percentage of deaths from drug overdoses did not differ between groups (4.8% in the prepandemic cohort vs. 5.1% in the pandemic cohort; P = .49).

In the pandemic cohort, fatal drug overdoses were 33% less likely among those who received OUD-related telehealth services (adjusted odds ratio, 0.67; 95% confidence interval, 0.48-0.92); 59% less likely among those who received MOUD from opioid treatment programs (aOR, 0.41; 95% CI, 0.25-0.68), and 38% less likely among those who received buprenorphine in office-based settings (aOR, 0.62; 95% CI, 0.43-0.91).

Risk of fatal overdose was significantly lower among women and those aged 65 years and older. There were no significant differences in risk based on urban or rural residency or on ethnicity.

“Against the backdrop of a highly potent illicit drug supply driven by illicit fentanyl and fentanyl analogues and historically large increases in overdose deaths during the COVID-19 pandemic, MOUD was still highly effective at reducing risk for fatal overdose,” Dr. Jones said.

While the use of buprenorphine in office-based settings was associated with a decreased risk of overdose death, use of extended-release naltrexone was not.

“Prior research has demonstrated the effectiveness of extended-release naltrexone in the treatment of opioid use disorder,” Dr. Jones said. “However, research has also shown that patients have challenges getting started, or inducted, on extended-release naltrexone.”

An earlier study by Dr. Jones and colleagues showed that rates of retention were lower with extended-release naltrexone, compared with buprenorphine in office-based settings or MOUD from opioid treatment programs.

The new study included only a small number of individuals who were receiving extended-release naltrexone, which may have influenced the findings. In addition, challenges with induction and retention may be driving the results, Dr. Jones noted.

“Efforts to improve induction and retention with extended-release naltrexone are important areas for future research and clinical practice,” he added.
 

An important engagement tool

A number of questions about telehealth care for OUD remain, including whether increased access to care accounts for the reduction in drug overdose risk that the investigators found or whether other factors are at play.

“There is still more we need to understand about telehealth, such as the quality of care provided and the particular aspects of care provided by telehealth and how this influences health outcomes,” Dr. Jones said.

The results also suggest treatments for OUD are still not finding their way to patients who might benefit, he added.

“Despite the positive findings and the prior research showing that MOUD is highly effective, we found that only one in five patients received telehealth services and only one in eight received any MOUD. This really underscores the need to expand these services across clinical settings,” he added.

These and earlier findings demonstrate the potential benefits of continuing pandemic-era expansion of OUD-related telehealth services and MOUD access, Dr. Jones said.

In preparation for the end of the public health emergency on May 1, the Drug Enforcement Agency recently released a proposal that would allow providers to prescribe a 30-day supply of buprenorphine, but for patients to receive additional prescriptions, a face-to-face meeting would be required. The proposal has drawn criticism from addiction medicine specialists.

The current study didn’t explore if or how the proposal might affect patients with OUD or whether it could blunt the positive effects of the findings.

“Prior research shows that keeping individuals engaged in treatment, including on medications, is a critical part of reducing the negative health and social impacts of opioid use disorder. Our results suggest that telehealth can be an important tool in helping patients engage in and stay connected in care,” said Dr. Jones.

The study was funded by the Centers for Disease Control and Prevention, the Centers for Medicare & Medicaid Services, and the National Institutes of Health. Dr. Johnson reports no relevant financial relationships.

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

Scientists have identified two new genes linked to schizophrenia and discovered that a third gene previously known to be involved in the disorder may also play a role in autism.

The genes were identified through a meta-analysis comparing gene sequences of 35,828 people with schizophrenia to 107,877 people without the condition.

The study builds on a report published last year that identified 10 genes with rare variants that are directly tied to schizophrenia risk. But that study, like most prior genetic analyses on psychiatric illnesses, was done on the DNA from people of European ancestry.

About 40% of the genetic samples included in this new work came from people of non-European ancestry, which researchers say makes it the most ethnically diverse schizophrenia genetics study to date.

Based on the findings, researchers concluded that the schizophrenia risk conferred by the rare genetic variants found on the new genes they discovered and on those previously identified is conserved across ethnicities.

The new genes, SRRM2 and AKAP11, contain rare protein-truncating variants (PTVs) that investigators say could be the cause of schizophrenia in some patients. The results could have significant implications for drug development.

Icahn School of Medicine at Mount Sinai

“It’s not curing the illness, but it is taking us a step closer so that we’re able to say that this may be the cause of the illness in a particular patient,” senior investigator Alexander Charney, MD, PhD, associate professor of psychiatry, genetics and genomic sciences, neuroscience, and neurosurgery, at Icahn School of Medicine at Mount Sinai, New York, said in an interview.

The findings were published online in Nature Genetics.

 

Schizophrenia’s genetic architecture

Prior studies suggest the genetic architecture of schizophrenia may be influenced by common single-nucleotide polymorphisms, copy number variants and rare PTVs.

Investigators note that rare PTVs are important because they can link disease risk directly to individual genes. But identifying the PTVs and the genes that harbor them requires large patient cohorts, far bigger than any single institution can provide.

Dr. Charney and other researchers are part of the Psychiatric Genomics Consortium, a collaboration of researchers from hundreds of institutions around the world established in 2007 to create large cohorts for genetic studies of psychiatric disease.

For this study, investigators sequenced a new cohort of 11,580 schizophrenia cases and 10,555 controls of diverse ancestries. The analysis showed that the findings previously established in predominantly European cohorts extended to non-European populations.

They then conducted a meta-analysis of the new cohort combined with datasets from earlier studies, creating a pooled sample of 35,828 cases and 107,877 controls.

This meta-analysis revealed two new genes linked to schizophrenia, SRRM2 and AKAP11. The third gene flagged in the study, PCLO, was previously implicated in schizophrenia but is now identified as having a shared risk for schizophrenia and autism.

The rare PVTs on the 12 genes identified so far through this type of study are probably only involved in a small fraction of schizophrenia cases, Dr. Charney acknowledged. However, the discovery could lead to new treatments that could benefit all patients with the disease, he added.

“There are multiple pathways to psychosis and there’s also multiple pathways to treat psychosis,” Dr. Charney said. “There’s reason to believe if you can find a mechanism by which a human being could develop a psychosis, then reversing that mechanism could help a lot of people who have psychosis for another reason.”
 

Importance of diverse cohorts

Commenting on the findings, Jennifer Gladys Mulle, MHS, PhD, associate professor of psychiatry at the Robert Wood Johnson Medical School at Rutgers University, Piscataway, N.J., noted that while genetic discoveries have led to new therapies in other medical conditions, that has not been the case with schizophrenia.

“In other disorders, having genetic findings have really opened a window into the molecular mechanisms, which has allowed us to develop pharmaceuticals and understand the disease process better,” said Dr. Mulle, who was not part of this study. “But because we haven’t had that in schizophrenia, it’s really held us back. Having genetic variants associated with schizophrenia may really help us understand the mechanism.”

The inclusion of diverse populations is also a key contribution of this study, Dr. Mulle added.

“So far a lot of the work we’ve done in genetics has been on people of European ancestry,” Dr. Mulle said. “The fact that they have found results that are generalizable across multiple ethnicities really suggests that if we develop pharmaceutical agents based on these findings, it will help many people.”

More attention has been paid recently to a growing problem in the study of genetics of psychiatric disorders: More than 95% of participants in genome-wide association studies that seek to identify gene variants linked to disease are of European ancestry.

Dr. Charney and his colleagues had that in mind when they designed the study.

“We can’t get to a place where genetics is clinically useful if we don’t know the extent to which a particular observation that’s found in one population is also true for other populations,” Dr. Charney said.

The study was funded by the National Institutes of Health. Dr. Charney and Dr. Mulle report no relevant financial relationships.

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

Scientists have identified two new genes linked to schizophrenia and discovered that a third gene previously known to be involved in the disorder may also play a role in autism.

The genes were identified through a meta-analysis comparing gene sequences of 35,828 people with schizophrenia to 107,877 people without the condition.

The study builds on a report published last year that identified 10 genes with rare variants that are directly tied to schizophrenia risk. But that study, like most prior genetic analyses on psychiatric illnesses, was done on the DNA from people of European ancestry.

About 40% of the genetic samples included in this new work came from people of non-European ancestry, which researchers say makes it the most ethnically diverse schizophrenia genetics study to date.

Based on the findings, researchers concluded that the schizophrenia risk conferred by the rare genetic variants found on the new genes they discovered and on those previously identified is conserved across ethnicities.

The new genes, SRRM2 and AKAP11, contain rare protein-truncating variants (PTVs) that investigators say could be the cause of schizophrenia in some patients. The results could have significant implications for drug development.

Icahn School of Medicine at Mount Sinai

“It’s not curing the illness, but it is taking us a step closer so that we’re able to say that this may be the cause of the illness in a particular patient,” senior investigator Alexander Charney, MD, PhD, associate professor of psychiatry, genetics and genomic sciences, neuroscience, and neurosurgery, at Icahn School of Medicine at Mount Sinai, New York, said in an interview.

The findings were published online in Nature Genetics.

 

Schizophrenia’s genetic architecture

Prior studies suggest the genetic architecture of schizophrenia may be influenced by common single-nucleotide polymorphisms, copy number variants and rare PTVs.

Investigators note that rare PTVs are important because they can link disease risk directly to individual genes. But identifying the PTVs and the genes that harbor them requires large patient cohorts, far bigger than any single institution can provide.

Dr. Charney and other researchers are part of the Psychiatric Genomics Consortium, a collaboration of researchers from hundreds of institutions around the world established in 2007 to create large cohorts for genetic studies of psychiatric disease.

For this study, investigators sequenced a new cohort of 11,580 schizophrenia cases and 10,555 controls of diverse ancestries. The analysis showed that the findings previously established in predominantly European cohorts extended to non-European populations.

They then conducted a meta-analysis of the new cohort combined with datasets from earlier studies, creating a pooled sample of 35,828 cases and 107,877 controls.

This meta-analysis revealed two new genes linked to schizophrenia, SRRM2 and AKAP11. The third gene flagged in the study, PCLO, was previously implicated in schizophrenia but is now identified as having a shared risk for schizophrenia and autism.

The rare PVTs on the 12 genes identified so far through this type of study are probably only involved in a small fraction of schizophrenia cases, Dr. Charney acknowledged. However, the discovery could lead to new treatments that could benefit all patients with the disease, he added.

“There are multiple pathways to psychosis and there’s also multiple pathways to treat psychosis,” Dr. Charney said. “There’s reason to believe if you can find a mechanism by which a human being could develop a psychosis, then reversing that mechanism could help a lot of people who have psychosis for another reason.”
 

Importance of diverse cohorts

Commenting on the findings, Jennifer Gladys Mulle, MHS, PhD, associate professor of psychiatry at the Robert Wood Johnson Medical School at Rutgers University, Piscataway, N.J., noted that while genetic discoveries have led to new therapies in other medical conditions, that has not been the case with schizophrenia.

“In other disorders, having genetic findings have really opened a window into the molecular mechanisms, which has allowed us to develop pharmaceuticals and understand the disease process better,” said Dr. Mulle, who was not part of this study. “But because we haven’t had that in schizophrenia, it’s really held us back. Having genetic variants associated with schizophrenia may really help us understand the mechanism.”

The inclusion of diverse populations is also a key contribution of this study, Dr. Mulle added.

“So far a lot of the work we’ve done in genetics has been on people of European ancestry,” Dr. Mulle said. “The fact that they have found results that are generalizable across multiple ethnicities really suggests that if we develop pharmaceutical agents based on these findings, it will help many people.”

More attention has been paid recently to a growing problem in the study of genetics of psychiatric disorders: More than 95% of participants in genome-wide association studies that seek to identify gene variants linked to disease are of European ancestry.

Dr. Charney and his colleagues had that in mind when they designed the study.

“We can’t get to a place where genetics is clinically useful if we don’t know the extent to which a particular observation that’s found in one population is also true for other populations,” Dr. Charney said.

The study was funded by the National Institutes of Health. Dr. Charney and Dr. Mulle report no relevant financial relationships.

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

Scientists have identified two new genes linked to schizophrenia and discovered that a third gene previously known to be involved in the disorder may also play a role in autism.

The genes were identified through a meta-analysis comparing gene sequences of 35,828 people with schizophrenia to 107,877 people without the condition.

The study builds on a report published last year that identified 10 genes with rare variants that are directly tied to schizophrenia risk. But that study, like most prior genetic analyses on psychiatric illnesses, was done on the DNA from people of European ancestry.

About 40% of the genetic samples included in this new work came from people of non-European ancestry, which researchers say makes it the most ethnically diverse schizophrenia genetics study to date.

Based on the findings, researchers concluded that the schizophrenia risk conferred by the rare genetic variants found on the new genes they discovered and on those previously identified is conserved across ethnicities.

The new genes, SRRM2 and AKAP11, contain rare protein-truncating variants (PTVs) that investigators say could be the cause of schizophrenia in some patients. The results could have significant implications for drug development.

Icahn School of Medicine at Mount Sinai

“It’s not curing the illness, but it is taking us a step closer so that we’re able to say that this may be the cause of the illness in a particular patient,” senior investigator Alexander Charney, MD, PhD, associate professor of psychiatry, genetics and genomic sciences, neuroscience, and neurosurgery, at Icahn School of Medicine at Mount Sinai, New York, said in an interview.

The findings were published online in Nature Genetics.

 

Schizophrenia’s genetic architecture

Prior studies suggest the genetic architecture of schizophrenia may be influenced by common single-nucleotide polymorphisms, copy number variants and rare PTVs.

Investigators note that rare PTVs are important because they can link disease risk directly to individual genes. But identifying the PTVs and the genes that harbor them requires large patient cohorts, far bigger than any single institution can provide.

Dr. Charney and other researchers are part of the Psychiatric Genomics Consortium, a collaboration of researchers from hundreds of institutions around the world established in 2007 to create large cohorts for genetic studies of psychiatric disease.

For this study, investigators sequenced a new cohort of 11,580 schizophrenia cases and 10,555 controls of diverse ancestries. The analysis showed that the findings previously established in predominantly European cohorts extended to non-European populations.

They then conducted a meta-analysis of the new cohort combined with datasets from earlier studies, creating a pooled sample of 35,828 cases and 107,877 controls.

This meta-analysis revealed two new genes linked to schizophrenia, SRRM2 and AKAP11. The third gene flagged in the study, PCLO, was previously implicated in schizophrenia but is now identified as having a shared risk for schizophrenia and autism.

The rare PVTs on the 12 genes identified so far through this type of study are probably only involved in a small fraction of schizophrenia cases, Dr. Charney acknowledged. However, the discovery could lead to new treatments that could benefit all patients with the disease, he added.

“There are multiple pathways to psychosis and there’s also multiple pathways to treat psychosis,” Dr. Charney said. “There’s reason to believe if you can find a mechanism by which a human being could develop a psychosis, then reversing that mechanism could help a lot of people who have psychosis for another reason.”
 

Importance of diverse cohorts

Commenting on the findings, Jennifer Gladys Mulle, MHS, PhD, associate professor of psychiatry at the Robert Wood Johnson Medical School at Rutgers University, Piscataway, N.J., noted that while genetic discoveries have led to new therapies in other medical conditions, that has not been the case with schizophrenia.

“In other disorders, having genetic findings have really opened a window into the molecular mechanisms, which has allowed us to develop pharmaceuticals and understand the disease process better,” said Dr. Mulle, who was not part of this study. “But because we haven’t had that in schizophrenia, it’s really held us back. Having genetic variants associated with schizophrenia may really help us understand the mechanism.”

The inclusion of diverse populations is also a key contribution of this study, Dr. Mulle added.

“So far a lot of the work we’ve done in genetics has been on people of European ancestry,” Dr. Mulle said. “The fact that they have found results that are generalizable across multiple ethnicities really suggests that if we develop pharmaceutical agents based on these findings, it will help many people.”

More attention has been paid recently to a growing problem in the study of genetics of psychiatric disorders: More than 95% of participants in genome-wide association studies that seek to identify gene variants linked to disease are of European ancestry.

Dr. Charney and his colleagues had that in mind when they designed the study.

“We can’t get to a place where genetics is clinically useful if we don’t know the extent to which a particular observation that’s found in one population is also true for other populations,” Dr. Charney said.

The study was funded by the National Institutes of Health. Dr. Charney and Dr. Mulle report no relevant financial relationships.

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

People with epilepsy have a twofold increased risk for death, compared with their counterparts without the condition, irrespective of comorbidities or disease severity, new research shows.

“To our knowledge, this is the only study that has assessed the cause-specific mortality risk among people with epilepsy according to age and disease course,” investigators led by Seo-Young Lee, MD, PhD, of Kangwon National University, Chuncheon, South Korea, write. “Understanding cause-specific mortality risk, particularly the risk of external causes, is important because they are mostly preventable.”

The findings were published online  in Neurology.
 

Higher mortality risk

For the study, researchers analyzed data from the National Health Insurance Service database in Korea from 2006 to 2017 and vital statistics from Statistics Korea from 2008 to 2017.

The study population included 138,998 patients with newly treated epilepsy, with an average at diagnosis of 48.6 years.

Over 665,928 person years of follow-up (mean follow-up, 4.79 years), 20.095 patients died.

People with epilepsy had more than twice the risk for death, compared with the overall population (standardized mortality ratio, 2.25; 95% confidence interval, 2.22-2.28). Mortality was highest in children aged 4 years or younger and was higher in the first year after diagnosis and in women at all age points.

People with epilepsy had a higher mortality risk, compared with the general public, regardless of how many anti-seizure medications they were taking. Those taking only one medication had a 156% higher risk for death (SMR, 1.56; 95% CI, 1.53-1.60), compared with 493% higher risk in those taking four or more medications (SMR, 4.93; 95% CI, 4.76-5.10).

Where patients lived also played a role in mortality risk. Living in a rural area was associated with a 247% higher risk for death, compared with people without epilepsy who lived in the same area (SMR, 2.47; 95% CI, 2.41-2.53), and the risk was 203% higher risk among those living in urban centers (SMR, 2.03; 95% CI, 1.98-2.09).

Although people with comorbidities had higher mortality rates, even those without any other health conditions had a 161% higher risk for death, compared with people without epilepsy (SMR, 1.61; 95% CI, 1.50-1.72).
 

Causes of death

The most frequent causes of death were malignant neoplasm and cerebrovascular disease, which researchers noted are thought to be underlying causes of epilepsy.

Among external causes of death, suicide was the most common cause (2.6%). The suicide rate was highest among younger patients and gradually decreased with age.

Deaths tied directly to epilepsy, transport accidents, or falls were lower in this study than had been previously reported, which may be due to adequate seizure control or because the number of older people with epilepsy and comorbidities is higher in Korea than that reported in other countries.

“To reduce mortality in people with epilepsy, comprehensive efforts [are needed], including a national policy against stigma of epilepsy and clinicians’ total management such as risk stratification, education about injury prevention, and monitoring for suicidal ideation with psychological intervention, as well as active control of seizures,” the authors write.
 

Generalizable findings

Joseph Sirven, MD, professor of neurology at Mayo Clinic Florida, Jacksonville, said that although the study included only Korean patients, the findings are applicable to other counties.

That researchers found patients with epilepsy were more than twice as likely to die prematurely, compared with the general population wasn’t particularly surprising, Dr. Sirven said.

“What struck me the most was the fact that even patients who were on a single drug and seemingly well controlled also had excess mortality reported,” Dr. Sirven said. “That these risks occur should be part of what we tell all patients with epilepsy so that they can better arm themselves with information and help to address some of the risks that this study showed.”

Another important finding is the risk for suicide in patients with epilepsy, especially those who are newly diagnosed, he said.

“When we treat a patient with epilepsy, it should not just be about seizures, but we need to inquire about the psychiatric comorbidities and more importantly manage them in a comprehensive manner,” Dr. Sirven said.

The study was funded by Soonchunhyang University Research Fund and the Korea Health Technology R&D Project. The study authors and Dr. Sirven report no relevant financial conflicts.

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

People with epilepsy have a twofold increased risk for death, compared with their counterparts without the condition, irrespective of comorbidities or disease severity, new research shows.

“To our knowledge, this is the only study that has assessed the cause-specific mortality risk among people with epilepsy according to age and disease course,” investigators led by Seo-Young Lee, MD, PhD, of Kangwon National University, Chuncheon, South Korea, write. “Understanding cause-specific mortality risk, particularly the risk of external causes, is important because they are mostly preventable.”

The findings were published online  in Neurology.
 

Higher mortality risk

For the study, researchers analyzed data from the National Health Insurance Service database in Korea from 2006 to 2017 and vital statistics from Statistics Korea from 2008 to 2017.

The study population included 138,998 patients with newly treated epilepsy, with an average at diagnosis of 48.6 years.

Over 665,928 person years of follow-up (mean follow-up, 4.79 years), 20.095 patients died.

People with epilepsy had more than twice the risk for death, compared with the overall population (standardized mortality ratio, 2.25; 95% confidence interval, 2.22-2.28). Mortality was highest in children aged 4 years or younger and was higher in the first year after diagnosis and in women at all age points.

People with epilepsy had a higher mortality risk, compared with the general public, regardless of how many anti-seizure medications they were taking. Those taking only one medication had a 156% higher risk for death (SMR, 1.56; 95% CI, 1.53-1.60), compared with 493% higher risk in those taking four or more medications (SMR, 4.93; 95% CI, 4.76-5.10).

Where patients lived also played a role in mortality risk. Living in a rural area was associated with a 247% higher risk for death, compared with people without epilepsy who lived in the same area (SMR, 2.47; 95% CI, 2.41-2.53), and the risk was 203% higher risk among those living in urban centers (SMR, 2.03; 95% CI, 1.98-2.09).

Although people with comorbidities had higher mortality rates, even those without any other health conditions had a 161% higher risk for death, compared with people without epilepsy (SMR, 1.61; 95% CI, 1.50-1.72).
 

Causes of death

The most frequent causes of death were malignant neoplasm and cerebrovascular disease, which researchers noted are thought to be underlying causes of epilepsy.

Among external causes of death, suicide was the most common cause (2.6%). The suicide rate was highest among younger patients and gradually decreased with age.

Deaths tied directly to epilepsy, transport accidents, or falls were lower in this study than had been previously reported, which may be due to adequate seizure control or because the number of older people with epilepsy and comorbidities is higher in Korea than that reported in other countries.

“To reduce mortality in people with epilepsy, comprehensive efforts [are needed], including a national policy against stigma of epilepsy and clinicians’ total management such as risk stratification, education about injury prevention, and monitoring for suicidal ideation with psychological intervention, as well as active control of seizures,” the authors write.
 

Generalizable findings

Joseph Sirven, MD, professor of neurology at Mayo Clinic Florida, Jacksonville, said that although the study included only Korean patients, the findings are applicable to other counties.

That researchers found patients with epilepsy were more than twice as likely to die prematurely, compared with the general population wasn’t particularly surprising, Dr. Sirven said.

“What struck me the most was the fact that even patients who were on a single drug and seemingly well controlled also had excess mortality reported,” Dr. Sirven said. “That these risks occur should be part of what we tell all patients with epilepsy so that they can better arm themselves with information and help to address some of the risks that this study showed.”

Another important finding is the risk for suicide in patients with epilepsy, especially those who are newly diagnosed, he said.

“When we treat a patient with epilepsy, it should not just be about seizures, but we need to inquire about the psychiatric comorbidities and more importantly manage them in a comprehensive manner,” Dr. Sirven said.

The study was funded by Soonchunhyang University Research Fund and the Korea Health Technology R&D Project. The study authors and Dr. Sirven report no relevant financial conflicts.

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

People with epilepsy have a twofold increased risk for death, compared with their counterparts without the condition, irrespective of comorbidities or disease severity, new research shows.

“To our knowledge, this is the only study that has assessed the cause-specific mortality risk among people with epilepsy according to age and disease course,” investigators led by Seo-Young Lee, MD, PhD, of Kangwon National University, Chuncheon, South Korea, write. “Understanding cause-specific mortality risk, particularly the risk of external causes, is important because they are mostly preventable.”

The findings were published online  in Neurology.
 

Higher mortality risk

For the study, researchers analyzed data from the National Health Insurance Service database in Korea from 2006 to 2017 and vital statistics from Statistics Korea from 2008 to 2017.

The study population included 138,998 patients with newly treated epilepsy, with an average at diagnosis of 48.6 years.

Over 665,928 person years of follow-up (mean follow-up, 4.79 years), 20.095 patients died.

People with epilepsy had more than twice the risk for death, compared with the overall population (standardized mortality ratio, 2.25; 95% confidence interval, 2.22-2.28). Mortality was highest in children aged 4 years or younger and was higher in the first year after diagnosis and in women at all age points.

People with epilepsy had a higher mortality risk, compared with the general public, regardless of how many anti-seizure medications they were taking. Those taking only one medication had a 156% higher risk for death (SMR, 1.56; 95% CI, 1.53-1.60), compared with 493% higher risk in those taking four or more medications (SMR, 4.93; 95% CI, 4.76-5.10).

Where patients lived also played a role in mortality risk. Living in a rural area was associated with a 247% higher risk for death, compared with people without epilepsy who lived in the same area (SMR, 2.47; 95% CI, 2.41-2.53), and the risk was 203% higher risk among those living in urban centers (SMR, 2.03; 95% CI, 1.98-2.09).

Although people with comorbidities had higher mortality rates, even those without any other health conditions had a 161% higher risk for death, compared with people without epilepsy (SMR, 1.61; 95% CI, 1.50-1.72).
 

Causes of death

The most frequent causes of death were malignant neoplasm and cerebrovascular disease, which researchers noted are thought to be underlying causes of epilepsy.

Among external causes of death, suicide was the most common cause (2.6%). The suicide rate was highest among younger patients and gradually decreased with age.

Deaths tied directly to epilepsy, transport accidents, or falls were lower in this study than had been previously reported, which may be due to adequate seizure control or because the number of older people with epilepsy and comorbidities is higher in Korea than that reported in other countries.

“To reduce mortality in people with epilepsy, comprehensive efforts [are needed], including a national policy against stigma of epilepsy and clinicians’ total management such as risk stratification, education about injury prevention, and monitoring for suicidal ideation with psychological intervention, as well as active control of seizures,” the authors write.
 

Generalizable findings

Joseph Sirven, MD, professor of neurology at Mayo Clinic Florida, Jacksonville, said that although the study included only Korean patients, the findings are applicable to other counties.

That researchers found patients with epilepsy were more than twice as likely to die prematurely, compared with the general population wasn’t particularly surprising, Dr. Sirven said.

“What struck me the most was the fact that even patients who were on a single drug and seemingly well controlled also had excess mortality reported,” Dr. Sirven said. “That these risks occur should be part of what we tell all patients with epilepsy so that they can better arm themselves with information and help to address some of the risks that this study showed.”

Another important finding is the risk for suicide in patients with epilepsy, especially those who are newly diagnosed, he said.

“When we treat a patient with epilepsy, it should not just be about seizures, but we need to inquire about the psychiatric comorbidities and more importantly manage them in a comprehensive manner,” Dr. Sirven said.

The study was funded by Soonchunhyang University Research Fund and the Korea Health Technology R&D Project. The study authors and Dr. Sirven report no relevant financial conflicts.

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

Older people with high levels of stress are nearly 40% more likely to have cognitive impairment than those with low stress, a new study shows.

Individuals with elevated stress levels also had higher rates of diabetes, hypertension, and other cardiovascular disease (CVD) risk factors. But even after controlling for those risk factors, stress remained an independent predictor of cognitive decline.

The national cohort study showed that the association between stress and cognition was similar between Black and White individuals and that those with controlled stress were less likely to have cognitive impairment than those with uncontrolled or new stress.

“We have known for a while that excess levels of stress can be harmful for the human body and the heart, but we are now adding more evidence that excess levels of stress can be harmful for cognition,” said lead investigator Ambar Kulshreshtha, MD, PhD, associate professor of family and preventive medicine and epidemiology at Emory University, Atlanta. “We were able to see that regardless of race or gender, stress is bad.”

The findings were published online  in JAMA Network Open.
 

Independent risk factor

For the study, investigators analyzed data from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, a national population-based cohort of Black and White participants aged 45 years or older, sampled from the U.S. population.

Participants completed a questionnaire designed to evaluate stress levels when they were enrolled in the study between 2003 and 2007 and again about 11 years after enrollment.

Of the 24,448 participants (41.6% Black) in the study, 22.9% reported elevated stress levels.

Those with high stress were more likely to be younger, female, Black, smokers, and have a higher body mass index and less likely to have a college degree and to be physically active. They also had a lower family income and were more likely to have cardiovascular disease risk factors, such as hypertension, diabetes, and dyslipidemia.

Participants with elevated levels of perceived stress were 37% more likely to have poor cognition after adjustment for sociodemographic variables, cardiovascular risk factors, and depression (adjusted odds ratio, 1.37; 95% confidence interval, 1.22-1.53).

There was no significant difference between Black and White participants.
 

Damaging consequences

Researchers also found a dose-response relationship, with the greatest cognitive decline found in people who reported high stress at both time points and those who had new stress at follow up (aOR, 1.16; 95% CI, 0.92-1.45), compared with those with resolved stress (aOR, 1.03; 95% CI, 0.81-1.32) or no stress (aOR, 0.81; 95% CI, 0.68-0.97).

A change in perceived stress by 1 unit was associated with 4% increased risk of cognitive impairment after adjusting for sociodemographic variables, CVD risk factors, lifestyle factors, and depressive symptoms (aOR, 1.04; 95% CI, 1.02-1.06).

Although the study didn’t reveal the mechanisms that might link stress and cognition, it does point to stress as a potentially modifiable risk factor for cognitive decline, Dr. Kulshreshtha said.

“One in three of my patients have had to deal with extra levels of stress and anxiety over the past few years,” said Dr. Kulshreshtha. “We as clinicians are aware that stress can have damaging consequences to the heart and other organs, and when we see patients who have these complaints, especially elderly patients, we should spend some time asking people about their stress and how they are managing it.”
 

Additional screening

Gregory Day, MD, a neurologist at the Mayo Clinic, Jacksonville, Fla., said that the findings help fill a void in the research about stress and cognition.

“It’s a potentially important association that’s easy for us to miss in clinical practice,” said Dr. Day, who was not a part of the study. “It’s one of those things that we can all recognize impacts health, but we have very few large, well thought out studies that give us the data we need to inform its place in clinical decision-making.”

In addition to its large sample size, the overrepresentation of diverse populations is a strength of the study and a contribution to the field, Dr. Day said.

“One question they don’t directly ask is, is this association maybe due to some differences in stress? And the answer from the paper is probably not, because it looks like when we control for these things, we don’t see big differences incident risk factors between race,” he added.

The findings also point to the need for clinicians, especially primary care physicians, to screen patients for stress during routine examinations.

“Every visit is an opportunity to screen for risk factors that are going to set people up for future brain health,” Dr. Day said. “In addition to screening for all of these other risk factors for brain health, maybe it’s worth including some more global assessment of stress in a standard screener.”

The study was funded by the National Institute of Neurological Disorders and Stroke, the National Institutes of Health, and the National Institute on Aging. Dr. Kulshreshtha and Dr. Day report no relevant financial relationships.

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

Older people with high levels of stress are nearly 40% more likely to have cognitive impairment than those with low stress, a new study shows.

Individuals with elevated stress levels also had higher rates of diabetes, hypertension, and other cardiovascular disease (CVD) risk factors. But even after controlling for those risk factors, stress remained an independent predictor of cognitive decline.

The national cohort study showed that the association between stress and cognition was similar between Black and White individuals and that those with controlled stress were less likely to have cognitive impairment than those with uncontrolled or new stress.

“We have known for a while that excess levels of stress can be harmful for the human body and the heart, but we are now adding more evidence that excess levels of stress can be harmful for cognition,” said lead investigator Ambar Kulshreshtha, MD, PhD, associate professor of family and preventive medicine and epidemiology at Emory University, Atlanta. “We were able to see that regardless of race or gender, stress is bad.”

The findings were published online  in JAMA Network Open.
 

Independent risk factor

For the study, investigators analyzed data from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, a national population-based cohort of Black and White participants aged 45 years or older, sampled from the U.S. population.

Participants completed a questionnaire designed to evaluate stress levels when they were enrolled in the study between 2003 and 2007 and again about 11 years after enrollment.

Of the 24,448 participants (41.6% Black) in the study, 22.9% reported elevated stress levels.

Those with high stress were more likely to be younger, female, Black, smokers, and have a higher body mass index and less likely to have a college degree and to be physically active. They also had a lower family income and were more likely to have cardiovascular disease risk factors, such as hypertension, diabetes, and dyslipidemia.

Participants with elevated levels of perceived stress were 37% more likely to have poor cognition after adjustment for sociodemographic variables, cardiovascular risk factors, and depression (adjusted odds ratio, 1.37; 95% confidence interval, 1.22-1.53).

There was no significant difference between Black and White participants.
 

Damaging consequences

Researchers also found a dose-response relationship, with the greatest cognitive decline found in people who reported high stress at both time points and those who had new stress at follow up (aOR, 1.16; 95% CI, 0.92-1.45), compared with those with resolved stress (aOR, 1.03; 95% CI, 0.81-1.32) or no stress (aOR, 0.81; 95% CI, 0.68-0.97).

A change in perceived stress by 1 unit was associated with 4% increased risk of cognitive impairment after adjusting for sociodemographic variables, CVD risk factors, lifestyle factors, and depressive symptoms (aOR, 1.04; 95% CI, 1.02-1.06).

Although the study didn’t reveal the mechanisms that might link stress and cognition, it does point to stress as a potentially modifiable risk factor for cognitive decline, Dr. Kulshreshtha said.

“One in three of my patients have had to deal with extra levels of stress and anxiety over the past few years,” said Dr. Kulshreshtha. “We as clinicians are aware that stress can have damaging consequences to the heart and other organs, and when we see patients who have these complaints, especially elderly patients, we should spend some time asking people about their stress and how they are managing it.”
 

Additional screening

Gregory Day, MD, a neurologist at the Mayo Clinic, Jacksonville, Fla., said that the findings help fill a void in the research about stress and cognition.

“It’s a potentially important association that’s easy for us to miss in clinical practice,” said Dr. Day, who was not a part of the study. “It’s one of those things that we can all recognize impacts health, but we have very few large, well thought out studies that give us the data we need to inform its place in clinical decision-making.”

In addition to its large sample size, the overrepresentation of diverse populations is a strength of the study and a contribution to the field, Dr. Day said.

“One question they don’t directly ask is, is this association maybe due to some differences in stress? And the answer from the paper is probably not, because it looks like when we control for these things, we don’t see big differences incident risk factors between race,” he added.

The findings also point to the need for clinicians, especially primary care physicians, to screen patients for stress during routine examinations.

“Every visit is an opportunity to screen for risk factors that are going to set people up for future brain health,” Dr. Day said. “In addition to screening for all of these other risk factors for brain health, maybe it’s worth including some more global assessment of stress in a standard screener.”

The study was funded by the National Institute of Neurological Disorders and Stroke, the National Institutes of Health, and the National Institute on Aging. Dr. Kulshreshtha and Dr. Day report no relevant financial relationships.

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

Older people with high levels of stress are nearly 40% more likely to have cognitive impairment than those with low stress, a new study shows.

Individuals with elevated stress levels also had higher rates of diabetes, hypertension, and other cardiovascular disease (CVD) risk factors. But even after controlling for those risk factors, stress remained an independent predictor of cognitive decline.

The national cohort study showed that the association between stress and cognition was similar between Black and White individuals and that those with controlled stress were less likely to have cognitive impairment than those with uncontrolled or new stress.

“We have known for a while that excess levels of stress can be harmful for the human body and the heart, but we are now adding more evidence that excess levels of stress can be harmful for cognition,” said lead investigator Ambar Kulshreshtha, MD, PhD, associate professor of family and preventive medicine and epidemiology at Emory University, Atlanta. “We were able to see that regardless of race or gender, stress is bad.”

The findings were published online  in JAMA Network Open.
 

Independent risk factor

For the study, investigators analyzed data from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, a national population-based cohort of Black and White participants aged 45 years or older, sampled from the U.S. population.

Participants completed a questionnaire designed to evaluate stress levels when they were enrolled in the study between 2003 and 2007 and again about 11 years after enrollment.

Of the 24,448 participants (41.6% Black) in the study, 22.9% reported elevated stress levels.

Those with high stress were more likely to be younger, female, Black, smokers, and have a higher body mass index and less likely to have a college degree and to be physically active. They also had a lower family income and were more likely to have cardiovascular disease risk factors, such as hypertension, diabetes, and dyslipidemia.

Participants with elevated levels of perceived stress were 37% more likely to have poor cognition after adjustment for sociodemographic variables, cardiovascular risk factors, and depression (adjusted odds ratio, 1.37; 95% confidence interval, 1.22-1.53).

There was no significant difference between Black and White participants.
 

Damaging consequences

Researchers also found a dose-response relationship, with the greatest cognitive decline found in people who reported high stress at both time points and those who had new stress at follow up (aOR, 1.16; 95% CI, 0.92-1.45), compared with those with resolved stress (aOR, 1.03; 95% CI, 0.81-1.32) or no stress (aOR, 0.81; 95% CI, 0.68-0.97).

A change in perceived stress by 1 unit was associated with 4% increased risk of cognitive impairment after adjusting for sociodemographic variables, CVD risk factors, lifestyle factors, and depressive symptoms (aOR, 1.04; 95% CI, 1.02-1.06).

Although the study didn’t reveal the mechanisms that might link stress and cognition, it does point to stress as a potentially modifiable risk factor for cognitive decline, Dr. Kulshreshtha said.

“One in three of my patients have had to deal with extra levels of stress and anxiety over the past few years,” said Dr. Kulshreshtha. “We as clinicians are aware that stress can have damaging consequences to the heart and other organs, and when we see patients who have these complaints, especially elderly patients, we should spend some time asking people about their stress and how they are managing it.”
 

Additional screening

Gregory Day, MD, a neurologist at the Mayo Clinic, Jacksonville, Fla., said that the findings help fill a void in the research about stress and cognition.

“It’s a potentially important association that’s easy for us to miss in clinical practice,” said Dr. Day, who was not a part of the study. “It’s one of those things that we can all recognize impacts health, but we have very few large, well thought out studies that give us the data we need to inform its place in clinical decision-making.”

In addition to its large sample size, the overrepresentation of diverse populations is a strength of the study and a contribution to the field, Dr. Day said.

“One question they don’t directly ask is, is this association maybe due to some differences in stress? And the answer from the paper is probably not, because it looks like when we control for these things, we don’t see big differences incident risk factors between race,” he added.

The findings also point to the need for clinicians, especially primary care physicians, to screen patients for stress during routine examinations.

“Every visit is an opportunity to screen for risk factors that are going to set people up for future brain health,” Dr. Day said. “In addition to screening for all of these other risk factors for brain health, maybe it’s worth including some more global assessment of stress in a standard screener.”

The study was funded by the National Institute of Neurological Disorders and Stroke, the National Institutes of Health, and the National Institute on Aging. Dr. Kulshreshtha and Dr. Day report no relevant financial relationships.

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

A once-daily oral stimulant medication for treatment of attention-deficit/hyperactivity disorder in individuals aged 6 years or older is safe and effective after 1 year of treatment, new research shows.

Results from a phase 3, multicenter dose optimization, open-label safety study of Azstarys (KemPharm) found that most treatment-emergent adverse events (TEAEs) were mild to moderate.

“This data show that Azstarys remains safe and effective for the treatment of ADHD when given for up to a year,” lead investigator Ann Childress, MD, president of the Center for Psychiatry and Behavioral Medicine, Las Vegas, said in an interview.

The study was published online  in the Journal of Child and Adolescent Psychopharmacology.

Safety at 1 year

The drug is a combination of extended-release serdexmethylphenidate (SDX), KemPharm’s prodrug of dexmethylphenidate (d-MPH), co-formulated with immediate-release d-MPH.

SDX is converted to d-MPH after it is absorbed in the gastrointestinal tract. The d-MPH is released gradually throughout the day, providing quick symptom control with the d-MPH and extended control with SDX.

As reported by this news organization, Azstarys was approved by the U.S. Food and Drug Administration in 2021 on the basis of results from a laboratory classroom phase 3 trial, which showed significant improvement in ADHD symptoms, compared with placebo.

For this study, the second phase 3 trial of Azstarys, investigators analyzed data from 282 children aged 6-12 years in the United States, including 70 who participated in an earlier 1-month efficacy trial as well.

After screening and a 3-week dose-optimization phase for new participants, patients received once-daily treatment with doses of 26.1 mg/5.2 mg, 39.2 mg/7.8 mg, or 52.3 mg/10.4 mg of SDX/d-MPH.

After 1 year of treatment, 60.1% of participants reported at least one TEAE, the majority of which were moderate. Twelve patients reported severe TEAEs. Six children (2.5%) discontinued the study due to a TEAE during the treatment phase.

Investigators also measured growth and changes in sleep with the Children’s Sleep Habits Questionnaire during the 12-month study. Sleep improved on most measures and the impact on growth was mild.

There were no life-threatening TEAEs and no deaths reported during the study.

The most common TEAEs during the treatment phase were decreased appetite, upper respiratory tract infection, nasopharyngitis, decreased weight, irritability, and increased weight.

Efficacy at 1 year

ADHD symptoms improved considerably after 1 month of treatment, with responses continuing at 1 year.

At baseline, participants’ mean ADHD Rating Scale-5 (ADHD-RS-5) score was 41.5. After 1 month of treatment, scores averaged 16.1, a decline of –25.3 (P < .001).

The mean score stabilized in the 12-15 range for the remainder of the study. After 1 year of treatment, ADHD symptoms had decreased approximately 70% from baseline.

Investigators found similar results in clinical severity. After 1 month of treatment, the average Clinical Global Impressions–Severity (CGI-S) scale score was 2.5, a decline of –2.2 (P < .0001).

CGI-S scale scores remained in the 2.2-2.4 range for the remainder of the study.

These results, combined with the results of the original classroom trial, suggest Azstarys may offer advantages over other ADHD drugs, Dr. Childress said.

“In the laboratory classroom trial, subjects taking Azstarys completed significantly more math problems than subjects taking placebo beginning at 30 minutes and up to 13 hours after dosing,” Dr. Childress said. “No other methylphenidate extended-release product currently marketed in the United States has a 13-hour duration of effect.”

‘Reassuring data’

Aditya Pawar, MD, a child and adolescent psychiatrist with the Kennedy Krieger Institute and an assistant professor of psychiatry and behavioral sciences at Johns Hopkins School of Medicine, Baltimore, said that the study suggests the drug may be a valuable addition to ADHD treatment options for pediatric patients.

“The study provides reassuring data on the safety of stimulants in patients without significant history of cardiac events or blood pressure changes, which are usual concerns among patients and clinicians despite the evidence supporting safety, said Dr. Pawar, who was not part of the study.

“Additionally, the 1-year data on efficacy and safety of a new stimulant medication is valuable for clinicians looking for sustained relief for their patients, despite the limitations of an open-label trial,” she added.

Overall, the safety data reported here are fairly consistent with the safety profile of other methylphenidates used for treating ADHD, Dr. Pawar said.

However, she noted, the study does have some limitations, including its open-label design and lack of blinding. The research also excluded children with autism, disruptive mood dysregulation disorders, and other common comorbidities of ADHD, which may limit the generalizability of the results.

“These comorbidities often require stimulants as a part of treatment and yet have a higher risk of side effects,” Dr. Pawar said. “Future studies with a broader population may be needed to better understand treatment effectiveness and potential risks.”

The study was funded by KemPharm. Dr. Childress serves as consultant for Aardvark, Arbor, Attentive, Cingulate, Ironshore, Neos Therapeutics, Neurocentria, Otsuka, Purdue, Rhodes, Sunovion, Tris Pharma, KemPharm, Supernus, Jazz, Corium, Tulex, and Lumos. Full disclosures are reported in the original article.

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

A once-daily oral stimulant medication for treatment of attention-deficit/hyperactivity disorder in individuals aged 6 years or older is safe and effective after 1 year of treatment, new research shows.

Results from a phase 3, multicenter dose optimization, open-label safety study of Azstarys (KemPharm) found that most treatment-emergent adverse events (TEAEs) were mild to moderate.

“This data show that Azstarys remains safe and effective for the treatment of ADHD when given for up to a year,” lead investigator Ann Childress, MD, president of the Center for Psychiatry and Behavioral Medicine, Las Vegas, said in an interview.

The study was published online  in the Journal of Child and Adolescent Psychopharmacology.

Safety at 1 year

The drug is a combination of extended-release serdexmethylphenidate (SDX), KemPharm’s prodrug of dexmethylphenidate (d-MPH), co-formulated with immediate-release d-MPH.

SDX is converted to d-MPH after it is absorbed in the gastrointestinal tract. The d-MPH is released gradually throughout the day, providing quick symptom control with the d-MPH and extended control with SDX.

As reported by this news organization, Azstarys was approved by the U.S. Food and Drug Administration in 2021 on the basis of results from a laboratory classroom phase 3 trial, which showed significant improvement in ADHD symptoms, compared with placebo.

For this study, the second phase 3 trial of Azstarys, investigators analyzed data from 282 children aged 6-12 years in the United States, including 70 who participated in an earlier 1-month efficacy trial as well.

After screening and a 3-week dose-optimization phase for new participants, patients received once-daily treatment with doses of 26.1 mg/5.2 mg, 39.2 mg/7.8 mg, or 52.3 mg/10.4 mg of SDX/d-MPH.

After 1 year of treatment, 60.1% of participants reported at least one TEAE, the majority of which were moderate. Twelve patients reported severe TEAEs. Six children (2.5%) discontinued the study due to a TEAE during the treatment phase.

Investigators also measured growth and changes in sleep with the Children’s Sleep Habits Questionnaire during the 12-month study. Sleep improved on most measures and the impact on growth was mild.

There were no life-threatening TEAEs and no deaths reported during the study.

The most common TEAEs during the treatment phase were decreased appetite, upper respiratory tract infection, nasopharyngitis, decreased weight, irritability, and increased weight.

Efficacy at 1 year

ADHD symptoms improved considerably after 1 month of treatment, with responses continuing at 1 year.

At baseline, participants’ mean ADHD Rating Scale-5 (ADHD-RS-5) score was 41.5. After 1 month of treatment, scores averaged 16.1, a decline of –25.3 (P < .001).

The mean score stabilized in the 12-15 range for the remainder of the study. After 1 year of treatment, ADHD symptoms had decreased approximately 70% from baseline.

Investigators found similar results in clinical severity. After 1 month of treatment, the average Clinical Global Impressions–Severity (CGI-S) scale score was 2.5, a decline of –2.2 (P < .0001).

CGI-S scale scores remained in the 2.2-2.4 range for the remainder of the study.

These results, combined with the results of the original classroom trial, suggest Azstarys may offer advantages over other ADHD drugs, Dr. Childress said.

“In the laboratory classroom trial, subjects taking Azstarys completed significantly more math problems than subjects taking placebo beginning at 30 minutes and up to 13 hours after dosing,” Dr. Childress said. “No other methylphenidate extended-release product currently marketed in the United States has a 13-hour duration of effect.”

‘Reassuring data’

Aditya Pawar, MD, a child and adolescent psychiatrist with the Kennedy Krieger Institute and an assistant professor of psychiatry and behavioral sciences at Johns Hopkins School of Medicine, Baltimore, said that the study suggests the drug may be a valuable addition to ADHD treatment options for pediatric patients.

“The study provides reassuring data on the safety of stimulants in patients without significant history of cardiac events or blood pressure changes, which are usual concerns among patients and clinicians despite the evidence supporting safety, said Dr. Pawar, who was not part of the study.

“Additionally, the 1-year data on efficacy and safety of a new stimulant medication is valuable for clinicians looking for sustained relief for their patients, despite the limitations of an open-label trial,” she added.

Overall, the safety data reported here are fairly consistent with the safety profile of other methylphenidates used for treating ADHD, Dr. Pawar said.

However, she noted, the study does have some limitations, including its open-label design and lack of blinding. The research also excluded children with autism, disruptive mood dysregulation disorders, and other common comorbidities of ADHD, which may limit the generalizability of the results.

“These comorbidities often require stimulants as a part of treatment and yet have a higher risk of side effects,” Dr. Pawar said. “Future studies with a broader population may be needed to better understand treatment effectiveness and potential risks.”

The study was funded by KemPharm. Dr. Childress serves as consultant for Aardvark, Arbor, Attentive, Cingulate, Ironshore, Neos Therapeutics, Neurocentria, Otsuka, Purdue, Rhodes, Sunovion, Tris Pharma, KemPharm, Supernus, Jazz, Corium, Tulex, and Lumos. Full disclosures are reported in the original article.

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

A once-daily oral stimulant medication for treatment of attention-deficit/hyperactivity disorder in individuals aged 6 years or older is safe and effective after 1 year of treatment, new research shows.

Results from a phase 3, multicenter dose optimization, open-label safety study of Azstarys (KemPharm) found that most treatment-emergent adverse events (TEAEs) were mild to moderate.

“This data show that Azstarys remains safe and effective for the treatment of ADHD when given for up to a year,” lead investigator Ann Childress, MD, president of the Center for Psychiatry and Behavioral Medicine, Las Vegas, said in an interview.

The study was published online  in the Journal of Child and Adolescent Psychopharmacology.

Safety at 1 year

The drug is a combination of extended-release serdexmethylphenidate (SDX), KemPharm’s prodrug of dexmethylphenidate (d-MPH), co-formulated with immediate-release d-MPH.

SDX is converted to d-MPH after it is absorbed in the gastrointestinal tract. The d-MPH is released gradually throughout the day, providing quick symptom control with the d-MPH and extended control with SDX.

As reported by this news organization, Azstarys was approved by the U.S. Food and Drug Administration in 2021 on the basis of results from a laboratory classroom phase 3 trial, which showed significant improvement in ADHD symptoms, compared with placebo.

For this study, the second phase 3 trial of Azstarys, investigators analyzed data from 282 children aged 6-12 years in the United States, including 70 who participated in an earlier 1-month efficacy trial as well.

After screening and a 3-week dose-optimization phase for new participants, patients received once-daily treatment with doses of 26.1 mg/5.2 mg, 39.2 mg/7.8 mg, or 52.3 mg/10.4 mg of SDX/d-MPH.

After 1 year of treatment, 60.1% of participants reported at least one TEAE, the majority of which were moderate. Twelve patients reported severe TEAEs. Six children (2.5%) discontinued the study due to a TEAE during the treatment phase.

Investigators also measured growth and changes in sleep with the Children’s Sleep Habits Questionnaire during the 12-month study. Sleep improved on most measures and the impact on growth was mild.

There were no life-threatening TEAEs and no deaths reported during the study.

The most common TEAEs during the treatment phase were decreased appetite, upper respiratory tract infection, nasopharyngitis, decreased weight, irritability, and increased weight.

Efficacy at 1 year

ADHD symptoms improved considerably after 1 month of treatment, with responses continuing at 1 year.

At baseline, participants’ mean ADHD Rating Scale-5 (ADHD-RS-5) score was 41.5. After 1 month of treatment, scores averaged 16.1, a decline of –25.3 (P < .001).

The mean score stabilized in the 12-15 range for the remainder of the study. After 1 year of treatment, ADHD symptoms had decreased approximately 70% from baseline.

Investigators found similar results in clinical severity. After 1 month of treatment, the average Clinical Global Impressions–Severity (CGI-S) scale score was 2.5, a decline of –2.2 (P < .0001).

CGI-S scale scores remained in the 2.2-2.4 range for the remainder of the study.

These results, combined with the results of the original classroom trial, suggest Azstarys may offer advantages over other ADHD drugs, Dr. Childress said.

“In the laboratory classroom trial, subjects taking Azstarys completed significantly more math problems than subjects taking placebo beginning at 30 minutes and up to 13 hours after dosing,” Dr. Childress said. “No other methylphenidate extended-release product currently marketed in the United States has a 13-hour duration of effect.”

‘Reassuring data’

Aditya Pawar, MD, a child and adolescent psychiatrist with the Kennedy Krieger Institute and an assistant professor of psychiatry and behavioral sciences at Johns Hopkins School of Medicine, Baltimore, said that the study suggests the drug may be a valuable addition to ADHD treatment options for pediatric patients.

“The study provides reassuring data on the safety of stimulants in patients without significant history of cardiac events or blood pressure changes, which are usual concerns among patients and clinicians despite the evidence supporting safety, said Dr. Pawar, who was not part of the study.

“Additionally, the 1-year data on efficacy and safety of a new stimulant medication is valuable for clinicians looking for sustained relief for their patients, despite the limitations of an open-label trial,” she added.

Overall, the safety data reported here are fairly consistent with the safety profile of other methylphenidates used for treating ADHD, Dr. Pawar said.

However, she noted, the study does have some limitations, including its open-label design and lack of blinding. The research also excluded children with autism, disruptive mood dysregulation disorders, and other common comorbidities of ADHD, which may limit the generalizability of the results.

“These comorbidities often require stimulants as a part of treatment and yet have a higher risk of side effects,” Dr. Pawar said. “Future studies with a broader population may be needed to better understand treatment effectiveness and potential risks.”

The study was funded by KemPharm. Dr. Childress serves as consultant for Aardvark, Arbor, Attentive, Cingulate, Ironshore, Neos Therapeutics, Neurocentria, Otsuka, Purdue, Rhodes, Sunovion, Tris Pharma, KemPharm, Supernus, Jazz, Corium, Tulex, and Lumos. Full disclosures are reported in the original article.

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