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‘Fascinating’ link between Alzheimer’s and COVID-19
The findings could lead to new treatment targets to slow progression and severity of both diseases.
Investigators found that a single genetic variant in the oligoadenylate synthetase 1 (OAS1) gene increases the risk for AD and that related variants in the same gene increase the likelihood of severe COVID-19 outcomes.
“These findings may allow us to identify new drug targets to slow progression of both diseases and reduce their severity,” Dervis Salih, PhD, senior research associate, UK Dementia Research Institute, University College London, said in an interview.
“Our work also suggests new approaches to treat both diseases with the same drugs,” Dr. Salih added.
The study was published online Oct. 7 in Brain.
Shared genetic network
The OAS1 gene is expressed in microglia, a type of immune cell that makes up around 10% of all cells in the brain.
In earlier work, investigators found evidence suggesting a link between the OAS1 gene and AD, but the function of the gene in microglia was unknown.
To further investigate the gene’s link to AD, they sequenced genetic data from 2,547 people – half with AD, and half without.
The genotyping analysis confirmed that the single-nucleotide polymorphism (SNP) rs1131454 within OAS1 is significantly associated with AD.
Given that the same OAS1 locus has recently been linked with severe COVID-19 outcomes, the researchers investigated four variants on the OAS1 gene.
Results indicate that SNPs within OAS1 associated with AD also show linkage to SNP variants associated with critical illness in COVID-19.
The rs1131454 (risk allele A) and rs4766676 (risk allele T) are associated with AD, and rs10735079 (risk allele A) and rs6489867 (risk allele T) are associated with critical illness with COVID-19, the investigators reported. All of these risk alleles dampen expression of OAS1.
“This study also provides strong new evidence that interferon signaling by the innate immune system plays a substantial role in the progression of Alzheimer’s,” said Dr. Salih.
“Identifying this shared genetic network in innate immune cells will allow us with future work to identify new biomarkers to track disease progression and also predict disease risk better for both disorders,” he added.
‘Fascinating’ link
In a statement from the UK nonprofit organization, Science Media Center, Kenneth Baillie, MBChB, with the University of Edinburgh, said this study builds on a discovery he and his colleagues made last year that OAS1 variants are associated with severe COVID-19.
“In the ISARIC4C study, we recently found that this is probably due to a change in the way cell membranes detect viruses, but this mechanism doesn’t explain the fascinating association with Alzheimer’s disease reported in this new work,” Dr. Baillie said.
“It is often the case that the same gene can have different roles in different parts of the body. Importantly, it doesn’t mean that having COVID-19 has any effect on your risk of Alzheimer’s,” he added.
Also weighing in on the new study, Jonathan Schott, MD, professor of neurology, University College London, noted that dementia is the “main preexisting health condition associated with COVID-19 mortality, accounting for about one in four deaths from COVID-19 between March and June 2020.
“While some of this excessive mortality may relate to people with dementia being overrepresented in care homes, which were particularly hard hit by the pandemic, or due to general increased vulnerability to infections, there have been questions as to whether there are common factors that might increase susceptibility both to developing dementia and to dying from COVID-19,” Dr. Schott explained.
This “elegant paper” provides evidence for the latter, “suggesting a common genetic mechanism both for Alzheimer’s disease and for severe COVID-19 infection,” Dr. Schott said.
“The identification of a genetic risk factor and elucidation of inflammatory pathways through which it may increase risk has important implications for our understanding of both diseases, with potential implications for novel treatments,” he added.
The study was funded by the UK Dementia Research Institute. The authors have disclosed no relevant financial relationships. Dr. Schott serves as chief medical officer for Alzheimer’s Research UK and is clinical adviser to the UK Dementia Research Institute. Dr. Baillie has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The findings could lead to new treatment targets to slow progression and severity of both diseases.
Investigators found that a single genetic variant in the oligoadenylate synthetase 1 (OAS1) gene increases the risk for AD and that related variants in the same gene increase the likelihood of severe COVID-19 outcomes.
“These findings may allow us to identify new drug targets to slow progression of both diseases and reduce their severity,” Dervis Salih, PhD, senior research associate, UK Dementia Research Institute, University College London, said in an interview.
“Our work also suggests new approaches to treat both diseases with the same drugs,” Dr. Salih added.
The study was published online Oct. 7 in Brain.
Shared genetic network
The OAS1 gene is expressed in microglia, a type of immune cell that makes up around 10% of all cells in the brain.
In earlier work, investigators found evidence suggesting a link between the OAS1 gene and AD, but the function of the gene in microglia was unknown.
To further investigate the gene’s link to AD, they sequenced genetic data from 2,547 people – half with AD, and half without.
The genotyping analysis confirmed that the single-nucleotide polymorphism (SNP) rs1131454 within OAS1 is significantly associated with AD.
Given that the same OAS1 locus has recently been linked with severe COVID-19 outcomes, the researchers investigated four variants on the OAS1 gene.
Results indicate that SNPs within OAS1 associated with AD also show linkage to SNP variants associated with critical illness in COVID-19.
The rs1131454 (risk allele A) and rs4766676 (risk allele T) are associated with AD, and rs10735079 (risk allele A) and rs6489867 (risk allele T) are associated with critical illness with COVID-19, the investigators reported. All of these risk alleles dampen expression of OAS1.
“This study also provides strong new evidence that interferon signaling by the innate immune system plays a substantial role in the progression of Alzheimer’s,” said Dr. Salih.
“Identifying this shared genetic network in innate immune cells will allow us with future work to identify new biomarkers to track disease progression and also predict disease risk better for both disorders,” he added.
‘Fascinating’ link
In a statement from the UK nonprofit organization, Science Media Center, Kenneth Baillie, MBChB, with the University of Edinburgh, said this study builds on a discovery he and his colleagues made last year that OAS1 variants are associated with severe COVID-19.
“In the ISARIC4C study, we recently found that this is probably due to a change in the way cell membranes detect viruses, but this mechanism doesn’t explain the fascinating association with Alzheimer’s disease reported in this new work,” Dr. Baillie said.
“It is often the case that the same gene can have different roles in different parts of the body. Importantly, it doesn’t mean that having COVID-19 has any effect on your risk of Alzheimer’s,” he added.
Also weighing in on the new study, Jonathan Schott, MD, professor of neurology, University College London, noted that dementia is the “main preexisting health condition associated with COVID-19 mortality, accounting for about one in four deaths from COVID-19 between March and June 2020.
“While some of this excessive mortality may relate to people with dementia being overrepresented in care homes, which were particularly hard hit by the pandemic, or due to general increased vulnerability to infections, there have been questions as to whether there are common factors that might increase susceptibility both to developing dementia and to dying from COVID-19,” Dr. Schott explained.
This “elegant paper” provides evidence for the latter, “suggesting a common genetic mechanism both for Alzheimer’s disease and for severe COVID-19 infection,” Dr. Schott said.
“The identification of a genetic risk factor and elucidation of inflammatory pathways through which it may increase risk has important implications for our understanding of both diseases, with potential implications for novel treatments,” he added.
The study was funded by the UK Dementia Research Institute. The authors have disclosed no relevant financial relationships. Dr. Schott serves as chief medical officer for Alzheimer’s Research UK and is clinical adviser to the UK Dementia Research Institute. Dr. Baillie has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The findings could lead to new treatment targets to slow progression and severity of both diseases.
Investigators found that a single genetic variant in the oligoadenylate synthetase 1 (OAS1) gene increases the risk for AD and that related variants in the same gene increase the likelihood of severe COVID-19 outcomes.
“These findings may allow us to identify new drug targets to slow progression of both diseases and reduce their severity,” Dervis Salih, PhD, senior research associate, UK Dementia Research Institute, University College London, said in an interview.
“Our work also suggests new approaches to treat both diseases with the same drugs,” Dr. Salih added.
The study was published online Oct. 7 in Brain.
Shared genetic network
The OAS1 gene is expressed in microglia, a type of immune cell that makes up around 10% of all cells in the brain.
In earlier work, investigators found evidence suggesting a link between the OAS1 gene and AD, but the function of the gene in microglia was unknown.
To further investigate the gene’s link to AD, they sequenced genetic data from 2,547 people – half with AD, and half without.
The genotyping analysis confirmed that the single-nucleotide polymorphism (SNP) rs1131454 within OAS1 is significantly associated with AD.
Given that the same OAS1 locus has recently been linked with severe COVID-19 outcomes, the researchers investigated four variants on the OAS1 gene.
Results indicate that SNPs within OAS1 associated with AD also show linkage to SNP variants associated with critical illness in COVID-19.
The rs1131454 (risk allele A) and rs4766676 (risk allele T) are associated with AD, and rs10735079 (risk allele A) and rs6489867 (risk allele T) are associated with critical illness with COVID-19, the investigators reported. All of these risk alleles dampen expression of OAS1.
“This study also provides strong new evidence that interferon signaling by the innate immune system plays a substantial role in the progression of Alzheimer’s,” said Dr. Salih.
“Identifying this shared genetic network in innate immune cells will allow us with future work to identify new biomarkers to track disease progression and also predict disease risk better for both disorders,” he added.
‘Fascinating’ link
In a statement from the UK nonprofit organization, Science Media Center, Kenneth Baillie, MBChB, with the University of Edinburgh, said this study builds on a discovery he and his colleagues made last year that OAS1 variants are associated with severe COVID-19.
“In the ISARIC4C study, we recently found that this is probably due to a change in the way cell membranes detect viruses, but this mechanism doesn’t explain the fascinating association with Alzheimer’s disease reported in this new work,” Dr. Baillie said.
“It is often the case that the same gene can have different roles in different parts of the body. Importantly, it doesn’t mean that having COVID-19 has any effect on your risk of Alzheimer’s,” he added.
Also weighing in on the new study, Jonathan Schott, MD, professor of neurology, University College London, noted that dementia is the “main preexisting health condition associated with COVID-19 mortality, accounting for about one in four deaths from COVID-19 between March and June 2020.
“While some of this excessive mortality may relate to people with dementia being overrepresented in care homes, which were particularly hard hit by the pandemic, or due to general increased vulnerability to infections, there have been questions as to whether there are common factors that might increase susceptibility both to developing dementia and to dying from COVID-19,” Dr. Schott explained.
This “elegant paper” provides evidence for the latter, “suggesting a common genetic mechanism both for Alzheimer’s disease and for severe COVID-19 infection,” Dr. Schott said.
“The identification of a genetic risk factor and elucidation of inflammatory pathways through which it may increase risk has important implications for our understanding of both diseases, with potential implications for novel treatments,” he added.
The study was funded by the UK Dementia Research Institute. The authors have disclosed no relevant financial relationships. Dr. Schott serves as chief medical officer for Alzheimer’s Research UK and is clinical adviser to the UK Dementia Research Institute. Dr. Baillie has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
New FDA guidance aims to cut sodium in processed foods
The Food and Drug Administration has issued voluntary, short-term sodium reduction targets for food manufacturers, chain restaurants, and food service operators for processed, packaged, and prepared foods, with an eye toward reducing diet-related conditions such as heart disease and obesity.
The new targets seek to decrease average sodium intake from approximately 3,400 mg/day to 3,000 mg/day, about a 12% reduction, over the next 2.5 years, acting FDA Commissioner Janet Woodcock, MD, and Susan Mayne, PhD, director of the FDA’s Center for Food Safety and Applied Nutrition, said in joint statement.
Although this reduction keeps the average intake above the recommended limit of 2,300 mg/day for individuals 14 years and older as per the Dietary Guidelines for Americans, “we know that even these modest reductions made slowly over the next few years will substantially decrease diet-related diseases,” they added.
The FDA first proposed recommendations for reducing sodium content in draft guidance released in 2016.
Since, then a number of companies in the food industry have already made changes to sodium content in their products, “which is encouraging, but additional support across all types of foods to help consumers meet recommended sodium limits is needed,” Dr. Woodcock and Dr. Mayne said.
They emphasized that the new guidance represents short-term goals that the food industry should work to meet as soon as possible to help optimize public health.
“We will continue our discussions with the food industry as we monitor the sodium content of the food supply to evaluate progress. In the future, we plan to issue revised, subsequent targets to further lower the sodium content incrementally and continue to help reduce sodium intake,” Dr. Woodcock and Dr. Mayne said.
AHA: A good first step that does not go far enough
In a statement, the American Heart Association said the new targets will play “a critical role in helping people across the country achieve healthier levels of sodium and improved well-being overall. These targets will be an important driver to reduce sodium consumption, which can have significant health benefits and lead to lower medical costs.”
“Lowering sodium levels in the food supply would reduce risk of hypertension, heart disease, stroke, heart attack, and death in addition to saving billions of dollars in health care costs over the next decade,” the AHA said.
But the AHA also said lowering sodium intake to 3,000 mg/day is not enough.
“Lowering sodium further to 2,300 mg could prevent an estimated 450,000 cases of cardiovascular disease, gain 2 million quality-adjusted life-years, and save approximately $40 billion in health care costs over a 20-year period,” the AHA said.
The AHA is urging the FDA to “follow [this] action with additional targets to further lower the amount of sodium in the food supply and help people in America attain an appropriate sodium intake.”
A version of this article first appeared on Medscape.com.
The Food and Drug Administration has issued voluntary, short-term sodium reduction targets for food manufacturers, chain restaurants, and food service operators for processed, packaged, and prepared foods, with an eye toward reducing diet-related conditions such as heart disease and obesity.
The new targets seek to decrease average sodium intake from approximately 3,400 mg/day to 3,000 mg/day, about a 12% reduction, over the next 2.5 years, acting FDA Commissioner Janet Woodcock, MD, and Susan Mayne, PhD, director of the FDA’s Center for Food Safety and Applied Nutrition, said in joint statement.
Although this reduction keeps the average intake above the recommended limit of 2,300 mg/day for individuals 14 years and older as per the Dietary Guidelines for Americans, “we know that even these modest reductions made slowly over the next few years will substantially decrease diet-related diseases,” they added.
The FDA first proposed recommendations for reducing sodium content in draft guidance released in 2016.
Since, then a number of companies in the food industry have already made changes to sodium content in their products, “which is encouraging, but additional support across all types of foods to help consumers meet recommended sodium limits is needed,” Dr. Woodcock and Dr. Mayne said.
They emphasized that the new guidance represents short-term goals that the food industry should work to meet as soon as possible to help optimize public health.
“We will continue our discussions with the food industry as we monitor the sodium content of the food supply to evaluate progress. In the future, we plan to issue revised, subsequent targets to further lower the sodium content incrementally and continue to help reduce sodium intake,” Dr. Woodcock and Dr. Mayne said.
AHA: A good first step that does not go far enough
In a statement, the American Heart Association said the new targets will play “a critical role in helping people across the country achieve healthier levels of sodium and improved well-being overall. These targets will be an important driver to reduce sodium consumption, which can have significant health benefits and lead to lower medical costs.”
“Lowering sodium levels in the food supply would reduce risk of hypertension, heart disease, stroke, heart attack, and death in addition to saving billions of dollars in health care costs over the next decade,” the AHA said.
But the AHA also said lowering sodium intake to 3,000 mg/day is not enough.
“Lowering sodium further to 2,300 mg could prevent an estimated 450,000 cases of cardiovascular disease, gain 2 million quality-adjusted life-years, and save approximately $40 billion in health care costs over a 20-year period,” the AHA said.
The AHA is urging the FDA to “follow [this] action with additional targets to further lower the amount of sodium in the food supply and help people in America attain an appropriate sodium intake.”
A version of this article first appeared on Medscape.com.
The Food and Drug Administration has issued voluntary, short-term sodium reduction targets for food manufacturers, chain restaurants, and food service operators for processed, packaged, and prepared foods, with an eye toward reducing diet-related conditions such as heart disease and obesity.
The new targets seek to decrease average sodium intake from approximately 3,400 mg/day to 3,000 mg/day, about a 12% reduction, over the next 2.5 years, acting FDA Commissioner Janet Woodcock, MD, and Susan Mayne, PhD, director of the FDA’s Center for Food Safety and Applied Nutrition, said in joint statement.
Although this reduction keeps the average intake above the recommended limit of 2,300 mg/day for individuals 14 years and older as per the Dietary Guidelines for Americans, “we know that even these modest reductions made slowly over the next few years will substantially decrease diet-related diseases,” they added.
The FDA first proposed recommendations for reducing sodium content in draft guidance released in 2016.
Since, then a number of companies in the food industry have already made changes to sodium content in their products, “which is encouraging, but additional support across all types of foods to help consumers meet recommended sodium limits is needed,” Dr. Woodcock and Dr. Mayne said.
They emphasized that the new guidance represents short-term goals that the food industry should work to meet as soon as possible to help optimize public health.
“We will continue our discussions with the food industry as we monitor the sodium content of the food supply to evaluate progress. In the future, we plan to issue revised, subsequent targets to further lower the sodium content incrementally and continue to help reduce sodium intake,” Dr. Woodcock and Dr. Mayne said.
AHA: A good first step that does not go far enough
In a statement, the American Heart Association said the new targets will play “a critical role in helping people across the country achieve healthier levels of sodium and improved well-being overall. These targets will be an important driver to reduce sodium consumption, which can have significant health benefits and lead to lower medical costs.”
“Lowering sodium levels in the food supply would reduce risk of hypertension, heart disease, stroke, heart attack, and death in addition to saving billions of dollars in health care costs over the next decade,” the AHA said.
But the AHA also said lowering sodium intake to 3,000 mg/day is not enough.
“Lowering sodium further to 2,300 mg could prevent an estimated 450,000 cases of cardiovascular disease, gain 2 million quality-adjusted life-years, and save approximately $40 billion in health care costs over a 20-year period,” the AHA said.
The AHA is urging the FDA to “follow [this] action with additional targets to further lower the amount of sodium in the food supply and help people in America attain an appropriate sodium intake.”
A version of this article first appeared on Medscape.com.
High-dose omega-3s tied to higher AFib risk
Taking high-doses of marine omega-3 fatty acids, more than 1 gram daily, may raise the risk for atrial fibrillation (AFib), according to a meta-analysis of relevant research.
However, the risk of developing AFib appears to be “relatively small” for those taking 1 gram or less of fish oil per day, Christine M. Albert, MD, chair of the department of cardiology at the Smidt Heart Institute at Cedars-Sinai, Los Angeles, told this news organization.
The study was published online Oct. 6 in the journal Circulation.
It’s estimated that 7.8% of U.S. adults – almost 19 million in all – take fish oil supplements, often unbeknownst to their health care providers, the researchers noted. Yet, the literature on the effects of omega-3 fatty acid supplementation on cardiovascular outcomes are mixed.
“Some, but not all” large-scale randomized controlled trials investigating the effects of marine omega-3 fatty acid supplements on cardiovascular outcomes have reported increased risks for AFib. The potential reasons for differing findings may be dose related, the authors note in their paper.
The goal of this meta-analysis was to “bring clarity, answers, and actionable information” to doctors and patients, said Dr. Albert. The results suggest, however, that there may not be a “straightforward answer” to whether fish oil is good or bad for AFib. Instead, the answer may depend on the dose, she added.
Pooled data
After screening 4,049 articles and abstracts, the researchers included in their analysis seven large-scale randomized controlled trials reporting cardiovascular outcomes of marine omega-3 fatty acids.
The trials reported results for AFib, either as prespecified outcome, adverse event, or a reason for hospitalization. Each had a minimum of 500 patients and a median follow-up of at least 1 year.
Trials examining the effects of omega-3 fatty acids on recurrent AFib in patients with established AFib or postoperative AFib were excluded.
The seven trials enrolled a total of 81,210 patients (mean age, 65 years; 39% women); 72.6% of participants were enrolled in clinical trials testing ≤1 gram of marine omega-3 fatty acids per day and 27.4% were enrolled in clinical trials testing >1 gram of the supplement per day. The weighted average follow-up was 4.9 years.
Overall, use of omega-3 fatty acids was associated with a 25% increased risk for AFib (hazard ratio, 1.25; 95% confidence interval, 1.07-1.46; P = .013).
In analyses stratified by dose, the risk for AFib was “significantly more pronounced” in trials testing high doses of marine omega-3 fatty acid supplements (>1 gram per day: HR, 1.49; 95% CI, 1.04-2.15; P = .042) compared with those testing lower doses (≤1 gram per day: HR, 1.12; 95% CI, 1.03-1.22; P = .024; P for interaction < .001).
In meta-regression, the HR for AFib increased per 1 gram increase in daily omega-3 fatty acid dose (HR. 1.11; 95% CI, 1.06-1.15; P = .001).
Risk-benefit balance
“This meta-analysis adds new evidence regarding the risk of AFib in patients taking marine omega-3 fatty acid supplements,” wrote Dr. Albert and colleagues.
“Since the benefit of omega-3 fatty acids also appears to be dose dependent, the associated risk of AFib should be balanced against the benefit on atherosclerotic cardiovascular outcomes,” they suggested.
They cautioned that the meta-analysis pooled aggregate-level trial data, not individual patient data. Therefore, subgroup analyses by age or other patient level characteristics were not possible.
The risk of developing AFib increases with advancing age and is more common in men than in women. Additional risk factors include elevated blood pressure, coronary artery disease, heart failure, heart valve defects, obesity, and diabetes.
The authors said the potential risk of developing AFib with high doses of omega-3 fatty acid supplements should be discussed with patients and they should know the signs and symptoms of the condition.
The study had no specific funding. Dr. Albert has received grants from St. Jude Medical, Abbott, and Roche Diagnostics.
A version of this article first appeared on Medscape.com.
Taking high-doses of marine omega-3 fatty acids, more than 1 gram daily, may raise the risk for atrial fibrillation (AFib), according to a meta-analysis of relevant research.
However, the risk of developing AFib appears to be “relatively small” for those taking 1 gram or less of fish oil per day, Christine M. Albert, MD, chair of the department of cardiology at the Smidt Heart Institute at Cedars-Sinai, Los Angeles, told this news organization.
The study was published online Oct. 6 in the journal Circulation.
It’s estimated that 7.8% of U.S. adults – almost 19 million in all – take fish oil supplements, often unbeknownst to their health care providers, the researchers noted. Yet, the literature on the effects of omega-3 fatty acid supplementation on cardiovascular outcomes are mixed.
“Some, but not all” large-scale randomized controlled trials investigating the effects of marine omega-3 fatty acid supplements on cardiovascular outcomes have reported increased risks for AFib. The potential reasons for differing findings may be dose related, the authors note in their paper.
The goal of this meta-analysis was to “bring clarity, answers, and actionable information” to doctors and patients, said Dr. Albert. The results suggest, however, that there may not be a “straightforward answer” to whether fish oil is good or bad for AFib. Instead, the answer may depend on the dose, she added.
Pooled data
After screening 4,049 articles and abstracts, the researchers included in their analysis seven large-scale randomized controlled trials reporting cardiovascular outcomes of marine omega-3 fatty acids.
The trials reported results for AFib, either as prespecified outcome, adverse event, or a reason for hospitalization. Each had a minimum of 500 patients and a median follow-up of at least 1 year.
Trials examining the effects of omega-3 fatty acids on recurrent AFib in patients with established AFib or postoperative AFib were excluded.
The seven trials enrolled a total of 81,210 patients (mean age, 65 years; 39% women); 72.6% of participants were enrolled in clinical trials testing ≤1 gram of marine omega-3 fatty acids per day and 27.4% were enrolled in clinical trials testing >1 gram of the supplement per day. The weighted average follow-up was 4.9 years.
Overall, use of omega-3 fatty acids was associated with a 25% increased risk for AFib (hazard ratio, 1.25; 95% confidence interval, 1.07-1.46; P = .013).
In analyses stratified by dose, the risk for AFib was “significantly more pronounced” in trials testing high doses of marine omega-3 fatty acid supplements (>1 gram per day: HR, 1.49; 95% CI, 1.04-2.15; P = .042) compared with those testing lower doses (≤1 gram per day: HR, 1.12; 95% CI, 1.03-1.22; P = .024; P for interaction < .001).
In meta-regression, the HR for AFib increased per 1 gram increase in daily omega-3 fatty acid dose (HR. 1.11; 95% CI, 1.06-1.15; P = .001).
Risk-benefit balance
“This meta-analysis adds new evidence regarding the risk of AFib in patients taking marine omega-3 fatty acid supplements,” wrote Dr. Albert and colleagues.
“Since the benefit of omega-3 fatty acids also appears to be dose dependent, the associated risk of AFib should be balanced against the benefit on atherosclerotic cardiovascular outcomes,” they suggested.
They cautioned that the meta-analysis pooled aggregate-level trial data, not individual patient data. Therefore, subgroup analyses by age or other patient level characteristics were not possible.
The risk of developing AFib increases with advancing age and is more common in men than in women. Additional risk factors include elevated blood pressure, coronary artery disease, heart failure, heart valve defects, obesity, and diabetes.
The authors said the potential risk of developing AFib with high doses of omega-3 fatty acid supplements should be discussed with patients and they should know the signs and symptoms of the condition.
The study had no specific funding. Dr. Albert has received grants from St. Jude Medical, Abbott, and Roche Diagnostics.
A version of this article first appeared on Medscape.com.
Taking high-doses of marine omega-3 fatty acids, more than 1 gram daily, may raise the risk for atrial fibrillation (AFib), according to a meta-analysis of relevant research.
However, the risk of developing AFib appears to be “relatively small” for those taking 1 gram or less of fish oil per day, Christine M. Albert, MD, chair of the department of cardiology at the Smidt Heart Institute at Cedars-Sinai, Los Angeles, told this news organization.
The study was published online Oct. 6 in the journal Circulation.
It’s estimated that 7.8% of U.S. adults – almost 19 million in all – take fish oil supplements, often unbeknownst to their health care providers, the researchers noted. Yet, the literature on the effects of omega-3 fatty acid supplementation on cardiovascular outcomes are mixed.
“Some, but not all” large-scale randomized controlled trials investigating the effects of marine omega-3 fatty acid supplements on cardiovascular outcomes have reported increased risks for AFib. The potential reasons for differing findings may be dose related, the authors note in their paper.
The goal of this meta-analysis was to “bring clarity, answers, and actionable information” to doctors and patients, said Dr. Albert. The results suggest, however, that there may not be a “straightforward answer” to whether fish oil is good or bad for AFib. Instead, the answer may depend on the dose, she added.
Pooled data
After screening 4,049 articles and abstracts, the researchers included in their analysis seven large-scale randomized controlled trials reporting cardiovascular outcomes of marine omega-3 fatty acids.
The trials reported results for AFib, either as prespecified outcome, adverse event, or a reason for hospitalization. Each had a minimum of 500 patients and a median follow-up of at least 1 year.
Trials examining the effects of omega-3 fatty acids on recurrent AFib in patients with established AFib or postoperative AFib were excluded.
The seven trials enrolled a total of 81,210 patients (mean age, 65 years; 39% women); 72.6% of participants were enrolled in clinical trials testing ≤1 gram of marine omega-3 fatty acids per day and 27.4% were enrolled in clinical trials testing >1 gram of the supplement per day. The weighted average follow-up was 4.9 years.
Overall, use of omega-3 fatty acids was associated with a 25% increased risk for AFib (hazard ratio, 1.25; 95% confidence interval, 1.07-1.46; P = .013).
In analyses stratified by dose, the risk for AFib was “significantly more pronounced” in trials testing high doses of marine omega-3 fatty acid supplements (>1 gram per day: HR, 1.49; 95% CI, 1.04-2.15; P = .042) compared with those testing lower doses (≤1 gram per day: HR, 1.12; 95% CI, 1.03-1.22; P = .024; P for interaction < .001).
In meta-regression, the HR for AFib increased per 1 gram increase in daily omega-3 fatty acid dose (HR. 1.11; 95% CI, 1.06-1.15; P = .001).
Risk-benefit balance
“This meta-analysis adds new evidence regarding the risk of AFib in patients taking marine omega-3 fatty acid supplements,” wrote Dr. Albert and colleagues.
“Since the benefit of omega-3 fatty acids also appears to be dose dependent, the associated risk of AFib should be balanced against the benefit on atherosclerotic cardiovascular outcomes,” they suggested.
They cautioned that the meta-analysis pooled aggregate-level trial data, not individual patient data. Therefore, subgroup analyses by age or other patient level characteristics were not possible.
The risk of developing AFib increases with advancing age and is more common in men than in women. Additional risk factors include elevated blood pressure, coronary artery disease, heart failure, heart valve defects, obesity, and diabetes.
The authors said the potential risk of developing AFib with high doses of omega-3 fatty acid supplements should be discussed with patients and they should know the signs and symptoms of the condition.
The study had no specific funding. Dr. Albert has received grants from St. Jude Medical, Abbott, and Roche Diagnostics.
A version of this article first appeared on Medscape.com.
Lie down for orthostatic hypotension assessment
New research shows that supine orthostatic hypotension is more common and better predicts falls and orthostatic symptoms than seated OH, supporting a supine OH protocol in clinical practice, the researchers say.
“Older adults at risk for falls undergoing assessment for OH should lie supine rather than sitting prior to standing to get the most informative OH assessment,” study author Stephen Juraschek, MD, PhD, Beth Israel Deaconess Medical Center/Harvard Medical School, Boston, said in an interview.
“The findings call for a change in current practice,” Dr. Juraschek said.
He presented the study Sept. 29 at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension.
The seated position for detecting OH is “commonly used for convenience. Since many clinics already perform a seated blood pressure, it saves time for people to stand shortly afterward,” he explained.
“It has also been thought that the two are interchangeable [i.e., the change in blood pressure from seated to standing was just a lower magnitude than the change from supine to standing]. However, we showed that the physiology is on average quite different, questioning prior perspectives on the interchangeability of the two protocols,” he added.
The researchers studied 522 adults (mean age, 76 years; 42% women) at high risk for falls and with vitamin D levels in the insufficient/deficient range participating in the Study to Understand Fall Reduction and Vitamin D (STURDY).
The study showed that vitamin D supplementation was not associated with OH or the main study outcome of falls.
The study used two different OH assessment protocols – seated to standing and supine to standing – and Dr. Juraschek’s team used the data to gauge the impact of supine and seated positions on OH prevalence and its relation with fall risk and orthostatic symptoms.
OH was defined as a drop in systolic BP of at least 20 mm Hg or diastolic BP of at least 10 mm Hg.
At baseline, mean BP was 129/68 mm Hg. Mean BP increased 3.4/2.6 mm Hg after sitting, but decreased 3.7/0.7 mm Hg after lying supine.
Of the 953 OH assessments (supine and seated), OH was detected in 14.8% of the supine measurements but in only 2.2% of the seated measures.
Supine OH better predicted falls (hazard ratio, 1.60; 95% CI, 0.98-2.61; P = .06) than seated OH (HR, 0.70; 95% CI, 0.30-1.60; P = .39).
Although both were nonsignificant, “potentially due to power,” the association with falls was stronger for supine OH than for seated OH, Dr. Juraschek said.
In addition, seated OH was not associated with orthostatic symptoms, whereas supine OH was significantly associated with a greater risk of fainting, blacking out, seeing spots, room spinning, and headache in the previous month (P = .048-.002).
Useful study confirms anecdotal evidence
This is a “useful study” from a “reputable” group, “and the results reveal what I would have expected,” Robert Carey, MD, University of Virginia, Charlottesville, who wasn’t involved in the study, said in an interview.
The findings, Dr. Carey said, show that measuring supine, compared with standing, “actually correlates much better with the untoward effects of orthostatic hypotension which are falls and symptoms such as dizziness and spots before your eyes.”
“Seated BP is mostly used for convenience and a little bit shorter protocol. Most clinical trials do seated orthostatic hypotension measurements. I’ve always taught my medical students and others to use the supine to standing because I’ve just anecdotally felt that this was a much better way of detecting true orthostatic hypotension and that’s how we do it at the University of Virginia Hospital,” Dr. Carey said.
The study had no funding. Dr. Juraschek and Dr. Carey have no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
New research shows that supine orthostatic hypotension is more common and better predicts falls and orthostatic symptoms than seated OH, supporting a supine OH protocol in clinical practice, the researchers say.
“Older adults at risk for falls undergoing assessment for OH should lie supine rather than sitting prior to standing to get the most informative OH assessment,” study author Stephen Juraschek, MD, PhD, Beth Israel Deaconess Medical Center/Harvard Medical School, Boston, said in an interview.
“The findings call for a change in current practice,” Dr. Juraschek said.
He presented the study Sept. 29 at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension.
The seated position for detecting OH is “commonly used for convenience. Since many clinics already perform a seated blood pressure, it saves time for people to stand shortly afterward,” he explained.
“It has also been thought that the two are interchangeable [i.e., the change in blood pressure from seated to standing was just a lower magnitude than the change from supine to standing]. However, we showed that the physiology is on average quite different, questioning prior perspectives on the interchangeability of the two protocols,” he added.
The researchers studied 522 adults (mean age, 76 years; 42% women) at high risk for falls and with vitamin D levels in the insufficient/deficient range participating in the Study to Understand Fall Reduction and Vitamin D (STURDY).
The study showed that vitamin D supplementation was not associated with OH or the main study outcome of falls.
The study used two different OH assessment protocols – seated to standing and supine to standing – and Dr. Juraschek’s team used the data to gauge the impact of supine and seated positions on OH prevalence and its relation with fall risk and orthostatic symptoms.
OH was defined as a drop in systolic BP of at least 20 mm Hg or diastolic BP of at least 10 mm Hg.
At baseline, mean BP was 129/68 mm Hg. Mean BP increased 3.4/2.6 mm Hg after sitting, but decreased 3.7/0.7 mm Hg after lying supine.
Of the 953 OH assessments (supine and seated), OH was detected in 14.8% of the supine measurements but in only 2.2% of the seated measures.
Supine OH better predicted falls (hazard ratio, 1.60; 95% CI, 0.98-2.61; P = .06) than seated OH (HR, 0.70; 95% CI, 0.30-1.60; P = .39).
Although both were nonsignificant, “potentially due to power,” the association with falls was stronger for supine OH than for seated OH, Dr. Juraschek said.
In addition, seated OH was not associated with orthostatic symptoms, whereas supine OH was significantly associated with a greater risk of fainting, blacking out, seeing spots, room spinning, and headache in the previous month (P = .048-.002).
Useful study confirms anecdotal evidence
This is a “useful study” from a “reputable” group, “and the results reveal what I would have expected,” Robert Carey, MD, University of Virginia, Charlottesville, who wasn’t involved in the study, said in an interview.
The findings, Dr. Carey said, show that measuring supine, compared with standing, “actually correlates much better with the untoward effects of orthostatic hypotension which are falls and symptoms such as dizziness and spots before your eyes.”
“Seated BP is mostly used for convenience and a little bit shorter protocol. Most clinical trials do seated orthostatic hypotension measurements. I’ve always taught my medical students and others to use the supine to standing because I’ve just anecdotally felt that this was a much better way of detecting true orthostatic hypotension and that’s how we do it at the University of Virginia Hospital,” Dr. Carey said.
The study had no funding. Dr. Juraschek and Dr. Carey have no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
New research shows that supine orthostatic hypotension is more common and better predicts falls and orthostatic symptoms than seated OH, supporting a supine OH protocol in clinical practice, the researchers say.
“Older adults at risk for falls undergoing assessment for OH should lie supine rather than sitting prior to standing to get the most informative OH assessment,” study author Stephen Juraschek, MD, PhD, Beth Israel Deaconess Medical Center/Harvard Medical School, Boston, said in an interview.
“The findings call for a change in current practice,” Dr. Juraschek said.
He presented the study Sept. 29 at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension.
The seated position for detecting OH is “commonly used for convenience. Since many clinics already perform a seated blood pressure, it saves time for people to stand shortly afterward,” he explained.
“It has also been thought that the two are interchangeable [i.e., the change in blood pressure from seated to standing was just a lower magnitude than the change from supine to standing]. However, we showed that the physiology is on average quite different, questioning prior perspectives on the interchangeability of the two protocols,” he added.
The researchers studied 522 adults (mean age, 76 years; 42% women) at high risk for falls and with vitamin D levels in the insufficient/deficient range participating in the Study to Understand Fall Reduction and Vitamin D (STURDY).
The study showed that vitamin D supplementation was not associated with OH or the main study outcome of falls.
The study used two different OH assessment protocols – seated to standing and supine to standing – and Dr. Juraschek’s team used the data to gauge the impact of supine and seated positions on OH prevalence and its relation with fall risk and orthostatic symptoms.
OH was defined as a drop in systolic BP of at least 20 mm Hg or diastolic BP of at least 10 mm Hg.
At baseline, mean BP was 129/68 mm Hg. Mean BP increased 3.4/2.6 mm Hg after sitting, but decreased 3.7/0.7 mm Hg after lying supine.
Of the 953 OH assessments (supine and seated), OH was detected in 14.8% of the supine measurements but in only 2.2% of the seated measures.
Supine OH better predicted falls (hazard ratio, 1.60; 95% CI, 0.98-2.61; P = .06) than seated OH (HR, 0.70; 95% CI, 0.30-1.60; P = .39).
Although both were nonsignificant, “potentially due to power,” the association with falls was stronger for supine OH than for seated OH, Dr. Juraschek said.
In addition, seated OH was not associated with orthostatic symptoms, whereas supine OH was significantly associated with a greater risk of fainting, blacking out, seeing spots, room spinning, and headache in the previous month (P = .048-.002).
Useful study confirms anecdotal evidence
This is a “useful study” from a “reputable” group, “and the results reveal what I would have expected,” Robert Carey, MD, University of Virginia, Charlottesville, who wasn’t involved in the study, said in an interview.
The findings, Dr. Carey said, show that measuring supine, compared with standing, “actually correlates much better with the untoward effects of orthostatic hypotension which are falls and symptoms such as dizziness and spots before your eyes.”
“Seated BP is mostly used for convenience and a little bit shorter protocol. Most clinical trials do seated orthostatic hypotension measurements. I’ve always taught my medical students and others to use the supine to standing because I’ve just anecdotally felt that this was a much better way of detecting true orthostatic hypotension and that’s how we do it at the University of Virginia Hospital,” Dr. Carey said.
The study had no funding. Dr. Juraschek and Dr. Carey have no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
Retraining the brain may eliminate chronic back pain
Psychological therapy that changes an individual’s beliefs about pain not only provides lasting chronic pain relief but also alters brain regions related to pain generation, new research shows.
In the first randomized controlled test of pain-reprocessing therapy (PRT), two-thirds of patients with chronic back pain (CBP) who received 4 weeks of PRT were pain free or nearly pain free afterward – and for most patients, relief was maintained for 1 year, the researchers found.
“Primary chronic back pain can be dramatically reduced or even eliminated by psychological treatment focused on changing how threatening we perceive the pain to be,” first author Yoni Ashar, PhD, department of psychiatry, Weill Cornell Medicine, New York, said in an interview.
“ given that large reductions in pain have rarely been observed in studies that tested psychological therapies for chronic back pain.
The study was published online Sept. 29, 2021, in JAMA Psychiatry.
Rethinking pain
CBP is a leading cause of disability, and treatment is often ineffective. In about 85% of cases of primary CBP, a definitive cause of the pain can’t be identified. In these cases, fear, avoidance, and beliefs that pain indicates injury may contribute to ongoing CBP.
PRT educates patients about the role of the brain in generating chronic pain; helps them reappraise their pain as they engage in movements that they had been afraid to undertake; and helps them address emotions that may exacerbate pain.
The study included 151 adults (54% women; mean age, 41 years) who had primary CBP of low to moderate severity (mean pain intensity, 4 of 10) for an average of 10 years.
A total of 50 participants were randomly allocated to undergo PRT (one telehealth session with a physician and eight PRT sessions over 4 weeks), 51 to receive placebo (subcutaneous saline injection in the back), and 50 to continue their routine, usual ongoing care.
Large group differences in pain were observed after treatment. The mean pain score was 1.18 in the PRT group, 2.84 in the placebo group, and 3.13 in the usual-care group. Hedges’ g was –1.14 for PRT versus placebo and –1.74 for PRT versus usual care (P < .001).
Two-thirds (66%) of adults in the PRT group were pain free or nearly pain free following treatment (pain-intensity score of 0 or 1 out of 10), compared with 20% of those in the placebo group and 10% of those who received usual care.
Treatment effects were maintained at 1-year follow-up. The mean pain score was 1.51 in the PRT group, 2.79 in the placebo group, and 3.00 in the usual-care group. Neither age nor sex moderated the effect of PRT on pain intensity.
Retraining the brain
The researchers said the effects of PRT on pain were mediated by lessening the belief that pain indicates tissue damage. Of note, PRT also reduced experimentally evoked back pain and spontaneous pain during functional MRI, with large effect sizes.
“The idea is that by thinking about the pain as safe rather than threatening, patients can alter the brain networks reinforcing the pain, and neutralize it,” Dr. Ashar said in a news release.
The authors noted that study participants were relatively well educated and active. The participants reported having longstanding low to moderate pain and disability at baseline.
The physician and therapists were experts in delivering PRT. Future studies should test generalizability to other patient populations, therapists, and treatment contexts.
“Our clinical experience shows that PRT is effective for other primary chronic pain conditions as well,” said Dr. Ashar, including primary knee pain and tension headache.
Restoring function
Commenting on the findings, Shaheen E. Lakhan, MD, PhD, neurologist and pain specialist in Newton, Mass., said he has long experience using psychological approaches to address pain, with good results.
“Imagine telling a person suffering from decades of chronic pain that your pain is all in your head. I’ve done that for years as a board-certified pain physician managing only the most severe and debilitating forms of pain. When used to ground brain retraining, I could ultimately restore function to people living with chronic pain,” Dr. Lakhan said.
“The statement is true – the brain ultimately processes signals from throughout the body, forms the perception of pain, and links it to emotional brain centers, among others. Pain is an important survival mechanism so that when your body is at threat of injury, you protect yourself from further damage and withdraw. The problem lies when pain outlasts its welcome and chronifies,” said Dr. Lakhan, senior vice president of research and development of Click Therapeutics in Boston.
The investigators in this study “eloquently prove” that with 4 weeks of PRT, patients can learn that chronic pain is largely a “brain-generated false alarm and that constantly affirming this truth can actually reduce or eliminate it,” Dr. Lakhan said.
“Further, the brain areas implicated with pain are calmed after going through the therapy to both resting pain and pain induced by extending the back,” he noted.
“Pain-reprocessing therapy can improve the lives of chronic [pain patients] who have low to moderate levels of pain and disability; however, much work needs to be done to make this scalable and universally available and covered by insurers as a treatment modality,” Dr. Lakhan added.
He cautioned that he has not seen therapies such as this work when there is significant depression, withdrawal, or lack of control over one’s situation such that one behaves in a helpless manner – “a terrible state of mind called learned helplessness.”
The study was funded by the National Institutes of Health, the National Center for Advancing Translational Sciences, the Radiological Society of North America, the German Research Foundation, the Psychophysiologic Disorders Association, the Foundation for the Study of the Therapeutic Encounter, and community donations. Dr. Ashar received grants from the National Institutes of Health during the conduct of the study and personal fees from UnitedHealth Group, Lin Health, Pain Reprocessing Therapy Center, and Mental Health Partners of Boulder County outside the submitted work. Dr. Lakhan disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Psychological therapy that changes an individual’s beliefs about pain not only provides lasting chronic pain relief but also alters brain regions related to pain generation, new research shows.
In the first randomized controlled test of pain-reprocessing therapy (PRT), two-thirds of patients with chronic back pain (CBP) who received 4 weeks of PRT were pain free or nearly pain free afterward – and for most patients, relief was maintained for 1 year, the researchers found.
“Primary chronic back pain can be dramatically reduced or even eliminated by psychological treatment focused on changing how threatening we perceive the pain to be,” first author Yoni Ashar, PhD, department of psychiatry, Weill Cornell Medicine, New York, said in an interview.
“ given that large reductions in pain have rarely been observed in studies that tested psychological therapies for chronic back pain.
The study was published online Sept. 29, 2021, in JAMA Psychiatry.
Rethinking pain
CBP is a leading cause of disability, and treatment is often ineffective. In about 85% of cases of primary CBP, a definitive cause of the pain can’t be identified. In these cases, fear, avoidance, and beliefs that pain indicates injury may contribute to ongoing CBP.
PRT educates patients about the role of the brain in generating chronic pain; helps them reappraise their pain as they engage in movements that they had been afraid to undertake; and helps them address emotions that may exacerbate pain.
The study included 151 adults (54% women; mean age, 41 years) who had primary CBP of low to moderate severity (mean pain intensity, 4 of 10) for an average of 10 years.
A total of 50 participants were randomly allocated to undergo PRT (one telehealth session with a physician and eight PRT sessions over 4 weeks), 51 to receive placebo (subcutaneous saline injection in the back), and 50 to continue their routine, usual ongoing care.
Large group differences in pain were observed after treatment. The mean pain score was 1.18 in the PRT group, 2.84 in the placebo group, and 3.13 in the usual-care group. Hedges’ g was –1.14 for PRT versus placebo and –1.74 for PRT versus usual care (P < .001).
Two-thirds (66%) of adults in the PRT group were pain free or nearly pain free following treatment (pain-intensity score of 0 or 1 out of 10), compared with 20% of those in the placebo group and 10% of those who received usual care.
Treatment effects were maintained at 1-year follow-up. The mean pain score was 1.51 in the PRT group, 2.79 in the placebo group, and 3.00 in the usual-care group. Neither age nor sex moderated the effect of PRT on pain intensity.
Retraining the brain
The researchers said the effects of PRT on pain were mediated by lessening the belief that pain indicates tissue damage. Of note, PRT also reduced experimentally evoked back pain and spontaneous pain during functional MRI, with large effect sizes.
“The idea is that by thinking about the pain as safe rather than threatening, patients can alter the brain networks reinforcing the pain, and neutralize it,” Dr. Ashar said in a news release.
The authors noted that study participants were relatively well educated and active. The participants reported having longstanding low to moderate pain and disability at baseline.
The physician and therapists were experts in delivering PRT. Future studies should test generalizability to other patient populations, therapists, and treatment contexts.
“Our clinical experience shows that PRT is effective for other primary chronic pain conditions as well,” said Dr. Ashar, including primary knee pain and tension headache.
Restoring function
Commenting on the findings, Shaheen E. Lakhan, MD, PhD, neurologist and pain specialist in Newton, Mass., said he has long experience using psychological approaches to address pain, with good results.
“Imagine telling a person suffering from decades of chronic pain that your pain is all in your head. I’ve done that for years as a board-certified pain physician managing only the most severe and debilitating forms of pain. When used to ground brain retraining, I could ultimately restore function to people living with chronic pain,” Dr. Lakhan said.
“The statement is true – the brain ultimately processes signals from throughout the body, forms the perception of pain, and links it to emotional brain centers, among others. Pain is an important survival mechanism so that when your body is at threat of injury, you protect yourself from further damage and withdraw. The problem lies when pain outlasts its welcome and chronifies,” said Dr. Lakhan, senior vice president of research and development of Click Therapeutics in Boston.
The investigators in this study “eloquently prove” that with 4 weeks of PRT, patients can learn that chronic pain is largely a “brain-generated false alarm and that constantly affirming this truth can actually reduce or eliminate it,” Dr. Lakhan said.
“Further, the brain areas implicated with pain are calmed after going through the therapy to both resting pain and pain induced by extending the back,” he noted.
“Pain-reprocessing therapy can improve the lives of chronic [pain patients] who have low to moderate levels of pain and disability; however, much work needs to be done to make this scalable and universally available and covered by insurers as a treatment modality,” Dr. Lakhan added.
He cautioned that he has not seen therapies such as this work when there is significant depression, withdrawal, or lack of control over one’s situation such that one behaves in a helpless manner – “a terrible state of mind called learned helplessness.”
The study was funded by the National Institutes of Health, the National Center for Advancing Translational Sciences, the Radiological Society of North America, the German Research Foundation, the Psychophysiologic Disorders Association, the Foundation for the Study of the Therapeutic Encounter, and community donations. Dr. Ashar received grants from the National Institutes of Health during the conduct of the study and personal fees from UnitedHealth Group, Lin Health, Pain Reprocessing Therapy Center, and Mental Health Partners of Boulder County outside the submitted work. Dr. Lakhan disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Psychological therapy that changes an individual’s beliefs about pain not only provides lasting chronic pain relief but also alters brain regions related to pain generation, new research shows.
In the first randomized controlled test of pain-reprocessing therapy (PRT), two-thirds of patients with chronic back pain (CBP) who received 4 weeks of PRT were pain free or nearly pain free afterward – and for most patients, relief was maintained for 1 year, the researchers found.
“Primary chronic back pain can be dramatically reduced or even eliminated by psychological treatment focused on changing how threatening we perceive the pain to be,” first author Yoni Ashar, PhD, department of psychiatry, Weill Cornell Medicine, New York, said in an interview.
“ given that large reductions in pain have rarely been observed in studies that tested psychological therapies for chronic back pain.
The study was published online Sept. 29, 2021, in JAMA Psychiatry.
Rethinking pain
CBP is a leading cause of disability, and treatment is often ineffective. In about 85% of cases of primary CBP, a definitive cause of the pain can’t be identified. In these cases, fear, avoidance, and beliefs that pain indicates injury may contribute to ongoing CBP.
PRT educates patients about the role of the brain in generating chronic pain; helps them reappraise their pain as they engage in movements that they had been afraid to undertake; and helps them address emotions that may exacerbate pain.
The study included 151 adults (54% women; mean age, 41 years) who had primary CBP of low to moderate severity (mean pain intensity, 4 of 10) for an average of 10 years.
A total of 50 participants were randomly allocated to undergo PRT (one telehealth session with a physician and eight PRT sessions over 4 weeks), 51 to receive placebo (subcutaneous saline injection in the back), and 50 to continue their routine, usual ongoing care.
Large group differences in pain were observed after treatment. The mean pain score was 1.18 in the PRT group, 2.84 in the placebo group, and 3.13 in the usual-care group. Hedges’ g was –1.14 for PRT versus placebo and –1.74 for PRT versus usual care (P < .001).
Two-thirds (66%) of adults in the PRT group were pain free or nearly pain free following treatment (pain-intensity score of 0 or 1 out of 10), compared with 20% of those in the placebo group and 10% of those who received usual care.
Treatment effects were maintained at 1-year follow-up. The mean pain score was 1.51 in the PRT group, 2.79 in the placebo group, and 3.00 in the usual-care group. Neither age nor sex moderated the effect of PRT on pain intensity.
Retraining the brain
The researchers said the effects of PRT on pain were mediated by lessening the belief that pain indicates tissue damage. Of note, PRT also reduced experimentally evoked back pain and spontaneous pain during functional MRI, with large effect sizes.
“The idea is that by thinking about the pain as safe rather than threatening, patients can alter the brain networks reinforcing the pain, and neutralize it,” Dr. Ashar said in a news release.
The authors noted that study participants were relatively well educated and active. The participants reported having longstanding low to moderate pain and disability at baseline.
The physician and therapists were experts in delivering PRT. Future studies should test generalizability to other patient populations, therapists, and treatment contexts.
“Our clinical experience shows that PRT is effective for other primary chronic pain conditions as well,” said Dr. Ashar, including primary knee pain and tension headache.
Restoring function
Commenting on the findings, Shaheen E. Lakhan, MD, PhD, neurologist and pain specialist in Newton, Mass., said he has long experience using psychological approaches to address pain, with good results.
“Imagine telling a person suffering from decades of chronic pain that your pain is all in your head. I’ve done that for years as a board-certified pain physician managing only the most severe and debilitating forms of pain. When used to ground brain retraining, I could ultimately restore function to people living with chronic pain,” Dr. Lakhan said.
“The statement is true – the brain ultimately processes signals from throughout the body, forms the perception of pain, and links it to emotional brain centers, among others. Pain is an important survival mechanism so that when your body is at threat of injury, you protect yourself from further damage and withdraw. The problem lies when pain outlasts its welcome and chronifies,” said Dr. Lakhan, senior vice president of research and development of Click Therapeutics in Boston.
The investigators in this study “eloquently prove” that with 4 weeks of PRT, patients can learn that chronic pain is largely a “brain-generated false alarm and that constantly affirming this truth can actually reduce or eliminate it,” Dr. Lakhan said.
“Further, the brain areas implicated with pain are calmed after going through the therapy to both resting pain and pain induced by extending the back,” he noted.
“Pain-reprocessing therapy can improve the lives of chronic [pain patients] who have low to moderate levels of pain and disability; however, much work needs to be done to make this scalable and universally available and covered by insurers as a treatment modality,” Dr. Lakhan added.
He cautioned that he has not seen therapies such as this work when there is significant depression, withdrawal, or lack of control over one’s situation such that one behaves in a helpless manner – “a terrible state of mind called learned helplessness.”
The study was funded by the National Institutes of Health, the National Center for Advancing Translational Sciences, the Radiological Society of North America, the German Research Foundation, the Psychophysiologic Disorders Association, the Foundation for the Study of the Therapeutic Encounter, and community donations. Dr. Ashar received grants from the National Institutes of Health during the conduct of the study and personal fees from UnitedHealth Group, Lin Health, Pain Reprocessing Therapy Center, and Mental Health Partners of Boulder County outside the submitted work. Dr. Lakhan disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Customized brain stimulation: New hope for severe depression
Personalized deep brain stimulation (DBS) appears to rapidly and effectively improve symptoms of treatment-resistant depression, new research suggests.
In a proof-of-concept study, investigators identified specific brain activity patterns responsible for a single patient’s severe depression and customized a DBS protocol to modulate the patterns. Results showed rapid and sustained improvement in depression scores.
“This study points the way to a new paradigm that is desperately needed in psychiatry,” Andrew Krystal, PhD, Weill Institute for Neurosciences, University of California, San Francisco, said in a news release.
“ by identifying and modulating the circuit in her brain that’s uniquely associated with her symptoms,” Dr. Krystal added.
The findings were published online Oct. 4 in Nature Medicine.
Closed-loop, on-demand stimulation
The patient was a 36-year-old woman with longstanding, severe, and treatment-resistant major depressive disorder. She was unresponsive to multiple antidepressant combinations and electroconvulsive therapy.
The researchers used intracranial electrophysiology and focal electrical stimulation to identify the specific pattern of electrical brain activity that correlated with her depressed mood.
They identified the right ventral striatum – which is involved in emotion, motivation, and reward – as the stimulation site that led to consistent, sustained, and dose-dependent improvement of symptoms and served as the neural biomarker.
In addition, the investigators identified a neural activity pattern in the amygdala that predicted both the mood symptoms, symptom severity, and stimulation efficacy.
The patient was implanted with the Food and Drug Administration–approved NeuroPace RNS System. The device was placed in the right hemisphere. A single sensing lead was positioned in the amygdala and the second stimulation lead was placed in the ventral striatum.
When the sensing lead detected the activity pattern associated with depression, the other lead delivered a tiny dose (1 milliampere/1 mA) of electricity for 6 seconds, which altered the neural activity and relieved mood symptoms.
Remission achieved
Once this personalized, closed-loop therapy was fully operational, the patient’s depression score on the Montgomery-Åsberg Depression Rating Scale (MADRS) dropped from 33 before turning treatment ON to 14 at the first ON-treatment assessment carried out after 12 days of stimulation. The score dropped below 10, representing remission, several months later.
The treatment also rapidly improved symptom severity, as measured daily with Hamilton Depression Rating Scale (HAMD-6) and visual analog scales.
“Success was predicated on a clinical mapping stage before chronic device placement, a strategy that has been utilized in epilepsy to map seizure foci in a personalized manner but has not previously been performed in other neuropsychiatric conditions,” the investigators wrote.
This patient represents “one of the first examples of precision psychiatry – a treatment tailored to an individual,” the study’s lead author, Katherine Scangos, MD, also with UCSF Weill Institute, said in an interview.
She added that the treatment “was personally tailored both spatially,” meaning at the brain location, and temporally – the time it was delivered.
“This is the first time a neural biomarker has been used to automatically trigger therapeutic stimulation in depression as a successful long-term treatment,” said Dr. Scangos. However, “we have a lot of work left to do,” she added.
“This study provides proof-of-principle that we can utilize a multimodal brain mapping approach to identify a personalized depression circuit and target that circuit with successful treatment. We will need to test the approach in more patients before we can determine its efficacy,” Dr. Scangos said.
First reliable biomarker in psychiatry
In a statement from the UK nonprofit Science Media Centre, Vladimir Litvak, PhD, with the Wellcome Centre for Human Neuroimaging, University College London, said that the study is interesting, noting that it is from “one of the leading groups in the field.”
The fact that depression symptoms can be treated in some patients by electrical stimulation of the ventral striatum is not new, Dr. Litvak said. However, what is “exciting” is that the authors identified a particular neural activity pattern in the amygdala as a reliable predictor of both symptom severity and stimulation effectiveness, he noted.
“Patterns of brain activity correlated with disease symptoms when testing over a large group of patients are commonly discovered. But there are just a handful of examples of patterns that are reliable enough to be predictive on a short time scale in a single patient,” said Dr. Litvak, who was not associated with the research.
“Furthermore, to my knowledge, this is the first example of such a reliable biomarker for psychiatric symptoms. The other examples were all for neurological disorders such as Parkinson’s disease, dystonia, and epilepsy,” he added.
He cautioned that this is a single case, but “if reproduced in additional patients, it will bring at least some psychiatric conditions into the domain of brain diseases that can be characterized and diagnosed objectively rather than based on symptoms alone.”
Dr. Litvak pointed out two other critical aspects of the study: the use of exploratory recordings and stimulation to determine the most effective treatment strategy, and the use of a closed-loop device that stimulates only when detecting the amygdala biomarker.
“It is hard to say based on this single case how important these will be in the future. There is no comparison to constant stimulation that might have worked as well because the implanted device used in the study is not suitable for that,” Dr. Litvak said.
It should also be noted that implanting multiple depth electrodes at different brain sites is a “traumatic invasive procedure only reserved to date for severe cases of drug-resistant epilepsy,” he said. “Furthermore, it only allows [researchers] to test a small number of candidate sites, so it relies heavily on prior knowledge.
“Once clinicians know better what to look for, it might be possible to avoid this procedure altogether by using noninvasive methods,” such as functional MRI or EEG, to match the right treatment option to a patient, Dr. Litvak concluded.
The research was funded by the National Institutes of Health, the Brain & Behavior Research Foundation, and the Ray and Dagmar Dolby Family Fund through the department of psychiatry at UCSF. Dr. Scangos has reported no relevant financial relationships. A complete list of author disclosures is available in the original article. Dr. Litvak is participating in a research funding application to search for electrophysiological biomarkers of depression symptoms using invasive recordings.
A version of this article first appeared on Medscape.com.
Personalized deep brain stimulation (DBS) appears to rapidly and effectively improve symptoms of treatment-resistant depression, new research suggests.
In a proof-of-concept study, investigators identified specific brain activity patterns responsible for a single patient’s severe depression and customized a DBS protocol to modulate the patterns. Results showed rapid and sustained improvement in depression scores.
“This study points the way to a new paradigm that is desperately needed in psychiatry,” Andrew Krystal, PhD, Weill Institute for Neurosciences, University of California, San Francisco, said in a news release.
“ by identifying and modulating the circuit in her brain that’s uniquely associated with her symptoms,” Dr. Krystal added.
The findings were published online Oct. 4 in Nature Medicine.
Closed-loop, on-demand stimulation
The patient was a 36-year-old woman with longstanding, severe, and treatment-resistant major depressive disorder. She was unresponsive to multiple antidepressant combinations and electroconvulsive therapy.
The researchers used intracranial electrophysiology and focal electrical stimulation to identify the specific pattern of electrical brain activity that correlated with her depressed mood.
They identified the right ventral striatum – which is involved in emotion, motivation, and reward – as the stimulation site that led to consistent, sustained, and dose-dependent improvement of symptoms and served as the neural biomarker.
In addition, the investigators identified a neural activity pattern in the amygdala that predicted both the mood symptoms, symptom severity, and stimulation efficacy.
The patient was implanted with the Food and Drug Administration–approved NeuroPace RNS System. The device was placed in the right hemisphere. A single sensing lead was positioned in the amygdala and the second stimulation lead was placed in the ventral striatum.
When the sensing lead detected the activity pattern associated with depression, the other lead delivered a tiny dose (1 milliampere/1 mA) of electricity for 6 seconds, which altered the neural activity and relieved mood symptoms.
Remission achieved
Once this personalized, closed-loop therapy was fully operational, the patient’s depression score on the Montgomery-Åsberg Depression Rating Scale (MADRS) dropped from 33 before turning treatment ON to 14 at the first ON-treatment assessment carried out after 12 days of stimulation. The score dropped below 10, representing remission, several months later.
The treatment also rapidly improved symptom severity, as measured daily with Hamilton Depression Rating Scale (HAMD-6) and visual analog scales.
“Success was predicated on a clinical mapping stage before chronic device placement, a strategy that has been utilized in epilepsy to map seizure foci in a personalized manner but has not previously been performed in other neuropsychiatric conditions,” the investigators wrote.
This patient represents “one of the first examples of precision psychiatry – a treatment tailored to an individual,” the study’s lead author, Katherine Scangos, MD, also with UCSF Weill Institute, said in an interview.
She added that the treatment “was personally tailored both spatially,” meaning at the brain location, and temporally – the time it was delivered.
“This is the first time a neural biomarker has been used to automatically trigger therapeutic stimulation in depression as a successful long-term treatment,” said Dr. Scangos. However, “we have a lot of work left to do,” she added.
“This study provides proof-of-principle that we can utilize a multimodal brain mapping approach to identify a personalized depression circuit and target that circuit with successful treatment. We will need to test the approach in more patients before we can determine its efficacy,” Dr. Scangos said.
First reliable biomarker in psychiatry
In a statement from the UK nonprofit Science Media Centre, Vladimir Litvak, PhD, with the Wellcome Centre for Human Neuroimaging, University College London, said that the study is interesting, noting that it is from “one of the leading groups in the field.”
The fact that depression symptoms can be treated in some patients by electrical stimulation of the ventral striatum is not new, Dr. Litvak said. However, what is “exciting” is that the authors identified a particular neural activity pattern in the amygdala as a reliable predictor of both symptom severity and stimulation effectiveness, he noted.
“Patterns of brain activity correlated with disease symptoms when testing over a large group of patients are commonly discovered. But there are just a handful of examples of patterns that are reliable enough to be predictive on a short time scale in a single patient,” said Dr. Litvak, who was not associated with the research.
“Furthermore, to my knowledge, this is the first example of such a reliable biomarker for psychiatric symptoms. The other examples were all for neurological disorders such as Parkinson’s disease, dystonia, and epilepsy,” he added.
He cautioned that this is a single case, but “if reproduced in additional patients, it will bring at least some psychiatric conditions into the domain of brain diseases that can be characterized and diagnosed objectively rather than based on symptoms alone.”
Dr. Litvak pointed out two other critical aspects of the study: the use of exploratory recordings and stimulation to determine the most effective treatment strategy, and the use of a closed-loop device that stimulates only when detecting the amygdala biomarker.
“It is hard to say based on this single case how important these will be in the future. There is no comparison to constant stimulation that might have worked as well because the implanted device used in the study is not suitable for that,” Dr. Litvak said.
It should also be noted that implanting multiple depth electrodes at different brain sites is a “traumatic invasive procedure only reserved to date for severe cases of drug-resistant epilepsy,” he said. “Furthermore, it only allows [researchers] to test a small number of candidate sites, so it relies heavily on prior knowledge.
“Once clinicians know better what to look for, it might be possible to avoid this procedure altogether by using noninvasive methods,” such as functional MRI or EEG, to match the right treatment option to a patient, Dr. Litvak concluded.
The research was funded by the National Institutes of Health, the Brain & Behavior Research Foundation, and the Ray and Dagmar Dolby Family Fund through the department of psychiatry at UCSF. Dr. Scangos has reported no relevant financial relationships. A complete list of author disclosures is available in the original article. Dr. Litvak is participating in a research funding application to search for electrophysiological biomarkers of depression symptoms using invasive recordings.
A version of this article first appeared on Medscape.com.
Personalized deep brain stimulation (DBS) appears to rapidly and effectively improve symptoms of treatment-resistant depression, new research suggests.
In a proof-of-concept study, investigators identified specific brain activity patterns responsible for a single patient’s severe depression and customized a DBS protocol to modulate the patterns. Results showed rapid and sustained improvement in depression scores.
“This study points the way to a new paradigm that is desperately needed in psychiatry,” Andrew Krystal, PhD, Weill Institute for Neurosciences, University of California, San Francisco, said in a news release.
“ by identifying and modulating the circuit in her brain that’s uniquely associated with her symptoms,” Dr. Krystal added.
The findings were published online Oct. 4 in Nature Medicine.
Closed-loop, on-demand stimulation
The patient was a 36-year-old woman with longstanding, severe, and treatment-resistant major depressive disorder. She was unresponsive to multiple antidepressant combinations and electroconvulsive therapy.
The researchers used intracranial electrophysiology and focal electrical stimulation to identify the specific pattern of electrical brain activity that correlated with her depressed mood.
They identified the right ventral striatum – which is involved in emotion, motivation, and reward – as the stimulation site that led to consistent, sustained, and dose-dependent improvement of symptoms and served as the neural biomarker.
In addition, the investigators identified a neural activity pattern in the amygdala that predicted both the mood symptoms, symptom severity, and stimulation efficacy.
The patient was implanted with the Food and Drug Administration–approved NeuroPace RNS System. The device was placed in the right hemisphere. A single sensing lead was positioned in the amygdala and the second stimulation lead was placed in the ventral striatum.
When the sensing lead detected the activity pattern associated with depression, the other lead delivered a tiny dose (1 milliampere/1 mA) of electricity for 6 seconds, which altered the neural activity and relieved mood symptoms.
Remission achieved
Once this personalized, closed-loop therapy was fully operational, the patient’s depression score on the Montgomery-Åsberg Depression Rating Scale (MADRS) dropped from 33 before turning treatment ON to 14 at the first ON-treatment assessment carried out after 12 days of stimulation. The score dropped below 10, representing remission, several months later.
The treatment also rapidly improved symptom severity, as measured daily with Hamilton Depression Rating Scale (HAMD-6) and visual analog scales.
“Success was predicated on a clinical mapping stage before chronic device placement, a strategy that has been utilized in epilepsy to map seizure foci in a personalized manner but has not previously been performed in other neuropsychiatric conditions,” the investigators wrote.
This patient represents “one of the first examples of precision psychiatry – a treatment tailored to an individual,” the study’s lead author, Katherine Scangos, MD, also with UCSF Weill Institute, said in an interview.
She added that the treatment “was personally tailored both spatially,” meaning at the brain location, and temporally – the time it was delivered.
“This is the first time a neural biomarker has been used to automatically trigger therapeutic stimulation in depression as a successful long-term treatment,” said Dr. Scangos. However, “we have a lot of work left to do,” she added.
“This study provides proof-of-principle that we can utilize a multimodal brain mapping approach to identify a personalized depression circuit and target that circuit with successful treatment. We will need to test the approach in more patients before we can determine its efficacy,” Dr. Scangos said.
First reliable biomarker in psychiatry
In a statement from the UK nonprofit Science Media Centre, Vladimir Litvak, PhD, with the Wellcome Centre for Human Neuroimaging, University College London, said that the study is interesting, noting that it is from “one of the leading groups in the field.”
The fact that depression symptoms can be treated in some patients by electrical stimulation of the ventral striatum is not new, Dr. Litvak said. However, what is “exciting” is that the authors identified a particular neural activity pattern in the amygdala as a reliable predictor of both symptom severity and stimulation effectiveness, he noted.
“Patterns of brain activity correlated with disease symptoms when testing over a large group of patients are commonly discovered. But there are just a handful of examples of patterns that are reliable enough to be predictive on a short time scale in a single patient,” said Dr. Litvak, who was not associated with the research.
“Furthermore, to my knowledge, this is the first example of such a reliable biomarker for psychiatric symptoms. The other examples were all for neurological disorders such as Parkinson’s disease, dystonia, and epilepsy,” he added.
He cautioned that this is a single case, but “if reproduced in additional patients, it will bring at least some psychiatric conditions into the domain of brain diseases that can be characterized and diagnosed objectively rather than based on symptoms alone.”
Dr. Litvak pointed out two other critical aspects of the study: the use of exploratory recordings and stimulation to determine the most effective treatment strategy, and the use of a closed-loop device that stimulates only when detecting the amygdala biomarker.
“It is hard to say based on this single case how important these will be in the future. There is no comparison to constant stimulation that might have worked as well because the implanted device used in the study is not suitable for that,” Dr. Litvak said.
It should also be noted that implanting multiple depth electrodes at different brain sites is a “traumatic invasive procedure only reserved to date for severe cases of drug-resistant epilepsy,” he said. “Furthermore, it only allows [researchers] to test a small number of candidate sites, so it relies heavily on prior knowledge.
“Once clinicians know better what to look for, it might be possible to avoid this procedure altogether by using noninvasive methods,” such as functional MRI or EEG, to match the right treatment option to a patient, Dr. Litvak concluded.
The research was funded by the National Institutes of Health, the Brain & Behavior Research Foundation, and the Ray and Dagmar Dolby Family Fund through the department of psychiatry at UCSF. Dr. Scangos has reported no relevant financial relationships. A complete list of author disclosures is available in the original article. Dr. Litvak is participating in a research funding application to search for electrophysiological biomarkers of depression symptoms using invasive recordings.
A version of this article first appeared on Medscape.com.
FDA clears first mobile rapid test for concussion
, the company has announced.
Eye-Sync is a virtual reality eye-tracking platform that provides objective measurements to aid in the assessment of concussion. It’s the first mobile, rapid test for concussion that has been cleared by the FDA, the company said.
As reported by this news organization, Eye-Sync received breakthrough designation from the FDA for this indication in March 2019.
The FDA initially cleared the Eye-Sync platform for recording, viewing, and analyzing eye movements to help clinicians identify visual tracking impairment.
The Eye-Sync technology uses a series of 60-second eye tracking assessments, neurocognitive batteries, symptom inventories, and standardized patient inventories to identify the type and severity of impairment after concussion.
“The platform generates customizable and interpretive reports that support clinical decision making and offers visual and vestibular therapies to remedy deficits and monitor improvement over time,” the company said.
In support of the application for use in concussion, SyncThink enrolled 1,655 children and adults into a clinical study that collected comprehensive patient and concussion-related data for over 12 months.
The company used these data to develop proprietary algorithms and deep learning models to identify a positive or negative indication of concussion.
The study showed that Eye-Sinc had sensitivity greater than 82% and specificity greater than 93%, “thereby providing clinicians with significant and actionable data when evaluating individuals with concussion,” the company said in a news release.
“The outcome of this study very clearly shows the effectiveness of our technology at detecting concussion and definitively demonstrates the clinical utility of Eye-Sinc,” SyncThink Chief Clinical Officer Scott Anderson said in the release.
“It also shows that the future of concussion diagnosis is no longer purely symptom-based but that of a technology driven multi-modal approach,” Mr. Anderson said.
A version of this article first appeared on Medscape.com.
, the company has announced.
Eye-Sync is a virtual reality eye-tracking platform that provides objective measurements to aid in the assessment of concussion. It’s the first mobile, rapid test for concussion that has been cleared by the FDA, the company said.
As reported by this news organization, Eye-Sync received breakthrough designation from the FDA for this indication in March 2019.
The FDA initially cleared the Eye-Sync platform for recording, viewing, and analyzing eye movements to help clinicians identify visual tracking impairment.
The Eye-Sync technology uses a series of 60-second eye tracking assessments, neurocognitive batteries, symptom inventories, and standardized patient inventories to identify the type and severity of impairment after concussion.
“The platform generates customizable and interpretive reports that support clinical decision making and offers visual and vestibular therapies to remedy deficits and monitor improvement over time,” the company said.
In support of the application for use in concussion, SyncThink enrolled 1,655 children and adults into a clinical study that collected comprehensive patient and concussion-related data for over 12 months.
The company used these data to develop proprietary algorithms and deep learning models to identify a positive or negative indication of concussion.
The study showed that Eye-Sinc had sensitivity greater than 82% and specificity greater than 93%, “thereby providing clinicians with significant and actionable data when evaluating individuals with concussion,” the company said in a news release.
“The outcome of this study very clearly shows the effectiveness of our technology at detecting concussion and definitively demonstrates the clinical utility of Eye-Sinc,” SyncThink Chief Clinical Officer Scott Anderson said in the release.
“It also shows that the future of concussion diagnosis is no longer purely symptom-based but that of a technology driven multi-modal approach,” Mr. Anderson said.
A version of this article first appeared on Medscape.com.
, the company has announced.
Eye-Sync is a virtual reality eye-tracking platform that provides objective measurements to aid in the assessment of concussion. It’s the first mobile, rapid test for concussion that has been cleared by the FDA, the company said.
As reported by this news organization, Eye-Sync received breakthrough designation from the FDA for this indication in March 2019.
The FDA initially cleared the Eye-Sync platform for recording, viewing, and analyzing eye movements to help clinicians identify visual tracking impairment.
The Eye-Sync technology uses a series of 60-second eye tracking assessments, neurocognitive batteries, symptom inventories, and standardized patient inventories to identify the type and severity of impairment after concussion.
“The platform generates customizable and interpretive reports that support clinical decision making and offers visual and vestibular therapies to remedy deficits and monitor improvement over time,” the company said.
In support of the application for use in concussion, SyncThink enrolled 1,655 children and adults into a clinical study that collected comprehensive patient and concussion-related data for over 12 months.
The company used these data to develop proprietary algorithms and deep learning models to identify a positive or negative indication of concussion.
The study showed that Eye-Sinc had sensitivity greater than 82% and specificity greater than 93%, “thereby providing clinicians with significant and actionable data when evaluating individuals with concussion,” the company said in a news release.
“The outcome of this study very clearly shows the effectiveness of our technology at detecting concussion and definitively demonstrates the clinical utility of Eye-Sinc,” SyncThink Chief Clinical Officer Scott Anderson said in the release.
“It also shows that the future of concussion diagnosis is no longer purely symptom-based but that of a technology driven multi-modal approach,” Mr. Anderson said.
A version of this article first appeared on Medscape.com.
Scientists who unlocked secrets of pain sensation win nobel prize
for their discoveries of receptors for temperature and touch.
Their discoveries paved the way for new treatments for a wide range of disease conditions, including chronic pain.
“Our ability to sense heat, cold, and touch is essential for survival and underpins our interaction with the world around us,” the Nobel committee, in Stockholm, said in a news release.
“In our daily lives we take these sensations for granted, but how are nerve impulses initiated so that temperature and pressure can be perceived? This question has been solved by this year’s Nobel Prize laureates,” the committee added.
Science heats up
Dr. Julius and his collaborators used capsaicin, a pungent compound found in chili peppers that produces a burning sensation, to identify TRPV1, an ion channel activated by painful heat.
“The discovery of TRPV1 was a major breakthrough leading the way to the unravelling of additional temperature-sensing receptors,” the committee said.
Both Dr. Julius and Dr. Patapoutian used menthol to identify another receptor called TRPM8 that is activated by cold. Additional ion channels related to TRPV1 and TRPM8 were identified and found to be activated by a range of different temperatures.
The discoveries fueled other scientists to investigate the roles of these channels in thermal sensation.
“Julius’ discovery of TRPV1 was the breakthrough that allowed us to understand how differences in temperature can induce electrical signals in the nervous system,” the committee noted.
Science under pressure
As the mechanisms for temperature sensation began to unravel, Dr. Patapoutian and his collaborators used cultured pressure-sensitive cells to identify an ion channel activated by mechanical stimuli in the skin and internal organs. It was given the name Piezo1, after the Greek word for pressure.
Through its similarity to Piezo1, a second gene was discovered and named Piezo2. Sensory neurons were found to express high levels of Piezo2 and further studies firmly established that Piezo1 and Piezo2 are ion channels that are directly activated by the exertion of pressure on cell membranes.
“The groundbreaking discoveries of the TRPV1, TRPM8, and Piezo channels by this year’s Nobel Prize laureates have allowed us to understand how heat, cold, and mechanical force can initiate the nerve impulses that allow us to perceive and adapt to the world around us,” the Nobel committee said.
Dr. Julius and Dr. Patapoutian will receive a gold medal and share the $1.14 million prize money.
A version of this article first appeared on Medscape.com.
for their discoveries of receptors for temperature and touch.
Their discoveries paved the way for new treatments for a wide range of disease conditions, including chronic pain.
“Our ability to sense heat, cold, and touch is essential for survival and underpins our interaction with the world around us,” the Nobel committee, in Stockholm, said in a news release.
“In our daily lives we take these sensations for granted, but how are nerve impulses initiated so that temperature and pressure can be perceived? This question has been solved by this year’s Nobel Prize laureates,” the committee added.
Science heats up
Dr. Julius and his collaborators used capsaicin, a pungent compound found in chili peppers that produces a burning sensation, to identify TRPV1, an ion channel activated by painful heat.
“The discovery of TRPV1 was a major breakthrough leading the way to the unravelling of additional temperature-sensing receptors,” the committee said.
Both Dr. Julius and Dr. Patapoutian used menthol to identify another receptor called TRPM8 that is activated by cold. Additional ion channels related to TRPV1 and TRPM8 were identified and found to be activated by a range of different temperatures.
The discoveries fueled other scientists to investigate the roles of these channels in thermal sensation.
“Julius’ discovery of TRPV1 was the breakthrough that allowed us to understand how differences in temperature can induce electrical signals in the nervous system,” the committee noted.
Science under pressure
As the mechanisms for temperature sensation began to unravel, Dr. Patapoutian and his collaborators used cultured pressure-sensitive cells to identify an ion channel activated by mechanical stimuli in the skin and internal organs. It was given the name Piezo1, after the Greek word for pressure.
Through its similarity to Piezo1, a second gene was discovered and named Piezo2. Sensory neurons were found to express high levels of Piezo2 and further studies firmly established that Piezo1 and Piezo2 are ion channels that are directly activated by the exertion of pressure on cell membranes.
“The groundbreaking discoveries of the TRPV1, TRPM8, and Piezo channels by this year’s Nobel Prize laureates have allowed us to understand how heat, cold, and mechanical force can initiate the nerve impulses that allow us to perceive and adapt to the world around us,” the Nobel committee said.
Dr. Julius and Dr. Patapoutian will receive a gold medal and share the $1.14 million prize money.
A version of this article first appeared on Medscape.com.
for their discoveries of receptors for temperature and touch.
Their discoveries paved the way for new treatments for a wide range of disease conditions, including chronic pain.
“Our ability to sense heat, cold, and touch is essential for survival and underpins our interaction with the world around us,” the Nobel committee, in Stockholm, said in a news release.
“In our daily lives we take these sensations for granted, but how are nerve impulses initiated so that temperature and pressure can be perceived? This question has been solved by this year’s Nobel Prize laureates,” the committee added.
Science heats up
Dr. Julius and his collaborators used capsaicin, a pungent compound found in chili peppers that produces a burning sensation, to identify TRPV1, an ion channel activated by painful heat.
“The discovery of TRPV1 was a major breakthrough leading the way to the unravelling of additional temperature-sensing receptors,” the committee said.
Both Dr. Julius and Dr. Patapoutian used menthol to identify another receptor called TRPM8 that is activated by cold. Additional ion channels related to TRPV1 and TRPM8 were identified and found to be activated by a range of different temperatures.
The discoveries fueled other scientists to investigate the roles of these channels in thermal sensation.
“Julius’ discovery of TRPV1 was the breakthrough that allowed us to understand how differences in temperature can induce electrical signals in the nervous system,” the committee noted.
Science under pressure
As the mechanisms for temperature sensation began to unravel, Dr. Patapoutian and his collaborators used cultured pressure-sensitive cells to identify an ion channel activated by mechanical stimuli in the skin and internal organs. It was given the name Piezo1, after the Greek word for pressure.
Through its similarity to Piezo1, a second gene was discovered and named Piezo2. Sensory neurons were found to express high levels of Piezo2 and further studies firmly established that Piezo1 and Piezo2 are ion channels that are directly activated by the exertion of pressure on cell membranes.
“The groundbreaking discoveries of the TRPV1, TRPM8, and Piezo channels by this year’s Nobel Prize laureates have allowed us to understand how heat, cold, and mechanical force can initiate the nerve impulses that allow us to perceive and adapt to the world around us,” the Nobel committee said.
Dr. Julius and Dr. Patapoutian will receive a gold medal and share the $1.14 million prize money.
A version of this article first appeared on Medscape.com.
There’s no place like home to diagnose hypertension
Adults who need to track their blood pressure to find out if they have hypertension prefer to do it at home rather than at a clinic or kiosk or with 24-hour ambulatory BP monitoring (ABPM), according to a new study.
“From a patient-centered perspective, home BP monitoring is the most acceptable method for diagnosing hypertension, although participants were willing to complete ABPM and appreciated its accuracy,” said Beverly Green, MD, MPH, of Kaiser Permanente Washington, Seattle.
Dr. Green presented the study Sept. 29 during the virtual American Heart Association Hypertension Scientific Sessions 2021.
“Health care professionals should work toward relying less on in-clinic visits to diagnose hypertension and supporting their patients in taking their blood pressure measurements at home,” Dr. Green said in an AHA news release.
“Home blood pressure monitoring is empowering and improves our ability to identify and treat hypertension, and to prevent strokes, heart attacks, heart failure, and cardiovascular death,” she added.
Convenience is key
The BP-CHECK study was a three-group, randomized, controlled diagnostic study that tested the accuracy and acceptability of office, home, and kiosk BP monitoring against the gold-standard – ABPM – for diagnosing hypertension. Dr. Green presented the results on patient adherence and acceptability of these methods.
Those assigned to clinic measurements were asked to return to the clinic for at least one additional BP check, as is routine in diagnosing hypertension in clinical practice.
Those in the home group were given and trained to use a Bluetooth/web-enabled home BP monitor and were asked to take their BP twice a day (morning and evening, with two measurements each time) for 5 days.
Those in the kiosk group were trained to use a BP kiosk with a smart card and were asked to return to the kiosk (or a nearby pharmacy with the same kiosk) on 3 separate days and measure their BP three times at each visit.
All participants were asked to complete their group-assigned diagnostic regimens in 3 weeks and then to complete 24-hour ABPM.
The trial enrolled 510 adults who presented to Kaiser Permanente Washington primary care clinics with elevated BP (mean, 150/88 mm Hg) but who had not yet been diagnosed with hypertension. Their mean age was 59 years, 80% of the study participants were White, and 51% were male.
Adherence to the monitoring regimen was highest in the home BP group (90.6%), followed by the clinic group (87.2%), and lowest in the kiosk group (67.9%). Adherence to ABPM among all participants was 91.6%.
Overall, acceptability was highest for the home BP group, followed by the clinic and kiosk groups; 24-hour ABPM monitoring was the least acceptable option.
Home was the “overwhelming” stated preference when asked before randomization and after, Dr. Green said.
The findings come as no surprise to Willie Lawrence Jr., MD, head of the AHA National Hypertension Control Initiative oversight committee. “Patients will do what’s most convenient for them,” he told this news organization.
“We know from other studies that really all you need to do is measure the blood pressure twice a day for 3 days. That will give you a good idea what that patient’s blood pressure is as it relates to future cardiac events,” said Dr. Lawrence, who wasn’t involved in the study.
“We should really begin to focus more on these home, self-measured blood pressures using validated devices, and that’s important because a lot of the devices out there aren’t validated,” he explained.
“Patients with hypertension should have a blood pressure monitor at home that is validated and should be instructed in how to use it properly,” Dr. Lawrence concluded.
Funding for the study was provided by the Patient-Centered Outcomes Research Institute. Dr. Green and Dr. Lawrence have no relevant disclosures.
A version of this article first appeared on Medscape.com.
Adults who need to track their blood pressure to find out if they have hypertension prefer to do it at home rather than at a clinic or kiosk or with 24-hour ambulatory BP monitoring (ABPM), according to a new study.
“From a patient-centered perspective, home BP monitoring is the most acceptable method for diagnosing hypertension, although participants were willing to complete ABPM and appreciated its accuracy,” said Beverly Green, MD, MPH, of Kaiser Permanente Washington, Seattle.
Dr. Green presented the study Sept. 29 during the virtual American Heart Association Hypertension Scientific Sessions 2021.
“Health care professionals should work toward relying less on in-clinic visits to diagnose hypertension and supporting their patients in taking their blood pressure measurements at home,” Dr. Green said in an AHA news release.
“Home blood pressure monitoring is empowering and improves our ability to identify and treat hypertension, and to prevent strokes, heart attacks, heart failure, and cardiovascular death,” she added.
Convenience is key
The BP-CHECK study was a three-group, randomized, controlled diagnostic study that tested the accuracy and acceptability of office, home, and kiosk BP monitoring against the gold-standard – ABPM – for diagnosing hypertension. Dr. Green presented the results on patient adherence and acceptability of these methods.
Those assigned to clinic measurements were asked to return to the clinic for at least one additional BP check, as is routine in diagnosing hypertension in clinical practice.
Those in the home group were given and trained to use a Bluetooth/web-enabled home BP monitor and were asked to take their BP twice a day (morning and evening, with two measurements each time) for 5 days.
Those in the kiosk group were trained to use a BP kiosk with a smart card and were asked to return to the kiosk (or a nearby pharmacy with the same kiosk) on 3 separate days and measure their BP three times at each visit.
All participants were asked to complete their group-assigned diagnostic regimens in 3 weeks and then to complete 24-hour ABPM.
The trial enrolled 510 adults who presented to Kaiser Permanente Washington primary care clinics with elevated BP (mean, 150/88 mm Hg) but who had not yet been diagnosed with hypertension. Their mean age was 59 years, 80% of the study participants were White, and 51% were male.
Adherence to the monitoring regimen was highest in the home BP group (90.6%), followed by the clinic group (87.2%), and lowest in the kiosk group (67.9%). Adherence to ABPM among all participants was 91.6%.
Overall, acceptability was highest for the home BP group, followed by the clinic and kiosk groups; 24-hour ABPM monitoring was the least acceptable option.
Home was the “overwhelming” stated preference when asked before randomization and after, Dr. Green said.
The findings come as no surprise to Willie Lawrence Jr., MD, head of the AHA National Hypertension Control Initiative oversight committee. “Patients will do what’s most convenient for them,” he told this news organization.
“We know from other studies that really all you need to do is measure the blood pressure twice a day for 3 days. That will give you a good idea what that patient’s blood pressure is as it relates to future cardiac events,” said Dr. Lawrence, who wasn’t involved in the study.
“We should really begin to focus more on these home, self-measured blood pressures using validated devices, and that’s important because a lot of the devices out there aren’t validated,” he explained.
“Patients with hypertension should have a blood pressure monitor at home that is validated and should be instructed in how to use it properly,” Dr. Lawrence concluded.
Funding for the study was provided by the Patient-Centered Outcomes Research Institute. Dr. Green and Dr. Lawrence have no relevant disclosures.
A version of this article first appeared on Medscape.com.
Adults who need to track their blood pressure to find out if they have hypertension prefer to do it at home rather than at a clinic or kiosk or with 24-hour ambulatory BP monitoring (ABPM), according to a new study.
“From a patient-centered perspective, home BP monitoring is the most acceptable method for diagnosing hypertension, although participants were willing to complete ABPM and appreciated its accuracy,” said Beverly Green, MD, MPH, of Kaiser Permanente Washington, Seattle.
Dr. Green presented the study Sept. 29 during the virtual American Heart Association Hypertension Scientific Sessions 2021.
“Health care professionals should work toward relying less on in-clinic visits to diagnose hypertension and supporting their patients in taking their blood pressure measurements at home,” Dr. Green said in an AHA news release.
“Home blood pressure monitoring is empowering and improves our ability to identify and treat hypertension, and to prevent strokes, heart attacks, heart failure, and cardiovascular death,” she added.
Convenience is key
The BP-CHECK study was a three-group, randomized, controlled diagnostic study that tested the accuracy and acceptability of office, home, and kiosk BP monitoring against the gold-standard – ABPM – for diagnosing hypertension. Dr. Green presented the results on patient adherence and acceptability of these methods.
Those assigned to clinic measurements were asked to return to the clinic for at least one additional BP check, as is routine in diagnosing hypertension in clinical practice.
Those in the home group were given and trained to use a Bluetooth/web-enabled home BP monitor and were asked to take their BP twice a day (morning and evening, with two measurements each time) for 5 days.
Those in the kiosk group were trained to use a BP kiosk with a smart card and were asked to return to the kiosk (or a nearby pharmacy with the same kiosk) on 3 separate days and measure their BP three times at each visit.
All participants were asked to complete their group-assigned diagnostic regimens in 3 weeks and then to complete 24-hour ABPM.
The trial enrolled 510 adults who presented to Kaiser Permanente Washington primary care clinics with elevated BP (mean, 150/88 mm Hg) but who had not yet been diagnosed with hypertension. Their mean age was 59 years, 80% of the study participants were White, and 51% were male.
Adherence to the monitoring regimen was highest in the home BP group (90.6%), followed by the clinic group (87.2%), and lowest in the kiosk group (67.9%). Adherence to ABPM among all participants was 91.6%.
Overall, acceptability was highest for the home BP group, followed by the clinic and kiosk groups; 24-hour ABPM monitoring was the least acceptable option.
Home was the “overwhelming” stated preference when asked before randomization and after, Dr. Green said.
The findings come as no surprise to Willie Lawrence Jr., MD, head of the AHA National Hypertension Control Initiative oversight committee. “Patients will do what’s most convenient for them,” he told this news organization.
“We know from other studies that really all you need to do is measure the blood pressure twice a day for 3 days. That will give you a good idea what that patient’s blood pressure is as it relates to future cardiac events,” said Dr. Lawrence, who wasn’t involved in the study.
“We should really begin to focus more on these home, self-measured blood pressures using validated devices, and that’s important because a lot of the devices out there aren’t validated,” he explained.
“Patients with hypertension should have a blood pressure monitor at home that is validated and should be instructed in how to use it properly,” Dr. Lawrence concluded.
Funding for the study was provided by the Patient-Centered Outcomes Research Institute. Dr. Green and Dr. Lawrence have no relevant disclosures.
A version of this article first appeared on Medscape.com.
Abnormal nighttime BP patterns risky in adults with diabetes
Adults with diabetes whose blood pressure does not drop as expected at night (nondipping), or whose BP increases during the night (reverse dipping) are at higher risk of dying than peers with normal nighttime BP patterns, a longitudinal study has shown.
“Reverse dippers have more than double the risk of death for any cause over 20 years, irrespective of blood pressure control,” study investigator Martina Chiriacò, MD, University of Pisa (Italy), said in an interview.
“Primary physicians and diabetologists should look for abnormal blood pressure dipping patterns in patients with diabetes through 24-hour ambulatory blood pressure monitoring,” she added.
Dr. Chiriacò presented the research Sept. 28 at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension.
Scarce data
Previous studies have shown that a nondipping BP pattern is linked to renal and cardiovascular disease, both in healthy individuals and in patients with hypertension or diabetes.
“Nevertheless, the long-term effect of nondipping on mortality in diabetes is still unclear; in particular, data on reverse dippers are extremely scarce,” Dr. Chiriacò explained.
To investigate, the researchers analyzed data on 349 adults with diabetes (81% type 2 diabetes) who were followed for more than 2 decades as part of the CHAMPION study, all with available 24-hour ambulatory BP monitoring (ABPM) and heart rate variability monitoring.
Dipping, nondipping, and reverse dipping were defined as a decline of at least 10%, a decline of less than 10%, and an increase of at least 0.1% in average night-time systolic BP, compared with average daytime SBP, respectively.
The cohort involved 166 (47.6%) dippers, 144 (41.2%) nondippers, and 39 (11.2%) reverse dippers.
Compared with dippers, nondippers and reverse dippers showed a progressively higher prevalence of cardiac autonomic neuropathy, low heart rate variability, 24-hour hypertension, isolated nocturnal hypertension, postural hypotension, and lower prevalence of white-coat hypertension.
During a median follow-up of 21 years, 136 patients died (39%).
Compared with dippers, reverse dippers and nondippers had an average reduction in survival of 2.5 years and 1.1 years, respectively, Dr. Chiriacò reported.
During follow-up, risk for all-cause mortality was about twofold higher for reverse dippers than for dippers (adjusted hazard ratio, 2.2; 95% confidence interval, 1.3-3.8; P = .003) and than for nondippers (adjusted HR, 1.8; 95% CI, 1.1-2.9; P = .34).
There was no significant difference in all-cause mortality risk between dippers and nondippers.
Notably, said Dr. Chiriacò, the one in five patients with isolated nocturnal hypertension had a reduction in survival similar to that seen in individuals with 24-hour sustained hypertension (average, 1.2 years).
Individuals with low heart rate variability over 24 hours had an average reduction in survival of 1.8 years.
Important underused diagnostic tool
“We believe that our study is important since it is the only available study with a follow-up longer than 20 years that explores the role of blood pressure patterns and heart rate variability as risk factors for all-cause mortality in diabetes,” Dr. Chiriacò said in an interview.
There are some available strategies to reduce BP during the night, she added. “The most tested and effective is the administration of anti-hypertensive medications in the evening rather than in the morning.”
Weighing in on the study, Maryann McLaughlin, MD, cardiologist at Mount Sinai Hospital, New York, said: “Interestingly, most physicians do not do 24-hour ambulatory blood pressure monitoring when they’re making the diagnosis of hypertension.”
“And really, the correct way to make a diagnosis of hypertension and rule out white-coat hypertension is either with a 24-hour ambulatory blood pressure monitor or use of home blood pressure monitors,” she said in an interview.
“The 24-hour ambulatory blood pressure monitor is an important diagnostic tool and a great way to really look at this issue of dipping, which is a very important physiologic parameter,” Dr. McLaughlin said.
“In our offices, we offer the 24-hour home ambulatory blood pressure monitor routinely. Most patients are receptive to it and they usually tolerate it pretty well,” Dr. McLaughlin said.
The study was funded by the University of Pisa. Dr. Chiriacò and Dr. McLaughlin have no relevant disclosures.
A version of this article first appeared on Medscape.com.
Adults with diabetes whose blood pressure does not drop as expected at night (nondipping), or whose BP increases during the night (reverse dipping) are at higher risk of dying than peers with normal nighttime BP patterns, a longitudinal study has shown.
“Reverse dippers have more than double the risk of death for any cause over 20 years, irrespective of blood pressure control,” study investigator Martina Chiriacò, MD, University of Pisa (Italy), said in an interview.
“Primary physicians and diabetologists should look for abnormal blood pressure dipping patterns in patients with diabetes through 24-hour ambulatory blood pressure monitoring,” she added.
Dr. Chiriacò presented the research Sept. 28 at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension.
Scarce data
Previous studies have shown that a nondipping BP pattern is linked to renal and cardiovascular disease, both in healthy individuals and in patients with hypertension or diabetes.
“Nevertheless, the long-term effect of nondipping on mortality in diabetes is still unclear; in particular, data on reverse dippers are extremely scarce,” Dr. Chiriacò explained.
To investigate, the researchers analyzed data on 349 adults with diabetes (81% type 2 diabetes) who were followed for more than 2 decades as part of the CHAMPION study, all with available 24-hour ambulatory BP monitoring (ABPM) and heart rate variability monitoring.
Dipping, nondipping, and reverse dipping were defined as a decline of at least 10%, a decline of less than 10%, and an increase of at least 0.1% in average night-time systolic BP, compared with average daytime SBP, respectively.
The cohort involved 166 (47.6%) dippers, 144 (41.2%) nondippers, and 39 (11.2%) reverse dippers.
Compared with dippers, nondippers and reverse dippers showed a progressively higher prevalence of cardiac autonomic neuropathy, low heart rate variability, 24-hour hypertension, isolated nocturnal hypertension, postural hypotension, and lower prevalence of white-coat hypertension.
During a median follow-up of 21 years, 136 patients died (39%).
Compared with dippers, reverse dippers and nondippers had an average reduction in survival of 2.5 years and 1.1 years, respectively, Dr. Chiriacò reported.
During follow-up, risk for all-cause mortality was about twofold higher for reverse dippers than for dippers (adjusted hazard ratio, 2.2; 95% confidence interval, 1.3-3.8; P = .003) and than for nondippers (adjusted HR, 1.8; 95% CI, 1.1-2.9; P = .34).
There was no significant difference in all-cause mortality risk between dippers and nondippers.
Notably, said Dr. Chiriacò, the one in five patients with isolated nocturnal hypertension had a reduction in survival similar to that seen in individuals with 24-hour sustained hypertension (average, 1.2 years).
Individuals with low heart rate variability over 24 hours had an average reduction in survival of 1.8 years.
Important underused diagnostic tool
“We believe that our study is important since it is the only available study with a follow-up longer than 20 years that explores the role of blood pressure patterns and heart rate variability as risk factors for all-cause mortality in diabetes,” Dr. Chiriacò said in an interview.
There are some available strategies to reduce BP during the night, she added. “The most tested and effective is the administration of anti-hypertensive medications in the evening rather than in the morning.”
Weighing in on the study, Maryann McLaughlin, MD, cardiologist at Mount Sinai Hospital, New York, said: “Interestingly, most physicians do not do 24-hour ambulatory blood pressure monitoring when they’re making the diagnosis of hypertension.”
“And really, the correct way to make a diagnosis of hypertension and rule out white-coat hypertension is either with a 24-hour ambulatory blood pressure monitor or use of home blood pressure monitors,” she said in an interview.
“The 24-hour ambulatory blood pressure monitor is an important diagnostic tool and a great way to really look at this issue of dipping, which is a very important physiologic parameter,” Dr. McLaughlin said.
“In our offices, we offer the 24-hour home ambulatory blood pressure monitor routinely. Most patients are receptive to it and they usually tolerate it pretty well,” Dr. McLaughlin said.
The study was funded by the University of Pisa. Dr. Chiriacò and Dr. McLaughlin have no relevant disclosures.
A version of this article first appeared on Medscape.com.
Adults with diabetes whose blood pressure does not drop as expected at night (nondipping), or whose BP increases during the night (reverse dipping) are at higher risk of dying than peers with normal nighttime BP patterns, a longitudinal study has shown.
“Reverse dippers have more than double the risk of death for any cause over 20 years, irrespective of blood pressure control,” study investigator Martina Chiriacò, MD, University of Pisa (Italy), said in an interview.
“Primary physicians and diabetologists should look for abnormal blood pressure dipping patterns in patients with diabetes through 24-hour ambulatory blood pressure monitoring,” she added.
Dr. Chiriacò presented the research Sept. 28 at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension.
Scarce data
Previous studies have shown that a nondipping BP pattern is linked to renal and cardiovascular disease, both in healthy individuals and in patients with hypertension or diabetes.
“Nevertheless, the long-term effect of nondipping on mortality in diabetes is still unclear; in particular, data on reverse dippers are extremely scarce,” Dr. Chiriacò explained.
To investigate, the researchers analyzed data on 349 adults with diabetes (81% type 2 diabetes) who were followed for more than 2 decades as part of the CHAMPION study, all with available 24-hour ambulatory BP monitoring (ABPM) and heart rate variability monitoring.
Dipping, nondipping, and reverse dipping were defined as a decline of at least 10%, a decline of less than 10%, and an increase of at least 0.1% in average night-time systolic BP, compared with average daytime SBP, respectively.
The cohort involved 166 (47.6%) dippers, 144 (41.2%) nondippers, and 39 (11.2%) reverse dippers.
Compared with dippers, nondippers and reverse dippers showed a progressively higher prevalence of cardiac autonomic neuropathy, low heart rate variability, 24-hour hypertension, isolated nocturnal hypertension, postural hypotension, and lower prevalence of white-coat hypertension.
During a median follow-up of 21 years, 136 patients died (39%).
Compared with dippers, reverse dippers and nondippers had an average reduction in survival of 2.5 years and 1.1 years, respectively, Dr. Chiriacò reported.
During follow-up, risk for all-cause mortality was about twofold higher for reverse dippers than for dippers (adjusted hazard ratio, 2.2; 95% confidence interval, 1.3-3.8; P = .003) and than for nondippers (adjusted HR, 1.8; 95% CI, 1.1-2.9; P = .34).
There was no significant difference in all-cause mortality risk between dippers and nondippers.
Notably, said Dr. Chiriacò, the one in five patients with isolated nocturnal hypertension had a reduction in survival similar to that seen in individuals with 24-hour sustained hypertension (average, 1.2 years).
Individuals with low heart rate variability over 24 hours had an average reduction in survival of 1.8 years.
Important underused diagnostic tool
“We believe that our study is important since it is the only available study with a follow-up longer than 20 years that explores the role of blood pressure patterns and heart rate variability as risk factors for all-cause mortality in diabetes,” Dr. Chiriacò said in an interview.
There are some available strategies to reduce BP during the night, she added. “The most tested and effective is the administration of anti-hypertensive medications in the evening rather than in the morning.”
Weighing in on the study, Maryann McLaughlin, MD, cardiologist at Mount Sinai Hospital, New York, said: “Interestingly, most physicians do not do 24-hour ambulatory blood pressure monitoring when they’re making the diagnosis of hypertension.”
“And really, the correct way to make a diagnosis of hypertension and rule out white-coat hypertension is either with a 24-hour ambulatory blood pressure monitor or use of home blood pressure monitors,” she said in an interview.
“The 24-hour ambulatory blood pressure monitor is an important diagnostic tool and a great way to really look at this issue of dipping, which is a very important physiologic parameter,” Dr. McLaughlin said.
“In our offices, we offer the 24-hour home ambulatory blood pressure monitor routinely. Most patients are receptive to it and they usually tolerate it pretty well,” Dr. McLaughlin said.
The study was funded by the University of Pisa. Dr. Chiriacò and Dr. McLaughlin have no relevant disclosures.
A version of this article first appeared on Medscape.com.