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Ulcerative colitis cases projected to top 2 million in eight countries by 2031
The data and analytics company’s report offers projections for diagnosed incident and prevalent cases of UC in the United States, United Kingdom, Germany, Spain, Japan, Italy, France, and Canada.
In 2031, the United States will have the highest number of diagnosed prevalent cases of UC, with 655,317 cases, whereas Canada will have the fewest, with 91,186 cases, the company projects.
“UC can occur at any age, although most people are diagnosed in their mid-thirties. Men and women are equally likely to be affected, but older men are more likely to be diagnosed than older women,” Bharti Prabhakar, MPH, associate project manager at GlobalData, said in a statement.
In all eight countries, adults aged 30-69 years accounted for more than 65% of the diagnosed prevalent cases of UC, whereas those younger than 20 years made up less than 3% of the cases, GlobalData noted.
Incidence also rising
Diagnosed incident cases of UC in the eight countries are expected to increase from 160,122 cases in 2021 to 168,467 cases in 2031, at an annual growth rate of 0.52%, the company said.
In 2031, the United States will have the highest number of diagnosed incident cases of UC, with 104,795 cases, and France will have the fewest, with 2972 cases, the company predicted.
GlobalData epidemiologists attribute the predicted increases in UC prevalence and incidence to changes in population dynamics in each country.
The forecast is supported by historical data obtained from peer-reviewed articles and population-based studies, the firm noted.
The methodology was kept consistent across the eight countries to allow for a meaningful comparison of the forecast incident and prevalent cases of UC across these markets, GlobalData added.
“UC can affect people of any racial or ethnic group,” Ms. Prabhakar stated. “Genes, abnormal immune reactions, the microbiome, diet, stress, and the environment have all been suggested as triggers, but there is no definite evidence that any one of these factors is the cause of UC.”
Western countries have reported high incidence and prevalence of UC, Ms. Prabhaker noted. “Therefore, environmental factors may either suppress or reinforce inherent predispositions for UC and might also be crucial in triggering disease onset.”
A version of this article originally appeared on Medscape.com.
The data and analytics company’s report offers projections for diagnosed incident and prevalent cases of UC in the United States, United Kingdom, Germany, Spain, Japan, Italy, France, and Canada.
In 2031, the United States will have the highest number of diagnosed prevalent cases of UC, with 655,317 cases, whereas Canada will have the fewest, with 91,186 cases, the company projects.
“UC can occur at any age, although most people are diagnosed in their mid-thirties. Men and women are equally likely to be affected, but older men are more likely to be diagnosed than older women,” Bharti Prabhakar, MPH, associate project manager at GlobalData, said in a statement.
In all eight countries, adults aged 30-69 years accounted for more than 65% of the diagnosed prevalent cases of UC, whereas those younger than 20 years made up less than 3% of the cases, GlobalData noted.
Incidence also rising
Diagnosed incident cases of UC in the eight countries are expected to increase from 160,122 cases in 2021 to 168,467 cases in 2031, at an annual growth rate of 0.52%, the company said.
In 2031, the United States will have the highest number of diagnosed incident cases of UC, with 104,795 cases, and France will have the fewest, with 2972 cases, the company predicted.
GlobalData epidemiologists attribute the predicted increases in UC prevalence and incidence to changes in population dynamics in each country.
The forecast is supported by historical data obtained from peer-reviewed articles and population-based studies, the firm noted.
The methodology was kept consistent across the eight countries to allow for a meaningful comparison of the forecast incident and prevalent cases of UC across these markets, GlobalData added.
“UC can affect people of any racial or ethnic group,” Ms. Prabhakar stated. “Genes, abnormal immune reactions, the microbiome, diet, stress, and the environment have all been suggested as triggers, but there is no definite evidence that any one of these factors is the cause of UC.”
Western countries have reported high incidence and prevalence of UC, Ms. Prabhaker noted. “Therefore, environmental factors may either suppress or reinforce inherent predispositions for UC and might also be crucial in triggering disease onset.”
A version of this article originally appeared on Medscape.com.
The data and analytics company’s report offers projections for diagnosed incident and prevalent cases of UC in the United States, United Kingdom, Germany, Spain, Japan, Italy, France, and Canada.
In 2031, the United States will have the highest number of diagnosed prevalent cases of UC, with 655,317 cases, whereas Canada will have the fewest, with 91,186 cases, the company projects.
“UC can occur at any age, although most people are diagnosed in their mid-thirties. Men and women are equally likely to be affected, but older men are more likely to be diagnosed than older women,” Bharti Prabhakar, MPH, associate project manager at GlobalData, said in a statement.
In all eight countries, adults aged 30-69 years accounted for more than 65% of the diagnosed prevalent cases of UC, whereas those younger than 20 years made up less than 3% of the cases, GlobalData noted.
Incidence also rising
Diagnosed incident cases of UC in the eight countries are expected to increase from 160,122 cases in 2021 to 168,467 cases in 2031, at an annual growth rate of 0.52%, the company said.
In 2031, the United States will have the highest number of diagnosed incident cases of UC, with 104,795 cases, and France will have the fewest, with 2972 cases, the company predicted.
GlobalData epidemiologists attribute the predicted increases in UC prevalence and incidence to changes in population dynamics in each country.
The forecast is supported by historical data obtained from peer-reviewed articles and population-based studies, the firm noted.
The methodology was kept consistent across the eight countries to allow for a meaningful comparison of the forecast incident and prevalent cases of UC across these markets, GlobalData added.
“UC can affect people of any racial or ethnic group,” Ms. Prabhakar stated. “Genes, abnormal immune reactions, the microbiome, diet, stress, and the environment have all been suggested as triggers, but there is no definite evidence that any one of these factors is the cause of UC.”
Western countries have reported high incidence and prevalence of UC, Ms. Prabhaker noted. “Therefore, environmental factors may either suppress or reinforce inherent predispositions for UC and might also be crucial in triggering disease onset.”
A version of this article originally appeared on Medscape.com.
AI helps predict ulcerative colitis remission/activity, flare-ups
The AI tool predicted UC disease activity with 89% accuracy and inflammation at the biopsy site with 80% accuracy. Its ability to stratify risk of UC flare was on par with human pathologists.
“This tool in the near future will speed up, simplify, and standardize histological assessment of ulcerative colitis and provide the clinician with accurate prognostic information in real time,” co–lead author Marietta Iacucci, MD, PhD, from the University of Birmingham (England), and University College Cork (Ireland), said in an interview.
“The tool needs to be refined and further validated before it is ready for daily clinical practice. That work is ongoing now,” Dr. Iacucci said.
The researchers describe their advanced AI-based computer-aided detection tool in a study published online in Gastroenterology.
‘Strong’ performance
They used 535 digitized biopsies from 273 patients with UC (mean age, 48 years; 41% women) to develop and test the tool. They used a subset of 118 to train it to distinguish remission from activity, 42 to calibrate it, and 375 to test it. An additional 154 biopsies from 58 patients with UC were used to externally validate the tool.
The model also was tested to predict the corresponding endoscopic assessment and occurrence of flares at 12 months.
UC disease activity was defined by three different histologic indices: the Robarts Histopathology Index (RHI), the Nancy Histological Index (NHI), and the newly developed PICaSSO Histologic Remission Index (PHRI).
The AI tool had “strong diagnostic performance to detect disease activity” (PHRI > 0) with an overall area under the receiver operating characteristic curve of 0.87 and sensitivity and specificity of 89% and 85%, respectively.
The researchers note that, while the AI tool was trained for the PHRI, its sensitivity for RHI and NHI histologic remission/activity was also high (94% and 89%, respectively).
Despite the different mix of severity grades, the AI model “maintained a good diagnostic performance, proving its applicability outside the original development setting,” they reported.
The AI tool could also predict the presence of endoscopic inflammation in the biopsy area with about 80% accuracy.
“Though imperfect, this result is consistent with human-assessed correlation between endoscopy and histology,” the researchers noted.
The model predicted the corresponding endoscopic remission/activity with 79% and 82% accuracy for UCEIS and PICaSSO, respectively.
The hazard ratios for disease flare-up between the AI system and pathologists assessed by PHRI was similar (4.64 and 3.56, respectively), “demonstrating the ability of the computer to stratify the risk of flare comparably well to pathologists,” they added.
Both histology and outcome prediction were confirmed in the external validation cohort.
The AI system delivered results in an average of 9.8 seconds per slide.
Potential ‘game changer’
UC is a “complex condition to predict, and developing machine learning–derived systems to make this diagnostic job quicker and more accurate could be a game changer,” Dr. Iacucci said in a news release.
With refinement, the AI tool will have an impact on both clinical trials and daily practice, the researchers wrote. In clinical practice, histological reporting remains “largely descriptive and nonstandard, thus would greatly benefit from a quick and objective assessment. Similarly, clinical trials in UC could efficiently overcome costly central readings.”
Assessing and measuring improvement in endoscopy and histology are difficult parts of treating UC, said David Hudesman, MD, codirector of the Inflammatory Bowel Disease Center at New York University Langone Health.
“We do not know how much improvement is associated with improved long-term outcomes,” Dr. Hudesman said in an interview. “For example, does a patient need complete healing or is 50% better enough?” Dr. Hudesman was not involved with the current research.
“This study showed that AI can predict – with good accuracy – endoscopy and histology scores, as well as 1-year patient outcomes. If this is validated in larger studies, AI can help determine if we should adjust/change therapies or continue, which is very important,” he said.
This research was supported by the National Institute for Health Research Birmingham Biomedical Research Centre. Dr. Iacucci and Dr. Hudesman reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The AI tool predicted UC disease activity with 89% accuracy and inflammation at the biopsy site with 80% accuracy. Its ability to stratify risk of UC flare was on par with human pathologists.
“This tool in the near future will speed up, simplify, and standardize histological assessment of ulcerative colitis and provide the clinician with accurate prognostic information in real time,” co–lead author Marietta Iacucci, MD, PhD, from the University of Birmingham (England), and University College Cork (Ireland), said in an interview.
“The tool needs to be refined and further validated before it is ready for daily clinical practice. That work is ongoing now,” Dr. Iacucci said.
The researchers describe their advanced AI-based computer-aided detection tool in a study published online in Gastroenterology.
‘Strong’ performance
They used 535 digitized biopsies from 273 patients with UC (mean age, 48 years; 41% women) to develop and test the tool. They used a subset of 118 to train it to distinguish remission from activity, 42 to calibrate it, and 375 to test it. An additional 154 biopsies from 58 patients with UC were used to externally validate the tool.
The model also was tested to predict the corresponding endoscopic assessment and occurrence of flares at 12 months.
UC disease activity was defined by three different histologic indices: the Robarts Histopathology Index (RHI), the Nancy Histological Index (NHI), and the newly developed PICaSSO Histologic Remission Index (PHRI).
The AI tool had “strong diagnostic performance to detect disease activity” (PHRI > 0) with an overall area under the receiver operating characteristic curve of 0.87 and sensitivity and specificity of 89% and 85%, respectively.
The researchers note that, while the AI tool was trained for the PHRI, its sensitivity for RHI and NHI histologic remission/activity was also high (94% and 89%, respectively).
Despite the different mix of severity grades, the AI model “maintained a good diagnostic performance, proving its applicability outside the original development setting,” they reported.
The AI tool could also predict the presence of endoscopic inflammation in the biopsy area with about 80% accuracy.
“Though imperfect, this result is consistent with human-assessed correlation between endoscopy and histology,” the researchers noted.
The model predicted the corresponding endoscopic remission/activity with 79% and 82% accuracy for UCEIS and PICaSSO, respectively.
The hazard ratios for disease flare-up between the AI system and pathologists assessed by PHRI was similar (4.64 and 3.56, respectively), “demonstrating the ability of the computer to stratify the risk of flare comparably well to pathologists,” they added.
Both histology and outcome prediction were confirmed in the external validation cohort.
The AI system delivered results in an average of 9.8 seconds per slide.
Potential ‘game changer’
UC is a “complex condition to predict, and developing machine learning–derived systems to make this diagnostic job quicker and more accurate could be a game changer,” Dr. Iacucci said in a news release.
With refinement, the AI tool will have an impact on both clinical trials and daily practice, the researchers wrote. In clinical practice, histological reporting remains “largely descriptive and nonstandard, thus would greatly benefit from a quick and objective assessment. Similarly, clinical trials in UC could efficiently overcome costly central readings.”
Assessing and measuring improvement in endoscopy and histology are difficult parts of treating UC, said David Hudesman, MD, codirector of the Inflammatory Bowel Disease Center at New York University Langone Health.
“We do not know how much improvement is associated with improved long-term outcomes,” Dr. Hudesman said in an interview. “For example, does a patient need complete healing or is 50% better enough?” Dr. Hudesman was not involved with the current research.
“This study showed that AI can predict – with good accuracy – endoscopy and histology scores, as well as 1-year patient outcomes. If this is validated in larger studies, AI can help determine if we should adjust/change therapies or continue, which is very important,” he said.
This research was supported by the National Institute for Health Research Birmingham Biomedical Research Centre. Dr. Iacucci and Dr. Hudesman reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The AI tool predicted UC disease activity with 89% accuracy and inflammation at the biopsy site with 80% accuracy. Its ability to stratify risk of UC flare was on par with human pathologists.
“This tool in the near future will speed up, simplify, and standardize histological assessment of ulcerative colitis and provide the clinician with accurate prognostic information in real time,” co–lead author Marietta Iacucci, MD, PhD, from the University of Birmingham (England), and University College Cork (Ireland), said in an interview.
“The tool needs to be refined and further validated before it is ready for daily clinical practice. That work is ongoing now,” Dr. Iacucci said.
The researchers describe their advanced AI-based computer-aided detection tool in a study published online in Gastroenterology.
‘Strong’ performance
They used 535 digitized biopsies from 273 patients with UC (mean age, 48 years; 41% women) to develop and test the tool. They used a subset of 118 to train it to distinguish remission from activity, 42 to calibrate it, and 375 to test it. An additional 154 biopsies from 58 patients with UC were used to externally validate the tool.
The model also was tested to predict the corresponding endoscopic assessment and occurrence of flares at 12 months.
UC disease activity was defined by three different histologic indices: the Robarts Histopathology Index (RHI), the Nancy Histological Index (NHI), and the newly developed PICaSSO Histologic Remission Index (PHRI).
The AI tool had “strong diagnostic performance to detect disease activity” (PHRI > 0) with an overall area under the receiver operating characteristic curve of 0.87 and sensitivity and specificity of 89% and 85%, respectively.
The researchers note that, while the AI tool was trained for the PHRI, its sensitivity for RHI and NHI histologic remission/activity was also high (94% and 89%, respectively).
Despite the different mix of severity grades, the AI model “maintained a good diagnostic performance, proving its applicability outside the original development setting,” they reported.
The AI tool could also predict the presence of endoscopic inflammation in the biopsy area with about 80% accuracy.
“Though imperfect, this result is consistent with human-assessed correlation between endoscopy and histology,” the researchers noted.
The model predicted the corresponding endoscopic remission/activity with 79% and 82% accuracy for UCEIS and PICaSSO, respectively.
The hazard ratios for disease flare-up between the AI system and pathologists assessed by PHRI was similar (4.64 and 3.56, respectively), “demonstrating the ability of the computer to stratify the risk of flare comparably well to pathologists,” they added.
Both histology and outcome prediction were confirmed in the external validation cohort.
The AI system delivered results in an average of 9.8 seconds per slide.
Potential ‘game changer’
UC is a “complex condition to predict, and developing machine learning–derived systems to make this diagnostic job quicker and more accurate could be a game changer,” Dr. Iacucci said in a news release.
With refinement, the AI tool will have an impact on both clinical trials and daily practice, the researchers wrote. In clinical practice, histological reporting remains “largely descriptive and nonstandard, thus would greatly benefit from a quick and objective assessment. Similarly, clinical trials in UC could efficiently overcome costly central readings.”
Assessing and measuring improvement in endoscopy and histology are difficult parts of treating UC, said David Hudesman, MD, codirector of the Inflammatory Bowel Disease Center at New York University Langone Health.
“We do not know how much improvement is associated with improved long-term outcomes,” Dr. Hudesman said in an interview. “For example, does a patient need complete healing or is 50% better enough?” Dr. Hudesman was not involved with the current research.
“This study showed that AI can predict – with good accuracy – endoscopy and histology scores, as well as 1-year patient outcomes. If this is validated in larger studies, AI can help determine if we should adjust/change therapies or continue, which is very important,” he said.
This research was supported by the National Institute for Health Research Birmingham Biomedical Research Centre. Dr. Iacucci and Dr. Hudesman reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM GASTROENTEROLOGY
FDA OKs first drug for Rett syndrome
Rett syndrome is a rare, genetic neurodevelopmental disorder that affects about 6,000-9,000 people in the United States, mostly females.
Symptoms typically present between 6 and 18 months of age, with patients experiencing a rapid decline with loss of fine motor and communication skills.
Trofinetide is a synthetic analogue of the amino-terminal tripeptide of insulinlike growth factor-1 (IGF-1), which occurs naturally in the brain. The drug is designed to treat the core symptoms of Rett syndrome by potentially reducing neuroinflammation and supporting synaptic function.
The approval of trofinetide was supported by results from the pivotal phase 3 LAVENDER study that tested the efficacy and safety of trofinetide vs. placebo in 187 female patients with Rett syndrome, aged 5-20 years.
A total of 93 participants were randomly assigned to twice-daily oral trofinetide, and 94 received placebo for 12 weeks.
After 12 weeks, trofinetide showed a statistically significant improvement from baseline, compared with placebo, on both the caregiver-assessed Rett Syndrome Behavior Questionnaire (RSBQ) and 7-point Clinical Global Impression-Improvement (CGI-I) scale.
The drug also outperformed placebo at 12 weeks in a key secondary endpoint: the composite score on the Communication and Symbolic Behavior Scales Developmental Profile Infant-Toddler Checklist-Social (CSBS-DP-IT Social), a scale on which caregivers assess nonverbal communication.
The most common adverse events with trofinetide treatment were diarrhea and vomiting. Almost all these events were considered mild or moderate.
‘Historic day’
“This is a historic day for the Rett syndrome community and a meaningful moment for the patients and caregivers who have eagerly awaited the arrival of an approved treatment for this condition,” Melissa Kennedy, MHA, chief executive officer of the International Rett Syndrome Foundation, said in a news release issued by Acadia.
“Rett syndrome is a complicated, devastating disease that affects not only the individual patient, but whole families. With today’s FDA decision, those impacted by Rett have a promising new treatment option that has demonstrated benefit across a variety of Rett symptoms, including those that impact the daily lives of those living with Rett and their loved ones,” Ms. Kennedy said.
Trofinetide is expected to be available in the United States by the end of April.
A version of this article first appeared on Medscape.com.
Rett syndrome is a rare, genetic neurodevelopmental disorder that affects about 6,000-9,000 people in the United States, mostly females.
Symptoms typically present between 6 and 18 months of age, with patients experiencing a rapid decline with loss of fine motor and communication skills.
Trofinetide is a synthetic analogue of the amino-terminal tripeptide of insulinlike growth factor-1 (IGF-1), which occurs naturally in the brain. The drug is designed to treat the core symptoms of Rett syndrome by potentially reducing neuroinflammation and supporting synaptic function.
The approval of trofinetide was supported by results from the pivotal phase 3 LAVENDER study that tested the efficacy and safety of trofinetide vs. placebo in 187 female patients with Rett syndrome, aged 5-20 years.
A total of 93 participants were randomly assigned to twice-daily oral trofinetide, and 94 received placebo for 12 weeks.
After 12 weeks, trofinetide showed a statistically significant improvement from baseline, compared with placebo, on both the caregiver-assessed Rett Syndrome Behavior Questionnaire (RSBQ) and 7-point Clinical Global Impression-Improvement (CGI-I) scale.
The drug also outperformed placebo at 12 weeks in a key secondary endpoint: the composite score on the Communication and Symbolic Behavior Scales Developmental Profile Infant-Toddler Checklist-Social (CSBS-DP-IT Social), a scale on which caregivers assess nonverbal communication.
The most common adverse events with trofinetide treatment were diarrhea and vomiting. Almost all these events were considered mild or moderate.
‘Historic day’
“This is a historic day for the Rett syndrome community and a meaningful moment for the patients and caregivers who have eagerly awaited the arrival of an approved treatment for this condition,” Melissa Kennedy, MHA, chief executive officer of the International Rett Syndrome Foundation, said in a news release issued by Acadia.
“Rett syndrome is a complicated, devastating disease that affects not only the individual patient, but whole families. With today’s FDA decision, those impacted by Rett have a promising new treatment option that has demonstrated benefit across a variety of Rett symptoms, including those that impact the daily lives of those living with Rett and their loved ones,” Ms. Kennedy said.
Trofinetide is expected to be available in the United States by the end of April.
A version of this article first appeared on Medscape.com.
Rett syndrome is a rare, genetic neurodevelopmental disorder that affects about 6,000-9,000 people in the United States, mostly females.
Symptoms typically present between 6 and 18 months of age, with patients experiencing a rapid decline with loss of fine motor and communication skills.
Trofinetide is a synthetic analogue of the amino-terminal tripeptide of insulinlike growth factor-1 (IGF-1), which occurs naturally in the brain. The drug is designed to treat the core symptoms of Rett syndrome by potentially reducing neuroinflammation and supporting synaptic function.
The approval of trofinetide was supported by results from the pivotal phase 3 LAVENDER study that tested the efficacy and safety of trofinetide vs. placebo in 187 female patients with Rett syndrome, aged 5-20 years.
A total of 93 participants were randomly assigned to twice-daily oral trofinetide, and 94 received placebo for 12 weeks.
After 12 weeks, trofinetide showed a statistically significant improvement from baseline, compared with placebo, on both the caregiver-assessed Rett Syndrome Behavior Questionnaire (RSBQ) and 7-point Clinical Global Impression-Improvement (CGI-I) scale.
The drug also outperformed placebo at 12 weeks in a key secondary endpoint: the composite score on the Communication and Symbolic Behavior Scales Developmental Profile Infant-Toddler Checklist-Social (CSBS-DP-IT Social), a scale on which caregivers assess nonverbal communication.
The most common adverse events with trofinetide treatment were diarrhea and vomiting. Almost all these events were considered mild or moderate.
‘Historic day’
“This is a historic day for the Rett syndrome community and a meaningful moment for the patients and caregivers who have eagerly awaited the arrival of an approved treatment for this condition,” Melissa Kennedy, MHA, chief executive officer of the International Rett Syndrome Foundation, said in a news release issued by Acadia.
“Rett syndrome is a complicated, devastating disease that affects not only the individual patient, but whole families. With today’s FDA decision, those impacted by Rett have a promising new treatment option that has demonstrated benefit across a variety of Rett symptoms, including those that impact the daily lives of those living with Rett and their loved ones,” Ms. Kennedy said.
Trofinetide is expected to be available in the United States by the end of April.
A version of this article first appeared on Medscape.com.
Two diets tied to lower Alzheimer’s pathology at autopsy
In a cohort of deceased older adults, those who had adhered to the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) and Mediterranean diets for nearly a decade before death had less global Alzheimer’s disease–related pathology, primarily less beta-amyloid, at autopsy.
Those who most closely followed these diets had almost 40% lower odds of having an Alzheimer’s disease diagnosis at death. The findings offer one mechanism by which healthy diets protect cognition.
“While our research doesn’t prove that a healthy diet resulted in fewer brain deposits of amyloid plaques ... we know there is a relationship, and following the MIND and Mediterranean diets may be one way that people can improve their brain health and protect cognition as they age,” study investigator Puja Agarwal, PhD, of RUSH University Medical Center in Chicago, said in a statement.
The study was published online in Neurology.
Green leafy veggies key
The MIND diet was pioneered by the late Martha Clare Morris, ScD, a Rush nutritional epidemiologist, who died of cancer in 2020 at age 64.
Although similar, the Mediterranean diet recommends vegetables, fruit, and three or more servings of fish per week, whereas the MIND diet prioritizes green leafy vegetables, such as spinach, kale, and collard greens, along with other vegetables. The MIND diet also prioritizes berries over other fruit and recommends one or more servings of fish per week. Both diets recommend small amounts of wine.
The current study focused on 581 older adults who died while participating in the Rush Memory and Aging Project (MAP). All participants agreed to undergo annual clinical evaluations and brain autopsy after death.
Participants completed annual food frequency questionnaires beginning at a mean age of 84. The mean age at death was 91. Mean follow-up was 6.8 years.
Around the time of death, 224 participants (39%) had a diagnosis of clinical dementia, and 383 participants (66%) had a pathologic Alzheimer’s disease diagnosis at time of death.
The researchers used a series of regression analyses to investigate the MIND and Mediterranean diets and dietary components associated with Alzheimer’s disease pathology. They controlled for age at death, sex, education, APO-epsilon 4 status, and total calories.
Overall, both diets were significantly associated with lower global Alzheimer’s disease pathology (MIND: beta = –0.022, P = .034; and Mediterranean: beta = –0.007, P = .039) – specifically, with less beta-amyloid (MIND: beta = –0.068, P = .050; and Mediterranean: beta = –0.040, P = .004).
The findings persisted when the analysis was further adjusted for physical activity, smoking, and vascular disease burden and when participants with mild cognitive impairment or dementia at the baseline dietary assessment were excluded.
Individuals who most closely followed the Mediterranean diet had average beta-amyloid load similar to being 18 years younger than peers with the lowest adherence. And those who most closely followed the MIND diet had average beta-amyloid amounts similar to being 12 years younger than those with the lowest adherence.
A MIND diet score 1 point higher corresponded to typical plaque deposition of participants who are 4.25 years younger in age.
Regarding individual dietary components, those who ate seven or more servings of green leafy vegetables weekly had less global Alzheimer’s disease pathology than peers who ate one or fewer (beta = –0.115, P = .0038). Those who ate seven or more servings per week had plaque amounts in their brains corresponding to being almost 19 years younger in comparison with those who ate the fewest servings per week.
“Our finding that eating more green leafy vegetables is in itself associated with fewer signs of Alzheimer’s disease in the brain is intriguing enough for people to consider adding more of these vegetables to their diet,” Dr. Agarwal said in the news release.
Previous data from the MAP cohort showed that adherence to the MIND diet can improve memory and thinking skills of older adults, even in the presence of Alzheimer’s disease pathology.
Novel study, intriguing results
Heather Snyder, PhD, vice president of medical and scientific relations with the Alzheimer’s Association, noted that a number of studies have linked overall nutrition – especially a balanced diet low in saturated fats and sugar and high in vegetables – with brain health, including cognition, as one ages.
This new study “takes what we know about the link between nutrition and risk for cognitive decline a step further by looking at the specific brain changes that occur in Alzheimer’s disease. The study found an association of certain nutrition behaviors with less of these Alzheimer’s brain changes,” said Dr. Snyder, who was not involved in the study.
“This is intriguing, and more research is needed to test via an intervention if healthy dietary behaviors can modify the presence of Alzheimer’s brain changes and reduce risk of cognitive decline.”
The Alzheimer’s Association is leading a 2-year clinical trial known as US POINTER to study how targeting known dementia risk factors in combination may reduce risk of cognitive decline in older adults. The MIND diet is being used in US POINTER.
“But while we work to find an exact ‘recipe’ for risk reduction, it’s important to eat a heart-healthy diet that incorporates nutrients that our bodies and brains need to be at their best,” Dr. Snyder said.
The study was funded by the National Institutes of Health. Dr. Agarwal and Dr. Snyder have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
In a cohort of deceased older adults, those who had adhered to the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) and Mediterranean diets for nearly a decade before death had less global Alzheimer’s disease–related pathology, primarily less beta-amyloid, at autopsy.
Those who most closely followed these diets had almost 40% lower odds of having an Alzheimer’s disease diagnosis at death. The findings offer one mechanism by which healthy diets protect cognition.
“While our research doesn’t prove that a healthy diet resulted in fewer brain deposits of amyloid plaques ... we know there is a relationship, and following the MIND and Mediterranean diets may be one way that people can improve their brain health and protect cognition as they age,” study investigator Puja Agarwal, PhD, of RUSH University Medical Center in Chicago, said in a statement.
The study was published online in Neurology.
Green leafy veggies key
The MIND diet was pioneered by the late Martha Clare Morris, ScD, a Rush nutritional epidemiologist, who died of cancer in 2020 at age 64.
Although similar, the Mediterranean diet recommends vegetables, fruit, and three or more servings of fish per week, whereas the MIND diet prioritizes green leafy vegetables, such as spinach, kale, and collard greens, along with other vegetables. The MIND diet also prioritizes berries over other fruit and recommends one or more servings of fish per week. Both diets recommend small amounts of wine.
The current study focused on 581 older adults who died while participating in the Rush Memory and Aging Project (MAP). All participants agreed to undergo annual clinical evaluations and brain autopsy after death.
Participants completed annual food frequency questionnaires beginning at a mean age of 84. The mean age at death was 91. Mean follow-up was 6.8 years.
Around the time of death, 224 participants (39%) had a diagnosis of clinical dementia, and 383 participants (66%) had a pathologic Alzheimer’s disease diagnosis at time of death.
The researchers used a series of regression analyses to investigate the MIND and Mediterranean diets and dietary components associated with Alzheimer’s disease pathology. They controlled for age at death, sex, education, APO-epsilon 4 status, and total calories.
Overall, both diets were significantly associated with lower global Alzheimer’s disease pathology (MIND: beta = –0.022, P = .034; and Mediterranean: beta = –0.007, P = .039) – specifically, with less beta-amyloid (MIND: beta = –0.068, P = .050; and Mediterranean: beta = –0.040, P = .004).
The findings persisted when the analysis was further adjusted for physical activity, smoking, and vascular disease burden and when participants with mild cognitive impairment or dementia at the baseline dietary assessment were excluded.
Individuals who most closely followed the Mediterranean diet had average beta-amyloid load similar to being 18 years younger than peers with the lowest adherence. And those who most closely followed the MIND diet had average beta-amyloid amounts similar to being 12 years younger than those with the lowest adherence.
A MIND diet score 1 point higher corresponded to typical plaque deposition of participants who are 4.25 years younger in age.
Regarding individual dietary components, those who ate seven or more servings of green leafy vegetables weekly had less global Alzheimer’s disease pathology than peers who ate one or fewer (beta = –0.115, P = .0038). Those who ate seven or more servings per week had plaque amounts in their brains corresponding to being almost 19 years younger in comparison with those who ate the fewest servings per week.
“Our finding that eating more green leafy vegetables is in itself associated with fewer signs of Alzheimer’s disease in the brain is intriguing enough for people to consider adding more of these vegetables to their diet,” Dr. Agarwal said in the news release.
Previous data from the MAP cohort showed that adherence to the MIND diet can improve memory and thinking skills of older adults, even in the presence of Alzheimer’s disease pathology.
Novel study, intriguing results
Heather Snyder, PhD, vice president of medical and scientific relations with the Alzheimer’s Association, noted that a number of studies have linked overall nutrition – especially a balanced diet low in saturated fats and sugar and high in vegetables – with brain health, including cognition, as one ages.
This new study “takes what we know about the link between nutrition and risk for cognitive decline a step further by looking at the specific brain changes that occur in Alzheimer’s disease. The study found an association of certain nutrition behaviors with less of these Alzheimer’s brain changes,” said Dr. Snyder, who was not involved in the study.
“This is intriguing, and more research is needed to test via an intervention if healthy dietary behaviors can modify the presence of Alzheimer’s brain changes and reduce risk of cognitive decline.”
The Alzheimer’s Association is leading a 2-year clinical trial known as US POINTER to study how targeting known dementia risk factors in combination may reduce risk of cognitive decline in older adults. The MIND diet is being used in US POINTER.
“But while we work to find an exact ‘recipe’ for risk reduction, it’s important to eat a heart-healthy diet that incorporates nutrients that our bodies and brains need to be at their best,” Dr. Snyder said.
The study was funded by the National Institutes of Health. Dr. Agarwal and Dr. Snyder have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
In a cohort of deceased older adults, those who had adhered to the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) and Mediterranean diets for nearly a decade before death had less global Alzheimer’s disease–related pathology, primarily less beta-amyloid, at autopsy.
Those who most closely followed these diets had almost 40% lower odds of having an Alzheimer’s disease diagnosis at death. The findings offer one mechanism by which healthy diets protect cognition.
“While our research doesn’t prove that a healthy diet resulted in fewer brain deposits of amyloid plaques ... we know there is a relationship, and following the MIND and Mediterranean diets may be one way that people can improve their brain health and protect cognition as they age,” study investigator Puja Agarwal, PhD, of RUSH University Medical Center in Chicago, said in a statement.
The study was published online in Neurology.
Green leafy veggies key
The MIND diet was pioneered by the late Martha Clare Morris, ScD, a Rush nutritional epidemiologist, who died of cancer in 2020 at age 64.
Although similar, the Mediterranean diet recommends vegetables, fruit, and three or more servings of fish per week, whereas the MIND diet prioritizes green leafy vegetables, such as spinach, kale, and collard greens, along with other vegetables. The MIND diet also prioritizes berries over other fruit and recommends one or more servings of fish per week. Both diets recommend small amounts of wine.
The current study focused on 581 older adults who died while participating in the Rush Memory and Aging Project (MAP). All participants agreed to undergo annual clinical evaluations and brain autopsy after death.
Participants completed annual food frequency questionnaires beginning at a mean age of 84. The mean age at death was 91. Mean follow-up was 6.8 years.
Around the time of death, 224 participants (39%) had a diagnosis of clinical dementia, and 383 participants (66%) had a pathologic Alzheimer’s disease diagnosis at time of death.
The researchers used a series of regression analyses to investigate the MIND and Mediterranean diets and dietary components associated with Alzheimer’s disease pathology. They controlled for age at death, sex, education, APO-epsilon 4 status, and total calories.
Overall, both diets were significantly associated with lower global Alzheimer’s disease pathology (MIND: beta = –0.022, P = .034; and Mediterranean: beta = –0.007, P = .039) – specifically, with less beta-amyloid (MIND: beta = –0.068, P = .050; and Mediterranean: beta = –0.040, P = .004).
The findings persisted when the analysis was further adjusted for physical activity, smoking, and vascular disease burden and when participants with mild cognitive impairment or dementia at the baseline dietary assessment were excluded.
Individuals who most closely followed the Mediterranean diet had average beta-amyloid load similar to being 18 years younger than peers with the lowest adherence. And those who most closely followed the MIND diet had average beta-amyloid amounts similar to being 12 years younger than those with the lowest adherence.
A MIND diet score 1 point higher corresponded to typical plaque deposition of participants who are 4.25 years younger in age.
Regarding individual dietary components, those who ate seven or more servings of green leafy vegetables weekly had less global Alzheimer’s disease pathology than peers who ate one or fewer (beta = –0.115, P = .0038). Those who ate seven or more servings per week had plaque amounts in their brains corresponding to being almost 19 years younger in comparison with those who ate the fewest servings per week.
“Our finding that eating more green leafy vegetables is in itself associated with fewer signs of Alzheimer’s disease in the brain is intriguing enough for people to consider adding more of these vegetables to their diet,” Dr. Agarwal said in the news release.
Previous data from the MAP cohort showed that adherence to the MIND diet can improve memory and thinking skills of older adults, even in the presence of Alzheimer’s disease pathology.
Novel study, intriguing results
Heather Snyder, PhD, vice president of medical and scientific relations with the Alzheimer’s Association, noted that a number of studies have linked overall nutrition – especially a balanced diet low in saturated fats and sugar and high in vegetables – with brain health, including cognition, as one ages.
This new study “takes what we know about the link between nutrition and risk for cognitive decline a step further by looking at the specific brain changes that occur in Alzheimer’s disease. The study found an association of certain nutrition behaviors with less of these Alzheimer’s brain changes,” said Dr. Snyder, who was not involved in the study.
“This is intriguing, and more research is needed to test via an intervention if healthy dietary behaviors can modify the presence of Alzheimer’s brain changes and reduce risk of cognitive decline.”
The Alzheimer’s Association is leading a 2-year clinical trial known as US POINTER to study how targeting known dementia risk factors in combination may reduce risk of cognitive decline in older adults. The MIND diet is being used in US POINTER.
“But while we work to find an exact ‘recipe’ for risk reduction, it’s important to eat a heart-healthy diet that incorporates nutrients that our bodies and brains need to be at their best,” Dr. Snyder said.
The study was funded by the National Institutes of Health. Dr. Agarwal and Dr. Snyder have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM NEUROLOGY
Breast cancer surgery timing matters, but is faster always better?
according to findings from a case series.
With no national quality metrics delineating optimal breast cancer surgery timing, the researchers recommend surgery before 8 weeks from breast cancer diagnosis.
“This time interval does not appear to have a detrimental association with cancer outcomes and allows for multidisciplinary care,” the researchers, led by Alyssa A. Wiener, MD, from University of Wisconsin–Madison, said.
But, in an accompanying editorial, two surgical oncologists questioned whether faster surgery is always better.
“Efficiency might associate with quality, but doesn’t always ensure it,” Rita Mukhtar, MD, and Laura Esserman, MD, with the division of surgical oncology, University of California, San Francisco, said.
The study and editorial were published online in JAMA Surgery.
Optimal timing for surgery?
Some studies have found worse survival outcomes for women who experience delays between breast cancer diagnosis and surgical treatment, but the optimal window for surgery and the point at which surgery becomes less advantageous remain unknown.
Using the National Cancer Database, Dr. Wiener and colleagues identified 373,334 women (median age, 61) who were diagnosed with stage I to stage III ductal or lobular breast cancer from 2010 to 2014 and followed up through 2019.
All women underwent surgery as their first course of treatment. Patients with prior breast cancer, those who had neoadjuvant or experimental therapy or missing receptor information, and those who were diagnosed with breast cancer on the date of their primary surgery were excluded.
Most patients had timely surgery. The median time to surgery was 30 days, and 88% of patients underwent surgery before the 57-day time point.
Only 12% of patients had surgery more than 8 weeks after their diagnosis. Factors associated with longer times to surgery included age younger than 45, having Medicaid or no insurance, and lower household income.
The overall 5-year survival for the cohort was high at 90%. On multivariable analysis, the researchers found no statistically significant association between time to surgery and overall survival when surgery was performed between 0 and 8 weeks.
However, women who had surgery 9 or more weeks after diagnosis had a significantly higher rate of death within 5 years, compared with those who had surgery performed between 0 and 4 weeks (hazard ratio, 1.15; P < .001). Performing surgery up to 9 weeks (57-63 days) post diagnosis also did not appear to be negatively associated with survival.
This study “highlights that time to treatment of breast cancer is important,” said Sarah P. Cate, MD, director, Breast Surgery Quality Program, Mount Sinai Health System, New York, who wasn’t involved in the study. “Surgery is only one-third of the treatment of breast cancer, so these patients who had longer delays to the OR may have also not started their postsurgery treatments in time.”
In addition, the study found that socioeconomic status – Medicaid or uninsured status and lower household incomes – was associated with longer times to surgery.
“Socioeconomic factors like these may be independently associated with worse outcomes and may contribute to some of the disparities in cancer outcomes observed for resource-limited patients due to delayed care,” the authors said.
Identifying 8 weeks as a goal for time to surgery can help uncover delays associated with socioeconomic factors and provide adequate time for decision-making, the researchers noted.
Is faster always better?
Dr. Wiener and colleagues cautioned, however, that their findings should be considered “hypothesis generating,” given that decision-making surrounding breast cancer surgery is complex.
Importantly, the authors noted, tumor characteristics, such as tumor size, nodal status, and receptor subtype, appeared to have a pronounced impact on overall survival, compared with timing of surgery. For instance, compared with a tumor size of 2 cm or fewer, larger tumors – those > 2 cm to ≤ 5 cm and > 5 cm – were associated with worse survival (HR, 1.80 and 2.62, respectively).
“This highlights that tumor biology is the primary driver of patients’ breast cancer outcomes,” the authors noted.
In an accompanying editorial, two surgical oncologists highlighted that faster may not always be better.
For instance, Dr. Mukhtar and Dr. Esserman explained, if a patient with a large node-positive, triple-negative breast cancer receives surgery within a week of diagnosis, “one must question whether this timely care represents quality care, as the opportunity to understand tumor response and affect breast cancer survival has been lost.”
The editorialists noted that time to surgery might also matter very little for indolent, screen-detected cancers, and time to treatment start might matter a lot for fast-growing, interval cancers.
In addition, they questioned whether including the socioeconomic factors highlighted in the overall model would “mitigate the association between time to surgery and survival seen in this study.”
Overall, “operating too soon could indicate lack of quality, while operating too late perhaps reflects lack of access to care,” the editorialists said.
This study was supported by grants from the National Cancer Institute and the National Institutes of Health. Dr. Wiener and Dr. Cate report no relevant financial relationships. Dr. Esserman is a member of the Blue Cross Medical advisory panel, is a board member of the Quantum Leap Healthcare Collaborative, and leads an investigator-initiated vaccine trial for high-risk ductal carcinoma in situ, which is funded by Merck.
A version of this article first appeared on Medscape.com.
according to findings from a case series.
With no national quality metrics delineating optimal breast cancer surgery timing, the researchers recommend surgery before 8 weeks from breast cancer diagnosis.
“This time interval does not appear to have a detrimental association with cancer outcomes and allows for multidisciplinary care,” the researchers, led by Alyssa A. Wiener, MD, from University of Wisconsin–Madison, said.
But, in an accompanying editorial, two surgical oncologists questioned whether faster surgery is always better.
“Efficiency might associate with quality, but doesn’t always ensure it,” Rita Mukhtar, MD, and Laura Esserman, MD, with the division of surgical oncology, University of California, San Francisco, said.
The study and editorial were published online in JAMA Surgery.
Optimal timing for surgery?
Some studies have found worse survival outcomes for women who experience delays between breast cancer diagnosis and surgical treatment, but the optimal window for surgery and the point at which surgery becomes less advantageous remain unknown.
Using the National Cancer Database, Dr. Wiener and colleagues identified 373,334 women (median age, 61) who were diagnosed with stage I to stage III ductal or lobular breast cancer from 2010 to 2014 and followed up through 2019.
All women underwent surgery as their first course of treatment. Patients with prior breast cancer, those who had neoadjuvant or experimental therapy or missing receptor information, and those who were diagnosed with breast cancer on the date of their primary surgery were excluded.
Most patients had timely surgery. The median time to surgery was 30 days, and 88% of patients underwent surgery before the 57-day time point.
Only 12% of patients had surgery more than 8 weeks after their diagnosis. Factors associated with longer times to surgery included age younger than 45, having Medicaid or no insurance, and lower household income.
The overall 5-year survival for the cohort was high at 90%. On multivariable analysis, the researchers found no statistically significant association between time to surgery and overall survival when surgery was performed between 0 and 8 weeks.
However, women who had surgery 9 or more weeks after diagnosis had a significantly higher rate of death within 5 years, compared with those who had surgery performed between 0 and 4 weeks (hazard ratio, 1.15; P < .001). Performing surgery up to 9 weeks (57-63 days) post diagnosis also did not appear to be negatively associated with survival.
This study “highlights that time to treatment of breast cancer is important,” said Sarah P. Cate, MD, director, Breast Surgery Quality Program, Mount Sinai Health System, New York, who wasn’t involved in the study. “Surgery is only one-third of the treatment of breast cancer, so these patients who had longer delays to the OR may have also not started their postsurgery treatments in time.”
In addition, the study found that socioeconomic status – Medicaid or uninsured status and lower household incomes – was associated with longer times to surgery.
“Socioeconomic factors like these may be independently associated with worse outcomes and may contribute to some of the disparities in cancer outcomes observed for resource-limited patients due to delayed care,” the authors said.
Identifying 8 weeks as a goal for time to surgery can help uncover delays associated with socioeconomic factors and provide adequate time for decision-making, the researchers noted.
Is faster always better?
Dr. Wiener and colleagues cautioned, however, that their findings should be considered “hypothesis generating,” given that decision-making surrounding breast cancer surgery is complex.
Importantly, the authors noted, tumor characteristics, such as tumor size, nodal status, and receptor subtype, appeared to have a pronounced impact on overall survival, compared with timing of surgery. For instance, compared with a tumor size of 2 cm or fewer, larger tumors – those > 2 cm to ≤ 5 cm and > 5 cm – were associated with worse survival (HR, 1.80 and 2.62, respectively).
“This highlights that tumor biology is the primary driver of patients’ breast cancer outcomes,” the authors noted.
In an accompanying editorial, two surgical oncologists highlighted that faster may not always be better.
For instance, Dr. Mukhtar and Dr. Esserman explained, if a patient with a large node-positive, triple-negative breast cancer receives surgery within a week of diagnosis, “one must question whether this timely care represents quality care, as the opportunity to understand tumor response and affect breast cancer survival has been lost.”
The editorialists noted that time to surgery might also matter very little for indolent, screen-detected cancers, and time to treatment start might matter a lot for fast-growing, interval cancers.
In addition, they questioned whether including the socioeconomic factors highlighted in the overall model would “mitigate the association between time to surgery and survival seen in this study.”
Overall, “operating too soon could indicate lack of quality, while operating too late perhaps reflects lack of access to care,” the editorialists said.
This study was supported by grants from the National Cancer Institute and the National Institutes of Health. Dr. Wiener and Dr. Cate report no relevant financial relationships. Dr. Esserman is a member of the Blue Cross Medical advisory panel, is a board member of the Quantum Leap Healthcare Collaborative, and leads an investigator-initiated vaccine trial for high-risk ductal carcinoma in situ, which is funded by Merck.
A version of this article first appeared on Medscape.com.
according to findings from a case series.
With no national quality metrics delineating optimal breast cancer surgery timing, the researchers recommend surgery before 8 weeks from breast cancer diagnosis.
“This time interval does not appear to have a detrimental association with cancer outcomes and allows for multidisciplinary care,” the researchers, led by Alyssa A. Wiener, MD, from University of Wisconsin–Madison, said.
But, in an accompanying editorial, two surgical oncologists questioned whether faster surgery is always better.
“Efficiency might associate with quality, but doesn’t always ensure it,” Rita Mukhtar, MD, and Laura Esserman, MD, with the division of surgical oncology, University of California, San Francisco, said.
The study and editorial were published online in JAMA Surgery.
Optimal timing for surgery?
Some studies have found worse survival outcomes for women who experience delays between breast cancer diagnosis and surgical treatment, but the optimal window for surgery and the point at which surgery becomes less advantageous remain unknown.
Using the National Cancer Database, Dr. Wiener and colleagues identified 373,334 women (median age, 61) who were diagnosed with stage I to stage III ductal or lobular breast cancer from 2010 to 2014 and followed up through 2019.
All women underwent surgery as their first course of treatment. Patients with prior breast cancer, those who had neoadjuvant or experimental therapy or missing receptor information, and those who were diagnosed with breast cancer on the date of their primary surgery were excluded.
Most patients had timely surgery. The median time to surgery was 30 days, and 88% of patients underwent surgery before the 57-day time point.
Only 12% of patients had surgery more than 8 weeks after their diagnosis. Factors associated with longer times to surgery included age younger than 45, having Medicaid or no insurance, and lower household income.
The overall 5-year survival for the cohort was high at 90%. On multivariable analysis, the researchers found no statistically significant association between time to surgery and overall survival when surgery was performed between 0 and 8 weeks.
However, women who had surgery 9 or more weeks after diagnosis had a significantly higher rate of death within 5 years, compared with those who had surgery performed between 0 and 4 weeks (hazard ratio, 1.15; P < .001). Performing surgery up to 9 weeks (57-63 days) post diagnosis also did not appear to be negatively associated with survival.
This study “highlights that time to treatment of breast cancer is important,” said Sarah P. Cate, MD, director, Breast Surgery Quality Program, Mount Sinai Health System, New York, who wasn’t involved in the study. “Surgery is only one-third of the treatment of breast cancer, so these patients who had longer delays to the OR may have also not started their postsurgery treatments in time.”
In addition, the study found that socioeconomic status – Medicaid or uninsured status and lower household incomes – was associated with longer times to surgery.
“Socioeconomic factors like these may be independently associated with worse outcomes and may contribute to some of the disparities in cancer outcomes observed for resource-limited patients due to delayed care,” the authors said.
Identifying 8 weeks as a goal for time to surgery can help uncover delays associated with socioeconomic factors and provide adequate time for decision-making, the researchers noted.
Is faster always better?
Dr. Wiener and colleagues cautioned, however, that their findings should be considered “hypothesis generating,” given that decision-making surrounding breast cancer surgery is complex.
Importantly, the authors noted, tumor characteristics, such as tumor size, nodal status, and receptor subtype, appeared to have a pronounced impact on overall survival, compared with timing of surgery. For instance, compared with a tumor size of 2 cm or fewer, larger tumors – those > 2 cm to ≤ 5 cm and > 5 cm – were associated with worse survival (HR, 1.80 and 2.62, respectively).
“This highlights that tumor biology is the primary driver of patients’ breast cancer outcomes,” the authors noted.
In an accompanying editorial, two surgical oncologists highlighted that faster may not always be better.
For instance, Dr. Mukhtar and Dr. Esserman explained, if a patient with a large node-positive, triple-negative breast cancer receives surgery within a week of diagnosis, “one must question whether this timely care represents quality care, as the opportunity to understand tumor response and affect breast cancer survival has been lost.”
The editorialists noted that time to surgery might also matter very little for indolent, screen-detected cancers, and time to treatment start might matter a lot for fast-growing, interval cancers.
In addition, they questioned whether including the socioeconomic factors highlighted in the overall model would “mitigate the association between time to surgery and survival seen in this study.”
Overall, “operating too soon could indicate lack of quality, while operating too late perhaps reflects lack of access to care,” the editorialists said.
This study was supported by grants from the National Cancer Institute and the National Institutes of Health. Dr. Wiener and Dr. Cate report no relevant financial relationships. Dr. Esserman is a member of the Blue Cross Medical advisory panel, is a board member of the Quantum Leap Healthcare Collaborative, and leads an investigator-initiated vaccine trial for high-risk ductal carcinoma in situ, which is funded by Merck.
A version of this article first appeared on Medscape.com.
FROM JAMA SURGERY
Black people are less likely to receive dementia meds
, preliminary data from a retrospective study show.
“There have been disparities regarding the use of cognition-enhancing medications in the treatment of dementia described in the literature, and disparities in the use of adjunctive treatments for other neuropsychiatric symptoms of dementia described in hospital and nursing home settings,” said study investigator Alice Hawkins, MD, with the department of neurology, Icahn School of Medicine at Mount Sinai, New York. “However, less is known about use of dementia medications that people take at home. Our study found disparities in this area as well,” Dr. Hawkins said.
The findings were released ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology.
More research needed
The researchers analyzed data on 3,655 Black and 12,885 White patients with a diagnosis of dementia who were seen at Mount Sinai. They evaluated utilization of five medication classes:
- cholinesterase inhibitors.
- N-methyl D-aspartate (NMDA) receptor antagonists.
- selective serotonin reuptake inhibitors (SSRIs).
- antipsychotics.
- benzodiazepines.
They found that Black patients with dementia received cognitive enhancers less often than White patients with dementia (20% vs. 30% for cholinesterase inhibitors; 10% vs. 17% for NMDA antagonists).
Black patients with dementia were also less likely to receive medications for behavioral and psychological symptom management, compared with White peers (24% vs. 40% for SSRIs; 18% vs. 22% for antipsychotics; and 18% vs. 37% for benzodiazepines).
These disparities remained even after controlling for factors such as demographics and insurance coverage.
“Larger systemic forces such as systemic racism, quality of care, and provider bias are harder to pin down, particularly in the medical record, though they all may be playing a role in perpetuating these inequities. More research will be needed to pinpoint all the factors that are contributing to these disparities,” said Dr. Hawkins.
The researchers found Black patients who were referred to a neurologist received cholinesterase inhibitors and NMDA antagonists at rates comparable with White patients. “Therefore, referrals to specialists such as neurologists may decrease the disparities for these prescriptions,” Dr. Hawkins said.
Crucial research
Commenting on the findings, Carl V. Hill, PhD, MPH, Alzheimer’s Association chief diversity, equity, and inclusion officer, said the study “adds to previous research that points to inequities in the administering of medications for dementia symptoms, and highlights the inequities we know exist in dementia care.”
“Cognitive enhancers and other behavioral/psychological management drugs, while they don’t stop, slow, or cure dementia, can offer relief for some of the challenging symptoms associated with diseases caused by dementia. If people aren’t being appropriately prescribed medications that may offer symptom relief from this challenging disease, it could lead to poorer health outcomes,” said Dr. Hill.
“These data underscore the importance of health disparities research that is crucial in uncovering inequities in dementia treatment, care, and research for Black individuals, as well as all underrepresented populations.
“We must create a society in which the underserved, disproportionately affected, and underrepresented are safe, cared for, and valued. This can be done through enhancing cultural competence in health care settings, improving representation within the health care system, and engaging and building trust with diverse communities,” Dr. Hill said.
The Alzheimer’s Association has partnered with more than 500 diverse community-based groups on disease education programs to ensure families have information and resources to navigate this devastating disease.
The study was supported by the American Academy of Neurology Resident Research Scholarship. Dr. Hawkins and Dr. Hill reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, preliminary data from a retrospective study show.
“There have been disparities regarding the use of cognition-enhancing medications in the treatment of dementia described in the literature, and disparities in the use of adjunctive treatments for other neuropsychiatric symptoms of dementia described in hospital and nursing home settings,” said study investigator Alice Hawkins, MD, with the department of neurology, Icahn School of Medicine at Mount Sinai, New York. “However, less is known about use of dementia medications that people take at home. Our study found disparities in this area as well,” Dr. Hawkins said.
The findings were released ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology.
More research needed
The researchers analyzed data on 3,655 Black and 12,885 White patients with a diagnosis of dementia who were seen at Mount Sinai. They evaluated utilization of five medication classes:
- cholinesterase inhibitors.
- N-methyl D-aspartate (NMDA) receptor antagonists.
- selective serotonin reuptake inhibitors (SSRIs).
- antipsychotics.
- benzodiazepines.
They found that Black patients with dementia received cognitive enhancers less often than White patients with dementia (20% vs. 30% for cholinesterase inhibitors; 10% vs. 17% for NMDA antagonists).
Black patients with dementia were also less likely to receive medications for behavioral and psychological symptom management, compared with White peers (24% vs. 40% for SSRIs; 18% vs. 22% for antipsychotics; and 18% vs. 37% for benzodiazepines).
These disparities remained even after controlling for factors such as demographics and insurance coverage.
“Larger systemic forces such as systemic racism, quality of care, and provider bias are harder to pin down, particularly in the medical record, though they all may be playing a role in perpetuating these inequities. More research will be needed to pinpoint all the factors that are contributing to these disparities,” said Dr. Hawkins.
The researchers found Black patients who were referred to a neurologist received cholinesterase inhibitors and NMDA antagonists at rates comparable with White patients. “Therefore, referrals to specialists such as neurologists may decrease the disparities for these prescriptions,” Dr. Hawkins said.
Crucial research
Commenting on the findings, Carl V. Hill, PhD, MPH, Alzheimer’s Association chief diversity, equity, and inclusion officer, said the study “adds to previous research that points to inequities in the administering of medications for dementia symptoms, and highlights the inequities we know exist in dementia care.”
“Cognitive enhancers and other behavioral/psychological management drugs, while they don’t stop, slow, or cure dementia, can offer relief for some of the challenging symptoms associated with diseases caused by dementia. If people aren’t being appropriately prescribed medications that may offer symptom relief from this challenging disease, it could lead to poorer health outcomes,” said Dr. Hill.
“These data underscore the importance of health disparities research that is crucial in uncovering inequities in dementia treatment, care, and research for Black individuals, as well as all underrepresented populations.
“We must create a society in which the underserved, disproportionately affected, and underrepresented are safe, cared for, and valued. This can be done through enhancing cultural competence in health care settings, improving representation within the health care system, and engaging and building trust with diverse communities,” Dr. Hill said.
The Alzheimer’s Association has partnered with more than 500 diverse community-based groups on disease education programs to ensure families have information and resources to navigate this devastating disease.
The study was supported by the American Academy of Neurology Resident Research Scholarship. Dr. Hawkins and Dr. Hill reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, preliminary data from a retrospective study show.
“There have been disparities regarding the use of cognition-enhancing medications in the treatment of dementia described in the literature, and disparities in the use of adjunctive treatments for other neuropsychiatric symptoms of dementia described in hospital and nursing home settings,” said study investigator Alice Hawkins, MD, with the department of neurology, Icahn School of Medicine at Mount Sinai, New York. “However, less is known about use of dementia medications that people take at home. Our study found disparities in this area as well,” Dr. Hawkins said.
The findings were released ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology.
More research needed
The researchers analyzed data on 3,655 Black and 12,885 White patients with a diagnosis of dementia who were seen at Mount Sinai. They evaluated utilization of five medication classes:
- cholinesterase inhibitors.
- N-methyl D-aspartate (NMDA) receptor antagonists.
- selective serotonin reuptake inhibitors (SSRIs).
- antipsychotics.
- benzodiazepines.
They found that Black patients with dementia received cognitive enhancers less often than White patients with dementia (20% vs. 30% for cholinesterase inhibitors; 10% vs. 17% for NMDA antagonists).
Black patients with dementia were also less likely to receive medications for behavioral and psychological symptom management, compared with White peers (24% vs. 40% for SSRIs; 18% vs. 22% for antipsychotics; and 18% vs. 37% for benzodiazepines).
These disparities remained even after controlling for factors such as demographics and insurance coverage.
“Larger systemic forces such as systemic racism, quality of care, and provider bias are harder to pin down, particularly in the medical record, though they all may be playing a role in perpetuating these inequities. More research will be needed to pinpoint all the factors that are contributing to these disparities,” said Dr. Hawkins.
The researchers found Black patients who were referred to a neurologist received cholinesterase inhibitors and NMDA antagonists at rates comparable with White patients. “Therefore, referrals to specialists such as neurologists may decrease the disparities for these prescriptions,” Dr. Hawkins said.
Crucial research
Commenting on the findings, Carl V. Hill, PhD, MPH, Alzheimer’s Association chief diversity, equity, and inclusion officer, said the study “adds to previous research that points to inequities in the administering of medications for dementia symptoms, and highlights the inequities we know exist in dementia care.”
“Cognitive enhancers and other behavioral/psychological management drugs, while they don’t stop, slow, or cure dementia, can offer relief for some of the challenging symptoms associated with diseases caused by dementia. If people aren’t being appropriately prescribed medications that may offer symptom relief from this challenging disease, it could lead to poorer health outcomes,” said Dr. Hill.
“These data underscore the importance of health disparities research that is crucial in uncovering inequities in dementia treatment, care, and research for Black individuals, as well as all underrepresented populations.
“We must create a society in which the underserved, disproportionately affected, and underrepresented are safe, cared for, and valued. This can be done through enhancing cultural competence in health care settings, improving representation within the health care system, and engaging and building trust with diverse communities,” Dr. Hill said.
The Alzheimer’s Association has partnered with more than 500 diverse community-based groups on disease education programs to ensure families have information and resources to navigate this devastating disease.
The study was supported by the American Academy of Neurology Resident Research Scholarship. Dr. Hawkins and Dr. Hill reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Childhood nightmares a prelude to cognitive problems, Parkinson’s?
new research shows.
Compared with children who never had distressing dreams between ages 7 and 11 years, those who had persistent distressing dreams were 76% more likely to develop cognitive impairment and roughly seven times more likely to develop PD by age 50 years.
It’s been shown previously that sleep problems in adulthood, including distressing dreams, can precede the onset of neurodegenerative diseases such as Alzheimer’s disease (AD) or PD by several years, and in some cases decades, study investigator Abidemi Otaiku, BMBS, University of Birmingham (England), told this news organization.
However, no studies have investigated whether distressing dreams during childhood might also be associated with increased risk for cognitive decline or PD.
“As such, these findings provide evidence for the first time that certain sleep problems in childhood (having regular distressing dreams) could be an early indicator of increased dementia and PD risk,” Dr. Otaiku said.
He noted that the findings build on previous studies which showed that regular nightmares in childhood could be an early indicator for psychiatric problems in adolescence, such as borderline personality disorder, attention-deficit/hyperactivity disorder, and psychosis.
The study was published online February 26 in The Lancet journal eClinicalMedicine.
Statistically significant
The prospective, longitudinal analysis used data from the 1958 British Birth Cohort Study, a prospective birth cohort which included all people born in Britain during a single week in 1958.
At age 7 years (in 1965) and 11 years (in 1969), mothers were asked to report whether their child experienced “bad dreams or night terrors” in the past 3 months, and cognitive impairment and PD were determined at age 50 (2008).
Among a total of 6,991 children (51% girls), 78.2% never had distressing dreams, 17.9% had transient distressing dreams (either at ages 7 or 11 years), and 3.8% had persistent distressing dreams (at both ages 7 and 11 years).
By age 50, 262 participants had developed cognitive impairment, and five had been diagnosed with PD.
After adjusting for all covariates, having more regular distressing dreams during childhood was “linearly and statistically significantly” associated with higher risk of developing cognitive impairment or PD by age 50 years (P = .037). This was the case in both boys and girls.
Compared with children who never had bad dreams, peers who had persistent distressing dreams (at ages 7 and 11 years) had an 85% increased risk for cognitive impairment or PD by age 50 (adjusted odds ratio, 1.85; 95% confidence interval, 1.10-3.11; P = .019).
The associations remained when incident cognitive impairment and incident PD were analyzed separately.
Compared with children who never had distressing dreams, children who had persistent distressing dreams were 76% more likely to develop cognitive impairment by age 50 years (aOR, 1.76; 95% CI, 1.03-2.99; P = .037), and were about seven times more likely to be diagnosed with PD by age 50 years (aOR, 7.35; 95% CI, 1.03-52.73; P = .047).
The linear association was statistically significant for PD (P = .050) and had a trend toward statistical significance for cognitive impairment (P = .074).
Mechanism unclear
“Early-life nightmares might be causally associated with cognitive impairment and PD, noncausally associated with cognitive impairment and PD, or both. At this stage it remains unclear which of the three options is correct. Therefore, further research on mechanisms is needed,” Dr. Otaiku told this news organization.
“One plausible noncausal explanation is that there are shared genetic factors which predispose individuals to having frequent nightmares in childhood, and to developing neurodegenerative diseases such as AD or PD in adulthood,” he added.
It’s also plausible that having regular nightmares throughout childhood could be a causal risk factor for cognitive impairment and PD by causing chronic sleep disruption, he noted.
“Chronic sleep disruption due to nightmares might lead to impaired glymphatic clearance during sleep – and thus greater accumulation of pathological proteins in the brain, such as amyloid-beta and alpha-synuclein,” Dr. Otaiku said.
Disrupted sleep throughout childhood might also impair normal brain development, which could make children’s brains less resilient to neuropathologic damage, he said.
Clinical implications?
There are established treatments for childhood nightmares, including nonpharmacologic approaches.
“For children who have regular nightmares that lead to impaired daytime functioning, it may well be a good idea for them to see a sleep physician to discuss whether treatment may be needed,” Dr. Otaiku said.
But should doctors treat children with persistent nightmares for the purpose of preventing neurodegenerative diseases in adulthood or psychiatric problems in adolescence?
“It’s an interesting possibility. However, more research is needed to confirm these epidemiological associations and to determine whether or not nightmares are a causal risk factor for these conditions,” Dr. Otaiku concluded.
The study received no external funding. Dr. Otaiku reports no relevant disclosures.
A version of this article first appeared on Medscape.com.
new research shows.
Compared with children who never had distressing dreams between ages 7 and 11 years, those who had persistent distressing dreams were 76% more likely to develop cognitive impairment and roughly seven times more likely to develop PD by age 50 years.
It’s been shown previously that sleep problems in adulthood, including distressing dreams, can precede the onset of neurodegenerative diseases such as Alzheimer’s disease (AD) or PD by several years, and in some cases decades, study investigator Abidemi Otaiku, BMBS, University of Birmingham (England), told this news organization.
However, no studies have investigated whether distressing dreams during childhood might also be associated with increased risk for cognitive decline or PD.
“As such, these findings provide evidence for the first time that certain sleep problems in childhood (having regular distressing dreams) could be an early indicator of increased dementia and PD risk,” Dr. Otaiku said.
He noted that the findings build on previous studies which showed that regular nightmares in childhood could be an early indicator for psychiatric problems in adolescence, such as borderline personality disorder, attention-deficit/hyperactivity disorder, and psychosis.
The study was published online February 26 in The Lancet journal eClinicalMedicine.
Statistically significant
The prospective, longitudinal analysis used data from the 1958 British Birth Cohort Study, a prospective birth cohort which included all people born in Britain during a single week in 1958.
At age 7 years (in 1965) and 11 years (in 1969), mothers were asked to report whether their child experienced “bad dreams or night terrors” in the past 3 months, and cognitive impairment and PD were determined at age 50 (2008).
Among a total of 6,991 children (51% girls), 78.2% never had distressing dreams, 17.9% had transient distressing dreams (either at ages 7 or 11 years), and 3.8% had persistent distressing dreams (at both ages 7 and 11 years).
By age 50, 262 participants had developed cognitive impairment, and five had been diagnosed with PD.
After adjusting for all covariates, having more regular distressing dreams during childhood was “linearly and statistically significantly” associated with higher risk of developing cognitive impairment or PD by age 50 years (P = .037). This was the case in both boys and girls.
Compared with children who never had bad dreams, peers who had persistent distressing dreams (at ages 7 and 11 years) had an 85% increased risk for cognitive impairment or PD by age 50 (adjusted odds ratio, 1.85; 95% confidence interval, 1.10-3.11; P = .019).
The associations remained when incident cognitive impairment and incident PD were analyzed separately.
Compared with children who never had distressing dreams, children who had persistent distressing dreams were 76% more likely to develop cognitive impairment by age 50 years (aOR, 1.76; 95% CI, 1.03-2.99; P = .037), and were about seven times more likely to be diagnosed with PD by age 50 years (aOR, 7.35; 95% CI, 1.03-52.73; P = .047).
The linear association was statistically significant for PD (P = .050) and had a trend toward statistical significance for cognitive impairment (P = .074).
Mechanism unclear
“Early-life nightmares might be causally associated with cognitive impairment and PD, noncausally associated with cognitive impairment and PD, or both. At this stage it remains unclear which of the three options is correct. Therefore, further research on mechanisms is needed,” Dr. Otaiku told this news organization.
“One plausible noncausal explanation is that there are shared genetic factors which predispose individuals to having frequent nightmares in childhood, and to developing neurodegenerative diseases such as AD or PD in adulthood,” he added.
It’s also plausible that having regular nightmares throughout childhood could be a causal risk factor for cognitive impairment and PD by causing chronic sleep disruption, he noted.
“Chronic sleep disruption due to nightmares might lead to impaired glymphatic clearance during sleep – and thus greater accumulation of pathological proteins in the brain, such as amyloid-beta and alpha-synuclein,” Dr. Otaiku said.
Disrupted sleep throughout childhood might also impair normal brain development, which could make children’s brains less resilient to neuropathologic damage, he said.
Clinical implications?
There are established treatments for childhood nightmares, including nonpharmacologic approaches.
“For children who have regular nightmares that lead to impaired daytime functioning, it may well be a good idea for them to see a sleep physician to discuss whether treatment may be needed,” Dr. Otaiku said.
But should doctors treat children with persistent nightmares for the purpose of preventing neurodegenerative diseases in adulthood or psychiatric problems in adolescence?
“It’s an interesting possibility. However, more research is needed to confirm these epidemiological associations and to determine whether or not nightmares are a causal risk factor for these conditions,” Dr. Otaiku concluded.
The study received no external funding. Dr. Otaiku reports no relevant disclosures.
A version of this article first appeared on Medscape.com.
new research shows.
Compared with children who never had distressing dreams between ages 7 and 11 years, those who had persistent distressing dreams were 76% more likely to develop cognitive impairment and roughly seven times more likely to develop PD by age 50 years.
It’s been shown previously that sleep problems in adulthood, including distressing dreams, can precede the onset of neurodegenerative diseases such as Alzheimer’s disease (AD) or PD by several years, and in some cases decades, study investigator Abidemi Otaiku, BMBS, University of Birmingham (England), told this news organization.
However, no studies have investigated whether distressing dreams during childhood might also be associated with increased risk for cognitive decline or PD.
“As such, these findings provide evidence for the first time that certain sleep problems in childhood (having regular distressing dreams) could be an early indicator of increased dementia and PD risk,” Dr. Otaiku said.
He noted that the findings build on previous studies which showed that regular nightmares in childhood could be an early indicator for psychiatric problems in adolescence, such as borderline personality disorder, attention-deficit/hyperactivity disorder, and psychosis.
The study was published online February 26 in The Lancet journal eClinicalMedicine.
Statistically significant
The prospective, longitudinal analysis used data from the 1958 British Birth Cohort Study, a prospective birth cohort which included all people born in Britain during a single week in 1958.
At age 7 years (in 1965) and 11 years (in 1969), mothers were asked to report whether their child experienced “bad dreams or night terrors” in the past 3 months, and cognitive impairment and PD were determined at age 50 (2008).
Among a total of 6,991 children (51% girls), 78.2% never had distressing dreams, 17.9% had transient distressing dreams (either at ages 7 or 11 years), and 3.8% had persistent distressing dreams (at both ages 7 and 11 years).
By age 50, 262 participants had developed cognitive impairment, and five had been diagnosed with PD.
After adjusting for all covariates, having more regular distressing dreams during childhood was “linearly and statistically significantly” associated with higher risk of developing cognitive impairment or PD by age 50 years (P = .037). This was the case in both boys and girls.
Compared with children who never had bad dreams, peers who had persistent distressing dreams (at ages 7 and 11 years) had an 85% increased risk for cognitive impairment or PD by age 50 (adjusted odds ratio, 1.85; 95% confidence interval, 1.10-3.11; P = .019).
The associations remained when incident cognitive impairment and incident PD were analyzed separately.
Compared with children who never had distressing dreams, children who had persistent distressing dreams were 76% more likely to develop cognitive impairment by age 50 years (aOR, 1.76; 95% CI, 1.03-2.99; P = .037), and were about seven times more likely to be diagnosed with PD by age 50 years (aOR, 7.35; 95% CI, 1.03-52.73; P = .047).
The linear association was statistically significant for PD (P = .050) and had a trend toward statistical significance for cognitive impairment (P = .074).
Mechanism unclear
“Early-life nightmares might be causally associated with cognitive impairment and PD, noncausally associated with cognitive impairment and PD, or both. At this stage it remains unclear which of the three options is correct. Therefore, further research on mechanisms is needed,” Dr. Otaiku told this news organization.
“One plausible noncausal explanation is that there are shared genetic factors which predispose individuals to having frequent nightmares in childhood, and to developing neurodegenerative diseases such as AD or PD in adulthood,” he added.
It’s also plausible that having regular nightmares throughout childhood could be a causal risk factor for cognitive impairment and PD by causing chronic sleep disruption, he noted.
“Chronic sleep disruption due to nightmares might lead to impaired glymphatic clearance during sleep – and thus greater accumulation of pathological proteins in the brain, such as amyloid-beta and alpha-synuclein,” Dr. Otaiku said.
Disrupted sleep throughout childhood might also impair normal brain development, which could make children’s brains less resilient to neuropathologic damage, he said.
Clinical implications?
There are established treatments for childhood nightmares, including nonpharmacologic approaches.
“For children who have regular nightmares that lead to impaired daytime functioning, it may well be a good idea for them to see a sleep physician to discuss whether treatment may be needed,” Dr. Otaiku said.
But should doctors treat children with persistent nightmares for the purpose of preventing neurodegenerative diseases in adulthood or psychiatric problems in adolescence?
“It’s an interesting possibility. However, more research is needed to confirm these epidemiological associations and to determine whether or not nightmares are a causal risk factor for these conditions,” Dr. Otaiku concluded.
The study received no external funding. Dr. Otaiku reports no relevant disclosures.
A version of this article first appeared on Medscape.com.
FROM ECLINICALMEDICINE
Even mild COVID is hard on the brain
early research suggests.
“Our results suggest a severe pattern of changes in how the brain communicates as well as its structure, mainly in people with anxiety and depression with long-COVID syndrome, which affects so many people,” study investigator Clarissa Yasuda, MD, PhD, from University of Campinas, São Paulo, said in a news release.
“The magnitude of these changes suggests that they could lead to problems with memory and thinking skills, so we need to be exploring holistic treatments even for people mildly affected by COVID-19,” Dr. Yasuda added.
The findings were released March 6 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology.
Brain shrinkage
Some studies have shown a high prevalence of symptoms of anxiety and depression in COVID-19 survivors, but few have investigated the associated cerebral changes, Dr. Yasuda told this news organization.
The study included 254 adults (177 women, 77 men, median age 41 years) who had mild COVID-19 a median of 82 days earlier. A total of 102 had symptoms of both anxiety and depression, and 152 had no such symptoms.
On brain imaging, those with COVID-19 and anxiety and depression had atrophy in the limbic area of the brain, which plays a role in memory and emotional processing.
No shrinkage in this area was evident in people who had COVID-19 without anxiety and depression or in a healthy control group of individuals without COVID-19.
The researchers also observed a “severe” pattern of abnormal cerebral functional connectivity in those with COVID-19 and anxiety and depression.
In this functional connectivity analysis, individuals with COVID-19 and anxiety and depression had widespread functional changes in each of the 12 networks assessed, while those with COVID-19 but without symptoms of anxiety and depression showed changes in only 5 networks.
Mechanisms unclear
“Unfortunately, the underpinning mechanisms associated with brain changes and neuropsychiatric dysfunction after COVID-19 infection are unclear,” Dr. Yasuda told this news organization.
“Some studies have demonstrated an association between symptoms of anxiety and depression with inflammation. However, we hypothesize that these cerebral alterations may result from a more complex interaction of social, psychological, and systemic stressors, including inflammation. It is indeed intriguing that such alterations are present in individuals who presented mild acute infection,” Dr. Yasuda added.
“Symptoms of anxiety and depression are frequently observed after COVID-19 and are part of long-COVID syndrome for some individuals. These symptoms require adequate treatment to improve the quality of life, cognition, and work capacity,” she said.
Treating these symptoms may induce “brain plasticity, which may result in some degree of gray matter increase and eventually prevent further structural and functional damage,” Dr. Yasuda said.
A limitation of the study was that symptoms of anxiety and depression were self-reported, meaning people may have misjudged or misreported symptoms.
Commenting on the findings for this news organization, Cyrus Raji, MD, PhD, with the Mallinckrodt Institute of Radiology, Washington University, St. Louis, said the idea that COVID-19 is bad for the brain isn’t new. Dr. Raji was not involved with the study.
Early in the pandemic, Dr. Raji and colleagues published a paper detailing COVID-19’s effects on the brain, and Dr. Raji followed it up with a TED talk on the subject.
“Within the growing framework of what we already know about COVID-19 infection and its adverse effects on the brain, this work incrementally adds to this knowledge by identifying functional and structural neuroimaging abnormalities related to anxiety and depression in persons suffering from COVID-19 infection,” Dr. Raji said.
The study was supported by the São Paulo Research Foundation. The authors have no relevant disclosures. Raji is a consultant for Brainreader, Apollo Health, Pacific Neuroscience Foundation, and Neurevolution LLC.
early research suggests.
“Our results suggest a severe pattern of changes in how the brain communicates as well as its structure, mainly in people with anxiety and depression with long-COVID syndrome, which affects so many people,” study investigator Clarissa Yasuda, MD, PhD, from University of Campinas, São Paulo, said in a news release.
“The magnitude of these changes suggests that they could lead to problems with memory and thinking skills, so we need to be exploring holistic treatments even for people mildly affected by COVID-19,” Dr. Yasuda added.
The findings were released March 6 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology.
Brain shrinkage
Some studies have shown a high prevalence of symptoms of anxiety and depression in COVID-19 survivors, but few have investigated the associated cerebral changes, Dr. Yasuda told this news organization.
The study included 254 adults (177 women, 77 men, median age 41 years) who had mild COVID-19 a median of 82 days earlier. A total of 102 had symptoms of both anxiety and depression, and 152 had no such symptoms.
On brain imaging, those with COVID-19 and anxiety and depression had atrophy in the limbic area of the brain, which plays a role in memory and emotional processing.
No shrinkage in this area was evident in people who had COVID-19 without anxiety and depression or in a healthy control group of individuals without COVID-19.
The researchers also observed a “severe” pattern of abnormal cerebral functional connectivity in those with COVID-19 and anxiety and depression.
In this functional connectivity analysis, individuals with COVID-19 and anxiety and depression had widespread functional changes in each of the 12 networks assessed, while those with COVID-19 but without symptoms of anxiety and depression showed changes in only 5 networks.
Mechanisms unclear
“Unfortunately, the underpinning mechanisms associated with brain changes and neuropsychiatric dysfunction after COVID-19 infection are unclear,” Dr. Yasuda told this news organization.
“Some studies have demonstrated an association between symptoms of anxiety and depression with inflammation. However, we hypothesize that these cerebral alterations may result from a more complex interaction of social, psychological, and systemic stressors, including inflammation. It is indeed intriguing that such alterations are present in individuals who presented mild acute infection,” Dr. Yasuda added.
“Symptoms of anxiety and depression are frequently observed after COVID-19 and are part of long-COVID syndrome for some individuals. These symptoms require adequate treatment to improve the quality of life, cognition, and work capacity,” she said.
Treating these symptoms may induce “brain plasticity, which may result in some degree of gray matter increase and eventually prevent further structural and functional damage,” Dr. Yasuda said.
A limitation of the study was that symptoms of anxiety and depression were self-reported, meaning people may have misjudged or misreported symptoms.
Commenting on the findings for this news organization, Cyrus Raji, MD, PhD, with the Mallinckrodt Institute of Radiology, Washington University, St. Louis, said the idea that COVID-19 is bad for the brain isn’t new. Dr. Raji was not involved with the study.
Early in the pandemic, Dr. Raji and colleagues published a paper detailing COVID-19’s effects on the brain, and Dr. Raji followed it up with a TED talk on the subject.
“Within the growing framework of what we already know about COVID-19 infection and its adverse effects on the brain, this work incrementally adds to this knowledge by identifying functional and structural neuroimaging abnormalities related to anxiety and depression in persons suffering from COVID-19 infection,” Dr. Raji said.
The study was supported by the São Paulo Research Foundation. The authors have no relevant disclosures. Raji is a consultant for Brainreader, Apollo Health, Pacific Neuroscience Foundation, and Neurevolution LLC.
early research suggests.
“Our results suggest a severe pattern of changes in how the brain communicates as well as its structure, mainly in people with anxiety and depression with long-COVID syndrome, which affects so many people,” study investigator Clarissa Yasuda, MD, PhD, from University of Campinas, São Paulo, said in a news release.
“The magnitude of these changes suggests that they could lead to problems with memory and thinking skills, so we need to be exploring holistic treatments even for people mildly affected by COVID-19,” Dr. Yasuda added.
The findings were released March 6 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology.
Brain shrinkage
Some studies have shown a high prevalence of symptoms of anxiety and depression in COVID-19 survivors, but few have investigated the associated cerebral changes, Dr. Yasuda told this news organization.
The study included 254 adults (177 women, 77 men, median age 41 years) who had mild COVID-19 a median of 82 days earlier. A total of 102 had symptoms of both anxiety and depression, and 152 had no such symptoms.
On brain imaging, those with COVID-19 and anxiety and depression had atrophy in the limbic area of the brain, which plays a role in memory and emotional processing.
No shrinkage in this area was evident in people who had COVID-19 without anxiety and depression or in a healthy control group of individuals without COVID-19.
The researchers also observed a “severe” pattern of abnormal cerebral functional connectivity in those with COVID-19 and anxiety and depression.
In this functional connectivity analysis, individuals with COVID-19 and anxiety and depression had widespread functional changes in each of the 12 networks assessed, while those with COVID-19 but without symptoms of anxiety and depression showed changes in only 5 networks.
Mechanisms unclear
“Unfortunately, the underpinning mechanisms associated with brain changes and neuropsychiatric dysfunction after COVID-19 infection are unclear,” Dr. Yasuda told this news organization.
“Some studies have demonstrated an association between symptoms of anxiety and depression with inflammation. However, we hypothesize that these cerebral alterations may result from a more complex interaction of social, psychological, and systemic stressors, including inflammation. It is indeed intriguing that such alterations are present in individuals who presented mild acute infection,” Dr. Yasuda added.
“Symptoms of anxiety and depression are frequently observed after COVID-19 and are part of long-COVID syndrome for some individuals. These symptoms require adequate treatment to improve the quality of life, cognition, and work capacity,” she said.
Treating these symptoms may induce “brain plasticity, which may result in some degree of gray matter increase and eventually prevent further structural and functional damage,” Dr. Yasuda said.
A limitation of the study was that symptoms of anxiety and depression were self-reported, meaning people may have misjudged or misreported symptoms.
Commenting on the findings for this news organization, Cyrus Raji, MD, PhD, with the Mallinckrodt Institute of Radiology, Washington University, St. Louis, said the idea that COVID-19 is bad for the brain isn’t new. Dr. Raji was not involved with the study.
Early in the pandemic, Dr. Raji and colleagues published a paper detailing COVID-19’s effects on the brain, and Dr. Raji followed it up with a TED talk on the subject.
“Within the growing framework of what we already know about COVID-19 infection and its adverse effects on the brain, this work incrementally adds to this knowledge by identifying functional and structural neuroimaging abnormalities related to anxiety and depression in persons suffering from COVID-19 infection,” Dr. Raji said.
The study was supported by the São Paulo Research Foundation. The authors have no relevant disclosures. Raji is a consultant for Brainreader, Apollo Health, Pacific Neuroscience Foundation, and Neurevolution LLC.
High CV risk factor burden in young adults a ‘smoldering’ crisis
New data show a high and rising burden of most cardiovascular (CV) risk factors among young adults aged 20-44 years in the United States.
In this age group, over the past 10 years, there has been an increase in the prevalence of diabetes and obesity, no improvement in the prevalence of hypertension, and a decrease in the prevalence of hyperlipidemia.
Yet medical treatment rates for CV risk factors are “surprisingly” low among young adults, study investigator Rishi Wadhera, MD, with Beth Israel Deaconess Medical Center and Harvard Medical School, both in Boston, told this news organization.
The findings are “extremely concerning. We’re witnessing a smoldering public health crisis. The onset of these risk factors earlier in life is associated with a higher lifetime risk of heart disease and potentially life-threatening,” Dr. Wadhera added.
The study was presented March 5 at the joint scientific sessions of the American College of Cardiology and the World Heart Federation and was simultaneously published in JAMA.
The burden of CV risk factors among young adults is “unacceptably high and increasing,” write the co-authors of a JAMA editorial.
“The time is now for aggressive preventive measures in young adults. Without immediate action there will continue to be a rise in heart disease and the burden it places on patients, families, and communities,” say Norrina Allen, PhD, and John Wilkins, MD, with Northwestern University, Chicago.
Preventing a tsunami of heart disease
The findings stem from a cross-sectional study of 12,294 U.S. adults aged 20-44 years (mean age, 32; 51% women) who participated in National Health and Nutrition Examination Survey (NHANES) cycles for 2009-2010 to 2017-2020.
Overall, the prevalence of hypertension was 9.3% in 2009-2010 and increased to 11.5% in 2017-2020. The prevalence of diabetes rose from 3.0% to 4.1%, and the prevalence of obesity rose from 32.7% to 40.9%. The prevalence of hyperlipidemia decreased from 40.5% to 36.1%.
Black adults consistently had high rates of hypertension during the study period – 16.2% in 2009-2010 and 20.1% in 2017-2020 – and significant increases in hypertension occurred among Mexican American adults (from 6.5% to 9.5%) and other Hispanic adults (from 4.4% to 10.5%), while Mexican American adults had a significant uptick in diabetes (from 4.3% to 7.5%).
Equally concerning, said Dr. Wadhera, is the fact that only about 55% of young adults with hypertension were receiving antihypertensive medication, and just 1 in 2 young adults with diabetes were receiving treatment. “These low rates were driven, in part, by many young adults not being aware of their diagnosis,” he noted.
The NHANES data also show that the percentage of young adults who were treated for hypertension and who achieved blood pressure control did not change significantly over the study period (65.0% in 2009-2010 and 74.8% in 2017-2020). Blood sugar control among young adults being treated for diabetes remained suboptimal throughout the study period (45.5% in 2009-2010 and 56.6% in 2017-2020).
“The fact that blood pressure control and glycemic control are so poor is really worrisome,” Jeffrey Berger, MD, director of the Center for the Prevention of Cardiovascular Disease at NYU Langone Heart, who wasn’t involved in the study, told this news organization.
“Even in the lipid control, while it did get a little bit better, it’s still only around 30%-40%. So, I think we have ways to go as a society,” Dr. Berger noted.
Double down on screening
Dr. Wadhera said “we need to double down on efforts to screen for and treat cardiovascular risk factors like high blood pressure and diabetes in young adults. We need to intensify clinical and public health interventions focused on primordial and primary prevention in young adults now so that we can avoid a tsunami of cardiovascular disease in the long term.”
“It’s critically important that young adults speak with their health care provider about whether – and when – they should undergo screening for high blood pressure, diabetes, and high cholesterol,” Dr. Wadhera added.
Dr. Berger said one problem is that younger people often have a “superman or superwoman” view and don’t comprehend that they are at risk for some of these conditions. Studies such as this “reinforce the idea that it’s never too young to be checked out.”
As a cardiologist who specializes in cardiovascular prevention, Dr. Berger said he sometimes hears patients say things like, “I don’t ever want to need a cardiologist,” or “I hope I never need a cardiologist.”
“My response is, ‘There are many different types of cardiologists,’ and I think it would really be helpful for many people to see a prevention-focused cardiologist way before they have problems,” he said in an interview.
“As a system, medicine has become very good at treating patients with different diseases. I think we need to get better in terms of preventing some of these problems,” Dr. Berger added.
In their editorial, Dr. Allen and Dr. Wilkins say the “foundation of cardiovascular health begins early in life. These worsening trends in risk factors highlight the importance of focusing on prevention in adolescence and young adulthood in order to promote cardiovascular health across the lifetime.”
The study was funded by a grant from the National Heart, Lung, and Blood Institute. Dr. Wadhera has served as a consultant for Abbott and CVS Health. Dr. Wilkins has received personal fees from 3M. Dr. Berger has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
New data show a high and rising burden of most cardiovascular (CV) risk factors among young adults aged 20-44 years in the United States.
In this age group, over the past 10 years, there has been an increase in the prevalence of diabetes and obesity, no improvement in the prevalence of hypertension, and a decrease in the prevalence of hyperlipidemia.
Yet medical treatment rates for CV risk factors are “surprisingly” low among young adults, study investigator Rishi Wadhera, MD, with Beth Israel Deaconess Medical Center and Harvard Medical School, both in Boston, told this news organization.
The findings are “extremely concerning. We’re witnessing a smoldering public health crisis. The onset of these risk factors earlier in life is associated with a higher lifetime risk of heart disease and potentially life-threatening,” Dr. Wadhera added.
The study was presented March 5 at the joint scientific sessions of the American College of Cardiology and the World Heart Federation and was simultaneously published in JAMA.
The burden of CV risk factors among young adults is “unacceptably high and increasing,” write the co-authors of a JAMA editorial.
“The time is now for aggressive preventive measures in young adults. Without immediate action there will continue to be a rise in heart disease and the burden it places on patients, families, and communities,” say Norrina Allen, PhD, and John Wilkins, MD, with Northwestern University, Chicago.
Preventing a tsunami of heart disease
The findings stem from a cross-sectional study of 12,294 U.S. adults aged 20-44 years (mean age, 32; 51% women) who participated in National Health and Nutrition Examination Survey (NHANES) cycles for 2009-2010 to 2017-2020.
Overall, the prevalence of hypertension was 9.3% in 2009-2010 and increased to 11.5% in 2017-2020. The prevalence of diabetes rose from 3.0% to 4.1%, and the prevalence of obesity rose from 32.7% to 40.9%. The prevalence of hyperlipidemia decreased from 40.5% to 36.1%.
Black adults consistently had high rates of hypertension during the study period – 16.2% in 2009-2010 and 20.1% in 2017-2020 – and significant increases in hypertension occurred among Mexican American adults (from 6.5% to 9.5%) and other Hispanic adults (from 4.4% to 10.5%), while Mexican American adults had a significant uptick in diabetes (from 4.3% to 7.5%).
Equally concerning, said Dr. Wadhera, is the fact that only about 55% of young adults with hypertension were receiving antihypertensive medication, and just 1 in 2 young adults with diabetes were receiving treatment. “These low rates were driven, in part, by many young adults not being aware of their diagnosis,” he noted.
The NHANES data also show that the percentage of young adults who were treated for hypertension and who achieved blood pressure control did not change significantly over the study period (65.0% in 2009-2010 and 74.8% in 2017-2020). Blood sugar control among young adults being treated for diabetes remained suboptimal throughout the study period (45.5% in 2009-2010 and 56.6% in 2017-2020).
“The fact that blood pressure control and glycemic control are so poor is really worrisome,” Jeffrey Berger, MD, director of the Center for the Prevention of Cardiovascular Disease at NYU Langone Heart, who wasn’t involved in the study, told this news organization.
“Even in the lipid control, while it did get a little bit better, it’s still only around 30%-40%. So, I think we have ways to go as a society,” Dr. Berger noted.
Double down on screening
Dr. Wadhera said “we need to double down on efforts to screen for and treat cardiovascular risk factors like high blood pressure and diabetes in young adults. We need to intensify clinical and public health interventions focused on primordial and primary prevention in young adults now so that we can avoid a tsunami of cardiovascular disease in the long term.”
“It’s critically important that young adults speak with their health care provider about whether – and when – they should undergo screening for high blood pressure, diabetes, and high cholesterol,” Dr. Wadhera added.
Dr. Berger said one problem is that younger people often have a “superman or superwoman” view and don’t comprehend that they are at risk for some of these conditions. Studies such as this “reinforce the idea that it’s never too young to be checked out.”
As a cardiologist who specializes in cardiovascular prevention, Dr. Berger said he sometimes hears patients say things like, “I don’t ever want to need a cardiologist,” or “I hope I never need a cardiologist.”
“My response is, ‘There are many different types of cardiologists,’ and I think it would really be helpful for many people to see a prevention-focused cardiologist way before they have problems,” he said in an interview.
“As a system, medicine has become very good at treating patients with different diseases. I think we need to get better in terms of preventing some of these problems,” Dr. Berger added.
In their editorial, Dr. Allen and Dr. Wilkins say the “foundation of cardiovascular health begins early in life. These worsening trends in risk factors highlight the importance of focusing on prevention in adolescence and young adulthood in order to promote cardiovascular health across the lifetime.”
The study was funded by a grant from the National Heart, Lung, and Blood Institute. Dr. Wadhera has served as a consultant for Abbott and CVS Health. Dr. Wilkins has received personal fees from 3M. Dr. Berger has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
New data show a high and rising burden of most cardiovascular (CV) risk factors among young adults aged 20-44 years in the United States.
In this age group, over the past 10 years, there has been an increase in the prevalence of diabetes and obesity, no improvement in the prevalence of hypertension, and a decrease in the prevalence of hyperlipidemia.
Yet medical treatment rates for CV risk factors are “surprisingly” low among young adults, study investigator Rishi Wadhera, MD, with Beth Israel Deaconess Medical Center and Harvard Medical School, both in Boston, told this news organization.
The findings are “extremely concerning. We’re witnessing a smoldering public health crisis. The onset of these risk factors earlier in life is associated with a higher lifetime risk of heart disease and potentially life-threatening,” Dr. Wadhera added.
The study was presented March 5 at the joint scientific sessions of the American College of Cardiology and the World Heart Federation and was simultaneously published in JAMA.
The burden of CV risk factors among young adults is “unacceptably high and increasing,” write the co-authors of a JAMA editorial.
“The time is now for aggressive preventive measures in young adults. Without immediate action there will continue to be a rise in heart disease and the burden it places on patients, families, and communities,” say Norrina Allen, PhD, and John Wilkins, MD, with Northwestern University, Chicago.
Preventing a tsunami of heart disease
The findings stem from a cross-sectional study of 12,294 U.S. adults aged 20-44 years (mean age, 32; 51% women) who participated in National Health and Nutrition Examination Survey (NHANES) cycles for 2009-2010 to 2017-2020.
Overall, the prevalence of hypertension was 9.3% in 2009-2010 and increased to 11.5% in 2017-2020. The prevalence of diabetes rose from 3.0% to 4.1%, and the prevalence of obesity rose from 32.7% to 40.9%. The prevalence of hyperlipidemia decreased from 40.5% to 36.1%.
Black adults consistently had high rates of hypertension during the study period – 16.2% in 2009-2010 and 20.1% in 2017-2020 – and significant increases in hypertension occurred among Mexican American adults (from 6.5% to 9.5%) and other Hispanic adults (from 4.4% to 10.5%), while Mexican American adults had a significant uptick in diabetes (from 4.3% to 7.5%).
Equally concerning, said Dr. Wadhera, is the fact that only about 55% of young adults with hypertension were receiving antihypertensive medication, and just 1 in 2 young adults with diabetes were receiving treatment. “These low rates were driven, in part, by many young adults not being aware of their diagnosis,” he noted.
The NHANES data also show that the percentage of young adults who were treated for hypertension and who achieved blood pressure control did not change significantly over the study period (65.0% in 2009-2010 and 74.8% in 2017-2020). Blood sugar control among young adults being treated for diabetes remained suboptimal throughout the study period (45.5% in 2009-2010 and 56.6% in 2017-2020).
“The fact that blood pressure control and glycemic control are so poor is really worrisome,” Jeffrey Berger, MD, director of the Center for the Prevention of Cardiovascular Disease at NYU Langone Heart, who wasn’t involved in the study, told this news organization.
“Even in the lipid control, while it did get a little bit better, it’s still only around 30%-40%. So, I think we have ways to go as a society,” Dr. Berger noted.
Double down on screening
Dr. Wadhera said “we need to double down on efforts to screen for and treat cardiovascular risk factors like high blood pressure and diabetes in young adults. We need to intensify clinical and public health interventions focused on primordial and primary prevention in young adults now so that we can avoid a tsunami of cardiovascular disease in the long term.”
“It’s critically important that young adults speak with their health care provider about whether – and when – they should undergo screening for high blood pressure, diabetes, and high cholesterol,” Dr. Wadhera added.
Dr. Berger said one problem is that younger people often have a “superman or superwoman” view and don’t comprehend that they are at risk for some of these conditions. Studies such as this “reinforce the idea that it’s never too young to be checked out.”
As a cardiologist who specializes in cardiovascular prevention, Dr. Berger said he sometimes hears patients say things like, “I don’t ever want to need a cardiologist,” or “I hope I never need a cardiologist.”
“My response is, ‘There are many different types of cardiologists,’ and I think it would really be helpful for many people to see a prevention-focused cardiologist way before they have problems,” he said in an interview.
“As a system, medicine has become very good at treating patients with different diseases. I think we need to get better in terms of preventing some of these problems,” Dr. Berger added.
In their editorial, Dr. Allen and Dr. Wilkins say the “foundation of cardiovascular health begins early in life. These worsening trends in risk factors highlight the importance of focusing on prevention in adolescence and young adulthood in order to promote cardiovascular health across the lifetime.”
The study was funded by a grant from the National Heart, Lung, and Blood Institute. Dr. Wadhera has served as a consultant for Abbott and CVS Health. Dr. Wilkins has received personal fees from 3M. Dr. Berger has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM ACC 2023
Aerobic, breathing exercises tied to faster concussion recovery
, preliminary findings from a new study suggest.
Heart rate variability biofeedback (HRVB) and progressive aerobic exercise (PAE) were each helpful on their own, but combining them led to even greater improvement in cognition, depression, and mood.
“Managing persistent concussion symptoms is particularly challenging as there are no standard therapies,” study investigator R. Davis Moore, PhD, from the University of South Carolina, Columbia, said in a news release.
“These therapies are inexpensive, easy to implement, and can be self-administered, making them feasible and accessible for everyone with persistent symptoms,” Dr. Moore noted.
The study was released early, ahead of its scheduled presentation in Boston at the annual meeting of the American Academy of Neurology.
Targeting autonomic dysfunction
Concussion can affect the autonomic nervous system, and it is “increasingly clear that this underlies the inability to tolerate exercise, problems with thinking skills, and mood issues in those with persisting symptoms,” Dr. Moore explained.
Preliminary research suggests that HRVB and PAE can improve cardio-autonomic dysfunction and clinical symptoms. However, until now, no study has evaluated whether there is additional benefit from combining the two.
The investigators randomly assigned 30 teens with postconcussive symptoms that had lasted more than 1 month to a 6-week intervention consisting of either HRVB, PAE, or HRVB plus PAE.
The HRVB group practiced resonant-frequency breathing using a handheld biofeedback device for 20 minutes 4 nights a week. The PAE group completed a 3-day-a-week aerobic exercise protocol that gradually increased in intensity and duration. The HRVB plus PAE group did both. Concussion symptoms, HRV, cognition, and mood were assessed at baseline and again 6 weeks later.
All participants experienced improvement in sleep, mood, cognition, and autonomic function, but those who received the combined biofeedback and exercise intervention experienced greater improvements than peers who engaged in exercise or received biofeedback alone.
The study’s top-line results, which were released ahead of the presentation, show that HRVB plus PAE is associated with a twofold greater reduction in symptom severity, compared with PAE only, and a 1.3 times greater reduction in symptom severity, compared with HRVB only.
Similarly, HRVB plus PAE led to a 1.2 times greater reduction in symptoms of depression, compared with PAE only, and a 1.3 times greater reduction, compared with HRVB only.
The combined group also experienced more than 1.4 times the reduction in total mood disturbance than was provided by exercise or biofeedback alone.
The combined group also experienced significantly greater improvements in attention and working memory, as well as greater changes in metrics of HRV, than the groups that participated in exercise or biofeedback alone.
Dr. Moore and colleagues caution that the current results are preliminary and that future studies are needed with larger groups of people.
A limitation of the study was that it did not include a control group of people with persistent postconcussive symptoms who received no intervention.
Complex problem
Commenting on the findings, neuroscientist José Posas, MD, director of the Ochsner Neurology Residency Program, New Orleans, who wasn’t involved in the study, said these preliminary results are “promising” but cited the small number of participants as a limitation.
Dr. Posas said the results “fit with what’s known about the role of postconcussion autonomic dysfunction in persisting postconcussive symptoms.
“Managing persistent concussion symptoms can be challenging,” he added, and this study supports “exercise as medicine” as well as taking a “mind-body, holistic approach” to postconcussion recovery, said Dr. Posas.
Also weighing in, Michael F. Bergeron, PhD, clinical and scientific advisor, Department of Performance Health, Women’s Tennis Association, noted that “each of these therapeutic interventions has been around for some time now. Neither is new.
“Heart rate variability biofeedback based on variation in heart rate corresponding to breathing has been shown to be effective in treating numerous conditions, including reducing (nonclinical) stress, anxiety, depression, anger, and posttraumatic stress disorder in veterans and in some instances enhancing athletic performance. Of course, the validity and reliability of the commercially available apps and devices are potential significant limitations, as well as the stability of the user’s technique,” Dr. Bergeron said.
“It’s also been recognized that low-level aerobic exercise treatment normalizes the cerebrovascular physiological dysfunction in patients with concussion by increasing CO2 sensitivity, which normalizes exercise ventilation and cerebral blood flow and thus reduces some symptoms,” Dr. Bergeron added.
“The combination of treatments is likely the novel aspect, which makes sense because brain injury is complex, and effective interventions need to utilize a complex, integrated biological systems approach across the multiple interdependent domains of influence,” Dr. Bergeron said.
The study was supported by the nonprofit Woodcock Institute at Texas Woman’s University. Dr. Moore, Dr. Bergeron, and Dr. Posas have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, preliminary findings from a new study suggest.
Heart rate variability biofeedback (HRVB) and progressive aerobic exercise (PAE) were each helpful on their own, but combining them led to even greater improvement in cognition, depression, and mood.
“Managing persistent concussion symptoms is particularly challenging as there are no standard therapies,” study investigator R. Davis Moore, PhD, from the University of South Carolina, Columbia, said in a news release.
“These therapies are inexpensive, easy to implement, and can be self-administered, making them feasible and accessible for everyone with persistent symptoms,” Dr. Moore noted.
The study was released early, ahead of its scheduled presentation in Boston at the annual meeting of the American Academy of Neurology.
Targeting autonomic dysfunction
Concussion can affect the autonomic nervous system, and it is “increasingly clear that this underlies the inability to tolerate exercise, problems with thinking skills, and mood issues in those with persisting symptoms,” Dr. Moore explained.
Preliminary research suggests that HRVB and PAE can improve cardio-autonomic dysfunction and clinical symptoms. However, until now, no study has evaluated whether there is additional benefit from combining the two.
The investigators randomly assigned 30 teens with postconcussive symptoms that had lasted more than 1 month to a 6-week intervention consisting of either HRVB, PAE, or HRVB plus PAE.
The HRVB group practiced resonant-frequency breathing using a handheld biofeedback device for 20 minutes 4 nights a week. The PAE group completed a 3-day-a-week aerobic exercise protocol that gradually increased in intensity and duration. The HRVB plus PAE group did both. Concussion symptoms, HRV, cognition, and mood were assessed at baseline and again 6 weeks later.
All participants experienced improvement in sleep, mood, cognition, and autonomic function, but those who received the combined biofeedback and exercise intervention experienced greater improvements than peers who engaged in exercise or received biofeedback alone.
The study’s top-line results, which were released ahead of the presentation, show that HRVB plus PAE is associated with a twofold greater reduction in symptom severity, compared with PAE only, and a 1.3 times greater reduction in symptom severity, compared with HRVB only.
Similarly, HRVB plus PAE led to a 1.2 times greater reduction in symptoms of depression, compared with PAE only, and a 1.3 times greater reduction, compared with HRVB only.
The combined group also experienced more than 1.4 times the reduction in total mood disturbance than was provided by exercise or biofeedback alone.
The combined group also experienced significantly greater improvements in attention and working memory, as well as greater changes in metrics of HRV, than the groups that participated in exercise or biofeedback alone.
Dr. Moore and colleagues caution that the current results are preliminary and that future studies are needed with larger groups of people.
A limitation of the study was that it did not include a control group of people with persistent postconcussive symptoms who received no intervention.
Complex problem
Commenting on the findings, neuroscientist José Posas, MD, director of the Ochsner Neurology Residency Program, New Orleans, who wasn’t involved in the study, said these preliminary results are “promising” but cited the small number of participants as a limitation.
Dr. Posas said the results “fit with what’s known about the role of postconcussion autonomic dysfunction in persisting postconcussive symptoms.
“Managing persistent concussion symptoms can be challenging,” he added, and this study supports “exercise as medicine” as well as taking a “mind-body, holistic approach” to postconcussion recovery, said Dr. Posas.
Also weighing in, Michael F. Bergeron, PhD, clinical and scientific advisor, Department of Performance Health, Women’s Tennis Association, noted that “each of these therapeutic interventions has been around for some time now. Neither is new.
“Heart rate variability biofeedback based on variation in heart rate corresponding to breathing has been shown to be effective in treating numerous conditions, including reducing (nonclinical) stress, anxiety, depression, anger, and posttraumatic stress disorder in veterans and in some instances enhancing athletic performance. Of course, the validity and reliability of the commercially available apps and devices are potential significant limitations, as well as the stability of the user’s technique,” Dr. Bergeron said.
“It’s also been recognized that low-level aerobic exercise treatment normalizes the cerebrovascular physiological dysfunction in patients with concussion by increasing CO2 sensitivity, which normalizes exercise ventilation and cerebral blood flow and thus reduces some symptoms,” Dr. Bergeron added.
“The combination of treatments is likely the novel aspect, which makes sense because brain injury is complex, and effective interventions need to utilize a complex, integrated biological systems approach across the multiple interdependent domains of influence,” Dr. Bergeron said.
The study was supported by the nonprofit Woodcock Institute at Texas Woman’s University. Dr. Moore, Dr. Bergeron, and Dr. Posas have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, preliminary findings from a new study suggest.
Heart rate variability biofeedback (HRVB) and progressive aerobic exercise (PAE) were each helpful on their own, but combining them led to even greater improvement in cognition, depression, and mood.
“Managing persistent concussion symptoms is particularly challenging as there are no standard therapies,” study investigator R. Davis Moore, PhD, from the University of South Carolina, Columbia, said in a news release.
“These therapies are inexpensive, easy to implement, and can be self-administered, making them feasible and accessible for everyone with persistent symptoms,” Dr. Moore noted.
The study was released early, ahead of its scheduled presentation in Boston at the annual meeting of the American Academy of Neurology.
Targeting autonomic dysfunction
Concussion can affect the autonomic nervous system, and it is “increasingly clear that this underlies the inability to tolerate exercise, problems with thinking skills, and mood issues in those with persisting symptoms,” Dr. Moore explained.
Preliminary research suggests that HRVB and PAE can improve cardio-autonomic dysfunction and clinical symptoms. However, until now, no study has evaluated whether there is additional benefit from combining the two.
The investigators randomly assigned 30 teens with postconcussive symptoms that had lasted more than 1 month to a 6-week intervention consisting of either HRVB, PAE, or HRVB plus PAE.
The HRVB group practiced resonant-frequency breathing using a handheld biofeedback device for 20 minutes 4 nights a week. The PAE group completed a 3-day-a-week aerobic exercise protocol that gradually increased in intensity and duration. The HRVB plus PAE group did both. Concussion symptoms, HRV, cognition, and mood were assessed at baseline and again 6 weeks later.
All participants experienced improvement in sleep, mood, cognition, and autonomic function, but those who received the combined biofeedback and exercise intervention experienced greater improvements than peers who engaged in exercise or received biofeedback alone.
The study’s top-line results, which were released ahead of the presentation, show that HRVB plus PAE is associated with a twofold greater reduction in symptom severity, compared with PAE only, and a 1.3 times greater reduction in symptom severity, compared with HRVB only.
Similarly, HRVB plus PAE led to a 1.2 times greater reduction in symptoms of depression, compared with PAE only, and a 1.3 times greater reduction, compared with HRVB only.
The combined group also experienced more than 1.4 times the reduction in total mood disturbance than was provided by exercise or biofeedback alone.
The combined group also experienced significantly greater improvements in attention and working memory, as well as greater changes in metrics of HRV, than the groups that participated in exercise or biofeedback alone.
Dr. Moore and colleagues caution that the current results are preliminary and that future studies are needed with larger groups of people.
A limitation of the study was that it did not include a control group of people with persistent postconcussive symptoms who received no intervention.
Complex problem
Commenting on the findings, neuroscientist José Posas, MD, director of the Ochsner Neurology Residency Program, New Orleans, who wasn’t involved in the study, said these preliminary results are “promising” but cited the small number of participants as a limitation.
Dr. Posas said the results “fit with what’s known about the role of postconcussion autonomic dysfunction in persisting postconcussive symptoms.
“Managing persistent concussion symptoms can be challenging,” he added, and this study supports “exercise as medicine” as well as taking a “mind-body, holistic approach” to postconcussion recovery, said Dr. Posas.
Also weighing in, Michael F. Bergeron, PhD, clinical and scientific advisor, Department of Performance Health, Women’s Tennis Association, noted that “each of these therapeutic interventions has been around for some time now. Neither is new.
“Heart rate variability biofeedback based on variation in heart rate corresponding to breathing has been shown to be effective in treating numerous conditions, including reducing (nonclinical) stress, anxiety, depression, anger, and posttraumatic stress disorder in veterans and in some instances enhancing athletic performance. Of course, the validity and reliability of the commercially available apps and devices are potential significant limitations, as well as the stability of the user’s technique,” Dr. Bergeron said.
“It’s also been recognized that low-level aerobic exercise treatment normalizes the cerebrovascular physiological dysfunction in patients with concussion by increasing CO2 sensitivity, which normalizes exercise ventilation and cerebral blood flow and thus reduces some symptoms,” Dr. Bergeron added.
“The combination of treatments is likely the novel aspect, which makes sense because brain injury is complex, and effective interventions need to utilize a complex, integrated biological systems approach across the multiple interdependent domains of influence,” Dr. Bergeron said.
The study was supported by the nonprofit Woodcock Institute at Texas Woman’s University. Dr. Moore, Dr. Bergeron, and Dr. Posas have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM AAN 2023