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Dietary fat tied to better cognition in older adults
, new research suggests.
The study provides important “pieces of the puzzle” of the diet and cognition connection, but the results aren’t “ready for prime time,” study investigator Roger S. McIntyre, MD, professor of psychiatry and pharmacology, University of Toronto, said in an interview.
“I don’t think we’re there yet when it comes to recommending supplementation to the general public,” said Dr. McIntyre, adding a larger “more compelling study” is needed.
The study was published online Jan. 14 in The American Journal of Geriatric Psychiatry.
Clinically meaningful?
Research shows that 25%-50% of community-dwelling adults aged 65-85 years have some cognitive impairment. Other evidence indicates cognition is affected by dietary fat intake.
Many lines of research show that alterations in lipid homeostasis can cause brain dysfunction, said Dr. McIntyre. “This shouldn’t surprise us because our brain is made up of protein, water, and fat.”
This new analysis used combined data from the 2011-2012 and 2013-2014 cycles of the National Health and Nutrition Examination Survey (NHANES), a series of ongoing cross-sectional surveys conducted by the Centers for Disease Control and Prevention. The data are collected in two phases, an in-home face-to-face interview and a physical examination.
Researchers obtained dietary intake information through two 24-hour dietary recall interviews. Dietary information included total energy (kcal/d), intakes in grams per day (g/d) of total fat, saturated fatty acid (SFAT), monounsaturated fatty acid (MUFA), PUFA, total omega-3 and total omega-6 fatty acids, and milligrams per day (mg/d) of cholesterol.
For cognitive function, the researchers used total and delayed recall scores of the Consortium to Establish a Registry for Alzheimer’s Disease (CERAD), the animal fluency test, and the digit symbol substitution test (DSST).
The study included 2,253 adults aged 60 years and older (mean age, 69.4 years) and 51% were non-Hispanic White individuals.
After adjustment for age, sex, race/ethnicity, educational attainment, smoking status, alcohol consumption, income, and total energy, dietary intake of PUFA and omega-6 fatty acid was positively associated with DSST.
The DSST score increased about 0.06 standard deviation (SD) (about 1 score) with each SD increase in these fatty acids (8.8 g/d for PUFA and 7.9 g/d for omega-6) (P values were .02 for PUFA and .01 for omega-6).
However, it’s unclear what an improvement of 1 DSST score means clinically, said Dr. McIntyre. “The P value is significant, but how does that translate? Does this mean a person can now think more clearly or function better?”
‘Million dollar question’ remains unanswered
The fact that omega-6, considered neuroinflammatory, was associated with improved DSST score illustrates the complexity of this field, said Dr. McIntyre.
“We’re learning that when it comes to inflammation, many of the molecules in our brain that are implicated as anti-inflammatory can also be pro-inflammatory, so bad guys can be good guys and good guys can be bad guys.”
It speaks to the notion of homeostasis, he added. “Just like a seesaw; when you push this part down, that part goes up.”
The analysis showed the animal fluency score increased about 0.05 SD (around 0.3 score) with each SD (1.1 g/d) increase in dietary intake of omega-3.
There were no significant associations between other dietary fat intake and cognitive performance.
The researchers investigated the role of oxidative stress and antioxidant biomarkers (gamma glutamyl transpeptidase [GGT], bilirubin, uric acid, and vitamin D).
Cells produce oxidative radicals that are normally “mopped up” by our “innate antioxidant capability,” said Dr. McIntyre. “But in states of cognitive impairment, these oxidative stress markers accumulate and they exceed what the normal innate response is able to manage.”
The study showed GGT levels decreased with increased PUFA and omega-6 fatty acid intakes; levels of bilirubin decreased with increase in most dietary fat intakes; uric acid levels decreased with MUFA intake and omega-6/omega-3 ratio; and vitamin D levels increased with omega-3 fatty acid intake but decreased with SFAT intake.
Causal mediation analysis showed the association between dietary intake of fatty acids and DSST performance was partially mediated by GGT levels. However, Dr. McIntyre emphasized that this does not prove causality.
“The million dollar question is, is this the sole explanation for the association? In other words, is it the oxidative stress that caused the cognitive impairment and therefore correcting it improved it, or is it the case that oxidative stress is a proxy of other activities that are also taking place?”
A ‘plausible’ link
In an editorial, Candida Rebello, PhD, of the department of integrated physiology and molecular medicine at Pennington Biomedical Research Center, Baton Rouge, La., said the finding that omega-3 and omega-6 fatty acids are positively associated with cognition in older adults makes some sense.
She noted that aging is associated with an overt inflammatory phenotype, and evidence shows these fatty acids are precursors for bioactive molecules that play a role in self-limiting the acute inflammatory response.
Dr. Rebello said the positive association of omega-6 fatty acid with cognition shown in this study contrasts with the “common belief” that increasing dietary intake of these fatty acids enhances inflammation, but agreed the association is “plausible.”
She said it’s “essential” to determine “the underlying mechanisms that regulate the diverse features of inflammation and sort out the processes that protect from neuronal damage and those that contribute towards it.”
She noted the ratio of omega-6 to omega-3 is about 15:1 in the present day Western diet, as opposed to a 1:1 ratio in diets of the past. Omega-3 fatty acids are found in fish oil supplements and fatty fish like mackerel and salmon, while cereal, grains, and vegetable oil are sources of omega-6.
Attaining a measure of balance of fatty acids in the diet may be a “prudent approach,” said Dr. Rebello. “Substituting some meat entrées with fatty fish and polyunsaturated vegetable oils with monounsaturated fats such as olive oil are small changes that are likely to garner adherence.”
Dr. Rebello noted that the study used NHANES food intake data, which rely on participant self-report and so may not be accurate.
The study received funding from the MOE (Ministry of Education in China) Project of Humanities and Social Sciences and the Research Startup Fund of Southwest University. Dr. McIntyre has received research grant support from CIHR/GACD/Chinese National Natural Research Foundation and speaker/consultation fees from Lundbeck, Janssen, Purdue, Pfizer, Otsuka, Takeda, Neurocrine, Sunovion, Bausch Health, Novo Nordisk, Kris, Sanofi, Eisai, Intra-Cellular, NewBridge Pharmaceuticals, and AbbVie. He is a CEO of Braxia Scientific Corp.
A version of this article first appeared on Medscape.com.
, new research suggests.
The study provides important “pieces of the puzzle” of the diet and cognition connection, but the results aren’t “ready for prime time,” study investigator Roger S. McIntyre, MD, professor of psychiatry and pharmacology, University of Toronto, said in an interview.
“I don’t think we’re there yet when it comes to recommending supplementation to the general public,” said Dr. McIntyre, adding a larger “more compelling study” is needed.
The study was published online Jan. 14 in The American Journal of Geriatric Psychiatry.
Clinically meaningful?
Research shows that 25%-50% of community-dwelling adults aged 65-85 years have some cognitive impairment. Other evidence indicates cognition is affected by dietary fat intake.
Many lines of research show that alterations in lipid homeostasis can cause brain dysfunction, said Dr. McIntyre. “This shouldn’t surprise us because our brain is made up of protein, water, and fat.”
This new analysis used combined data from the 2011-2012 and 2013-2014 cycles of the National Health and Nutrition Examination Survey (NHANES), a series of ongoing cross-sectional surveys conducted by the Centers for Disease Control and Prevention. The data are collected in two phases, an in-home face-to-face interview and a physical examination.
Researchers obtained dietary intake information through two 24-hour dietary recall interviews. Dietary information included total energy (kcal/d), intakes in grams per day (g/d) of total fat, saturated fatty acid (SFAT), monounsaturated fatty acid (MUFA), PUFA, total omega-3 and total omega-6 fatty acids, and milligrams per day (mg/d) of cholesterol.
For cognitive function, the researchers used total and delayed recall scores of the Consortium to Establish a Registry for Alzheimer’s Disease (CERAD), the animal fluency test, and the digit symbol substitution test (DSST).
The study included 2,253 adults aged 60 years and older (mean age, 69.4 years) and 51% were non-Hispanic White individuals.
After adjustment for age, sex, race/ethnicity, educational attainment, smoking status, alcohol consumption, income, and total energy, dietary intake of PUFA and omega-6 fatty acid was positively associated with DSST.
The DSST score increased about 0.06 standard deviation (SD) (about 1 score) with each SD increase in these fatty acids (8.8 g/d for PUFA and 7.9 g/d for omega-6) (P values were .02 for PUFA and .01 for omega-6).
However, it’s unclear what an improvement of 1 DSST score means clinically, said Dr. McIntyre. “The P value is significant, but how does that translate? Does this mean a person can now think more clearly or function better?”
‘Million dollar question’ remains unanswered
The fact that omega-6, considered neuroinflammatory, was associated with improved DSST score illustrates the complexity of this field, said Dr. McIntyre.
“We’re learning that when it comes to inflammation, many of the molecules in our brain that are implicated as anti-inflammatory can also be pro-inflammatory, so bad guys can be good guys and good guys can be bad guys.”
It speaks to the notion of homeostasis, he added. “Just like a seesaw; when you push this part down, that part goes up.”
The analysis showed the animal fluency score increased about 0.05 SD (around 0.3 score) with each SD (1.1 g/d) increase in dietary intake of omega-3.
There were no significant associations between other dietary fat intake and cognitive performance.
The researchers investigated the role of oxidative stress and antioxidant biomarkers (gamma glutamyl transpeptidase [GGT], bilirubin, uric acid, and vitamin D).
Cells produce oxidative radicals that are normally “mopped up” by our “innate antioxidant capability,” said Dr. McIntyre. “But in states of cognitive impairment, these oxidative stress markers accumulate and they exceed what the normal innate response is able to manage.”
The study showed GGT levels decreased with increased PUFA and omega-6 fatty acid intakes; levels of bilirubin decreased with increase in most dietary fat intakes; uric acid levels decreased with MUFA intake and omega-6/omega-3 ratio; and vitamin D levels increased with omega-3 fatty acid intake but decreased with SFAT intake.
Causal mediation analysis showed the association between dietary intake of fatty acids and DSST performance was partially mediated by GGT levels. However, Dr. McIntyre emphasized that this does not prove causality.
“The million dollar question is, is this the sole explanation for the association? In other words, is it the oxidative stress that caused the cognitive impairment and therefore correcting it improved it, or is it the case that oxidative stress is a proxy of other activities that are also taking place?”
A ‘plausible’ link
In an editorial, Candida Rebello, PhD, of the department of integrated physiology and molecular medicine at Pennington Biomedical Research Center, Baton Rouge, La., said the finding that omega-3 and omega-6 fatty acids are positively associated with cognition in older adults makes some sense.
She noted that aging is associated with an overt inflammatory phenotype, and evidence shows these fatty acids are precursors for bioactive molecules that play a role in self-limiting the acute inflammatory response.
Dr. Rebello said the positive association of omega-6 fatty acid with cognition shown in this study contrasts with the “common belief” that increasing dietary intake of these fatty acids enhances inflammation, but agreed the association is “plausible.”
She said it’s “essential” to determine “the underlying mechanisms that regulate the diverse features of inflammation and sort out the processes that protect from neuronal damage and those that contribute towards it.”
She noted the ratio of omega-6 to omega-3 is about 15:1 in the present day Western diet, as opposed to a 1:1 ratio in diets of the past. Omega-3 fatty acids are found in fish oil supplements and fatty fish like mackerel and salmon, while cereal, grains, and vegetable oil are sources of omega-6.
Attaining a measure of balance of fatty acids in the diet may be a “prudent approach,” said Dr. Rebello. “Substituting some meat entrées with fatty fish and polyunsaturated vegetable oils with monounsaturated fats such as olive oil are small changes that are likely to garner adherence.”
Dr. Rebello noted that the study used NHANES food intake data, which rely on participant self-report and so may not be accurate.
The study received funding from the MOE (Ministry of Education in China) Project of Humanities and Social Sciences and the Research Startup Fund of Southwest University. Dr. McIntyre has received research grant support from CIHR/GACD/Chinese National Natural Research Foundation and speaker/consultation fees from Lundbeck, Janssen, Purdue, Pfizer, Otsuka, Takeda, Neurocrine, Sunovion, Bausch Health, Novo Nordisk, Kris, Sanofi, Eisai, Intra-Cellular, NewBridge Pharmaceuticals, and AbbVie. He is a CEO of Braxia Scientific Corp.
A version of this article first appeared on Medscape.com.
, new research suggests.
The study provides important “pieces of the puzzle” of the diet and cognition connection, but the results aren’t “ready for prime time,” study investigator Roger S. McIntyre, MD, professor of psychiatry and pharmacology, University of Toronto, said in an interview.
“I don’t think we’re there yet when it comes to recommending supplementation to the general public,” said Dr. McIntyre, adding a larger “more compelling study” is needed.
The study was published online Jan. 14 in The American Journal of Geriatric Psychiatry.
Clinically meaningful?
Research shows that 25%-50% of community-dwelling adults aged 65-85 years have some cognitive impairment. Other evidence indicates cognition is affected by dietary fat intake.
Many lines of research show that alterations in lipid homeostasis can cause brain dysfunction, said Dr. McIntyre. “This shouldn’t surprise us because our brain is made up of protein, water, and fat.”
This new analysis used combined data from the 2011-2012 and 2013-2014 cycles of the National Health and Nutrition Examination Survey (NHANES), a series of ongoing cross-sectional surveys conducted by the Centers for Disease Control and Prevention. The data are collected in two phases, an in-home face-to-face interview and a physical examination.
Researchers obtained dietary intake information through two 24-hour dietary recall interviews. Dietary information included total energy (kcal/d), intakes in grams per day (g/d) of total fat, saturated fatty acid (SFAT), monounsaturated fatty acid (MUFA), PUFA, total omega-3 and total omega-6 fatty acids, and milligrams per day (mg/d) of cholesterol.
For cognitive function, the researchers used total and delayed recall scores of the Consortium to Establish a Registry for Alzheimer’s Disease (CERAD), the animal fluency test, and the digit symbol substitution test (DSST).
The study included 2,253 adults aged 60 years and older (mean age, 69.4 years) and 51% were non-Hispanic White individuals.
After adjustment for age, sex, race/ethnicity, educational attainment, smoking status, alcohol consumption, income, and total energy, dietary intake of PUFA and omega-6 fatty acid was positively associated with DSST.
The DSST score increased about 0.06 standard deviation (SD) (about 1 score) with each SD increase in these fatty acids (8.8 g/d for PUFA and 7.9 g/d for omega-6) (P values were .02 for PUFA and .01 for omega-6).
However, it’s unclear what an improvement of 1 DSST score means clinically, said Dr. McIntyre. “The P value is significant, but how does that translate? Does this mean a person can now think more clearly or function better?”
‘Million dollar question’ remains unanswered
The fact that omega-6, considered neuroinflammatory, was associated with improved DSST score illustrates the complexity of this field, said Dr. McIntyre.
“We’re learning that when it comes to inflammation, many of the molecules in our brain that are implicated as anti-inflammatory can also be pro-inflammatory, so bad guys can be good guys and good guys can be bad guys.”
It speaks to the notion of homeostasis, he added. “Just like a seesaw; when you push this part down, that part goes up.”
The analysis showed the animal fluency score increased about 0.05 SD (around 0.3 score) with each SD (1.1 g/d) increase in dietary intake of omega-3.
There were no significant associations between other dietary fat intake and cognitive performance.
The researchers investigated the role of oxidative stress and antioxidant biomarkers (gamma glutamyl transpeptidase [GGT], bilirubin, uric acid, and vitamin D).
Cells produce oxidative radicals that are normally “mopped up” by our “innate antioxidant capability,” said Dr. McIntyre. “But in states of cognitive impairment, these oxidative stress markers accumulate and they exceed what the normal innate response is able to manage.”
The study showed GGT levels decreased with increased PUFA and omega-6 fatty acid intakes; levels of bilirubin decreased with increase in most dietary fat intakes; uric acid levels decreased with MUFA intake and omega-6/omega-3 ratio; and vitamin D levels increased with omega-3 fatty acid intake but decreased with SFAT intake.
Causal mediation analysis showed the association between dietary intake of fatty acids and DSST performance was partially mediated by GGT levels. However, Dr. McIntyre emphasized that this does not prove causality.
“The million dollar question is, is this the sole explanation for the association? In other words, is it the oxidative stress that caused the cognitive impairment and therefore correcting it improved it, or is it the case that oxidative stress is a proxy of other activities that are also taking place?”
A ‘plausible’ link
In an editorial, Candida Rebello, PhD, of the department of integrated physiology and molecular medicine at Pennington Biomedical Research Center, Baton Rouge, La., said the finding that omega-3 and omega-6 fatty acids are positively associated with cognition in older adults makes some sense.
She noted that aging is associated with an overt inflammatory phenotype, and evidence shows these fatty acids are precursors for bioactive molecules that play a role in self-limiting the acute inflammatory response.
Dr. Rebello said the positive association of omega-6 fatty acid with cognition shown in this study contrasts with the “common belief” that increasing dietary intake of these fatty acids enhances inflammation, but agreed the association is “plausible.”
She said it’s “essential” to determine “the underlying mechanisms that regulate the diverse features of inflammation and sort out the processes that protect from neuronal damage and those that contribute towards it.”
She noted the ratio of omega-6 to omega-3 is about 15:1 in the present day Western diet, as opposed to a 1:1 ratio in diets of the past. Omega-3 fatty acids are found in fish oil supplements and fatty fish like mackerel and salmon, while cereal, grains, and vegetable oil are sources of omega-6.
Attaining a measure of balance of fatty acids in the diet may be a “prudent approach,” said Dr. Rebello. “Substituting some meat entrées with fatty fish and polyunsaturated vegetable oils with monounsaturated fats such as olive oil are small changes that are likely to garner adherence.”
Dr. Rebello noted that the study used NHANES food intake data, which rely on participant self-report and so may not be accurate.
The study received funding from the MOE (Ministry of Education in China) Project of Humanities and Social Sciences and the Research Startup Fund of Southwest University. Dr. McIntyre has received research grant support from CIHR/GACD/Chinese National Natural Research Foundation and speaker/consultation fees from Lundbeck, Janssen, Purdue, Pfizer, Otsuka, Takeda, Neurocrine, Sunovion, Bausch Health, Novo Nordisk, Kris, Sanofi, Eisai, Intra-Cellular, NewBridge Pharmaceuticals, and AbbVie. He is a CEO of Braxia Scientific Corp.
A version of this article first appeared on Medscape.com.
AHA annual stats update highlights heart-brain connection
“For several years now, the AHA and the scientific community have increasingly recognized the connections between cardiovascular health and brain health, so it was time for us to cement this into its own chapter, which we highlight as the brain health chapter,” Connie W. Tsao, MD, MPH, chair of the statistical update writing group, with Harvard Medical School, Boston, said in an AHA podcast.
“The global rate of brain disease is quickly outpacing heart disease,” Mitchell S. V. Elkind, MD, immediate past president of the AHA, added in a news release.
“The rate of deaths from Alzheimer’s disease and other dementias rose more than twice as much in the past decade compared to the rate of deaths from heart disease, and that is something we must address,” said Dr. Elkind, with Columbia University Vagelos College of Physicians and Surgeons in New York.
“It’s becoming more evident that reducing vascular disease risk factors can make a real difference in helping people live longer, healthier lives, free of heart disease and brain disease,” Dr. Elkind added.
The AHA’s Heart Disease and Stroke Statistics – 2022 Update was published online January 26 in Circulation).
The report highlights some of the research connecting heart and brain health, including the following:
- A meta-analysis of 139 studies showed that people with midlife hypertension were five times more likely to experience impairment on global cognition and about twice as likely to experience reduced executive function, dementia, and Alzheimer’s disease.
- A meta-analysis of four longitudinal studies found that the risk for dementia associated with heart failure was increased nearly twofold.
- In the large prospective Atherosclerosis Risk in Communities (ARIC) Neurocognitive Study, atrial fibrillation was associated with greater cognitive decline and dementia over 20 years.
- A meta-analysis of 10 prospective studies (including 24,801 participants) showed that coronary heart disease (CHD) was associated with a 40% increased risk of poor cognitive outcomes, including dementia, cognitive impairment, or cognitive decline.
“This new chapter on brain health was a critical one to add,” Dr. Tsao said in the news release.
“The data we’ve collected brings to light the strong correlations between heart health and brain health and makes it an easy story to tell -- what’s good for the heart is good for the brain,” Dr. Tsao added.
Along with the new chapter on brain health, the 2022 statistical update provides the latest statistics and heart disease and stroke. Among the highlights:
- Cardiovascular disease (CVD) remains the leading cause of death worldwide. In the United States in 2019, CVD, listed as the underlying cause of death, accounted for 874,613 deaths, about 2,396 deaths each day. On average, someone dies of CVD every 36 seconds.
- CVD claims more lives each year in the United States than all forms of cancer and chronic lower respiratory disease combined.
- In 2019, CHD was the leading cause (41.3%) of deaths attributable to CVD, followed by other CVD (17.3%), stroke (17.2%), hypertension (11.7%), heart failure (9.9%), and diseases of the arteries (2.8%).
- In 2019, stroke accounted for roughly 1 in every 19 deaths in the United States. On average, someone in the United States has a stroke every 40 seconds and someone dies of stroke every 3 minutes 30 seconds. When considered separately from other CVD, stroke ranks number five among all causes of death in the United States.
While the annual statistics update aims to be a contemporary update of annual heart disease and stroke statistics over the past year, it also examines trends over time, Dr. Tsao explains in the podcast.
“One noteworthy point is that we saw a decline in the rate of cardiovascular mortality over the past three decades or so until about 2010. But over the past decade now, we’re also seeing a rise in these numbers,” she said.
This could be due to rising rates of obesity, diabetes, and poor hypertension control, as well as other lifestyle behaviors, Tsao said.
Key risk factor data
Each year, the statistical update gauges the cardiovascular health of Americans by tracking seven key health factors and behaviors that increase risk for heart disease and stroke. Below is a snapshot of the latest risk factor data.
Smoking
In 2019, smoking was the leading risk factor for years of life lost to premature death and the third leading risk factor for years of life lived with disability or injury.
According to the 2020 surgeon general’s report on smoking cessation, more than 480,000 Americans die as a result of cigarette smoking, and more than 41,000 die of secondhand smoke exposure each year (roughly 1 in 5 deaths annually).
One in 7 adults are current smokers, 1 in 6 female adults are current smokers, and 1 in 5 high school students use e-cigarettes.
Physical inactivity
In 2018, 25.4% of U.S. adults did not engage in leisure-time physical activity, and only 24.0% met the 2018 Physical Activity Guidelines for Americans for both aerobic and muscle strengthening.
Among U.S. high school students in 2019, only 44.1% were physically active for 60 minutes or more on at least 5 days of the week.
Nutrition
While there is some evidence that Americans are improving their diet, fewer than 10% of U.S. adults met guidelines for whole grain, whole fruit, and nonstarchy vegetable consumption each day in 2017–2018.
Overweight/obesity
The prevalence of obesity among adults increased from 1999–2000 through 2017–2018 from 30.5% to 42.4%. Overall prevalence of obesity and severe obesity in U.S. youth 2 to 19 years of age increased from 13.9% to 19.3% and 2.6% to 6.1% between 1999–2000 and 2017–2018.
Cholesterol
Close to 94 million (38.1%) U.S. adults have total cholesterol of 200 mg/dL or higher, according to 2015–2018 data; about 28.0 million (11.5%) have total cholesterol of 240 mg/dL or higher; and 27.8% have high levels of low-density lipoprotein cholesterol (130 mg/dL or higher).
Diabetes
In 2019, 87,647 U.S. deaths were attributed to diabetes; data show that 9.8 million U.S. adults have undiagnosed diabetes, 28.2 million have diagnosed diabetes, and 113.6 million have prediabetes.
Hypertension
A total of 121.5 million (47.3%) U.S. adults have hypertension, based on 2015–2018 data. In 2019, 102,072 U.S. deaths were primarily attributable to hypertension.
This statistical update was prepared by a volunteer writing group on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Disclosures for the writing committee are listed with the original article.
A version of this article first appeared on Medscape.com.
“For several years now, the AHA and the scientific community have increasingly recognized the connections between cardiovascular health and brain health, so it was time for us to cement this into its own chapter, which we highlight as the brain health chapter,” Connie W. Tsao, MD, MPH, chair of the statistical update writing group, with Harvard Medical School, Boston, said in an AHA podcast.
“The global rate of brain disease is quickly outpacing heart disease,” Mitchell S. V. Elkind, MD, immediate past president of the AHA, added in a news release.
“The rate of deaths from Alzheimer’s disease and other dementias rose more than twice as much in the past decade compared to the rate of deaths from heart disease, and that is something we must address,” said Dr. Elkind, with Columbia University Vagelos College of Physicians and Surgeons in New York.
“It’s becoming more evident that reducing vascular disease risk factors can make a real difference in helping people live longer, healthier lives, free of heart disease and brain disease,” Dr. Elkind added.
The AHA’s Heart Disease and Stroke Statistics – 2022 Update was published online January 26 in Circulation).
The report highlights some of the research connecting heart and brain health, including the following:
- A meta-analysis of 139 studies showed that people with midlife hypertension were five times more likely to experience impairment on global cognition and about twice as likely to experience reduced executive function, dementia, and Alzheimer’s disease.
- A meta-analysis of four longitudinal studies found that the risk for dementia associated with heart failure was increased nearly twofold.
- In the large prospective Atherosclerosis Risk in Communities (ARIC) Neurocognitive Study, atrial fibrillation was associated with greater cognitive decline and dementia over 20 years.
- A meta-analysis of 10 prospective studies (including 24,801 participants) showed that coronary heart disease (CHD) was associated with a 40% increased risk of poor cognitive outcomes, including dementia, cognitive impairment, or cognitive decline.
“This new chapter on brain health was a critical one to add,” Dr. Tsao said in the news release.
“The data we’ve collected brings to light the strong correlations between heart health and brain health and makes it an easy story to tell -- what’s good for the heart is good for the brain,” Dr. Tsao added.
Along with the new chapter on brain health, the 2022 statistical update provides the latest statistics and heart disease and stroke. Among the highlights:
- Cardiovascular disease (CVD) remains the leading cause of death worldwide. In the United States in 2019, CVD, listed as the underlying cause of death, accounted for 874,613 deaths, about 2,396 deaths each day. On average, someone dies of CVD every 36 seconds.
- CVD claims more lives each year in the United States than all forms of cancer and chronic lower respiratory disease combined.
- In 2019, CHD was the leading cause (41.3%) of deaths attributable to CVD, followed by other CVD (17.3%), stroke (17.2%), hypertension (11.7%), heart failure (9.9%), and diseases of the arteries (2.8%).
- In 2019, stroke accounted for roughly 1 in every 19 deaths in the United States. On average, someone in the United States has a stroke every 40 seconds and someone dies of stroke every 3 minutes 30 seconds. When considered separately from other CVD, stroke ranks number five among all causes of death in the United States.
While the annual statistics update aims to be a contemporary update of annual heart disease and stroke statistics over the past year, it also examines trends over time, Dr. Tsao explains in the podcast.
“One noteworthy point is that we saw a decline in the rate of cardiovascular mortality over the past three decades or so until about 2010. But over the past decade now, we’re also seeing a rise in these numbers,” she said.
This could be due to rising rates of obesity, diabetes, and poor hypertension control, as well as other lifestyle behaviors, Tsao said.
Key risk factor data
Each year, the statistical update gauges the cardiovascular health of Americans by tracking seven key health factors and behaviors that increase risk for heart disease and stroke. Below is a snapshot of the latest risk factor data.
Smoking
In 2019, smoking was the leading risk factor for years of life lost to premature death and the third leading risk factor for years of life lived with disability or injury.
According to the 2020 surgeon general’s report on smoking cessation, more than 480,000 Americans die as a result of cigarette smoking, and more than 41,000 die of secondhand smoke exposure each year (roughly 1 in 5 deaths annually).
One in 7 adults are current smokers, 1 in 6 female adults are current smokers, and 1 in 5 high school students use e-cigarettes.
Physical inactivity
In 2018, 25.4% of U.S. adults did not engage in leisure-time physical activity, and only 24.0% met the 2018 Physical Activity Guidelines for Americans for both aerobic and muscle strengthening.
Among U.S. high school students in 2019, only 44.1% were physically active for 60 minutes or more on at least 5 days of the week.
Nutrition
While there is some evidence that Americans are improving their diet, fewer than 10% of U.S. adults met guidelines for whole grain, whole fruit, and nonstarchy vegetable consumption each day in 2017–2018.
Overweight/obesity
The prevalence of obesity among adults increased from 1999–2000 through 2017–2018 from 30.5% to 42.4%. Overall prevalence of obesity and severe obesity in U.S. youth 2 to 19 years of age increased from 13.9% to 19.3% and 2.6% to 6.1% between 1999–2000 and 2017–2018.
Cholesterol
Close to 94 million (38.1%) U.S. adults have total cholesterol of 200 mg/dL or higher, according to 2015–2018 data; about 28.0 million (11.5%) have total cholesterol of 240 mg/dL or higher; and 27.8% have high levels of low-density lipoprotein cholesterol (130 mg/dL or higher).
Diabetes
In 2019, 87,647 U.S. deaths were attributed to diabetes; data show that 9.8 million U.S. adults have undiagnosed diabetes, 28.2 million have diagnosed diabetes, and 113.6 million have prediabetes.
Hypertension
A total of 121.5 million (47.3%) U.S. adults have hypertension, based on 2015–2018 data. In 2019, 102,072 U.S. deaths were primarily attributable to hypertension.
This statistical update was prepared by a volunteer writing group on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Disclosures for the writing committee are listed with the original article.
A version of this article first appeared on Medscape.com.
“For several years now, the AHA and the scientific community have increasingly recognized the connections between cardiovascular health and brain health, so it was time for us to cement this into its own chapter, which we highlight as the brain health chapter,” Connie W. Tsao, MD, MPH, chair of the statistical update writing group, with Harvard Medical School, Boston, said in an AHA podcast.
“The global rate of brain disease is quickly outpacing heart disease,” Mitchell S. V. Elkind, MD, immediate past president of the AHA, added in a news release.
“The rate of deaths from Alzheimer’s disease and other dementias rose more than twice as much in the past decade compared to the rate of deaths from heart disease, and that is something we must address,” said Dr. Elkind, with Columbia University Vagelos College of Physicians and Surgeons in New York.
“It’s becoming more evident that reducing vascular disease risk factors can make a real difference in helping people live longer, healthier lives, free of heart disease and brain disease,” Dr. Elkind added.
The AHA’s Heart Disease and Stroke Statistics – 2022 Update was published online January 26 in Circulation).
The report highlights some of the research connecting heart and brain health, including the following:
- A meta-analysis of 139 studies showed that people with midlife hypertension were five times more likely to experience impairment on global cognition and about twice as likely to experience reduced executive function, dementia, and Alzheimer’s disease.
- A meta-analysis of four longitudinal studies found that the risk for dementia associated with heart failure was increased nearly twofold.
- In the large prospective Atherosclerosis Risk in Communities (ARIC) Neurocognitive Study, atrial fibrillation was associated with greater cognitive decline and dementia over 20 years.
- A meta-analysis of 10 prospective studies (including 24,801 participants) showed that coronary heart disease (CHD) was associated with a 40% increased risk of poor cognitive outcomes, including dementia, cognitive impairment, or cognitive decline.
“This new chapter on brain health was a critical one to add,” Dr. Tsao said in the news release.
“The data we’ve collected brings to light the strong correlations between heart health and brain health and makes it an easy story to tell -- what’s good for the heart is good for the brain,” Dr. Tsao added.
Along with the new chapter on brain health, the 2022 statistical update provides the latest statistics and heart disease and stroke. Among the highlights:
- Cardiovascular disease (CVD) remains the leading cause of death worldwide. In the United States in 2019, CVD, listed as the underlying cause of death, accounted for 874,613 deaths, about 2,396 deaths each day. On average, someone dies of CVD every 36 seconds.
- CVD claims more lives each year in the United States than all forms of cancer and chronic lower respiratory disease combined.
- In 2019, CHD was the leading cause (41.3%) of deaths attributable to CVD, followed by other CVD (17.3%), stroke (17.2%), hypertension (11.7%), heart failure (9.9%), and diseases of the arteries (2.8%).
- In 2019, stroke accounted for roughly 1 in every 19 deaths in the United States. On average, someone in the United States has a stroke every 40 seconds and someone dies of stroke every 3 minutes 30 seconds. When considered separately from other CVD, stroke ranks number five among all causes of death in the United States.
While the annual statistics update aims to be a contemporary update of annual heart disease and stroke statistics over the past year, it also examines trends over time, Dr. Tsao explains in the podcast.
“One noteworthy point is that we saw a decline in the rate of cardiovascular mortality over the past three decades or so until about 2010. But over the past decade now, we’re also seeing a rise in these numbers,” she said.
This could be due to rising rates of obesity, diabetes, and poor hypertension control, as well as other lifestyle behaviors, Tsao said.
Key risk factor data
Each year, the statistical update gauges the cardiovascular health of Americans by tracking seven key health factors and behaviors that increase risk for heart disease and stroke. Below is a snapshot of the latest risk factor data.
Smoking
In 2019, smoking was the leading risk factor for years of life lost to premature death and the third leading risk factor for years of life lived with disability or injury.
According to the 2020 surgeon general’s report on smoking cessation, more than 480,000 Americans die as a result of cigarette smoking, and more than 41,000 die of secondhand smoke exposure each year (roughly 1 in 5 deaths annually).
One in 7 adults are current smokers, 1 in 6 female adults are current smokers, and 1 in 5 high school students use e-cigarettes.
Physical inactivity
In 2018, 25.4% of U.S. adults did not engage in leisure-time physical activity, and only 24.0% met the 2018 Physical Activity Guidelines for Americans for both aerobic and muscle strengthening.
Among U.S. high school students in 2019, only 44.1% were physically active for 60 minutes or more on at least 5 days of the week.
Nutrition
While there is some evidence that Americans are improving their diet, fewer than 10% of U.S. adults met guidelines for whole grain, whole fruit, and nonstarchy vegetable consumption each day in 2017–2018.
Overweight/obesity
The prevalence of obesity among adults increased from 1999–2000 through 2017–2018 from 30.5% to 42.4%. Overall prevalence of obesity and severe obesity in U.S. youth 2 to 19 years of age increased from 13.9% to 19.3% and 2.6% to 6.1% between 1999–2000 and 2017–2018.
Cholesterol
Close to 94 million (38.1%) U.S. adults have total cholesterol of 200 mg/dL or higher, according to 2015–2018 data; about 28.0 million (11.5%) have total cholesterol of 240 mg/dL or higher; and 27.8% have high levels of low-density lipoprotein cholesterol (130 mg/dL or higher).
Diabetes
In 2019, 87,647 U.S. deaths were attributed to diabetes; data show that 9.8 million U.S. adults have undiagnosed diabetes, 28.2 million have diagnosed diabetes, and 113.6 million have prediabetes.
Hypertension
A total of 121.5 million (47.3%) U.S. adults have hypertension, based on 2015–2018 data. In 2019, 102,072 U.S. deaths were primarily attributable to hypertension.
This statistical update was prepared by a volunteer writing group on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Disclosures for the writing committee are listed with the original article.
A version of this article first appeared on Medscape.com.
Screen time in first year may raise autism risk at age 3
Boys exposed to at least 2 hours a day of screen time by 1 year of age were significantly more likely to have an autism spectrum disorder (ASD) diagnosis at 3 years, based on data from more than 80,000 children.
The World Health Organization and the American Academy of Pediatrics recommend against any screen time for infants up to 1 year of age and 18 months of age, respectively, wrote Megumi Kushima, MA, of the University of Yamanashi (Japan), and colleagues on behalf of the Japan Environment and Children’s Study Group.
The extent to which screen time duration in infancy is associated with subsequent ASD diagnosis remains unclear, the researchers said. The ongoing COVID-19 pandemic has increased screen time among children worldwide, which makes an examination of the impact of screen time on children’s health an important public health issue.
In a study published in JAMA Pediatrics, the researchers recruited pregnant women between 2011 and 2014; data were analyzed in December 2020. The final study population included 84,030 mother-child pairs. The primary exposure of screen time at 1 year of age was assessed by questionnaire, in which mothers were asked to report their number of hours they let their child watch TV or DVDs daily. Responses were none (no screen time), less than 1 hour, 1 hour or more but less than 2 hours, 2 hours or more but less than 4 hours, and 4 hours or more.
The primary outcome was ASD diagnosis at 3 years of age, and mothers were asked via questionnaire whether their 3-year-old had been diagnosed with ASD from age 2.
The study was conducted by the Japan Environment and Children’s Study Group at 15 regional centers across Japan.
Overall, 330 children had received an ASD diagnosis at age 3 years, a prevalence of 0.4%. Of these, 251 (76%) were boys, and 79 (24%) were girls. Independent of ASD, the most common response for screen time was less than 1 hour, which was reported by 27,707 mothers. The proportion of children with ASD at age 3 increased as screen time at age 1 increased, the percentages were 5.8%, 22.3%, 30.2%, and 31.7% for children with no screen time, less than 1 hour, 1 to less than 2 hours, and 2 to less than 4 hours, respectively. The percentage of children with ASD diagnoses who had 4 hours or more of daily screen time was 10%.
Logistic regression analysis showed that longer screen time at age 1 year was significantly associated with higher odds of ASD at 3 years in boys, but not in girls. The researchers controlled for variables including maternal maltreatment and children’s predisposition to ASD. Among boys, the adjusted odds ratios for screen times of less than 1 hour, 1 hour to less than 2 hours, 2 hours to less than 4 hours, and more than 4 hours were 1.38, 2.16, 3.48, and 3.02, respectively.
Screen time at age 3 years was not associated with ASD diagnosis at age 3 years, potentially “because the association with environmental factors on brain development varies with age,” the researchers noted.
The study findings were limited by several factors including the reliance on parental reports of screen time and potential for reporting bias, the researchers noted. Other limitations included the possible missed diagnoses of mild ASD cases at 3 years, and the inability to consider variables such as childcare environment, living conditions, diseases, genetics, and disabilities.
However, the results were strengthened by the large study population and examination of screen time in early childhood, they said. More research is needed to examine other factors that contribute to the association between ASD and screen time, but given the rapid increase in device use in children, “it is necessary to review its health effects on infants and control excessive screen time.”
Strong study, but some gaps appear
The study is strong in many respects, Karalyn Kinsella, MD, a pediatrician in private practice in Cheshire, Conn., said in an interview.
However, “what I am not sure they addressed is that children on the spectrum are often not entertained by basic toys and may be hard to manage behaviorally,” Dr. Kinsella said. Consequently, parents may be more inclined to offer screen time as a way to pacify children with behavioral difficulties. “Parents also may see that their children are happier interacting with devices, so they may be more apt to let them continue with screen time.We know screen time is not good for the developing brain, however; I worry that the message from this study is that screen time causes autism in boys.
“What I would have liked to know from the parents who allowed more screen time was why they were offering it,” Dr. Kinsella said. “Was it because their child was difficult behaviorally or because that is the one place that they seemed to have satisfaction? To me, that would indicate the reverse hypothesis.” That said, the study findings “remind us to counsel families about screen time, especially in the age of COVID-19. Kids are home much longer than usual, which ultimately leads to more screen time.”
The study was funded by the Japanese Ministry of Environment. The researchers had no financial conflicts to disclose. Dr. Kinsella had no financial conflicts to disclose, but serves as a member of the Pediatric News editorial advisory board.
Boys exposed to at least 2 hours a day of screen time by 1 year of age were significantly more likely to have an autism spectrum disorder (ASD) diagnosis at 3 years, based on data from more than 80,000 children.
The World Health Organization and the American Academy of Pediatrics recommend against any screen time for infants up to 1 year of age and 18 months of age, respectively, wrote Megumi Kushima, MA, of the University of Yamanashi (Japan), and colleagues on behalf of the Japan Environment and Children’s Study Group.
The extent to which screen time duration in infancy is associated with subsequent ASD diagnosis remains unclear, the researchers said. The ongoing COVID-19 pandemic has increased screen time among children worldwide, which makes an examination of the impact of screen time on children’s health an important public health issue.
In a study published in JAMA Pediatrics, the researchers recruited pregnant women between 2011 and 2014; data were analyzed in December 2020. The final study population included 84,030 mother-child pairs. The primary exposure of screen time at 1 year of age was assessed by questionnaire, in which mothers were asked to report their number of hours they let their child watch TV or DVDs daily. Responses were none (no screen time), less than 1 hour, 1 hour or more but less than 2 hours, 2 hours or more but less than 4 hours, and 4 hours or more.
The primary outcome was ASD diagnosis at 3 years of age, and mothers were asked via questionnaire whether their 3-year-old had been diagnosed with ASD from age 2.
The study was conducted by the Japan Environment and Children’s Study Group at 15 regional centers across Japan.
Overall, 330 children had received an ASD diagnosis at age 3 years, a prevalence of 0.4%. Of these, 251 (76%) were boys, and 79 (24%) were girls. Independent of ASD, the most common response for screen time was less than 1 hour, which was reported by 27,707 mothers. The proportion of children with ASD at age 3 increased as screen time at age 1 increased, the percentages were 5.8%, 22.3%, 30.2%, and 31.7% for children with no screen time, less than 1 hour, 1 to less than 2 hours, and 2 to less than 4 hours, respectively. The percentage of children with ASD diagnoses who had 4 hours or more of daily screen time was 10%.
Logistic regression analysis showed that longer screen time at age 1 year was significantly associated with higher odds of ASD at 3 years in boys, but not in girls. The researchers controlled for variables including maternal maltreatment and children’s predisposition to ASD. Among boys, the adjusted odds ratios for screen times of less than 1 hour, 1 hour to less than 2 hours, 2 hours to less than 4 hours, and more than 4 hours were 1.38, 2.16, 3.48, and 3.02, respectively.
Screen time at age 3 years was not associated with ASD diagnosis at age 3 years, potentially “because the association with environmental factors on brain development varies with age,” the researchers noted.
The study findings were limited by several factors including the reliance on parental reports of screen time and potential for reporting bias, the researchers noted. Other limitations included the possible missed diagnoses of mild ASD cases at 3 years, and the inability to consider variables such as childcare environment, living conditions, diseases, genetics, and disabilities.
However, the results were strengthened by the large study population and examination of screen time in early childhood, they said. More research is needed to examine other factors that contribute to the association between ASD and screen time, but given the rapid increase in device use in children, “it is necessary to review its health effects on infants and control excessive screen time.”
Strong study, but some gaps appear
The study is strong in many respects, Karalyn Kinsella, MD, a pediatrician in private practice in Cheshire, Conn., said in an interview.
However, “what I am not sure they addressed is that children on the spectrum are often not entertained by basic toys and may be hard to manage behaviorally,” Dr. Kinsella said. Consequently, parents may be more inclined to offer screen time as a way to pacify children with behavioral difficulties. “Parents also may see that their children are happier interacting with devices, so they may be more apt to let them continue with screen time.We know screen time is not good for the developing brain, however; I worry that the message from this study is that screen time causes autism in boys.
“What I would have liked to know from the parents who allowed more screen time was why they were offering it,” Dr. Kinsella said. “Was it because their child was difficult behaviorally or because that is the one place that they seemed to have satisfaction? To me, that would indicate the reverse hypothesis.” That said, the study findings “remind us to counsel families about screen time, especially in the age of COVID-19. Kids are home much longer than usual, which ultimately leads to more screen time.”
The study was funded by the Japanese Ministry of Environment. The researchers had no financial conflicts to disclose. Dr. Kinsella had no financial conflicts to disclose, but serves as a member of the Pediatric News editorial advisory board.
Boys exposed to at least 2 hours a day of screen time by 1 year of age were significantly more likely to have an autism spectrum disorder (ASD) diagnosis at 3 years, based on data from more than 80,000 children.
The World Health Organization and the American Academy of Pediatrics recommend against any screen time for infants up to 1 year of age and 18 months of age, respectively, wrote Megumi Kushima, MA, of the University of Yamanashi (Japan), and colleagues on behalf of the Japan Environment and Children’s Study Group.
The extent to which screen time duration in infancy is associated with subsequent ASD diagnosis remains unclear, the researchers said. The ongoing COVID-19 pandemic has increased screen time among children worldwide, which makes an examination of the impact of screen time on children’s health an important public health issue.
In a study published in JAMA Pediatrics, the researchers recruited pregnant women between 2011 and 2014; data were analyzed in December 2020. The final study population included 84,030 mother-child pairs. The primary exposure of screen time at 1 year of age was assessed by questionnaire, in which mothers were asked to report their number of hours they let their child watch TV or DVDs daily. Responses were none (no screen time), less than 1 hour, 1 hour or more but less than 2 hours, 2 hours or more but less than 4 hours, and 4 hours or more.
The primary outcome was ASD diagnosis at 3 years of age, and mothers were asked via questionnaire whether their 3-year-old had been diagnosed with ASD from age 2.
The study was conducted by the Japan Environment and Children’s Study Group at 15 regional centers across Japan.
Overall, 330 children had received an ASD diagnosis at age 3 years, a prevalence of 0.4%. Of these, 251 (76%) were boys, and 79 (24%) were girls. Independent of ASD, the most common response for screen time was less than 1 hour, which was reported by 27,707 mothers. The proportion of children with ASD at age 3 increased as screen time at age 1 increased, the percentages were 5.8%, 22.3%, 30.2%, and 31.7% for children with no screen time, less than 1 hour, 1 to less than 2 hours, and 2 to less than 4 hours, respectively. The percentage of children with ASD diagnoses who had 4 hours or more of daily screen time was 10%.
Logistic regression analysis showed that longer screen time at age 1 year was significantly associated with higher odds of ASD at 3 years in boys, but not in girls. The researchers controlled for variables including maternal maltreatment and children’s predisposition to ASD. Among boys, the adjusted odds ratios for screen times of less than 1 hour, 1 hour to less than 2 hours, 2 hours to less than 4 hours, and more than 4 hours were 1.38, 2.16, 3.48, and 3.02, respectively.
Screen time at age 3 years was not associated with ASD diagnosis at age 3 years, potentially “because the association with environmental factors on brain development varies with age,” the researchers noted.
The study findings were limited by several factors including the reliance on parental reports of screen time and potential for reporting bias, the researchers noted. Other limitations included the possible missed diagnoses of mild ASD cases at 3 years, and the inability to consider variables such as childcare environment, living conditions, diseases, genetics, and disabilities.
However, the results were strengthened by the large study population and examination of screen time in early childhood, they said. More research is needed to examine other factors that contribute to the association between ASD and screen time, but given the rapid increase in device use in children, “it is necessary to review its health effects on infants and control excessive screen time.”
Strong study, but some gaps appear
The study is strong in many respects, Karalyn Kinsella, MD, a pediatrician in private practice in Cheshire, Conn., said in an interview.
However, “what I am not sure they addressed is that children on the spectrum are often not entertained by basic toys and may be hard to manage behaviorally,” Dr. Kinsella said. Consequently, parents may be more inclined to offer screen time as a way to pacify children with behavioral difficulties. “Parents also may see that their children are happier interacting with devices, so they may be more apt to let them continue with screen time.We know screen time is not good for the developing brain, however; I worry that the message from this study is that screen time causes autism in boys.
“What I would have liked to know from the parents who allowed more screen time was why they were offering it,” Dr. Kinsella said. “Was it because their child was difficult behaviorally or because that is the one place that they seemed to have satisfaction? To me, that would indicate the reverse hypothesis.” That said, the study findings “remind us to counsel families about screen time, especially in the age of COVID-19. Kids are home much longer than usual, which ultimately leads to more screen time.”
The study was funded by the Japanese Ministry of Environment. The researchers had no financial conflicts to disclose. Dr. Kinsella had no financial conflicts to disclose, but serves as a member of the Pediatric News editorial advisory board.
FROM JAMA PEDIATRICS
Men with hypersexual disorder may have oxytocin overload
Men with hypersexual disorder showed higher levels of oxytocin in their blood than did healthy control men without the disorder, in a study with 102 participants.
Hypersexual disorder (HD) is characterized by “excessive and persistent sexual behaviors in relation to various mood states, with an impulsivity component and experienced loss of control,” John Flanagan, MD, of the Karolinska Institutet in Stockholm and colleagues wrote. Although HD is not included as a separate diagnosis in the current DSM, the similar disorder of compulsive sexual behavior is included in the ICD.
Data on the pathophysiology of HD are limited, although a previous study by corresponding author Andreas Chatzittofis, MD, and colleagues showed evidence of neuroendocrine dysregulation in men with HD, and prompted the current study to explore the possible involvement of the oxytocinergic system in HD.
In the current study, published in the Journal of Clinical Endocrinology & Metabolism, the researchers identified 64 men with HD and 38 healthy male controls. The patients were help-seeking men older than 18 years diagnosed with HD who presented to a single center in Sweden during 2013-2014. The men were included in a randomized clinical trial of cognitive-behavioral therapy for HD, and 30 of them participated in a 7-week CBT program.
Oxytocin, secreted by the pituitary gland, is known to play a role in sexual behavior, but has not been examined in HD men, the researchers said. At baseline, the mean plasma oxytocin was 31.0 pM in the HD patients, which was significantly higher than the mean 16.9 pM in healthy controls (P < .001). However, the 30 HD men who underwent CBT showed significant improvement in oxytocin levels, from a mean pretreatment level of 30.5 to a mean posttreatment level of 20.2 pM (P = .0000019).
The study findings were limited by several factors, including the lack of data on oxytocin for a wait list or control group, as well as the inability to control for confounding factors such as diet, physical activity, ethnicity, and stress, and a lack of data on sexual activity prior to oxytocin measurements, the researchers noted.
However, “although there is no clear consensus at this point, previous studies support the use of oxytocin plasma levels as a surrogate variable for [cerebrospinal fluid] oxytocin activity,” the researchers wrote in their discussion. The current study findings support the potential of oxytocin as a biomarker for HD diagnostics and also as a measure of disease severity. Larger studies to confirm the findings, especially those that exclude potential confounders, would be valuable.
Oxytocin may be treatment target
The study is important because of the lack of knowledge regarding the pathophysiology underlying hypersexual disorder, Dr. Chatzittofis of the University of Cyprus, Nicosia, said in an interview. “This is the first study to indicate a role for oxytocin’s involvement” in hypersexual disorder in men. Dr. Chatzittofis led a team in a previous study that showed an association between HD in men and dysregulation of the hypothalamic pituitary adrenal axis.
In the current study, “we discovered that men with compulsive sexual behavior disorder had higher oxytocin levels, compared with healthy men,” said Dr. Chatzittofis, adding that the take-home message for clinicians is the potential of CBT for treatment. “Cognitive-behavior therapy led to a reduction in both hypersexual behavior and oxytocin levels.” The results suggest that oxytocin plays an important role in sex addiction.
Consequently, oxytocin may be a potential drug target for future pharmacologic treatment of hypersexual disorder, he added.
The study was supported by the Swedish Research Council, the Stockholm County Council, and by a partnership between Umeå University and Västerbotten County Council. The researchers had no financial conflicts to disclose.
Men with hypersexual disorder showed higher levels of oxytocin in their blood than did healthy control men without the disorder, in a study with 102 participants.
Hypersexual disorder (HD) is characterized by “excessive and persistent sexual behaviors in relation to various mood states, with an impulsivity component and experienced loss of control,” John Flanagan, MD, of the Karolinska Institutet in Stockholm and colleagues wrote. Although HD is not included as a separate diagnosis in the current DSM, the similar disorder of compulsive sexual behavior is included in the ICD.
Data on the pathophysiology of HD are limited, although a previous study by corresponding author Andreas Chatzittofis, MD, and colleagues showed evidence of neuroendocrine dysregulation in men with HD, and prompted the current study to explore the possible involvement of the oxytocinergic system in HD.
In the current study, published in the Journal of Clinical Endocrinology & Metabolism, the researchers identified 64 men with HD and 38 healthy male controls. The patients were help-seeking men older than 18 years diagnosed with HD who presented to a single center in Sweden during 2013-2014. The men were included in a randomized clinical trial of cognitive-behavioral therapy for HD, and 30 of them participated in a 7-week CBT program.
Oxytocin, secreted by the pituitary gland, is known to play a role in sexual behavior, but has not been examined in HD men, the researchers said. At baseline, the mean plasma oxytocin was 31.0 pM in the HD patients, which was significantly higher than the mean 16.9 pM in healthy controls (P < .001). However, the 30 HD men who underwent CBT showed significant improvement in oxytocin levels, from a mean pretreatment level of 30.5 to a mean posttreatment level of 20.2 pM (P = .0000019).
The study findings were limited by several factors, including the lack of data on oxytocin for a wait list or control group, as well as the inability to control for confounding factors such as diet, physical activity, ethnicity, and stress, and a lack of data on sexual activity prior to oxytocin measurements, the researchers noted.
However, “although there is no clear consensus at this point, previous studies support the use of oxytocin plasma levels as a surrogate variable for [cerebrospinal fluid] oxytocin activity,” the researchers wrote in their discussion. The current study findings support the potential of oxytocin as a biomarker for HD diagnostics and also as a measure of disease severity. Larger studies to confirm the findings, especially those that exclude potential confounders, would be valuable.
Oxytocin may be treatment target
The study is important because of the lack of knowledge regarding the pathophysiology underlying hypersexual disorder, Dr. Chatzittofis of the University of Cyprus, Nicosia, said in an interview. “This is the first study to indicate a role for oxytocin’s involvement” in hypersexual disorder in men. Dr. Chatzittofis led a team in a previous study that showed an association between HD in men and dysregulation of the hypothalamic pituitary adrenal axis.
In the current study, “we discovered that men with compulsive sexual behavior disorder had higher oxytocin levels, compared with healthy men,” said Dr. Chatzittofis, adding that the take-home message for clinicians is the potential of CBT for treatment. “Cognitive-behavior therapy led to a reduction in both hypersexual behavior and oxytocin levels.” The results suggest that oxytocin plays an important role in sex addiction.
Consequently, oxytocin may be a potential drug target for future pharmacologic treatment of hypersexual disorder, he added.
The study was supported by the Swedish Research Council, the Stockholm County Council, and by a partnership between Umeå University and Västerbotten County Council. The researchers had no financial conflicts to disclose.
Men with hypersexual disorder showed higher levels of oxytocin in their blood than did healthy control men without the disorder, in a study with 102 participants.
Hypersexual disorder (HD) is characterized by “excessive and persistent sexual behaviors in relation to various mood states, with an impulsivity component and experienced loss of control,” John Flanagan, MD, of the Karolinska Institutet in Stockholm and colleagues wrote. Although HD is not included as a separate diagnosis in the current DSM, the similar disorder of compulsive sexual behavior is included in the ICD.
Data on the pathophysiology of HD are limited, although a previous study by corresponding author Andreas Chatzittofis, MD, and colleagues showed evidence of neuroendocrine dysregulation in men with HD, and prompted the current study to explore the possible involvement of the oxytocinergic system in HD.
In the current study, published in the Journal of Clinical Endocrinology & Metabolism, the researchers identified 64 men with HD and 38 healthy male controls. The patients were help-seeking men older than 18 years diagnosed with HD who presented to a single center in Sweden during 2013-2014. The men were included in a randomized clinical trial of cognitive-behavioral therapy for HD, and 30 of them participated in a 7-week CBT program.
Oxytocin, secreted by the pituitary gland, is known to play a role in sexual behavior, but has not been examined in HD men, the researchers said. At baseline, the mean plasma oxytocin was 31.0 pM in the HD patients, which was significantly higher than the mean 16.9 pM in healthy controls (P < .001). However, the 30 HD men who underwent CBT showed significant improvement in oxytocin levels, from a mean pretreatment level of 30.5 to a mean posttreatment level of 20.2 pM (P = .0000019).
The study findings were limited by several factors, including the lack of data on oxytocin for a wait list or control group, as well as the inability to control for confounding factors such as diet, physical activity, ethnicity, and stress, and a lack of data on sexual activity prior to oxytocin measurements, the researchers noted.
However, “although there is no clear consensus at this point, previous studies support the use of oxytocin plasma levels as a surrogate variable for [cerebrospinal fluid] oxytocin activity,” the researchers wrote in their discussion. The current study findings support the potential of oxytocin as a biomarker for HD diagnostics and also as a measure of disease severity. Larger studies to confirm the findings, especially those that exclude potential confounders, would be valuable.
Oxytocin may be treatment target
The study is important because of the lack of knowledge regarding the pathophysiology underlying hypersexual disorder, Dr. Chatzittofis of the University of Cyprus, Nicosia, said in an interview. “This is the first study to indicate a role for oxytocin’s involvement” in hypersexual disorder in men. Dr. Chatzittofis led a team in a previous study that showed an association between HD in men and dysregulation of the hypothalamic pituitary adrenal axis.
In the current study, “we discovered that men with compulsive sexual behavior disorder had higher oxytocin levels, compared with healthy men,” said Dr. Chatzittofis, adding that the take-home message for clinicians is the potential of CBT for treatment. “Cognitive-behavior therapy led to a reduction in both hypersexual behavior and oxytocin levels.” The results suggest that oxytocin plays an important role in sex addiction.
Consequently, oxytocin may be a potential drug target for future pharmacologic treatment of hypersexual disorder, he added.
The study was supported by the Swedish Research Council, the Stockholm County Council, and by a partnership between Umeå University and Västerbotten County Council. The researchers had no financial conflicts to disclose.
FROM THE JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
Ischemic stroke rates higher in young women than young men
Young women appear to be at a higher risk of ischemic stroke than young men, according to a new systematic review of studies on this topic.
The review included 19 studies that reported on sex-specific stroke incidence among young adults and found that overall, in young adults aged 18-35 years, there were 44% more women with ischemic strokes than men.
This gap narrowed in the age group 35-45 years, for which there was conflicting evidence whether more men or women have ischemic strokes.
“An assertion that young women may be disproportionately at risk of ischemic stroke represents a significant departure from our current scientific understanding and may have important implications about the etiology of ischemic strokes in young adults,” the authors note.
“One of the take-home messages from this study is that stroke happens across the entire age spectrum, including young adults, even if they do not have traditional risk factors,” study coauthor Sharon N. Poisson, MD, associate professor of neurology at the University of Colorado Anschutz Medical Campus, Denver, told this news organization.
“If a young person presents with focal neurological symptoms, the possibility of a stroke should not be discounted just because they may not fit the typical profile of a stroke patient. We need more education of the population that young people – including young women – can have a stroke and that fast action to call emergency services is critical,” she said.
The study was published online Jan. 24 in the journal Stroke as part of a special “Go Red for Women” spotlight issue.
The researchers note that historically it has been believed that men have a higher incidence of stroke in every age group until very old age. However, recent evidence focused on the young adult age group has reported that there are more young women (ages 18-45) with ischemic strokes compared with young men, suggesting that young women may be disproportionately at risk compared with their male counterparts.
Pointing out that a better understanding of these sex differences is important in implementing strategies that can more effectively prevent and treat strokes in this age group, the researchers conducted the current review to synthesize the updated evidence.
They searched PubMed from January 2008 to July 2021 for relevant studies that were population-based and reported stroke incidence by sex or sex-specific incidence rate ratios of young adults age 45 and younger. Statistical synthesis was performed to estimate sex difference by age group (less than or equal to 35, 35-45 and less than or equal to 45 years) and stroke type.
They found 19 relevant studies, including three that reported on overlapping data, with a total of 69,793 young adults (33,775 women and 36,018 men).
Nine studies did not show a statistically significant sex difference among young adults less than or equal to 45 years. Three studies found higher rates of ischemic stroke among men among young adults less than or equal to 30 to 35 years. Four studies showed more women with ischemic strokes among young adults less than or equal to 35 years.
Overall, there was an effect of a significantly higher incidence of ischemic stroke in women younger than age 35 years, with an incidence rate ratio (IRR) of 1.44. In the 35- to 45-year age group, there was a nonsignificant sex difference in the rate of ischemic stroke, with a slight trend toward a higher incidence in women (IRR, 1.08).
“In this study the sex difference was not clear in the 35-45 age group. But in the age group of over 45 years we know that men have a higher risk of stroke than women, which is probably related to a higher level of atherosclerotic risk factors,” Dr. Poisson commented.
“Interpreting data on stroke in young people is challenging, as stroke is not so common in this population,” she said. “Combining multiple studies helps, but this also introduces a lot of variability, so we need to interpret these results with some caution. However, this is certainly intriguing data and suggests that something interesting may be going on in young adults,” she added. “These observations give us an initial clue that we need to look further into this issue.”
The study did not look at the possible mechanisms behind the results, as the current data came from administrative datasets that are limited in terms of the information collected.
But Dr. Poisson noted that the traditional risk factors for stroke are high blood pressure and the usual atherosclerotic factors such as high cholesterol.
“These are normally more common in men than in women, and myocardial infarction is more common in younger men than in younger women. But the observation that young women may have a higher risk of stroke than young men suggests that something different may be going on in the mechanism for stroke.”
She pointed out that women have some unique risk factors for stroke, including oral contraceptive use, pregnancy, and the postpartum period, particularly pre-eclampsia during pregnancy. In addition, migraine, especially migraine with aura, is associated with an increased stroke risk, and migraine is more common in young women than in young men.
“We don’t completely understand the role of these risk factors, but they may contribute to the results that we found,” Dr. Poisson commented. “The role of estrogen in stroke is complicated. While estrogen is generally thought to be protective against atherosclerotic risk factors, it also increases risk of clotting, so high estrogen states like pregnancy increase risk of stroke,” she added.
To better understand what is happening, prospectively collected clinical data on younger patients who have had a stroke are needed. Some such studies are underway, but a concerted effort to do this in a large, multicenter registry would be desirable, Dr. Poisson said.
She noted that the presentation of a stroke in young people would be similar to that in the older population, with the most recent acronym to help recognize stroke symptoms being “BE FAST” – balance, eyes (vision), face (drooping), arm, speech (slurred), time (call emergency services quickly).
Call for more women in clinical trials
In an accompanying commentary, Cheryl Bushnell, MD, professor of neurology at Wake Forest School of Medicine, Winston-Salem, N.C., and Moira Kapral, MD, professor in medicine and health policy at the University of Toronto, say these findings support the need for further study to understand and address the causes and risk factors of stroke in young women.
However, they point out that representation and reporting of women in clinical trials of acute stroke continues to be suboptimal, and they call for improved incorporation of sex and gender into study design, analysis, and interpretation, which they say is critical for producing research that is broadly generalizable and applicable to different populations.
Coauthor Stacey L. Daugherty, MD, is funded by the National Institutes of Health. Dr. Poisson and Dr. Kapral have disclosed no relevant financial relationships. Dr. Bushnell reports ownership interest in Care Directions.
A version of this article first appeared on Medscape.com.
Young women appear to be at a higher risk of ischemic stroke than young men, according to a new systematic review of studies on this topic.
The review included 19 studies that reported on sex-specific stroke incidence among young adults and found that overall, in young adults aged 18-35 years, there were 44% more women with ischemic strokes than men.
This gap narrowed in the age group 35-45 years, for which there was conflicting evidence whether more men or women have ischemic strokes.
“An assertion that young women may be disproportionately at risk of ischemic stroke represents a significant departure from our current scientific understanding and may have important implications about the etiology of ischemic strokes in young adults,” the authors note.
“One of the take-home messages from this study is that stroke happens across the entire age spectrum, including young adults, even if they do not have traditional risk factors,” study coauthor Sharon N. Poisson, MD, associate professor of neurology at the University of Colorado Anschutz Medical Campus, Denver, told this news organization.
“If a young person presents with focal neurological symptoms, the possibility of a stroke should not be discounted just because they may not fit the typical profile of a stroke patient. We need more education of the population that young people – including young women – can have a stroke and that fast action to call emergency services is critical,” she said.
The study was published online Jan. 24 in the journal Stroke as part of a special “Go Red for Women” spotlight issue.
The researchers note that historically it has been believed that men have a higher incidence of stroke in every age group until very old age. However, recent evidence focused on the young adult age group has reported that there are more young women (ages 18-45) with ischemic strokes compared with young men, suggesting that young women may be disproportionately at risk compared with their male counterparts.
Pointing out that a better understanding of these sex differences is important in implementing strategies that can more effectively prevent and treat strokes in this age group, the researchers conducted the current review to synthesize the updated evidence.
They searched PubMed from January 2008 to July 2021 for relevant studies that were population-based and reported stroke incidence by sex or sex-specific incidence rate ratios of young adults age 45 and younger. Statistical synthesis was performed to estimate sex difference by age group (less than or equal to 35, 35-45 and less than or equal to 45 years) and stroke type.
They found 19 relevant studies, including three that reported on overlapping data, with a total of 69,793 young adults (33,775 women and 36,018 men).
Nine studies did not show a statistically significant sex difference among young adults less than or equal to 45 years. Three studies found higher rates of ischemic stroke among men among young adults less than or equal to 30 to 35 years. Four studies showed more women with ischemic strokes among young adults less than or equal to 35 years.
Overall, there was an effect of a significantly higher incidence of ischemic stroke in women younger than age 35 years, with an incidence rate ratio (IRR) of 1.44. In the 35- to 45-year age group, there was a nonsignificant sex difference in the rate of ischemic stroke, with a slight trend toward a higher incidence in women (IRR, 1.08).
“In this study the sex difference was not clear in the 35-45 age group. But in the age group of over 45 years we know that men have a higher risk of stroke than women, which is probably related to a higher level of atherosclerotic risk factors,” Dr. Poisson commented.
“Interpreting data on stroke in young people is challenging, as stroke is not so common in this population,” she said. “Combining multiple studies helps, but this also introduces a lot of variability, so we need to interpret these results with some caution. However, this is certainly intriguing data and suggests that something interesting may be going on in young adults,” she added. “These observations give us an initial clue that we need to look further into this issue.”
The study did not look at the possible mechanisms behind the results, as the current data came from administrative datasets that are limited in terms of the information collected.
But Dr. Poisson noted that the traditional risk factors for stroke are high blood pressure and the usual atherosclerotic factors such as high cholesterol.
“These are normally more common in men than in women, and myocardial infarction is more common in younger men than in younger women. But the observation that young women may have a higher risk of stroke than young men suggests that something different may be going on in the mechanism for stroke.”
She pointed out that women have some unique risk factors for stroke, including oral contraceptive use, pregnancy, and the postpartum period, particularly pre-eclampsia during pregnancy. In addition, migraine, especially migraine with aura, is associated with an increased stroke risk, and migraine is more common in young women than in young men.
“We don’t completely understand the role of these risk factors, but they may contribute to the results that we found,” Dr. Poisson commented. “The role of estrogen in stroke is complicated. While estrogen is generally thought to be protective against atherosclerotic risk factors, it also increases risk of clotting, so high estrogen states like pregnancy increase risk of stroke,” she added.
To better understand what is happening, prospectively collected clinical data on younger patients who have had a stroke are needed. Some such studies are underway, but a concerted effort to do this in a large, multicenter registry would be desirable, Dr. Poisson said.
She noted that the presentation of a stroke in young people would be similar to that in the older population, with the most recent acronym to help recognize stroke symptoms being “BE FAST” – balance, eyes (vision), face (drooping), arm, speech (slurred), time (call emergency services quickly).
Call for more women in clinical trials
In an accompanying commentary, Cheryl Bushnell, MD, professor of neurology at Wake Forest School of Medicine, Winston-Salem, N.C., and Moira Kapral, MD, professor in medicine and health policy at the University of Toronto, say these findings support the need for further study to understand and address the causes and risk factors of stroke in young women.
However, they point out that representation and reporting of women in clinical trials of acute stroke continues to be suboptimal, and they call for improved incorporation of sex and gender into study design, analysis, and interpretation, which they say is critical for producing research that is broadly generalizable and applicable to different populations.
Coauthor Stacey L. Daugherty, MD, is funded by the National Institutes of Health. Dr. Poisson and Dr. Kapral have disclosed no relevant financial relationships. Dr. Bushnell reports ownership interest in Care Directions.
A version of this article first appeared on Medscape.com.
Young women appear to be at a higher risk of ischemic stroke than young men, according to a new systematic review of studies on this topic.
The review included 19 studies that reported on sex-specific stroke incidence among young adults and found that overall, in young adults aged 18-35 years, there were 44% more women with ischemic strokes than men.
This gap narrowed in the age group 35-45 years, for which there was conflicting evidence whether more men or women have ischemic strokes.
“An assertion that young women may be disproportionately at risk of ischemic stroke represents a significant departure from our current scientific understanding and may have important implications about the etiology of ischemic strokes in young adults,” the authors note.
“One of the take-home messages from this study is that stroke happens across the entire age spectrum, including young adults, even if they do not have traditional risk factors,” study coauthor Sharon N. Poisson, MD, associate professor of neurology at the University of Colorado Anschutz Medical Campus, Denver, told this news organization.
“If a young person presents with focal neurological symptoms, the possibility of a stroke should not be discounted just because they may not fit the typical profile of a stroke patient. We need more education of the population that young people – including young women – can have a stroke and that fast action to call emergency services is critical,” she said.
The study was published online Jan. 24 in the journal Stroke as part of a special “Go Red for Women” spotlight issue.
The researchers note that historically it has been believed that men have a higher incidence of stroke in every age group until very old age. However, recent evidence focused on the young adult age group has reported that there are more young women (ages 18-45) with ischemic strokes compared with young men, suggesting that young women may be disproportionately at risk compared with their male counterparts.
Pointing out that a better understanding of these sex differences is important in implementing strategies that can more effectively prevent and treat strokes in this age group, the researchers conducted the current review to synthesize the updated evidence.
They searched PubMed from January 2008 to July 2021 for relevant studies that were population-based and reported stroke incidence by sex or sex-specific incidence rate ratios of young adults age 45 and younger. Statistical synthesis was performed to estimate sex difference by age group (less than or equal to 35, 35-45 and less than or equal to 45 years) and stroke type.
They found 19 relevant studies, including three that reported on overlapping data, with a total of 69,793 young adults (33,775 women and 36,018 men).
Nine studies did not show a statistically significant sex difference among young adults less than or equal to 45 years. Three studies found higher rates of ischemic stroke among men among young adults less than or equal to 30 to 35 years. Four studies showed more women with ischemic strokes among young adults less than or equal to 35 years.
Overall, there was an effect of a significantly higher incidence of ischemic stroke in women younger than age 35 years, with an incidence rate ratio (IRR) of 1.44. In the 35- to 45-year age group, there was a nonsignificant sex difference in the rate of ischemic stroke, with a slight trend toward a higher incidence in women (IRR, 1.08).
“In this study the sex difference was not clear in the 35-45 age group. But in the age group of over 45 years we know that men have a higher risk of stroke than women, which is probably related to a higher level of atherosclerotic risk factors,” Dr. Poisson commented.
“Interpreting data on stroke in young people is challenging, as stroke is not so common in this population,” she said. “Combining multiple studies helps, but this also introduces a lot of variability, so we need to interpret these results with some caution. However, this is certainly intriguing data and suggests that something interesting may be going on in young adults,” she added. “These observations give us an initial clue that we need to look further into this issue.”
The study did not look at the possible mechanisms behind the results, as the current data came from administrative datasets that are limited in terms of the information collected.
But Dr. Poisson noted that the traditional risk factors for stroke are high blood pressure and the usual atherosclerotic factors such as high cholesterol.
“These are normally more common in men than in women, and myocardial infarction is more common in younger men than in younger women. But the observation that young women may have a higher risk of stroke than young men suggests that something different may be going on in the mechanism for stroke.”
She pointed out that women have some unique risk factors for stroke, including oral contraceptive use, pregnancy, and the postpartum period, particularly pre-eclampsia during pregnancy. In addition, migraine, especially migraine with aura, is associated with an increased stroke risk, and migraine is more common in young women than in young men.
“We don’t completely understand the role of these risk factors, but they may contribute to the results that we found,” Dr. Poisson commented. “The role of estrogen in stroke is complicated. While estrogen is generally thought to be protective against atherosclerotic risk factors, it also increases risk of clotting, so high estrogen states like pregnancy increase risk of stroke,” she added.
To better understand what is happening, prospectively collected clinical data on younger patients who have had a stroke are needed. Some such studies are underway, but a concerted effort to do this in a large, multicenter registry would be desirable, Dr. Poisson said.
She noted that the presentation of a stroke in young people would be similar to that in the older population, with the most recent acronym to help recognize stroke symptoms being “BE FAST” – balance, eyes (vision), face (drooping), arm, speech (slurred), time (call emergency services quickly).
Call for more women in clinical trials
In an accompanying commentary, Cheryl Bushnell, MD, professor of neurology at Wake Forest School of Medicine, Winston-Salem, N.C., and Moira Kapral, MD, professor in medicine and health policy at the University of Toronto, say these findings support the need for further study to understand and address the causes and risk factors of stroke in young women.
However, they point out that representation and reporting of women in clinical trials of acute stroke continues to be suboptimal, and they call for improved incorporation of sex and gender into study design, analysis, and interpretation, which they say is critical for producing research that is broadly generalizable and applicable to different populations.
Coauthor Stacey L. Daugherty, MD, is funded by the National Institutes of Health. Dr. Poisson and Dr. Kapral have disclosed no relevant financial relationships. Dr. Bushnell reports ownership interest in Care Directions.
A version of this article first appeared on Medscape.com.
Yoga maneuver may prevent vasovagal syncope
The tadasana exercise – a movement-based contemplative practice that gradually corrects orthostatic imbalance by strengthening protective neuromuscular reflexes – practiced for just 15 minutes twice a day, was associated with the complete elimination of episodes of vasovagal syncope for many patients.
“These exercises are very easy to perform, inexpensive, and very effective. This is a very easy fix for a scary and potentially dangerous condition,” lead author Hygriv Rao, MD, said in an interview. “We are excited about these results. We thought it would work, but we did not expect it to be so effective. It seems to work for almost all patients.
“We found that, with the tadasana maneuver, episodes of full syncope, where the patient actually loses consciousness, ceased completely, and episodes of near-syncope, where the patient feels faint but does not completely pass out, were greatly reduced,” Dr. Rao added. “The actual loss of consciousness, which is the most dangerous part, is practically gone. This gives a lot of confidence to patients and their families.”
The researchers reported their initial results from a pilot study of the technique in a letter to JACC: Clinical Electrophysiology that was published online Jan. 26, 2022.
Dr. Rao, a cardiologist at the KIMS Hospitals, Hyderabad, India, explained that vasovagal syncope is a brief loss of consciousness caused by a neurologically induced drop in blood pressure caused by faulty neuromuscular reflexes.
It is typically triggered by emotional stress, prolonged standing, or getting up from a sitting position too quickly.
Very few treatments have been shown effective, with current management approaches involving avoiding triggers, increasing fluids, and if the individual feels an episode coming on, they can take steps to stop it by lying down, raising their legs, or lowering their head to increase blood flow to the brain.
“Recently, there has been a lot of interest in yoga as a preventative therapy for vasovagal syncope,” Dr. Rao noted. “We considered various yoga positions and we chose the tadasana maneuver to study in this context as it resembles exercises sometimes given to patients with vasovagal syncope but with some differences including the addition of synchronized breathing, which may help stabilize autonomic tone.”
For the tadasana maneuver, the individual stands straight with their feet together, arms by their side (against a wall if they need support), and alternatively lift the front and back part of their feet.
They first lift their toes with their weight resting on the ball of their feet, then after a few seconds they raise their heels with their weight on the front of the foot. Then after a few more seconds they lift their arms over their shoulders, stretching upward while standing on their toes.
These movements are synchronized with breathing exercises, with the individual taking a deep breath in as they lift their arms and breathing out again on lowering the arms.
“Each movement takes a few seconds, and each cycle of movements takes about 2 minutes. If this is performed 8 times, then this would take about 15 minutes. We recommend this 15-minute routine twice a day,” Dr. Rao said.
For the current study, 113 patients diagnosed with recurrent vasovagal disorder were counseled to practice standard physical maneuvers and maintain adequate hydration. Medications were prescribed at the discretion of the treating physician.
Of these, 61 patients were additionally trained to practice the tadasana maneuver and asked to practice the movement for 15 minutes twice a day. The mean durations of symptoms and follow-up in the two groups were similar. The average follow-up was about 20 months.
Results showed that episodes of both near-syncope and syncope decreased in both groups but there was a much larger reduction in the patients practicing the tadasana maneuver.
Before treatment, the 52 patients in the conventional group experienced 163 syncope or near-syncope events. At follow-up, 22 symptom recurrences occurred in 12 patients (23%). Total mean events per patient declined from 3 to 0.4.
Full syncope events in this group declined from 65 in 32 patients to 2 in 2 patients (mean per patient, 1.3 to 1), and near-syncope events fell from 98 in 34 patients to 20 in 10 patients (mean per patient, 2.0 to 0.4).
In the tadasana group, 61 patients had 378 syncope/near-syncope events before treatment; at follow-up, only 6 events occurred in 5 patients (8%). Per patient, total events declined from a mean of 6 to 0.1.
Full syncope events fell from 108 in 48 patients to 0 (mean per patient, 1.8 to 0), and near-syncope events declined from 269 in 33 patients to 6 in 5 patients (mean per patient, 4.4 to 0.1).
“This combination of exercise and breathing influences the neuromuscular reflex malfunction that occurs in vasovagal syncope,” Dr. Rao noted. “The movements focus on strengthening neuromuscular reflexes in the quadriceps and the calf muscles, which can increase the blood circulation and venous return, thus preventing blood pooling in the lower body.”
The researchers said this pilot study offers three main findings. First, both conventional therapy and conventional plus tadasana therapy appeared to benefit patients, compared with their respective baseline symptom burden. Second, application of tadasana as an adjunctive treatment was associated with fewer total event recurrences (that is, syncope and near-syncope combined), and third, tadasana was well tolerated, with no adverse events reported.
“The reduction in total events (i.e., syncope and near-syncope events), compared with pretreatment numbers, was substantial and most tadasana patients were managed without any pharmacotherapy,” the authors reported.
Dr. Rao noted that at baseline almost all patients in both groups were taking medications for the condition, but during the study these medications were reduced as fewer episodes occurred. At the end of the follow-up, 80% of the conventional group were still taking medication, compared with just 14% of those in the tadasana group.
Patients had an initial training session in person with a yoga instructor and then received follow-on training by video online. Dr. Rao said there was a very high rate of compliance, “almost 100%.”
He reports that a total of 200 patients have now been treated with this approach at his hospital with very similar results to those seen in the initial study.
This work was supported in part by a grant from the Dr Earl E. Bakken Family in support of heart-brain research. Dr. Rao disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The tadasana exercise – a movement-based contemplative practice that gradually corrects orthostatic imbalance by strengthening protective neuromuscular reflexes – practiced for just 15 minutes twice a day, was associated with the complete elimination of episodes of vasovagal syncope for many patients.
“These exercises are very easy to perform, inexpensive, and very effective. This is a very easy fix for a scary and potentially dangerous condition,” lead author Hygriv Rao, MD, said in an interview. “We are excited about these results. We thought it would work, but we did not expect it to be so effective. It seems to work for almost all patients.
“We found that, with the tadasana maneuver, episodes of full syncope, where the patient actually loses consciousness, ceased completely, and episodes of near-syncope, where the patient feels faint but does not completely pass out, were greatly reduced,” Dr. Rao added. “The actual loss of consciousness, which is the most dangerous part, is practically gone. This gives a lot of confidence to patients and their families.”
The researchers reported their initial results from a pilot study of the technique in a letter to JACC: Clinical Electrophysiology that was published online Jan. 26, 2022.
Dr. Rao, a cardiologist at the KIMS Hospitals, Hyderabad, India, explained that vasovagal syncope is a brief loss of consciousness caused by a neurologically induced drop in blood pressure caused by faulty neuromuscular reflexes.
It is typically triggered by emotional stress, prolonged standing, or getting up from a sitting position too quickly.
Very few treatments have been shown effective, with current management approaches involving avoiding triggers, increasing fluids, and if the individual feels an episode coming on, they can take steps to stop it by lying down, raising their legs, or lowering their head to increase blood flow to the brain.
“Recently, there has been a lot of interest in yoga as a preventative therapy for vasovagal syncope,” Dr. Rao noted. “We considered various yoga positions and we chose the tadasana maneuver to study in this context as it resembles exercises sometimes given to patients with vasovagal syncope but with some differences including the addition of synchronized breathing, which may help stabilize autonomic tone.”
For the tadasana maneuver, the individual stands straight with their feet together, arms by their side (against a wall if they need support), and alternatively lift the front and back part of their feet.
They first lift their toes with their weight resting on the ball of their feet, then after a few seconds they raise their heels with their weight on the front of the foot. Then after a few more seconds they lift their arms over their shoulders, stretching upward while standing on their toes.
These movements are synchronized with breathing exercises, with the individual taking a deep breath in as they lift their arms and breathing out again on lowering the arms.
“Each movement takes a few seconds, and each cycle of movements takes about 2 minutes. If this is performed 8 times, then this would take about 15 minutes. We recommend this 15-minute routine twice a day,” Dr. Rao said.
For the current study, 113 patients diagnosed with recurrent vasovagal disorder were counseled to practice standard physical maneuvers and maintain adequate hydration. Medications were prescribed at the discretion of the treating physician.
Of these, 61 patients were additionally trained to practice the tadasana maneuver and asked to practice the movement for 15 minutes twice a day. The mean durations of symptoms and follow-up in the two groups were similar. The average follow-up was about 20 months.
Results showed that episodes of both near-syncope and syncope decreased in both groups but there was a much larger reduction in the patients practicing the tadasana maneuver.
Before treatment, the 52 patients in the conventional group experienced 163 syncope or near-syncope events. At follow-up, 22 symptom recurrences occurred in 12 patients (23%). Total mean events per patient declined from 3 to 0.4.
Full syncope events in this group declined from 65 in 32 patients to 2 in 2 patients (mean per patient, 1.3 to 1), and near-syncope events fell from 98 in 34 patients to 20 in 10 patients (mean per patient, 2.0 to 0.4).
In the tadasana group, 61 patients had 378 syncope/near-syncope events before treatment; at follow-up, only 6 events occurred in 5 patients (8%). Per patient, total events declined from a mean of 6 to 0.1.
Full syncope events fell from 108 in 48 patients to 0 (mean per patient, 1.8 to 0), and near-syncope events declined from 269 in 33 patients to 6 in 5 patients (mean per patient, 4.4 to 0.1).
“This combination of exercise and breathing influences the neuromuscular reflex malfunction that occurs in vasovagal syncope,” Dr. Rao noted. “The movements focus on strengthening neuromuscular reflexes in the quadriceps and the calf muscles, which can increase the blood circulation and venous return, thus preventing blood pooling in the lower body.”
The researchers said this pilot study offers three main findings. First, both conventional therapy and conventional plus tadasana therapy appeared to benefit patients, compared with their respective baseline symptom burden. Second, application of tadasana as an adjunctive treatment was associated with fewer total event recurrences (that is, syncope and near-syncope combined), and third, tadasana was well tolerated, with no adverse events reported.
“The reduction in total events (i.e., syncope and near-syncope events), compared with pretreatment numbers, was substantial and most tadasana patients were managed without any pharmacotherapy,” the authors reported.
Dr. Rao noted that at baseline almost all patients in both groups were taking medications for the condition, but during the study these medications were reduced as fewer episodes occurred. At the end of the follow-up, 80% of the conventional group were still taking medication, compared with just 14% of those in the tadasana group.
Patients had an initial training session in person with a yoga instructor and then received follow-on training by video online. Dr. Rao said there was a very high rate of compliance, “almost 100%.”
He reports that a total of 200 patients have now been treated with this approach at his hospital with very similar results to those seen in the initial study.
This work was supported in part by a grant from the Dr Earl E. Bakken Family in support of heart-brain research. Dr. Rao disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The tadasana exercise – a movement-based contemplative practice that gradually corrects orthostatic imbalance by strengthening protective neuromuscular reflexes – practiced for just 15 minutes twice a day, was associated with the complete elimination of episodes of vasovagal syncope for many patients.
“These exercises are very easy to perform, inexpensive, and very effective. This is a very easy fix for a scary and potentially dangerous condition,” lead author Hygriv Rao, MD, said in an interview. “We are excited about these results. We thought it would work, but we did not expect it to be so effective. It seems to work for almost all patients.
“We found that, with the tadasana maneuver, episodes of full syncope, where the patient actually loses consciousness, ceased completely, and episodes of near-syncope, where the patient feels faint but does not completely pass out, were greatly reduced,” Dr. Rao added. “The actual loss of consciousness, which is the most dangerous part, is practically gone. This gives a lot of confidence to patients and their families.”
The researchers reported their initial results from a pilot study of the technique in a letter to JACC: Clinical Electrophysiology that was published online Jan. 26, 2022.
Dr. Rao, a cardiologist at the KIMS Hospitals, Hyderabad, India, explained that vasovagal syncope is a brief loss of consciousness caused by a neurologically induced drop in blood pressure caused by faulty neuromuscular reflexes.
It is typically triggered by emotional stress, prolonged standing, or getting up from a sitting position too quickly.
Very few treatments have been shown effective, with current management approaches involving avoiding triggers, increasing fluids, and if the individual feels an episode coming on, they can take steps to stop it by lying down, raising their legs, or lowering their head to increase blood flow to the brain.
“Recently, there has been a lot of interest in yoga as a preventative therapy for vasovagal syncope,” Dr. Rao noted. “We considered various yoga positions and we chose the tadasana maneuver to study in this context as it resembles exercises sometimes given to patients with vasovagal syncope but with some differences including the addition of synchronized breathing, which may help stabilize autonomic tone.”
For the tadasana maneuver, the individual stands straight with their feet together, arms by their side (against a wall if they need support), and alternatively lift the front and back part of their feet.
They first lift their toes with their weight resting on the ball of their feet, then after a few seconds they raise their heels with their weight on the front of the foot. Then after a few more seconds they lift their arms over their shoulders, stretching upward while standing on their toes.
These movements are synchronized with breathing exercises, with the individual taking a deep breath in as they lift their arms and breathing out again on lowering the arms.
“Each movement takes a few seconds, and each cycle of movements takes about 2 minutes. If this is performed 8 times, then this would take about 15 minutes. We recommend this 15-minute routine twice a day,” Dr. Rao said.
For the current study, 113 patients diagnosed with recurrent vasovagal disorder were counseled to practice standard physical maneuvers and maintain adequate hydration. Medications were prescribed at the discretion of the treating physician.
Of these, 61 patients were additionally trained to practice the tadasana maneuver and asked to practice the movement for 15 minutes twice a day. The mean durations of symptoms and follow-up in the two groups were similar. The average follow-up was about 20 months.
Results showed that episodes of both near-syncope and syncope decreased in both groups but there was a much larger reduction in the patients practicing the tadasana maneuver.
Before treatment, the 52 patients in the conventional group experienced 163 syncope or near-syncope events. At follow-up, 22 symptom recurrences occurred in 12 patients (23%). Total mean events per patient declined from 3 to 0.4.
Full syncope events in this group declined from 65 in 32 patients to 2 in 2 patients (mean per patient, 1.3 to 1), and near-syncope events fell from 98 in 34 patients to 20 in 10 patients (mean per patient, 2.0 to 0.4).
In the tadasana group, 61 patients had 378 syncope/near-syncope events before treatment; at follow-up, only 6 events occurred in 5 patients (8%). Per patient, total events declined from a mean of 6 to 0.1.
Full syncope events fell from 108 in 48 patients to 0 (mean per patient, 1.8 to 0), and near-syncope events declined from 269 in 33 patients to 6 in 5 patients (mean per patient, 4.4 to 0.1).
“This combination of exercise and breathing influences the neuromuscular reflex malfunction that occurs in vasovagal syncope,” Dr. Rao noted. “The movements focus on strengthening neuromuscular reflexes in the quadriceps and the calf muscles, which can increase the blood circulation and venous return, thus preventing blood pooling in the lower body.”
The researchers said this pilot study offers three main findings. First, both conventional therapy and conventional plus tadasana therapy appeared to benefit patients, compared with their respective baseline symptom burden. Second, application of tadasana as an adjunctive treatment was associated with fewer total event recurrences (that is, syncope and near-syncope combined), and third, tadasana was well tolerated, with no adverse events reported.
“The reduction in total events (i.e., syncope and near-syncope events), compared with pretreatment numbers, was substantial and most tadasana patients were managed without any pharmacotherapy,” the authors reported.
Dr. Rao noted that at baseline almost all patients in both groups were taking medications for the condition, but during the study these medications were reduced as fewer episodes occurred. At the end of the follow-up, 80% of the conventional group were still taking medication, compared with just 14% of those in the tadasana group.
Patients had an initial training session in person with a yoga instructor and then received follow-on training by video online. Dr. Rao said there was a very high rate of compliance, “almost 100%.”
He reports that a total of 200 patients have now been treated with this approach at his hospital with very similar results to those seen in the initial study.
This work was supported in part by a grant from the Dr Earl E. Bakken Family in support of heart-brain research. Dr. Rao disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JACC: CLINICAL ELECTROPHYSIOLOGY
Brain stimulation for improved memory?
Electrical brain stimulation may have the potential to improve verbal memory, results of a small study of patients with epilepsy suggest.
Investigators observed improvements in patients implanted with a responsive neurostimulation system (RNS) to control seizures, in that the patients had improved word recall when the system was activated.
Beyond epilepsy, “we suspect that our results would be broadly applicable regardless of the underlying condition, for example, memory loss with Alzheimer’s disease or traumatic brain injury,” Zulfi Haneef, MBBS, MD, associate professor of neurology, Baylor College of Medicine, Houston, said in an interview.
“Mental health conditions such as depression or psychosis could also benefit from targeted electrical stimulation. While we focused on enhancing a preferred brain function [such as memory], parallel areas of research may target enhancing function [such as weakness following stroke] or suppressing function [to manage conditions such as chronic pain,]” Dr. Haneef added.
The study was published online Jan. 17, 2022, in Neurosurgery.
As reported by this news organization, Following implantation of the system, patients attend the clinic for adjustments about every 8-12 weeks.
The investigators studied 17 patients with epilepsy and RNS implants who attended the clinic for routine appointments. A clinical neuropsychologist administered the Hopkins Verbal Learning Test–Revised (HVLT-R), a well-validated list-learning measure of memory and verbal learning.
Patients were read a list of 12 semantically related words and asked to recall the list after three different learning trials. Active or sham stimulation was performed for every third word presented for immediate recall.
The investigators found that the HVLT-R delayed recall raw score was higher for the stimulation condition, compared with the nonstimulation condition (paired t-test, P = .04; effect size, d = 0.627).
“The patients were not aware of when the RNS system was being activated. We alternated when patients were undergoing stimulation versus no stimulation, and still found that when patients’ RNS systems were activated, their memory recall score was greater than when there was no stimulation,” Dr. Haneef said in a release.
This suggests the “human memory can be potentially improved by direct electrical brain stimulation at extremely low currents,” Dr. Haneef said in an interview.
Most patients in the study had stimulation of the hippocampus, the brain’s memory center.
“Moving forward we would want to look at how different patterns or standardized stimulation patterns affect memory. Ultimately, the underlying brain rhythms responsible for these changes in brain function need to be understood so that a more targeted and precise application of electrical stimulation can be achieved,” Dr. Haneef said.
The researchers also caution that, for this preliminary study, no follow-up testing was conducted to determine whether the memory improvement was transient and settled back to baseline after a specified period.
However, they note, this study lays the groundwork for larger-scale and extensive studies examining the nuanced effects of brain stimulation on human cognition and memory.
The study was funded by the Mike Hogg Foundation. Dr. Haneef and two coauthors received coverage for travel expenses but no honorarium for a NeuroPace advisory meeting.
A version of this article first appeared on Medscape.com.
Electrical brain stimulation may have the potential to improve verbal memory, results of a small study of patients with epilepsy suggest.
Investigators observed improvements in patients implanted with a responsive neurostimulation system (RNS) to control seizures, in that the patients had improved word recall when the system was activated.
Beyond epilepsy, “we suspect that our results would be broadly applicable regardless of the underlying condition, for example, memory loss with Alzheimer’s disease or traumatic brain injury,” Zulfi Haneef, MBBS, MD, associate professor of neurology, Baylor College of Medicine, Houston, said in an interview.
“Mental health conditions such as depression or psychosis could also benefit from targeted electrical stimulation. While we focused on enhancing a preferred brain function [such as memory], parallel areas of research may target enhancing function [such as weakness following stroke] or suppressing function [to manage conditions such as chronic pain,]” Dr. Haneef added.
The study was published online Jan. 17, 2022, in Neurosurgery.
As reported by this news organization, Following implantation of the system, patients attend the clinic for adjustments about every 8-12 weeks.
The investigators studied 17 patients with epilepsy and RNS implants who attended the clinic for routine appointments. A clinical neuropsychologist administered the Hopkins Verbal Learning Test–Revised (HVLT-R), a well-validated list-learning measure of memory and verbal learning.
Patients were read a list of 12 semantically related words and asked to recall the list after three different learning trials. Active or sham stimulation was performed for every third word presented for immediate recall.
The investigators found that the HVLT-R delayed recall raw score was higher for the stimulation condition, compared with the nonstimulation condition (paired t-test, P = .04; effect size, d = 0.627).
“The patients were not aware of when the RNS system was being activated. We alternated when patients were undergoing stimulation versus no stimulation, and still found that when patients’ RNS systems were activated, their memory recall score was greater than when there was no stimulation,” Dr. Haneef said in a release.
This suggests the “human memory can be potentially improved by direct electrical brain stimulation at extremely low currents,” Dr. Haneef said in an interview.
Most patients in the study had stimulation of the hippocampus, the brain’s memory center.
“Moving forward we would want to look at how different patterns or standardized stimulation patterns affect memory. Ultimately, the underlying brain rhythms responsible for these changes in brain function need to be understood so that a more targeted and precise application of electrical stimulation can be achieved,” Dr. Haneef said.
The researchers also caution that, for this preliminary study, no follow-up testing was conducted to determine whether the memory improvement was transient and settled back to baseline after a specified period.
However, they note, this study lays the groundwork for larger-scale and extensive studies examining the nuanced effects of brain stimulation on human cognition and memory.
The study was funded by the Mike Hogg Foundation. Dr. Haneef and two coauthors received coverage for travel expenses but no honorarium for a NeuroPace advisory meeting.
A version of this article first appeared on Medscape.com.
Electrical brain stimulation may have the potential to improve verbal memory, results of a small study of patients with epilepsy suggest.
Investigators observed improvements in patients implanted with a responsive neurostimulation system (RNS) to control seizures, in that the patients had improved word recall when the system was activated.
Beyond epilepsy, “we suspect that our results would be broadly applicable regardless of the underlying condition, for example, memory loss with Alzheimer’s disease or traumatic brain injury,” Zulfi Haneef, MBBS, MD, associate professor of neurology, Baylor College of Medicine, Houston, said in an interview.
“Mental health conditions such as depression or psychosis could also benefit from targeted electrical stimulation. While we focused on enhancing a preferred brain function [such as memory], parallel areas of research may target enhancing function [such as weakness following stroke] or suppressing function [to manage conditions such as chronic pain,]” Dr. Haneef added.
The study was published online Jan. 17, 2022, in Neurosurgery.
As reported by this news organization, Following implantation of the system, patients attend the clinic for adjustments about every 8-12 weeks.
The investigators studied 17 patients with epilepsy and RNS implants who attended the clinic for routine appointments. A clinical neuropsychologist administered the Hopkins Verbal Learning Test–Revised (HVLT-R), a well-validated list-learning measure of memory and verbal learning.
Patients were read a list of 12 semantically related words and asked to recall the list after three different learning trials. Active or sham stimulation was performed for every third word presented for immediate recall.
The investigators found that the HVLT-R delayed recall raw score was higher for the stimulation condition, compared with the nonstimulation condition (paired t-test, P = .04; effect size, d = 0.627).
“The patients were not aware of when the RNS system was being activated. We alternated when patients were undergoing stimulation versus no stimulation, and still found that when patients’ RNS systems were activated, their memory recall score was greater than when there was no stimulation,” Dr. Haneef said in a release.
This suggests the “human memory can be potentially improved by direct electrical brain stimulation at extremely low currents,” Dr. Haneef said in an interview.
Most patients in the study had stimulation of the hippocampus, the brain’s memory center.
“Moving forward we would want to look at how different patterns or standardized stimulation patterns affect memory. Ultimately, the underlying brain rhythms responsible for these changes in brain function need to be understood so that a more targeted and precise application of electrical stimulation can be achieved,” Dr. Haneef said.
The researchers also caution that, for this preliminary study, no follow-up testing was conducted to determine whether the memory improvement was transient and settled back to baseline after a specified period.
However, they note, this study lays the groundwork for larger-scale and extensive studies examining the nuanced effects of brain stimulation on human cognition and memory.
The study was funded by the Mike Hogg Foundation. Dr. Haneef and two coauthors received coverage for travel expenses but no honorarium for a NeuroPace advisory meeting.
A version of this article first appeared on Medscape.com.
FROM NEUROSURGERY
Early, subtle, cardiac changes tied to midlife cognitive decline
new research suggests.
Cardiovascular disease risk factors such as high blood pressure, high cholesterol, and diabetes have been associated with an increased risk for cognitive impairment, but much less is known about heart structure and function and the risks for cognition.
“We showed for the first time that, even before the occurrence of cardiovascular disease, people with abnormalities in cardiac structure and function as early as in young adulthood have lower midlife cognition,” investigators Laure Rouch, PharmD, PhD, and Kristine Yaffe, MD, both with the department of psychiatry, University of California, San Francisco, said in a joint email.
“This study reminds us that heart health is key to brain health and that the overlap and interplay between the two is not limited to patients with end-stage heart disease,” Dr. Rouch and Dr. Yaffe said.
The findings were published online Jan. 26, 2022, in Neurology.
Heart/brain connection
The analysis included 2,653 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study.
Echocardiograms were obtained at year 5, 25, and 30 study visits – at mean ages of 30, 50, and 55 years, respectively. At year 30, participants underwent a standard battery of tests measuring global cognition, processing speed, executive function, delayed verbal memory, and verbal fluency.
Over 25 years, there was an average increase in left ventricular mass of 0.27 g/m2 per year – from a mean of 80.5 g/m2 in year 5 to 86.0 g/m2 in year 30.
Left atrial volume increased by an average of 0.42 mL/m2 per year, from 16 mL/m2 in year 5 to 26 mL/m2 in year 30.
Left ventricular ejection fraction (LVEF) decreased by 0.11% per year, from 63.3% in year 5 to 59.7% in year 30.
After adjustment for demographics and education, an increase in left ventricular mass of at least 1 standard deviation over 25 years was associated with lower cognition on most tests (P ≤ .02).
An increase in left atrial volume over the study period was associated with lower global cognition (P = .04), whereas a decrease in LVEF was not associated with cognition. Further adjustment for cardiovascular risk factors yielded similar results.
“A more effective collaboration is needed between cardiologists and neurologists to promote healthy brain aging,” Dr. Rouch and Dr. Yaffe said.
“Echocardiography is a widely available, relatively inexpensive, and noninvasive imaging method that could be integrated into a risk assessment for cognitive impairment,” they added.
Looking ahead, the investigators noted there is a need for further research to determine whether interventions to improve cardiac structure and diastolic function could also benefit brain health.
They should also investigate the role of arterial stiffness and cerebral small vessel disease in the relationship between cardiac structure, function, and cognition, the researchers added.
First structural biomarker
Commenting on the study, Shaheen E. Lakhan, MD, PhD, a neurologist in Newton, Mass., said the study is important because, “thus far, the connections have really been physiological parameters,” such as blood pressure and cognitive health.
“This is really strong evidence of a structural cardiac biomarker that can be measured before and independent of changes in physiology or diseased state,” said Dr. Lakhan, who was not involved with the research.
As more and more interventions are being introduced for addressing disorders of cognition, “this potential structural finding may serve as a solid biomarker to determine” what lifestyle or drug therapy should be taken, he added.
Also weighing in on the findings, Pierre Fayad, MD, professor in the department of neurological sciences and director of the Nebraska Stroke Center, University of Nebraska Medical Center, Omaha, said CARDIA is “an important study” providing “precious data.”
The reported changes in cardiac structure and function “precede the clinical symptomatology, as the follow-up stops before they enter into later adulthood, where the risk of clinical events dramatically rises. Meaning these patients still have not had stroke, congestive heart failure, heart attack or dementia, but some of them could be on that trajectory later in their life,” Dr. Fayad told this news organization.
Documenting such changes over time is “valuable to give an insight into what leads us to such progression,” he noted.
How reliably predictive the findings are for eventual clinical cognitive impairment “will need to be confirmed and verified” in future studies, he added.
“If verified, it could be helpful to provide interventions to those with the left atrial volume enlargement marker and see their effectiveness at preventing eventual clinical cognitive impairment,” said Dr. Fayad.
The CARDIA study is supported by the National Heart, Lung, and Blood Institute in collaboration with the University of Alabama at Birmingham, Northwestern University, the University of Minnesota, and the Kaiser Foundation Research Institute. Rouch, Lakhan, and Dr. Fayad have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
Cardiovascular disease risk factors such as high blood pressure, high cholesterol, and diabetes have been associated with an increased risk for cognitive impairment, but much less is known about heart structure and function and the risks for cognition.
“We showed for the first time that, even before the occurrence of cardiovascular disease, people with abnormalities in cardiac structure and function as early as in young adulthood have lower midlife cognition,” investigators Laure Rouch, PharmD, PhD, and Kristine Yaffe, MD, both with the department of psychiatry, University of California, San Francisco, said in a joint email.
“This study reminds us that heart health is key to brain health and that the overlap and interplay between the two is not limited to patients with end-stage heart disease,” Dr. Rouch and Dr. Yaffe said.
The findings were published online Jan. 26, 2022, in Neurology.
Heart/brain connection
The analysis included 2,653 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study.
Echocardiograms were obtained at year 5, 25, and 30 study visits – at mean ages of 30, 50, and 55 years, respectively. At year 30, participants underwent a standard battery of tests measuring global cognition, processing speed, executive function, delayed verbal memory, and verbal fluency.
Over 25 years, there was an average increase in left ventricular mass of 0.27 g/m2 per year – from a mean of 80.5 g/m2 in year 5 to 86.0 g/m2 in year 30.
Left atrial volume increased by an average of 0.42 mL/m2 per year, from 16 mL/m2 in year 5 to 26 mL/m2 in year 30.
Left ventricular ejection fraction (LVEF) decreased by 0.11% per year, from 63.3% in year 5 to 59.7% in year 30.
After adjustment for demographics and education, an increase in left ventricular mass of at least 1 standard deviation over 25 years was associated with lower cognition on most tests (P ≤ .02).
An increase in left atrial volume over the study period was associated with lower global cognition (P = .04), whereas a decrease in LVEF was not associated with cognition. Further adjustment for cardiovascular risk factors yielded similar results.
“A more effective collaboration is needed between cardiologists and neurologists to promote healthy brain aging,” Dr. Rouch and Dr. Yaffe said.
“Echocardiography is a widely available, relatively inexpensive, and noninvasive imaging method that could be integrated into a risk assessment for cognitive impairment,” they added.
Looking ahead, the investigators noted there is a need for further research to determine whether interventions to improve cardiac structure and diastolic function could also benefit brain health.
They should also investigate the role of arterial stiffness and cerebral small vessel disease in the relationship between cardiac structure, function, and cognition, the researchers added.
First structural biomarker
Commenting on the study, Shaheen E. Lakhan, MD, PhD, a neurologist in Newton, Mass., said the study is important because, “thus far, the connections have really been physiological parameters,” such as blood pressure and cognitive health.
“This is really strong evidence of a structural cardiac biomarker that can be measured before and independent of changes in physiology or diseased state,” said Dr. Lakhan, who was not involved with the research.
As more and more interventions are being introduced for addressing disorders of cognition, “this potential structural finding may serve as a solid biomarker to determine” what lifestyle or drug therapy should be taken, he added.
Also weighing in on the findings, Pierre Fayad, MD, professor in the department of neurological sciences and director of the Nebraska Stroke Center, University of Nebraska Medical Center, Omaha, said CARDIA is “an important study” providing “precious data.”
The reported changes in cardiac structure and function “precede the clinical symptomatology, as the follow-up stops before they enter into later adulthood, where the risk of clinical events dramatically rises. Meaning these patients still have not had stroke, congestive heart failure, heart attack or dementia, but some of them could be on that trajectory later in their life,” Dr. Fayad told this news organization.
Documenting such changes over time is “valuable to give an insight into what leads us to such progression,” he noted.
How reliably predictive the findings are for eventual clinical cognitive impairment “will need to be confirmed and verified” in future studies, he added.
“If verified, it could be helpful to provide interventions to those with the left atrial volume enlargement marker and see their effectiveness at preventing eventual clinical cognitive impairment,” said Dr. Fayad.
The CARDIA study is supported by the National Heart, Lung, and Blood Institute in collaboration with the University of Alabama at Birmingham, Northwestern University, the University of Minnesota, and the Kaiser Foundation Research Institute. Rouch, Lakhan, and Dr. Fayad have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
Cardiovascular disease risk factors such as high blood pressure, high cholesterol, and diabetes have been associated with an increased risk for cognitive impairment, but much less is known about heart structure and function and the risks for cognition.
“We showed for the first time that, even before the occurrence of cardiovascular disease, people with abnormalities in cardiac structure and function as early as in young adulthood have lower midlife cognition,” investigators Laure Rouch, PharmD, PhD, and Kristine Yaffe, MD, both with the department of psychiatry, University of California, San Francisco, said in a joint email.
“This study reminds us that heart health is key to brain health and that the overlap and interplay between the two is not limited to patients with end-stage heart disease,” Dr. Rouch and Dr. Yaffe said.
The findings were published online Jan. 26, 2022, in Neurology.
Heart/brain connection
The analysis included 2,653 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study.
Echocardiograms were obtained at year 5, 25, and 30 study visits – at mean ages of 30, 50, and 55 years, respectively. At year 30, participants underwent a standard battery of tests measuring global cognition, processing speed, executive function, delayed verbal memory, and verbal fluency.
Over 25 years, there was an average increase in left ventricular mass of 0.27 g/m2 per year – from a mean of 80.5 g/m2 in year 5 to 86.0 g/m2 in year 30.
Left atrial volume increased by an average of 0.42 mL/m2 per year, from 16 mL/m2 in year 5 to 26 mL/m2 in year 30.
Left ventricular ejection fraction (LVEF) decreased by 0.11% per year, from 63.3% in year 5 to 59.7% in year 30.
After adjustment for demographics and education, an increase in left ventricular mass of at least 1 standard deviation over 25 years was associated with lower cognition on most tests (P ≤ .02).
An increase in left atrial volume over the study period was associated with lower global cognition (P = .04), whereas a decrease in LVEF was not associated with cognition. Further adjustment for cardiovascular risk factors yielded similar results.
“A more effective collaboration is needed between cardiologists and neurologists to promote healthy brain aging,” Dr. Rouch and Dr. Yaffe said.
“Echocardiography is a widely available, relatively inexpensive, and noninvasive imaging method that could be integrated into a risk assessment for cognitive impairment,” they added.
Looking ahead, the investigators noted there is a need for further research to determine whether interventions to improve cardiac structure and diastolic function could also benefit brain health.
They should also investigate the role of arterial stiffness and cerebral small vessel disease in the relationship between cardiac structure, function, and cognition, the researchers added.
First structural biomarker
Commenting on the study, Shaheen E. Lakhan, MD, PhD, a neurologist in Newton, Mass., said the study is important because, “thus far, the connections have really been physiological parameters,” such as blood pressure and cognitive health.
“This is really strong evidence of a structural cardiac biomarker that can be measured before and independent of changes in physiology or diseased state,” said Dr. Lakhan, who was not involved with the research.
As more and more interventions are being introduced for addressing disorders of cognition, “this potential structural finding may serve as a solid biomarker to determine” what lifestyle or drug therapy should be taken, he added.
Also weighing in on the findings, Pierre Fayad, MD, professor in the department of neurological sciences and director of the Nebraska Stroke Center, University of Nebraska Medical Center, Omaha, said CARDIA is “an important study” providing “precious data.”
The reported changes in cardiac structure and function “precede the clinical symptomatology, as the follow-up stops before they enter into later adulthood, where the risk of clinical events dramatically rises. Meaning these patients still have not had stroke, congestive heart failure, heart attack or dementia, but some of them could be on that trajectory later in their life,” Dr. Fayad told this news organization.
Documenting such changes over time is “valuable to give an insight into what leads us to such progression,” he noted.
How reliably predictive the findings are for eventual clinical cognitive impairment “will need to be confirmed and verified” in future studies, he added.
“If verified, it could be helpful to provide interventions to those with the left atrial volume enlargement marker and see their effectiveness at preventing eventual clinical cognitive impairment,” said Dr. Fayad.
The CARDIA study is supported by the National Heart, Lung, and Blood Institute in collaboration with the University of Alabama at Birmingham, Northwestern University, the University of Minnesota, and the Kaiser Foundation Research Institute. Rouch, Lakhan, and Dr. Fayad have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM NEUROLOGY
Berries, red wine linked to lower mortality in Parkinson’s disease
(PD), new research suggests.
In a prospective analysis of more than 1,200 participants with an eventual PD diagnosis, those who ate three or more servings of flavonoid-rich foods a week had a 70% lower mortality versus those consuming one or fewer servings of such foods per month.
“Adopting a healthy dietary pattern that is high in colorful fruits and veggies like berries, even after a Parkinson diagnosis, could slow disease progression and improve survival rate,” study investigator Xiang Gao, MD, PhD, professor and director, Nutritional Epidemiology Lab, department of nutritional sciences, Penn State University, University Park, said in an interview.
The findings were published online Jan. 26, 2022, in Neurology.
First evidence of survival advantage
Flavonoids are plant-derived polyphenolic molecules found in fruits such as berries, apples, and oranges; vegetables such as kale and broccoli; and beverages, including tea and red wine. They are the dietary components that give many foods their vibrant color.
Certain flavonoids have been shown previously to have antioxidant and anti-inflammatory properties.
A previous study by Dr. Gao and colleagues showed that flavonoids were associated with a lower future risk for developing PD. However, it did not provide evidence these nutrients improved survival rates among PD patients.
The new analysis included participants from the ongoing Nurses’ Health Study (NHS) of female registered nurses, which began in 1976, and male participants from the ongoing Health Professionals Follow-up Study (HPFS), which began in 1986.
All participants answered questionnaires at baseline and then biennially to update information on demographics, lifestyle, medical history, and occurrence of chronic disease.
Using validated food-frequency questionnaires completed every 4 years, researchers assessed dietary intakes of total flavonoid, six flavonoid subclasses, and flavonoid-rich foods such as tea, apples, berries, oranges and orange juice, and red wine.
They examined flavonoid intake both before and after a PD diagnosis to minimize the potential for reverse causality. The investigators noted that patients with PD have difficulty swallowing and handling food and cutlery, which could impact their consumption of flavonoid-rich foods.
Frequency of consumption of flavonoid-rich foods was categorized into four groups: one or less servings per month (the reference group), one to three servings per month, one to two servings per week, and three or more servings per week.
The analysis included 599 women and 652 men who were newly diagnosed with PD. The mean age at PD diagnosis was 72 years, and the mean time between the last prediagnosis dietary assessment and PD diagnosis was 32 months.
The primary outcome measure was all-cause mortality. There were 528 deaths in men and 416 deaths in women during an average of 33 years of follow-up.
Neuroprotective pathway?
After controlling for age, lifestyle behaviors, medical history, and total energy and caffeine intake, results showed that higher total flavonoid intake before PD diagnosis was associated with a lower risk for all-cause mortality after diagnosis in men, with a hazard ratio of 0.53 (95% confidence interval, 0.39-0.71) when comparing the highest and lowest quartiles (P for trend < .001).
However, this association was not found in women (HR, 0.93; 95% CI, 0.68-1.28; P for trend = .69).
The pooled HR was 0.70 (95% CI, 0.40-1.22; P for trend = .25) with significant heterogeneity (P = .01).
There were significant associations between a higher prediagnosis intake of certain flavonoids and lower mortality risk. The pooled HR comparing the highest versus lowest intake quartiles was 0.66 for anthocyanin, 0.78 for flavones, and 0.69 for flavan-3-ols (P < .05 for all).
Compared with participants who consumed less than one serving a month, those consuming more than three servings a week prediagnosis of berries or red wine had a lower mortality risk (pooled HR, 0.77; 95% CI, 0.58-1.02 for berries and HR, 0.68; 95% CI, 0.51-0.91 for red wine).
After PD diagnosis, higher flavonoid consumption was associated with better survival rates in both men and women.
It’s unclear why there was a gender difference in the association between prediagnosis flavonoid intake and mortality but not for postdiagnosis flavonoid intakes, Dr. Gao said.
A potential neuroprotective pathway by which flavonoids reduce mortality in PD involves direct radical scavenging, which lowers oxidative stress and chronic neuroinflammation levels, he noted.
“Certain flavonoids, for example, anthocyanins, have been shown to exert antiapoptosis effects and protect cognition and motor functions. They could also increase dopamine release,” Dr. Gao added.
Study limitations included not having detailed information on participants’ PD disease severity and that both the NHS and HPFS include predominantly White health care professionals, which limits the generalizability of the results, the investigators noted.
No direct link
Commenting on the findings, Michael S. Okun, MD, medical advisor at the Parkinson’s Foundation and director of the Norman Fixel Institute for Neurological Diseases, University of Florida Health, Gainesville, said the study adds to growing evidence suggesting “subsets of flavonoids and especially berries and wine will have benefits pre- and post–Parkinson’s disease diagnosis.”
However, he emphasized that patients should not take up drinking red wine just to improve survival.
“We don’t recommend that folks who are already diagnosed with Parkinson’s drink alcohol, especially without physician supervision,” said Dr. Okun, who was not involved with the research.
Also commenting for this article, Gunter Kuhnle, PhD, professor of nutrition and food science, University of Reading (England), said because the study doesn’t appear to adjust for socioeconomic status, the results may be driven by factors such as income and education and not food intake.
The study found a beneficial association with anthocyanins, which are mainly found in expensive berries, and with flavan-3-ols found mainly in tea, which in the United States is often a marker of higher income, said Dr. Kuhnle.
The advantage of assessing dietary intake of flavonoids using a food-frequency questionnaire, as was done in this study, is that it captures long-term patterns. However, the disadvantage is a loss in “resolution” by combining similar foods, Dr. Kuhnle noted.
Since flavonoids are found in most fruits and vegetables, high flavonoid intake “might simply be a marker of fruit and vegetable intake and therefore a ‘healthy’ dietary pattern,” he concluded.
The study received funding from the National Institute of Neurological Disorders and Stroke. Dr. Gao and Dr. Okun reported no relevant financial relationships. Dr. Kuhnle has conducted research into the associations between flavanol and health, some of which has been funded by Mars.
A version of this article first appeared on Medscape.com.
(PD), new research suggests.
In a prospective analysis of more than 1,200 participants with an eventual PD diagnosis, those who ate three or more servings of flavonoid-rich foods a week had a 70% lower mortality versus those consuming one or fewer servings of such foods per month.
“Adopting a healthy dietary pattern that is high in colorful fruits and veggies like berries, even after a Parkinson diagnosis, could slow disease progression and improve survival rate,” study investigator Xiang Gao, MD, PhD, professor and director, Nutritional Epidemiology Lab, department of nutritional sciences, Penn State University, University Park, said in an interview.
The findings were published online Jan. 26, 2022, in Neurology.
First evidence of survival advantage
Flavonoids are plant-derived polyphenolic molecules found in fruits such as berries, apples, and oranges; vegetables such as kale and broccoli; and beverages, including tea and red wine. They are the dietary components that give many foods their vibrant color.
Certain flavonoids have been shown previously to have antioxidant and anti-inflammatory properties.
A previous study by Dr. Gao and colleagues showed that flavonoids were associated with a lower future risk for developing PD. However, it did not provide evidence these nutrients improved survival rates among PD patients.
The new analysis included participants from the ongoing Nurses’ Health Study (NHS) of female registered nurses, which began in 1976, and male participants from the ongoing Health Professionals Follow-up Study (HPFS), which began in 1986.
All participants answered questionnaires at baseline and then biennially to update information on demographics, lifestyle, medical history, and occurrence of chronic disease.
Using validated food-frequency questionnaires completed every 4 years, researchers assessed dietary intakes of total flavonoid, six flavonoid subclasses, and flavonoid-rich foods such as tea, apples, berries, oranges and orange juice, and red wine.
They examined flavonoid intake both before and after a PD diagnosis to minimize the potential for reverse causality. The investigators noted that patients with PD have difficulty swallowing and handling food and cutlery, which could impact their consumption of flavonoid-rich foods.
Frequency of consumption of flavonoid-rich foods was categorized into four groups: one or less servings per month (the reference group), one to three servings per month, one to two servings per week, and three or more servings per week.
The analysis included 599 women and 652 men who were newly diagnosed with PD. The mean age at PD diagnosis was 72 years, and the mean time between the last prediagnosis dietary assessment and PD diagnosis was 32 months.
The primary outcome measure was all-cause mortality. There were 528 deaths in men and 416 deaths in women during an average of 33 years of follow-up.
Neuroprotective pathway?
After controlling for age, lifestyle behaviors, medical history, and total energy and caffeine intake, results showed that higher total flavonoid intake before PD diagnosis was associated with a lower risk for all-cause mortality after diagnosis in men, with a hazard ratio of 0.53 (95% confidence interval, 0.39-0.71) when comparing the highest and lowest quartiles (P for trend < .001).
However, this association was not found in women (HR, 0.93; 95% CI, 0.68-1.28; P for trend = .69).
The pooled HR was 0.70 (95% CI, 0.40-1.22; P for trend = .25) with significant heterogeneity (P = .01).
There were significant associations between a higher prediagnosis intake of certain flavonoids and lower mortality risk. The pooled HR comparing the highest versus lowest intake quartiles was 0.66 for anthocyanin, 0.78 for flavones, and 0.69 for flavan-3-ols (P < .05 for all).
Compared with participants who consumed less than one serving a month, those consuming more than three servings a week prediagnosis of berries or red wine had a lower mortality risk (pooled HR, 0.77; 95% CI, 0.58-1.02 for berries and HR, 0.68; 95% CI, 0.51-0.91 for red wine).
After PD diagnosis, higher flavonoid consumption was associated with better survival rates in both men and women.
It’s unclear why there was a gender difference in the association between prediagnosis flavonoid intake and mortality but not for postdiagnosis flavonoid intakes, Dr. Gao said.
A potential neuroprotective pathway by which flavonoids reduce mortality in PD involves direct radical scavenging, which lowers oxidative stress and chronic neuroinflammation levels, he noted.
“Certain flavonoids, for example, anthocyanins, have been shown to exert antiapoptosis effects and protect cognition and motor functions. They could also increase dopamine release,” Dr. Gao added.
Study limitations included not having detailed information on participants’ PD disease severity and that both the NHS and HPFS include predominantly White health care professionals, which limits the generalizability of the results, the investigators noted.
No direct link
Commenting on the findings, Michael S. Okun, MD, medical advisor at the Parkinson’s Foundation and director of the Norman Fixel Institute for Neurological Diseases, University of Florida Health, Gainesville, said the study adds to growing evidence suggesting “subsets of flavonoids and especially berries and wine will have benefits pre- and post–Parkinson’s disease diagnosis.”
However, he emphasized that patients should not take up drinking red wine just to improve survival.
“We don’t recommend that folks who are already diagnosed with Parkinson’s drink alcohol, especially without physician supervision,” said Dr. Okun, who was not involved with the research.
Also commenting for this article, Gunter Kuhnle, PhD, professor of nutrition and food science, University of Reading (England), said because the study doesn’t appear to adjust for socioeconomic status, the results may be driven by factors such as income and education and not food intake.
The study found a beneficial association with anthocyanins, which are mainly found in expensive berries, and with flavan-3-ols found mainly in tea, which in the United States is often a marker of higher income, said Dr. Kuhnle.
The advantage of assessing dietary intake of flavonoids using a food-frequency questionnaire, as was done in this study, is that it captures long-term patterns. However, the disadvantage is a loss in “resolution” by combining similar foods, Dr. Kuhnle noted.
Since flavonoids are found in most fruits and vegetables, high flavonoid intake “might simply be a marker of fruit and vegetable intake and therefore a ‘healthy’ dietary pattern,” he concluded.
The study received funding from the National Institute of Neurological Disorders and Stroke. Dr. Gao and Dr. Okun reported no relevant financial relationships. Dr. Kuhnle has conducted research into the associations between flavanol and health, some of which has been funded by Mars.
A version of this article first appeared on Medscape.com.
(PD), new research suggests.
In a prospective analysis of more than 1,200 participants with an eventual PD diagnosis, those who ate three or more servings of flavonoid-rich foods a week had a 70% lower mortality versus those consuming one or fewer servings of such foods per month.
“Adopting a healthy dietary pattern that is high in colorful fruits and veggies like berries, even after a Parkinson diagnosis, could slow disease progression and improve survival rate,” study investigator Xiang Gao, MD, PhD, professor and director, Nutritional Epidemiology Lab, department of nutritional sciences, Penn State University, University Park, said in an interview.
The findings were published online Jan. 26, 2022, in Neurology.
First evidence of survival advantage
Flavonoids are plant-derived polyphenolic molecules found in fruits such as berries, apples, and oranges; vegetables such as kale and broccoli; and beverages, including tea and red wine. They are the dietary components that give many foods their vibrant color.
Certain flavonoids have been shown previously to have antioxidant and anti-inflammatory properties.
A previous study by Dr. Gao and colleagues showed that flavonoids were associated with a lower future risk for developing PD. However, it did not provide evidence these nutrients improved survival rates among PD patients.
The new analysis included participants from the ongoing Nurses’ Health Study (NHS) of female registered nurses, which began in 1976, and male participants from the ongoing Health Professionals Follow-up Study (HPFS), which began in 1986.
All participants answered questionnaires at baseline and then biennially to update information on demographics, lifestyle, medical history, and occurrence of chronic disease.
Using validated food-frequency questionnaires completed every 4 years, researchers assessed dietary intakes of total flavonoid, six flavonoid subclasses, and flavonoid-rich foods such as tea, apples, berries, oranges and orange juice, and red wine.
They examined flavonoid intake both before and after a PD diagnosis to minimize the potential for reverse causality. The investigators noted that patients with PD have difficulty swallowing and handling food and cutlery, which could impact their consumption of flavonoid-rich foods.
Frequency of consumption of flavonoid-rich foods was categorized into four groups: one or less servings per month (the reference group), one to three servings per month, one to two servings per week, and three or more servings per week.
The analysis included 599 women and 652 men who were newly diagnosed with PD. The mean age at PD diagnosis was 72 years, and the mean time between the last prediagnosis dietary assessment and PD diagnosis was 32 months.
The primary outcome measure was all-cause mortality. There were 528 deaths in men and 416 deaths in women during an average of 33 years of follow-up.
Neuroprotective pathway?
After controlling for age, lifestyle behaviors, medical history, and total energy and caffeine intake, results showed that higher total flavonoid intake before PD diagnosis was associated with a lower risk for all-cause mortality after diagnosis in men, with a hazard ratio of 0.53 (95% confidence interval, 0.39-0.71) when comparing the highest and lowest quartiles (P for trend < .001).
However, this association was not found in women (HR, 0.93; 95% CI, 0.68-1.28; P for trend = .69).
The pooled HR was 0.70 (95% CI, 0.40-1.22; P for trend = .25) with significant heterogeneity (P = .01).
There were significant associations between a higher prediagnosis intake of certain flavonoids and lower mortality risk. The pooled HR comparing the highest versus lowest intake quartiles was 0.66 for anthocyanin, 0.78 for flavones, and 0.69 for flavan-3-ols (P < .05 for all).
Compared with participants who consumed less than one serving a month, those consuming more than three servings a week prediagnosis of berries or red wine had a lower mortality risk (pooled HR, 0.77; 95% CI, 0.58-1.02 for berries and HR, 0.68; 95% CI, 0.51-0.91 for red wine).
After PD diagnosis, higher flavonoid consumption was associated with better survival rates in both men and women.
It’s unclear why there was a gender difference in the association between prediagnosis flavonoid intake and mortality but not for postdiagnosis flavonoid intakes, Dr. Gao said.
A potential neuroprotective pathway by which flavonoids reduce mortality in PD involves direct radical scavenging, which lowers oxidative stress and chronic neuroinflammation levels, he noted.
“Certain flavonoids, for example, anthocyanins, have been shown to exert antiapoptosis effects and protect cognition and motor functions. They could also increase dopamine release,” Dr. Gao added.
Study limitations included not having detailed information on participants’ PD disease severity and that both the NHS and HPFS include predominantly White health care professionals, which limits the generalizability of the results, the investigators noted.
No direct link
Commenting on the findings, Michael S. Okun, MD, medical advisor at the Parkinson’s Foundation and director of the Norman Fixel Institute for Neurological Diseases, University of Florida Health, Gainesville, said the study adds to growing evidence suggesting “subsets of flavonoids and especially berries and wine will have benefits pre- and post–Parkinson’s disease diagnosis.”
However, he emphasized that patients should not take up drinking red wine just to improve survival.
“We don’t recommend that folks who are already diagnosed with Parkinson’s drink alcohol, especially without physician supervision,” said Dr. Okun, who was not involved with the research.
Also commenting for this article, Gunter Kuhnle, PhD, professor of nutrition and food science, University of Reading (England), said because the study doesn’t appear to adjust for socioeconomic status, the results may be driven by factors such as income and education and not food intake.
The study found a beneficial association with anthocyanins, which are mainly found in expensive berries, and with flavan-3-ols found mainly in tea, which in the United States is often a marker of higher income, said Dr. Kuhnle.
The advantage of assessing dietary intake of flavonoids using a food-frequency questionnaire, as was done in this study, is that it captures long-term patterns. However, the disadvantage is a loss in “resolution” by combining similar foods, Dr. Kuhnle noted.
Since flavonoids are found in most fruits and vegetables, high flavonoid intake “might simply be a marker of fruit and vegetable intake and therefore a ‘healthy’ dietary pattern,” he concluded.
The study received funding from the National Institute of Neurological Disorders and Stroke. Dr. Gao and Dr. Okun reported no relevant financial relationships. Dr. Kuhnle has conducted research into the associations between flavanol and health, some of which has been funded by Mars.
A version of this article first appeared on Medscape.com.
FROM NEUROLOGY
Novel biomarker found for Alzheimer’s disease
The study covered in this summary was published in medRxiv.org as a preprint and has not yet been peer reviewed.
Key takeaways
- Estimated beta-amyloid (Aβ42) cellular uptake can be more than two times greater in AD patients compared to cognitively normal subjects. A less pronounced yet increased uptake rate was also observed in patients with late-onset mild cognitive impairment (MCI). This increased uptake may prove to be a key mechanism defining age-related AD progression.
- The increased cellular amyloid uptake in AD and LMCI may lead to quicker disease progression, but early-onset MCI may result from increased production of toxic amyloid metabolites.
Why this matters
- Additional biomarkers for AD could greatly aid diagnosis and course prediction, as they are currently limited to PET scan analysis of amyloid plaque deposits and concentration of Aβ42 in cerebrospinal fluid (CSF).
- Amyloid deposits found by PET have a positive correlation with AD diagnosis. In contrast, CSF-Aβ42 and AD diagnosis or cognitive decline are negatively correlated. Normal cognition (NC) is associated with higher CSF beta-amyloid levels, but previous research has not explained why CSF-Aβ42 levels can be equivalent in patients with NC but high amyloid load and patients with AD and low amyloid load.
Study design
- The authors of this retrospective study used anonymized data obtained from the Alzheimer’s’s Disease Neuroimaging Initiative (ADNI). ADNI’s goal has been to test whether serial MRI scans, PET scans, biomarkers, and clinical/neuropsychological assessment can be combined to measure the progression of MCI and AD.
- Study subjects had either an AD diagnosis or NC and were divided into two groups: low amyloid load and high amyloid load. The fraction of patients with an AD diagnosis was calculated as a function of CSF-Aβ42.
- Calculations and statistical comparisons were performed using Microsoft Excel and custom-written C++ programs.
Key results
- The lowest levels of CSF-Aβ42 correlated with the highest percentage of AD-diagnosed patients, estimated to be 27% in subjects with low amyloid deposit density and 65% in those with high deposit density.
- The relationship between CSF-Aβ42 levels and amyloid load can be described using a simple mathematical model: Amyloid concentration in the interstitial cells is equal to the synthesis rate divided by the density of amyloid deposits plus the sum of the rate of amyloid removal through the CSF and the cellular amyloid uptake rate.
- AD and late-onset MCI patients had a significantly higher amyloid removal rate compared to NC subjects.
- Early-onset MCI patients had Aβ42 turnover similar to that of NC subjects, pointing to a different underlying mechanism such as enzymatic disbalance.
Limitations
- The model used to explain amyloid exchange between the interstitial space and the CSF is oversimplified; the actual process is more complex.
- Synthesis and uptake rates of Aβ42 vary throughout areas of the brain. The model assumes a homogeneous distribution within the interstitial compartment.
Study disclosures
- Research reported in this publication was not supported by any external funding. Data collection and sharing for this project were funded by ADNI.
A version of this article first appeared on Medscape.com.
The study covered in this summary was published in medRxiv.org as a preprint and has not yet been peer reviewed.
Key takeaways
- Estimated beta-amyloid (Aβ42) cellular uptake can be more than two times greater in AD patients compared to cognitively normal subjects. A less pronounced yet increased uptake rate was also observed in patients with late-onset mild cognitive impairment (MCI). This increased uptake may prove to be a key mechanism defining age-related AD progression.
- The increased cellular amyloid uptake in AD and LMCI may lead to quicker disease progression, but early-onset MCI may result from increased production of toxic amyloid metabolites.
Why this matters
- Additional biomarkers for AD could greatly aid diagnosis and course prediction, as they are currently limited to PET scan analysis of amyloid plaque deposits and concentration of Aβ42 in cerebrospinal fluid (CSF).
- Amyloid deposits found by PET have a positive correlation with AD diagnosis. In contrast, CSF-Aβ42 and AD diagnosis or cognitive decline are negatively correlated. Normal cognition (NC) is associated with higher CSF beta-amyloid levels, but previous research has not explained why CSF-Aβ42 levels can be equivalent in patients with NC but high amyloid load and patients with AD and low amyloid load.
Study design
- The authors of this retrospective study used anonymized data obtained from the Alzheimer’s’s Disease Neuroimaging Initiative (ADNI). ADNI’s goal has been to test whether serial MRI scans, PET scans, biomarkers, and clinical/neuropsychological assessment can be combined to measure the progression of MCI and AD.
- Study subjects had either an AD diagnosis or NC and were divided into two groups: low amyloid load and high amyloid load. The fraction of patients with an AD diagnosis was calculated as a function of CSF-Aβ42.
- Calculations and statistical comparisons were performed using Microsoft Excel and custom-written C++ programs.
Key results
- The lowest levels of CSF-Aβ42 correlated with the highest percentage of AD-diagnosed patients, estimated to be 27% in subjects with low amyloid deposit density and 65% in those with high deposit density.
- The relationship between CSF-Aβ42 levels and amyloid load can be described using a simple mathematical model: Amyloid concentration in the interstitial cells is equal to the synthesis rate divided by the density of amyloid deposits plus the sum of the rate of amyloid removal through the CSF and the cellular amyloid uptake rate.
- AD and late-onset MCI patients had a significantly higher amyloid removal rate compared to NC subjects.
- Early-onset MCI patients had Aβ42 turnover similar to that of NC subjects, pointing to a different underlying mechanism such as enzymatic disbalance.
Limitations
- The model used to explain amyloid exchange between the interstitial space and the CSF is oversimplified; the actual process is more complex.
- Synthesis and uptake rates of Aβ42 vary throughout areas of the brain. The model assumes a homogeneous distribution within the interstitial compartment.
Study disclosures
- Research reported in this publication was not supported by any external funding. Data collection and sharing for this project were funded by ADNI.
A version of this article first appeared on Medscape.com.
The study covered in this summary was published in medRxiv.org as a preprint and has not yet been peer reviewed.
Key takeaways
- Estimated beta-amyloid (Aβ42) cellular uptake can be more than two times greater in AD patients compared to cognitively normal subjects. A less pronounced yet increased uptake rate was also observed in patients with late-onset mild cognitive impairment (MCI). This increased uptake may prove to be a key mechanism defining age-related AD progression.
- The increased cellular amyloid uptake in AD and LMCI may lead to quicker disease progression, but early-onset MCI may result from increased production of toxic amyloid metabolites.
Why this matters
- Additional biomarkers for AD could greatly aid diagnosis and course prediction, as they are currently limited to PET scan analysis of amyloid plaque deposits and concentration of Aβ42 in cerebrospinal fluid (CSF).
- Amyloid deposits found by PET have a positive correlation with AD diagnosis. In contrast, CSF-Aβ42 and AD diagnosis or cognitive decline are negatively correlated. Normal cognition (NC) is associated with higher CSF beta-amyloid levels, but previous research has not explained why CSF-Aβ42 levels can be equivalent in patients with NC but high amyloid load and patients with AD and low amyloid load.
Study design
- The authors of this retrospective study used anonymized data obtained from the Alzheimer’s’s Disease Neuroimaging Initiative (ADNI). ADNI’s goal has been to test whether serial MRI scans, PET scans, biomarkers, and clinical/neuropsychological assessment can be combined to measure the progression of MCI and AD.
- Study subjects had either an AD diagnosis or NC and were divided into two groups: low amyloid load and high amyloid load. The fraction of patients with an AD diagnosis was calculated as a function of CSF-Aβ42.
- Calculations and statistical comparisons were performed using Microsoft Excel and custom-written C++ programs.
Key results
- The lowest levels of CSF-Aβ42 correlated with the highest percentage of AD-diagnosed patients, estimated to be 27% in subjects with low amyloid deposit density and 65% in those with high deposit density.
- The relationship between CSF-Aβ42 levels and amyloid load can be described using a simple mathematical model: Amyloid concentration in the interstitial cells is equal to the synthesis rate divided by the density of amyloid deposits plus the sum of the rate of amyloid removal through the CSF and the cellular amyloid uptake rate.
- AD and late-onset MCI patients had a significantly higher amyloid removal rate compared to NC subjects.
- Early-onset MCI patients had Aβ42 turnover similar to that of NC subjects, pointing to a different underlying mechanism such as enzymatic disbalance.
Limitations
- The model used to explain amyloid exchange between the interstitial space and the CSF is oversimplified; the actual process is more complex.
- Synthesis and uptake rates of Aβ42 vary throughout areas of the brain. The model assumes a homogeneous distribution within the interstitial compartment.
Study disclosures
- Research reported in this publication was not supported by any external funding. Data collection and sharing for this project were funded by ADNI.
A version of this article first appeared on Medscape.com.