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Alzheimer's Association International Conference 2015 (AAIC)
VIDEO: Postoperative cognitive decline hits women hardest
WASHINGTON – Postoperative cognitive decline, which occurs in roughly 20% of elderly patients who undergo major surgery, strikes older women with greater severity than it does similarly aged men, according to a retrospective analysis of data collected from 527 older Americans.
“We looked at the sex difference in postoperative cognitive decline and Alzheimer’s disease because of the sex difference in Alzheimer’s disease, where about two-thirds of patients are women,” Dr. Katie J. Schenning said in an interview during the Alzheimer’s Association International Conference 2015. “We know that a lot of the pathologic changes that happen to the brain after anesthesia and surgery are similar to the changes that happen in Alzheimer’s disease patients. But at this point that is all we can say about a link between the two. It is currently unknown whether there is a clear relationship between postoperative cognitive decline and Alzheimer’s disease,” said Dr. Schenning, an anesthesiologist at Oregon Health & Science University in Portland.
She and her associates studied data collected longitudinally from two cohorts, the Oregon Brain Aging Study and the Intelligent Systems for Assessment of Aging Changes. At baseline, the average age of the enrollees in the combined group was 83 years, and just under two-thirds were women. During follow-up, 182 of the participants underwent a total of 331 major surgeries, with some undergoing more than one surgery. The most common form of surgery was orthopedic, done in one-third of the patients, followed by general surgery, in a quarter.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
The researchers running both studies collected data annually from participants using a battery of neuropsychological evaluations, brain MRIs, and information on their general health. Retrospective analysis of the data showed that following surgery, people showed evidence of statistically significant and clinically meaningful declines in several measures, compared with those who did not undergo surgery, including deficits measured by the Mini-Mental State Examination, instrumental activities of daily living, and logical memory delayed recall. The trajectory of these declines was significantly steeper in women following surgery, compared with men following surgery, Dr. Schenning reported in a poster at the meeting. In addition, the MRI scans showed ventricular enlargement in the postsurgical women but not in men, a change that is characteristic of neuropathology.
“Women who underwent surgery had a more rapid rate of decline in measures of cognition and function than women who did not have surgery, and it affected women in more categories than in men,” Dr. Schenning said.
The risk for postoperative cognitive decline “is one of the things that patients should take into consideration before undergoing elective surgery, especially if they are older or have pre-existing cognitive impairment,” Dr. Schenning suggested. The enhanced risk for postsurgical cognitive decline faced by older women and even the somewhat lesser risk that exists for older men “is certainly something that patients should discuss with their surgeon, anesthesiologist, and family members,” she said.
Dr. Schenning had no disclosures.
On Twitter @mitchelzoler
WASHINGTON – Postoperative cognitive decline, which occurs in roughly 20% of elderly patients who undergo major surgery, strikes older women with greater severity than it does similarly aged men, according to a retrospective analysis of data collected from 527 older Americans.
“We looked at the sex difference in postoperative cognitive decline and Alzheimer’s disease because of the sex difference in Alzheimer’s disease, where about two-thirds of patients are women,” Dr. Katie J. Schenning said in an interview during the Alzheimer’s Association International Conference 2015. “We know that a lot of the pathologic changes that happen to the brain after anesthesia and surgery are similar to the changes that happen in Alzheimer’s disease patients. But at this point that is all we can say about a link between the two. It is currently unknown whether there is a clear relationship between postoperative cognitive decline and Alzheimer’s disease,” said Dr. Schenning, an anesthesiologist at Oregon Health & Science University in Portland.
She and her associates studied data collected longitudinally from two cohorts, the Oregon Brain Aging Study and the Intelligent Systems for Assessment of Aging Changes. At baseline, the average age of the enrollees in the combined group was 83 years, and just under two-thirds were women. During follow-up, 182 of the participants underwent a total of 331 major surgeries, with some undergoing more than one surgery. The most common form of surgery was orthopedic, done in one-third of the patients, followed by general surgery, in a quarter.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
The researchers running both studies collected data annually from participants using a battery of neuropsychological evaluations, brain MRIs, and information on their general health. Retrospective analysis of the data showed that following surgery, people showed evidence of statistically significant and clinically meaningful declines in several measures, compared with those who did not undergo surgery, including deficits measured by the Mini-Mental State Examination, instrumental activities of daily living, and logical memory delayed recall. The trajectory of these declines was significantly steeper in women following surgery, compared with men following surgery, Dr. Schenning reported in a poster at the meeting. In addition, the MRI scans showed ventricular enlargement in the postsurgical women but not in men, a change that is characteristic of neuropathology.
“Women who underwent surgery had a more rapid rate of decline in measures of cognition and function than women who did not have surgery, and it affected women in more categories than in men,” Dr. Schenning said.
The risk for postoperative cognitive decline “is one of the things that patients should take into consideration before undergoing elective surgery, especially if they are older or have pre-existing cognitive impairment,” Dr. Schenning suggested. The enhanced risk for postsurgical cognitive decline faced by older women and even the somewhat lesser risk that exists for older men “is certainly something that patients should discuss with their surgeon, anesthesiologist, and family members,” she said.
Dr. Schenning had no disclosures.
On Twitter @mitchelzoler
WASHINGTON – Postoperative cognitive decline, which occurs in roughly 20% of elderly patients who undergo major surgery, strikes older women with greater severity than it does similarly aged men, according to a retrospective analysis of data collected from 527 older Americans.
“We looked at the sex difference in postoperative cognitive decline and Alzheimer’s disease because of the sex difference in Alzheimer’s disease, where about two-thirds of patients are women,” Dr. Katie J. Schenning said in an interview during the Alzheimer’s Association International Conference 2015. “We know that a lot of the pathologic changes that happen to the brain after anesthesia and surgery are similar to the changes that happen in Alzheimer’s disease patients. But at this point that is all we can say about a link between the two. It is currently unknown whether there is a clear relationship between postoperative cognitive decline and Alzheimer’s disease,” said Dr. Schenning, an anesthesiologist at Oregon Health & Science University in Portland.
She and her associates studied data collected longitudinally from two cohorts, the Oregon Brain Aging Study and the Intelligent Systems for Assessment of Aging Changes. At baseline, the average age of the enrollees in the combined group was 83 years, and just under two-thirds were women. During follow-up, 182 of the participants underwent a total of 331 major surgeries, with some undergoing more than one surgery. The most common form of surgery was orthopedic, done in one-third of the patients, followed by general surgery, in a quarter.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
The researchers running both studies collected data annually from participants using a battery of neuropsychological evaluations, brain MRIs, and information on their general health. Retrospective analysis of the data showed that following surgery, people showed evidence of statistically significant and clinically meaningful declines in several measures, compared with those who did not undergo surgery, including deficits measured by the Mini-Mental State Examination, instrumental activities of daily living, and logical memory delayed recall. The trajectory of these declines was significantly steeper in women following surgery, compared with men following surgery, Dr. Schenning reported in a poster at the meeting. In addition, the MRI scans showed ventricular enlargement in the postsurgical women but not in men, a change that is characteristic of neuropathology.
“Women who underwent surgery had a more rapid rate of decline in measures of cognition and function than women who did not have surgery, and it affected women in more categories than in men,” Dr. Schenning said.
The risk for postoperative cognitive decline “is one of the things that patients should take into consideration before undergoing elective surgery, especially if they are older or have pre-existing cognitive impairment,” Dr. Schenning suggested. The enhanced risk for postsurgical cognitive decline faced by older women and even the somewhat lesser risk that exists for older men “is certainly something that patients should discuss with their surgeon, anesthesiologist, and family members,” she said.
Dr. Schenning had no disclosures.
On Twitter @mitchelzoler
AT AAIC 2015
Estrogen Therapy Linked to Brain Atrophy in Women With Diabetes
WASHINGTON – Women with type 2 diabetes who take estrogen therapy showed lower total gray matter volume, with atrophy particularly evident in the hippocampus.
A new analysis of the Women’s Health Initiative Memory study suggested that these hormone therapy–related decrements in brain volume seem to stabilize in the years after treatment ends. However, said Christina E. Hugenschmidt, Ph.D., the findings also suggested caution when considering a prescription for estrogen therapy for a woman with emerging or frank diabetes.
“The concern is that prescribing estrogen to a woman with diabetes could increase her risk of brain atrophy,” she said at the Alzheimer’s Association International Conference 2015.
Dr. Hugenschmidt of Wake Forest University, Winston-Salem, N.C., reviewed data from the Women’s Health Initiate Memory Study–MRI (WHIMS-MRI).
The parallel placebo-controlled trial randomized women aged 65 years and older to placebo, or 0.625 mg conjugated equine estrogen with or without 2.5 mg progesterone. They were all free of cognitive decline at baseline.
Dr. Hugenschmidt focused on 1,400 women who underwent two magnetic resonance imaging brain scans: one 2.5 years after beginning the study and another about 5 years after that. The primary outcomes were total brain volume, including any ischemic lesions, total gray matter, total white matter, frontal lobe and hippocampal volume, and ischemic white matter lesion load.
At enrollment, the women were a mean age of 70 years old; 124 had type 2 diabetes. About 42% had long-standing disease of 10 years or longer. Not surprisingly, there were some significant differences between the diabetic and nondiabetic groups: Body mass index, waist girth, and waist/hip ratio were all significantly larger in the women with diabetes.
At the first scan, women with diabetes who had been randomized to estrogen therapy had about 18 cc less total brain volume than those without diabetes. The brain volumes of women with diabetes who were taking placebo were nearly identical to those of the nondiabetic women, regardless of what treatment they were taking.
The difference seemed to be driven by a loss of gray matter, Dr. Hugenschmidt said. There was no significant effect on white matter. The hippocampus appeared to have a similar amount of shrinkage. However, she added, there were no differences in cognitive scores on the Mini Mental State Exam.
Insulin use didn’t appear to ameliorate the findings of smaller brain volume among those with diabetes. Atrophy didn’t progress, however; findings at the same scan were similar.
The findings may be linked to the suppression of a natural process that occurs during the perimenopausal transition, Dr. Hugenschmidt said. Estrogen is crucial in maintaining the brain’s energy metabolism. It works by increasing glucose transport and aerobic glycolysis. But during this time of life, as estrogen wanes, it becomes uncoupled from the glucose metabolism pathway. The female brain then begins to use ketone bodies as its primary source of energy. Intact estrogen levels normally downregulate the use of alternative energy sources before menopause; supplementing them seems to prevent this transition from occurring.
“Among older women with diabetes for whom the glucose-based energy metabolism promoted by estrogen is already compromised, this downregulation of alternative energy sources may lead to increased atrophy of gray matter, which has a greater metabolic demand relative to white matter,” Dr. Hugenschmidt and her colleagues wrote in a paper published in Neurology (2015 July 10 [doi:10.1212/WNL.0000000000001816]).
Dr. Hugenschmidt reported having no relevant financial disclosures.
WASHINGTON – Women with type 2 diabetes who take estrogen therapy showed lower total gray matter volume, with atrophy particularly evident in the hippocampus.
A new analysis of the Women’s Health Initiative Memory study suggested that these hormone therapy–related decrements in brain volume seem to stabilize in the years after treatment ends. However, said Christina E. Hugenschmidt, Ph.D., the findings also suggested caution when considering a prescription for estrogen therapy for a woman with emerging or frank diabetes.
“The concern is that prescribing estrogen to a woman with diabetes could increase her risk of brain atrophy,” she said at the Alzheimer’s Association International Conference 2015.
Dr. Hugenschmidt of Wake Forest University, Winston-Salem, N.C., reviewed data from the Women’s Health Initiate Memory Study–MRI (WHIMS-MRI).
The parallel placebo-controlled trial randomized women aged 65 years and older to placebo, or 0.625 mg conjugated equine estrogen with or without 2.5 mg progesterone. They were all free of cognitive decline at baseline.
Dr. Hugenschmidt focused on 1,400 women who underwent two magnetic resonance imaging brain scans: one 2.5 years after beginning the study and another about 5 years after that. The primary outcomes were total brain volume, including any ischemic lesions, total gray matter, total white matter, frontal lobe and hippocampal volume, and ischemic white matter lesion load.
At enrollment, the women were a mean age of 70 years old; 124 had type 2 diabetes. About 42% had long-standing disease of 10 years or longer. Not surprisingly, there were some significant differences between the diabetic and nondiabetic groups: Body mass index, waist girth, and waist/hip ratio were all significantly larger in the women with diabetes.
At the first scan, women with diabetes who had been randomized to estrogen therapy had about 18 cc less total brain volume than those without diabetes. The brain volumes of women with diabetes who were taking placebo were nearly identical to those of the nondiabetic women, regardless of what treatment they were taking.
The difference seemed to be driven by a loss of gray matter, Dr. Hugenschmidt said. There was no significant effect on white matter. The hippocampus appeared to have a similar amount of shrinkage. However, she added, there were no differences in cognitive scores on the Mini Mental State Exam.
Insulin use didn’t appear to ameliorate the findings of smaller brain volume among those with diabetes. Atrophy didn’t progress, however; findings at the same scan were similar.
The findings may be linked to the suppression of a natural process that occurs during the perimenopausal transition, Dr. Hugenschmidt said. Estrogen is crucial in maintaining the brain’s energy metabolism. It works by increasing glucose transport and aerobic glycolysis. But during this time of life, as estrogen wanes, it becomes uncoupled from the glucose metabolism pathway. The female brain then begins to use ketone bodies as its primary source of energy. Intact estrogen levels normally downregulate the use of alternative energy sources before menopause; supplementing them seems to prevent this transition from occurring.
“Among older women with diabetes for whom the glucose-based energy metabolism promoted by estrogen is already compromised, this downregulation of alternative energy sources may lead to increased atrophy of gray matter, which has a greater metabolic demand relative to white matter,” Dr. Hugenschmidt and her colleagues wrote in a paper published in Neurology (2015 July 10 [doi:10.1212/WNL.0000000000001816]).
Dr. Hugenschmidt reported having no relevant financial disclosures.
WASHINGTON – Women with type 2 diabetes who take estrogen therapy showed lower total gray matter volume, with atrophy particularly evident in the hippocampus.
A new analysis of the Women’s Health Initiative Memory study suggested that these hormone therapy–related decrements in brain volume seem to stabilize in the years after treatment ends. However, said Christina E. Hugenschmidt, Ph.D., the findings also suggested caution when considering a prescription for estrogen therapy for a woman with emerging or frank diabetes.
“The concern is that prescribing estrogen to a woman with diabetes could increase her risk of brain atrophy,” she said at the Alzheimer’s Association International Conference 2015.
Dr. Hugenschmidt of Wake Forest University, Winston-Salem, N.C., reviewed data from the Women’s Health Initiate Memory Study–MRI (WHIMS-MRI).
The parallel placebo-controlled trial randomized women aged 65 years and older to placebo, or 0.625 mg conjugated equine estrogen with or without 2.5 mg progesterone. They were all free of cognitive decline at baseline.
Dr. Hugenschmidt focused on 1,400 women who underwent two magnetic resonance imaging brain scans: one 2.5 years after beginning the study and another about 5 years after that. The primary outcomes were total brain volume, including any ischemic lesions, total gray matter, total white matter, frontal lobe and hippocampal volume, and ischemic white matter lesion load.
At enrollment, the women were a mean age of 70 years old; 124 had type 2 diabetes. About 42% had long-standing disease of 10 years or longer. Not surprisingly, there were some significant differences between the diabetic and nondiabetic groups: Body mass index, waist girth, and waist/hip ratio were all significantly larger in the women with diabetes.
At the first scan, women with diabetes who had been randomized to estrogen therapy had about 18 cc less total brain volume than those without diabetes. The brain volumes of women with diabetes who were taking placebo were nearly identical to those of the nondiabetic women, regardless of what treatment they were taking.
The difference seemed to be driven by a loss of gray matter, Dr. Hugenschmidt said. There was no significant effect on white matter. The hippocampus appeared to have a similar amount of shrinkage. However, she added, there were no differences in cognitive scores on the Mini Mental State Exam.
Insulin use didn’t appear to ameliorate the findings of smaller brain volume among those with diabetes. Atrophy didn’t progress, however; findings at the same scan were similar.
The findings may be linked to the suppression of a natural process that occurs during the perimenopausal transition, Dr. Hugenschmidt said. Estrogen is crucial in maintaining the brain’s energy metabolism. It works by increasing glucose transport and aerobic glycolysis. But during this time of life, as estrogen wanes, it becomes uncoupled from the glucose metabolism pathway. The female brain then begins to use ketone bodies as its primary source of energy. Intact estrogen levels normally downregulate the use of alternative energy sources before menopause; supplementing them seems to prevent this transition from occurring.
“Among older women with diabetes for whom the glucose-based energy metabolism promoted by estrogen is already compromised, this downregulation of alternative energy sources may lead to increased atrophy of gray matter, which has a greater metabolic demand relative to white matter,” Dr. Hugenschmidt and her colleagues wrote in a paper published in Neurology (2015 July 10 [doi:10.1212/WNL.0000000000001816]).
Dr. Hugenschmidt reported having no relevant financial disclosures.
AT AAIC 2015
Estrogen therapy linked to brain atrophy in women with diabetes
WASHINGTON – Women with type 2 diabetes who take estrogen therapy showed lower total gray matter volume, with atrophy particularly evident in the hippocampus.
A new analysis of the Women’s Health Initiative Memory study suggested that these hormone therapy–related decrements in brain volume seem to stabilize in the years after treatment ends. However, said Christina E. Hugenschmidt, Ph.D., the findings also suggested caution when considering a prescription for estrogen therapy for a woman with emerging or frank diabetes.
“The concern is that prescribing estrogen to a woman with diabetes could increase her risk of brain atrophy,” she said at the Alzheimer’s Association International Conference 2015.
Dr. Hugenschmidt of Wake Forest University, Winston-Salem, N.C., reviewed data from the Women’s Health Initiate Memory Study–MRI (WHIMS-MRI).
The parallel placebo-controlled trial randomized women aged 65 years and older to placebo, or 0.625 mg conjugated equine estrogen with or without 2.5 mg progesterone. They were all free of cognitive decline at baseline.
Dr. Hugenschmidt focused on 1,400 women who underwent two magnetic resonance imaging brain scans: one 2.5 years after beginning the study and another about 5 years after that. The primary outcomes were total brain volume, including any ischemic lesions, total gray matter, total white matter, frontal lobe and hippocampal volume, and ischemic white matter lesion load.
At enrollment, the women were a mean age of 70 years old; 124 had type 2 diabetes. About 42% had long-standing disease of 10 years or longer. Not surprisingly, there were some significant differences between the diabetic and nondiabetic groups: Body mass index, waist girth, and waist/hip ratio were all significantly larger in the women with diabetes.
At the first scan, women with diabetes who had been randomized to estrogen therapy had about 18 cc less total brain volume than those without diabetes. The brain volumes of women with diabetes who were taking placebo were nearly identical to those of the nondiabetic women, regardless of what treatment they were taking.
The difference seemed to be driven by a loss of gray matter, Dr. Hugenschmidt said. There was no significant effect on white matter. The hippocampus appeared to have a similar amount of shrinkage. However, she added, there were no differences in cognitive scores on the Mini Mental State Exam.
Insulin use didn’t appear to ameliorate the findings of smaller brain volume among those with diabetes. Atrophy didn’t progress, however; findings at the same scan were similar.
The findings may be linked to the suppression of a natural process that occurs during the perimenopausal transition, Dr. Hugenschmidt said. Estrogen is crucial in maintaining the brain’s energy metabolism. It works by increasing glucose transport and aerobic glycolysis. But during this time of life, as estrogen wanes, it becomes uncoupled from the glucose metabolism pathway. The female brain then begins to use ketone bodies as its primary source of energy. Intact estrogen levels normally downregulate the use of alternative energy sources before menopause; supplementing them seems to prevent this transition from occurring.
“Among older women with diabetes for whom the glucose-based energy metabolism promoted by estrogen is already compromised, this downregulation of alternative energy sources may lead to increased atrophy of gray matter, which has a greater metabolic demand relative to white matter,” Dr. Hugenschmidt and her colleagues wrote in a paper published in Neurology (2015 July 10 [doi:10.1212/WNL.0000000000001816]).
Dr. Hugenschmidt reported having no relevant financial disclosures.
On Twitter @Alz_Gal
WASHINGTON – Women with type 2 diabetes who take estrogen therapy showed lower total gray matter volume, with atrophy particularly evident in the hippocampus.
A new analysis of the Women’s Health Initiative Memory study suggested that these hormone therapy–related decrements in brain volume seem to stabilize in the years after treatment ends. However, said Christina E. Hugenschmidt, Ph.D., the findings also suggested caution when considering a prescription for estrogen therapy for a woman with emerging or frank diabetes.
“The concern is that prescribing estrogen to a woman with diabetes could increase her risk of brain atrophy,” she said at the Alzheimer’s Association International Conference 2015.
Dr. Hugenschmidt of Wake Forest University, Winston-Salem, N.C., reviewed data from the Women’s Health Initiate Memory Study–MRI (WHIMS-MRI).
The parallel placebo-controlled trial randomized women aged 65 years and older to placebo, or 0.625 mg conjugated equine estrogen with or without 2.5 mg progesterone. They were all free of cognitive decline at baseline.
Dr. Hugenschmidt focused on 1,400 women who underwent two magnetic resonance imaging brain scans: one 2.5 years after beginning the study and another about 5 years after that. The primary outcomes were total brain volume, including any ischemic lesions, total gray matter, total white matter, frontal lobe and hippocampal volume, and ischemic white matter lesion load.
At enrollment, the women were a mean age of 70 years old; 124 had type 2 diabetes. About 42% had long-standing disease of 10 years or longer. Not surprisingly, there were some significant differences between the diabetic and nondiabetic groups: Body mass index, waist girth, and waist/hip ratio were all significantly larger in the women with diabetes.
At the first scan, women with diabetes who had been randomized to estrogen therapy had about 18 cc less total brain volume than those without diabetes. The brain volumes of women with diabetes who were taking placebo were nearly identical to those of the nondiabetic women, regardless of what treatment they were taking.
The difference seemed to be driven by a loss of gray matter, Dr. Hugenschmidt said. There was no significant effect on white matter. The hippocampus appeared to have a similar amount of shrinkage. However, she added, there were no differences in cognitive scores on the Mini Mental State Exam.
Insulin use didn’t appear to ameliorate the findings of smaller brain volume among those with diabetes. Atrophy didn’t progress, however; findings at the same scan were similar.
The findings may be linked to the suppression of a natural process that occurs during the perimenopausal transition, Dr. Hugenschmidt said. Estrogen is crucial in maintaining the brain’s energy metabolism. It works by increasing glucose transport and aerobic glycolysis. But during this time of life, as estrogen wanes, it becomes uncoupled from the glucose metabolism pathway. The female brain then begins to use ketone bodies as its primary source of energy. Intact estrogen levels normally downregulate the use of alternative energy sources before menopause; supplementing them seems to prevent this transition from occurring.
“Among older women with diabetes for whom the glucose-based energy metabolism promoted by estrogen is already compromised, this downregulation of alternative energy sources may lead to increased atrophy of gray matter, which has a greater metabolic demand relative to white matter,” Dr. Hugenschmidt and her colleagues wrote in a paper published in Neurology (2015 July 10 [doi:10.1212/WNL.0000000000001816]).
Dr. Hugenschmidt reported having no relevant financial disclosures.
On Twitter @Alz_Gal
WASHINGTON – Women with type 2 diabetes who take estrogen therapy showed lower total gray matter volume, with atrophy particularly evident in the hippocampus.
A new analysis of the Women’s Health Initiative Memory study suggested that these hormone therapy–related decrements in brain volume seem to stabilize in the years after treatment ends. However, said Christina E. Hugenschmidt, Ph.D., the findings also suggested caution when considering a prescription for estrogen therapy for a woman with emerging or frank diabetes.
“The concern is that prescribing estrogen to a woman with diabetes could increase her risk of brain atrophy,” she said at the Alzheimer’s Association International Conference 2015.
Dr. Hugenschmidt of Wake Forest University, Winston-Salem, N.C., reviewed data from the Women’s Health Initiate Memory Study–MRI (WHIMS-MRI).
The parallel placebo-controlled trial randomized women aged 65 years and older to placebo, or 0.625 mg conjugated equine estrogen with or without 2.5 mg progesterone. They were all free of cognitive decline at baseline.
Dr. Hugenschmidt focused on 1,400 women who underwent two magnetic resonance imaging brain scans: one 2.5 years after beginning the study and another about 5 years after that. The primary outcomes were total brain volume, including any ischemic lesions, total gray matter, total white matter, frontal lobe and hippocampal volume, and ischemic white matter lesion load.
At enrollment, the women were a mean age of 70 years old; 124 had type 2 diabetes. About 42% had long-standing disease of 10 years or longer. Not surprisingly, there were some significant differences between the diabetic and nondiabetic groups: Body mass index, waist girth, and waist/hip ratio were all significantly larger in the women with diabetes.
At the first scan, women with diabetes who had been randomized to estrogen therapy had about 18 cc less total brain volume than those without diabetes. The brain volumes of women with diabetes who were taking placebo were nearly identical to those of the nondiabetic women, regardless of what treatment they were taking.
The difference seemed to be driven by a loss of gray matter, Dr. Hugenschmidt said. There was no significant effect on white matter. The hippocampus appeared to have a similar amount of shrinkage. However, she added, there were no differences in cognitive scores on the Mini Mental State Exam.
Insulin use didn’t appear to ameliorate the findings of smaller brain volume among those with diabetes. Atrophy didn’t progress, however; findings at the same scan were similar.
The findings may be linked to the suppression of a natural process that occurs during the perimenopausal transition, Dr. Hugenschmidt said. Estrogen is crucial in maintaining the brain’s energy metabolism. It works by increasing glucose transport and aerobic glycolysis. But during this time of life, as estrogen wanes, it becomes uncoupled from the glucose metabolism pathway. The female brain then begins to use ketone bodies as its primary source of energy. Intact estrogen levels normally downregulate the use of alternative energy sources before menopause; supplementing them seems to prevent this transition from occurring.
“Among older women with diabetes for whom the glucose-based energy metabolism promoted by estrogen is already compromised, this downregulation of alternative energy sources may lead to increased atrophy of gray matter, which has a greater metabolic demand relative to white matter,” Dr. Hugenschmidt and her colleagues wrote in a paper published in Neurology (2015 July 10 [doi:10.1212/WNL.0000000000001816]).
Dr. Hugenschmidt reported having no relevant financial disclosures.
On Twitter @Alz_Gal
AT AAIC 2015
Key clinical point: Prescribing estrogen therapy for older women with type 2 diabetes could increase the risk of brain atrophy.
Major finding: Older women with type 2 diabetes who took estrogen therapy had about an 18-cc lower total brain volume than women with diabetes who took placebo and than women without the disease.
Data source: WHIMS-MRI was a large parallel-group study that examined the effect of hormone therapy on the brain and cognition in postmenopausal women.
Disclosures: Dr. Hugenschmidt reported having no relevant financial disclosures.
VIDEO: Investigating the role of plasmalogens in Alzheimer’s disease
WASHINGTON – Could a ubiquitous lipid – manufactured in the liver – be one of the root causes of Alzheimer’s disease? Plasmalogens are important in maintaining cell membrane permeability and effective neurotransmission. They also appear to influence the production of toxic forms of amyloid-beta by affecting the activity of alpha-secretase. What are they, and how strong could their influence in Alzheimer’s be? Dayan Goodenowe, Ph.D., explains at the Alzheimer’s Association International Conference 2015.
Dr. Goodenowe is the founder and CEO of Phenomenome Discoveries, which holds patents on measuring plasmalogen levels and is developing a plasmalogen therapeutic.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
On Twitter @alz_gal
WASHINGTON – Could a ubiquitous lipid – manufactured in the liver – be one of the root causes of Alzheimer’s disease? Plasmalogens are important in maintaining cell membrane permeability and effective neurotransmission. They also appear to influence the production of toxic forms of amyloid-beta by affecting the activity of alpha-secretase. What are they, and how strong could their influence in Alzheimer’s be? Dayan Goodenowe, Ph.D., explains at the Alzheimer’s Association International Conference 2015.
Dr. Goodenowe is the founder and CEO of Phenomenome Discoveries, which holds patents on measuring plasmalogen levels and is developing a plasmalogen therapeutic.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
On Twitter @alz_gal
WASHINGTON – Could a ubiquitous lipid – manufactured in the liver – be one of the root causes of Alzheimer’s disease? Plasmalogens are important in maintaining cell membrane permeability and effective neurotransmission. They also appear to influence the production of toxic forms of amyloid-beta by affecting the activity of alpha-secretase. What are they, and how strong could their influence in Alzheimer’s be? Dayan Goodenowe, Ph.D., explains at the Alzheimer’s Association International Conference 2015.
Dr. Goodenowe is the founder and CEO of Phenomenome Discoveries, which holds patents on measuring plasmalogen levels and is developing a plasmalogen therapeutic.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
On Twitter @alz_gal
AT AAIC 2015
VIDEO: Dementia Rate Doubled in Type 1 Diabetics
WASHINGTON – Improved management of patients with type 1 diabetes and the resulting increased longevity it has fostered has produced a new medical concern that few patients faced in the past: their risk for developing dementia as they age into their 60s, 70s, and beyond.
That risk, which turns out to be nearly double that of people without diabetes, closely matches the higher risk faced by patients with type 2 diabetes, based on analysis of data collected during 2002-2014 from more than 490,000 people aged 60 years or older enrolled in the Kaiser Permanente Medical Care Program of Northern California, Rachel Whitmer, Ph.D. reported at the Alzheimer’s Association International Conference 2015.
Her study tracked the dementia incidence in 334 of these Kaiser Permanente enrollees with type 1 diabetes and no dementia at baseline and found the rate ran 73% higher when compared with controls without any type of diabetes in the cohort after adjustment for sex, race, and vascular complications such as hypertension, stroke, and peripheral vascular disease. The patients with type 1 diabetes averaged 71 years old at baseline and their follow-up averaged 7 years. This is the first study to look at the incidence of dementia in elderly patients with type 1 diabetes, Dr. Whitmer said in an interview during the meeting.
Physicians who care for patients with type 1 diabetes should be aware of this increased risk, be on the lookout for signs of developing dementia in these patients, and use the increased risk to help motivate type 1 diabetes patients to be vigilant in controlling their disease to help avoid the microvascular complications that likely contribute to their dementia risk. Patients with type 1 diabetes are especially vulnerable to the consequences of cognitive impairment as they must maintain complex self-management routines of blood glucose monitoring, insulin administration, and keeping close tabs on their diet and exercise, Dr. Whitmer noted.
In 2013, she and her associates published a simple and easy-to-use tool for clinicians to assess the dementia risk in individual patients with type 2 diabetes (Lancet Diabetes Endocrinol. 2013;3:183-90). Further study of the risk factors that contribute to dementia onset in patients with type 1 diabetes will hopefully lead to creation of a similar risk-assessment tool for use in type 1 patients, said Dr. Whitmer, an epidemiologist at the Kaiser Permanente Northern California Division of Research in Oakland.
Dr. Whitmer had no disclosures.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
WASHINGTON – Improved management of patients with type 1 diabetes and the resulting increased longevity it has fostered has produced a new medical concern that few patients faced in the past: their risk for developing dementia as they age into their 60s, 70s, and beyond.
That risk, which turns out to be nearly double that of people without diabetes, closely matches the higher risk faced by patients with type 2 diabetes, based on analysis of data collected during 2002-2014 from more than 490,000 people aged 60 years or older enrolled in the Kaiser Permanente Medical Care Program of Northern California, Rachel Whitmer, Ph.D. reported at the Alzheimer’s Association International Conference 2015.
Her study tracked the dementia incidence in 334 of these Kaiser Permanente enrollees with type 1 diabetes and no dementia at baseline and found the rate ran 73% higher when compared with controls without any type of diabetes in the cohort after adjustment for sex, race, and vascular complications such as hypertension, stroke, and peripheral vascular disease. The patients with type 1 diabetes averaged 71 years old at baseline and their follow-up averaged 7 years. This is the first study to look at the incidence of dementia in elderly patients with type 1 diabetes, Dr. Whitmer said in an interview during the meeting.
Physicians who care for patients with type 1 diabetes should be aware of this increased risk, be on the lookout for signs of developing dementia in these patients, and use the increased risk to help motivate type 1 diabetes patients to be vigilant in controlling their disease to help avoid the microvascular complications that likely contribute to their dementia risk. Patients with type 1 diabetes are especially vulnerable to the consequences of cognitive impairment as they must maintain complex self-management routines of blood glucose monitoring, insulin administration, and keeping close tabs on their diet and exercise, Dr. Whitmer noted.
In 2013, she and her associates published a simple and easy-to-use tool for clinicians to assess the dementia risk in individual patients with type 2 diabetes (Lancet Diabetes Endocrinol. 2013;3:183-90). Further study of the risk factors that contribute to dementia onset in patients with type 1 diabetes will hopefully lead to creation of a similar risk-assessment tool for use in type 1 patients, said Dr. Whitmer, an epidemiologist at the Kaiser Permanente Northern California Division of Research in Oakland.
Dr. Whitmer had no disclosures.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
WASHINGTON – Improved management of patients with type 1 diabetes and the resulting increased longevity it has fostered has produced a new medical concern that few patients faced in the past: their risk for developing dementia as they age into their 60s, 70s, and beyond.
That risk, which turns out to be nearly double that of people without diabetes, closely matches the higher risk faced by patients with type 2 diabetes, based on analysis of data collected during 2002-2014 from more than 490,000 people aged 60 years or older enrolled in the Kaiser Permanente Medical Care Program of Northern California, Rachel Whitmer, Ph.D. reported at the Alzheimer’s Association International Conference 2015.
Her study tracked the dementia incidence in 334 of these Kaiser Permanente enrollees with type 1 diabetes and no dementia at baseline and found the rate ran 73% higher when compared with controls without any type of diabetes in the cohort after adjustment for sex, race, and vascular complications such as hypertension, stroke, and peripheral vascular disease. The patients with type 1 diabetes averaged 71 years old at baseline and their follow-up averaged 7 years. This is the first study to look at the incidence of dementia in elderly patients with type 1 diabetes, Dr. Whitmer said in an interview during the meeting.
Physicians who care for patients with type 1 diabetes should be aware of this increased risk, be on the lookout for signs of developing dementia in these patients, and use the increased risk to help motivate type 1 diabetes patients to be vigilant in controlling their disease to help avoid the microvascular complications that likely contribute to their dementia risk. Patients with type 1 diabetes are especially vulnerable to the consequences of cognitive impairment as they must maintain complex self-management routines of blood glucose monitoring, insulin administration, and keeping close tabs on their diet and exercise, Dr. Whitmer noted.
In 2013, she and her associates published a simple and easy-to-use tool for clinicians to assess the dementia risk in individual patients with type 2 diabetes (Lancet Diabetes Endocrinol. 2013;3:183-90). Further study of the risk factors that contribute to dementia onset in patients with type 1 diabetes will hopefully lead to creation of a similar risk-assessment tool for use in type 1 patients, said Dr. Whitmer, an epidemiologist at the Kaiser Permanente Northern California Division of Research in Oakland.
Dr. Whitmer had no disclosures.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
AT AAIC 2015
VIDEO: Dementia risk doubled in type 1 diabetes patients
WASHINGTON – Improved management of patients with type 1 diabetes and the resulting increased longevity it has fostered has produced a new medical concern that few patients faced in the past: their risk for developing dementia as they age into their 60s, 70s, and beyond.
That risk, which turns out to be nearly double that of people without diabetes, closely matches the higher risk faced by patients with type 2 diabetes, based on analysis of data collected during 2002-2014 from more than 490,000 people aged 60 years or older enrolled in the Kaiser Permanente Medical Care Program of Northern California, Rachel Whitmer, Ph.D. reported at the Alzheimer’s Association International Conference 2015.
Her study tracked the dementia incidence in 334 of these Kaiser Permanente enrollees with type 1 diabetes and no dementia at baseline and found the rate ran 73% higher when compared with controls without any type of diabetes in the cohort after adjustment for sex, race, and vascular complications such as hypertension, stroke, and peripheral vascular disease. The patients with type 1 diabetes averaged 71 years old at baseline and their follow-up averaged 7 years. This is the first study to look at the incidence of dementia in elderly patients with type 1 diabetes, Dr. Whitmer said in an interview during the meeting.
Physicians who care for patients with type 1 diabetes should be aware of this increased risk, be on the lookout for signs of developing dementia in these patients, and use the increased risk to help motivate type 1 diabetes patients to be vigilant in controlling their disease to help avoid the microvascular complications that likely contribute to their dementia risk. Patients with type 1 diabetes are especially vulnerable to the consequences of cognitive impairment as they must maintain complex self-management routines of blood glucose monitoring, insulin administration, and keeping close tabs on their diet and exercise, Dr. Whitmer noted.
In 2013, she and her associates published a simple and easy-to-use tool for clinicians to assess the dementia risk in individual patients with type 2 diabetes (Lancet Diabetes Endocrinol. 2013;3:183-90). Further study of the risk factors that contribute to dementia onset in patients with type 1 diabetes will hopefully lead to creation of a similar risk-assessment tool for use in type 1 patients, said Dr. Whitmer, an epidemiologist at the Kaiser Permanente Northern California Division of Research in Oakland.
Dr. Whitmer had no disclosures.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
On Twitter @mitchelzoler
WASHINGTON – Improved management of patients with type 1 diabetes and the resulting increased longevity it has fostered has produced a new medical concern that few patients faced in the past: their risk for developing dementia as they age into their 60s, 70s, and beyond.
That risk, which turns out to be nearly double that of people without diabetes, closely matches the higher risk faced by patients with type 2 diabetes, based on analysis of data collected during 2002-2014 from more than 490,000 people aged 60 years or older enrolled in the Kaiser Permanente Medical Care Program of Northern California, Rachel Whitmer, Ph.D. reported at the Alzheimer’s Association International Conference 2015.
Her study tracked the dementia incidence in 334 of these Kaiser Permanente enrollees with type 1 diabetes and no dementia at baseline and found the rate ran 73% higher when compared with controls without any type of diabetes in the cohort after adjustment for sex, race, and vascular complications such as hypertension, stroke, and peripheral vascular disease. The patients with type 1 diabetes averaged 71 years old at baseline and their follow-up averaged 7 years. This is the first study to look at the incidence of dementia in elderly patients with type 1 diabetes, Dr. Whitmer said in an interview during the meeting.
Physicians who care for patients with type 1 diabetes should be aware of this increased risk, be on the lookout for signs of developing dementia in these patients, and use the increased risk to help motivate type 1 diabetes patients to be vigilant in controlling their disease to help avoid the microvascular complications that likely contribute to their dementia risk. Patients with type 1 diabetes are especially vulnerable to the consequences of cognitive impairment as they must maintain complex self-management routines of blood glucose monitoring, insulin administration, and keeping close tabs on their diet and exercise, Dr. Whitmer noted.
In 2013, she and her associates published a simple and easy-to-use tool for clinicians to assess the dementia risk in individual patients with type 2 diabetes (Lancet Diabetes Endocrinol. 2013;3:183-90). Further study of the risk factors that contribute to dementia onset in patients with type 1 diabetes will hopefully lead to creation of a similar risk-assessment tool for use in type 1 patients, said Dr. Whitmer, an epidemiologist at the Kaiser Permanente Northern California Division of Research in Oakland.
Dr. Whitmer had no disclosures.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
On Twitter @mitchelzoler
WASHINGTON – Improved management of patients with type 1 diabetes and the resulting increased longevity it has fostered has produced a new medical concern that few patients faced in the past: their risk for developing dementia as they age into their 60s, 70s, and beyond.
That risk, which turns out to be nearly double that of people without diabetes, closely matches the higher risk faced by patients with type 2 diabetes, based on analysis of data collected during 2002-2014 from more than 490,000 people aged 60 years or older enrolled in the Kaiser Permanente Medical Care Program of Northern California, Rachel Whitmer, Ph.D. reported at the Alzheimer’s Association International Conference 2015.
Her study tracked the dementia incidence in 334 of these Kaiser Permanente enrollees with type 1 diabetes and no dementia at baseline and found the rate ran 73% higher when compared with controls without any type of diabetes in the cohort after adjustment for sex, race, and vascular complications such as hypertension, stroke, and peripheral vascular disease. The patients with type 1 diabetes averaged 71 years old at baseline and their follow-up averaged 7 years. This is the first study to look at the incidence of dementia in elderly patients with type 1 diabetes, Dr. Whitmer said in an interview during the meeting.
Physicians who care for patients with type 1 diabetes should be aware of this increased risk, be on the lookout for signs of developing dementia in these patients, and use the increased risk to help motivate type 1 diabetes patients to be vigilant in controlling their disease to help avoid the microvascular complications that likely contribute to their dementia risk. Patients with type 1 diabetes are especially vulnerable to the consequences of cognitive impairment as they must maintain complex self-management routines of blood glucose monitoring, insulin administration, and keeping close tabs on their diet and exercise, Dr. Whitmer noted.
In 2013, she and her associates published a simple and easy-to-use tool for clinicians to assess the dementia risk in individual patients with type 2 diabetes (Lancet Diabetes Endocrinol. 2013;3:183-90). Further study of the risk factors that contribute to dementia onset in patients with type 1 diabetes will hopefully lead to creation of a similar risk-assessment tool for use in type 1 patients, said Dr. Whitmer, an epidemiologist at the Kaiser Permanente Northern California Division of Research in Oakland.
Dr. Whitmer had no disclosures.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
On Twitter @mitchelzoler
AT AAIC 2015
AAIC: Sedentary Early Adulthood May Mean Worse Cognitive Functioning Later
WASHINGTON – Couch-potato time in youth may reach far into a person’s future, doubling the risk of cognitive decline in older years.
Data extracted from a 25-year-long cardiovascular risk study show that individuals who get less than the recommended amount of exercise and also sit in front of a TV for hours were twice as likely to experience cognitive decline as were those who had one individual factor, Dr. Kristine Yaffe said at the Alzheimer’s Association International Conference 2015.
“This pattern of low physical activity and sedentary behavior is associated with worse cognitive function even in midlife,” said Dr. Yaffe of the University of California, San Francisco. “It sets the stage for what happens over the next 20-30 years.”
It’s an especially important message for young people, who are spending more and more time in front of electronic devices and simultaneously decreasing time for physical exercise, said Dr. Yaffe, who presented the data on behalf of her colleague, Tina Hoang of the Northern California Institute of Research and Education, San Francisco.
“We all need to understand that physical activity is not just important for our weight and heart, but also for our brain. This needs to be a public health issue,” Dr. Yaffe said.
She presented a subanalysis of the CARDIA study (Coronary Artery Risk Development in Young Adults). CARDIA examines the development and determinants of clinical and subclinical cardiovascular disease and its risk factors. It began in 1985 with about 5,000 subjects aged 18-30 years. They have been followed regularly since then.
The CARDIA subanalysis comprised 3,375 individuals who had undergone three cognitive tests at the end of their follow-up periods: the Stroop Test of color naming, the Digit Symbol Substitution Test (DSST), and the Rey Auditory Verbal Learning Test (RAVLT). At each visit, subjects completed a questionnaire that assessed physical activity and television viewing over time.
Long-term patterns of low physical activity (approximately less than 300 calories per 50-minute session, three times a week) occurred in 17%, and long-term patterns of high TV viewing (at least 4 hours daily) in 11%. The investigators compared these groups to those who had neither activity pattern in multivariate regression analyses that controlled for age, race, gender, education, smoking, alcohol use, body mass index, and hypertension.
At the end of their follow-up, people who sustained a low physical activity pattern but did not have high TV viewing were almost twice as likely to have declined on both the DSST and Stroop (odds ratios, 1.82 and 1.38, respectively). The RAVLT was not significantly affected.
Those with high TV viewing alone were also significantly more likely to show cognitive decline on the DSST and Stroop (OR, 1.34 and 1.61, respectively). Again, the RAVLT was not significantly affected.
The group was then trichotomized according to activity level. Both those in the high- and intermediate-activity groups enjoyed what Dr. Yaffe called “a modest protective effect” against dementia. The combination of low physical activity and lots of TV time, which occurred in 3% of patients in the subanalysis, more than doubled the odds for cognitive decline on the Stroop and DSST (OR, 2.45 and 2.38, respectively).
There are likely two mechanisms of protection in the high and intermediate activity groups, Dr. Yaffe said. One seems intuitive: Exercise reduces the risk of atherosclerosis, which occurs not only in coronary vessels but in the brain’s vasculature as well.
The other is more abstruse.
“We know from rodent models, which are now backed up by human imaging results, that physical exercise increases plasticity in the hippocampus, preserving volume. Physical activity seems to have a direct effect on the hippocampus.”
The National Heart, Lung, and Blood Institute sponsors the CARDIA study. Neither Dr. Yaffe nor Ms. Hoang had any relevant financial disclosures.
WASHINGTON – Couch-potato time in youth may reach far into a person’s future, doubling the risk of cognitive decline in older years.
Data extracted from a 25-year-long cardiovascular risk study show that individuals who get less than the recommended amount of exercise and also sit in front of a TV for hours were twice as likely to experience cognitive decline as were those who had one individual factor, Dr. Kristine Yaffe said at the Alzheimer’s Association International Conference 2015.
“This pattern of low physical activity and sedentary behavior is associated with worse cognitive function even in midlife,” said Dr. Yaffe of the University of California, San Francisco. “It sets the stage for what happens over the next 20-30 years.”
It’s an especially important message for young people, who are spending more and more time in front of electronic devices and simultaneously decreasing time for physical exercise, said Dr. Yaffe, who presented the data on behalf of her colleague, Tina Hoang of the Northern California Institute of Research and Education, San Francisco.
“We all need to understand that physical activity is not just important for our weight and heart, but also for our brain. This needs to be a public health issue,” Dr. Yaffe said.
She presented a subanalysis of the CARDIA study (Coronary Artery Risk Development in Young Adults). CARDIA examines the development and determinants of clinical and subclinical cardiovascular disease and its risk factors. It began in 1985 with about 5,000 subjects aged 18-30 years. They have been followed regularly since then.
The CARDIA subanalysis comprised 3,375 individuals who had undergone three cognitive tests at the end of their follow-up periods: the Stroop Test of color naming, the Digit Symbol Substitution Test (DSST), and the Rey Auditory Verbal Learning Test (RAVLT). At each visit, subjects completed a questionnaire that assessed physical activity and television viewing over time.
Long-term patterns of low physical activity (approximately less than 300 calories per 50-minute session, three times a week) occurred in 17%, and long-term patterns of high TV viewing (at least 4 hours daily) in 11%. The investigators compared these groups to those who had neither activity pattern in multivariate regression analyses that controlled for age, race, gender, education, smoking, alcohol use, body mass index, and hypertension.
At the end of their follow-up, people who sustained a low physical activity pattern but did not have high TV viewing were almost twice as likely to have declined on both the DSST and Stroop (odds ratios, 1.82 and 1.38, respectively). The RAVLT was not significantly affected.
Those with high TV viewing alone were also significantly more likely to show cognitive decline on the DSST and Stroop (OR, 1.34 and 1.61, respectively). Again, the RAVLT was not significantly affected.
The group was then trichotomized according to activity level. Both those in the high- and intermediate-activity groups enjoyed what Dr. Yaffe called “a modest protective effect” against dementia. The combination of low physical activity and lots of TV time, which occurred in 3% of patients in the subanalysis, more than doubled the odds for cognitive decline on the Stroop and DSST (OR, 2.45 and 2.38, respectively).
There are likely two mechanisms of protection in the high and intermediate activity groups, Dr. Yaffe said. One seems intuitive: Exercise reduces the risk of atherosclerosis, which occurs not only in coronary vessels but in the brain’s vasculature as well.
The other is more abstruse.
“We know from rodent models, which are now backed up by human imaging results, that physical exercise increases plasticity in the hippocampus, preserving volume. Physical activity seems to have a direct effect on the hippocampus.”
The National Heart, Lung, and Blood Institute sponsors the CARDIA study. Neither Dr. Yaffe nor Ms. Hoang had any relevant financial disclosures.
WASHINGTON – Couch-potato time in youth may reach far into a person’s future, doubling the risk of cognitive decline in older years.
Data extracted from a 25-year-long cardiovascular risk study show that individuals who get less than the recommended amount of exercise and also sit in front of a TV for hours were twice as likely to experience cognitive decline as were those who had one individual factor, Dr. Kristine Yaffe said at the Alzheimer’s Association International Conference 2015.
“This pattern of low physical activity and sedentary behavior is associated with worse cognitive function even in midlife,” said Dr. Yaffe of the University of California, San Francisco. “It sets the stage for what happens over the next 20-30 years.”
It’s an especially important message for young people, who are spending more and more time in front of electronic devices and simultaneously decreasing time for physical exercise, said Dr. Yaffe, who presented the data on behalf of her colleague, Tina Hoang of the Northern California Institute of Research and Education, San Francisco.
“We all need to understand that physical activity is not just important for our weight and heart, but also for our brain. This needs to be a public health issue,” Dr. Yaffe said.
She presented a subanalysis of the CARDIA study (Coronary Artery Risk Development in Young Adults). CARDIA examines the development and determinants of clinical and subclinical cardiovascular disease and its risk factors. It began in 1985 with about 5,000 subjects aged 18-30 years. They have been followed regularly since then.
The CARDIA subanalysis comprised 3,375 individuals who had undergone three cognitive tests at the end of their follow-up periods: the Stroop Test of color naming, the Digit Symbol Substitution Test (DSST), and the Rey Auditory Verbal Learning Test (RAVLT). At each visit, subjects completed a questionnaire that assessed physical activity and television viewing over time.
Long-term patterns of low physical activity (approximately less than 300 calories per 50-minute session, three times a week) occurred in 17%, and long-term patterns of high TV viewing (at least 4 hours daily) in 11%. The investigators compared these groups to those who had neither activity pattern in multivariate regression analyses that controlled for age, race, gender, education, smoking, alcohol use, body mass index, and hypertension.
At the end of their follow-up, people who sustained a low physical activity pattern but did not have high TV viewing were almost twice as likely to have declined on both the DSST and Stroop (odds ratios, 1.82 and 1.38, respectively). The RAVLT was not significantly affected.
Those with high TV viewing alone were also significantly more likely to show cognitive decline on the DSST and Stroop (OR, 1.34 and 1.61, respectively). Again, the RAVLT was not significantly affected.
The group was then trichotomized according to activity level. Both those in the high- and intermediate-activity groups enjoyed what Dr. Yaffe called “a modest protective effect” against dementia. The combination of low physical activity and lots of TV time, which occurred in 3% of patients in the subanalysis, more than doubled the odds for cognitive decline on the Stroop and DSST (OR, 2.45 and 2.38, respectively).
There are likely two mechanisms of protection in the high and intermediate activity groups, Dr. Yaffe said. One seems intuitive: Exercise reduces the risk of atherosclerosis, which occurs not only in coronary vessels but in the brain’s vasculature as well.
The other is more abstruse.
“We know from rodent models, which are now backed up by human imaging results, that physical exercise increases plasticity in the hippocampus, preserving volume. Physical activity seems to have a direct effect on the hippocampus.”
The National Heart, Lung, and Blood Institute sponsors the CARDIA study. Neither Dr. Yaffe nor Ms. Hoang had any relevant financial disclosures.
AT AAIC 2015
AAIC: Sedentary early adulthood may mean worse cognitive functioning later
WASHINGTON – Couch-potato time in youth may reach far into a person’s future, doubling the risk of cognitive decline in older years.
Data extracted from a 25-year-long cardiovascular risk study show that individuals who get less than the recommended amount of exercise and also sit in front of a TV for hours were twice as likely to experience cognitive decline as were those who had one individual factor, Dr. Kristine Yaffe said at the Alzheimer’s Association International Conference 2015.
“This pattern of low physical activity and sedentary behavior is associated with worse cognitive function even in midlife,” said Dr. Yaffe of the University of California, San Francisco. “It sets the stage for what happens over the next 20-30 years.”
It’s an especially important message for young people, who are spending more and more time in front of electronic devices and simultaneously decreasing time for physical exercise, said Dr. Yaffe, who presented the data on behalf of her colleague, Tina Hoang of the Northern California Institute of Research and Education, San Francisco.
“We all need to understand that physical activity is not just important for our weight and heart, but also for our brain. This needs to be a public health issue,” Dr. Yaffe said.
She presented a subanalysis of the CARDIA study (Coronary Artery Risk Development in Young Adults). CARDIA examines the development and determinants of clinical and subclinical cardiovascular disease and its risk factors. It began in 1985 with about 5,000 subjects aged 18-30 years. They have been followed regularly since then.
The CARDIA subanalysis comprised 3,375 individuals who had undergone three cognitive tests at the end of their follow-up periods: the Stroop Test of color naming, the Digit Symbol Substitution Test (DSST), and the Rey Auditory Verbal Learning Test (RAVLT). At each visit, subjects completed a questionnaire that assessed physical activity and television viewing over time.
Long-term patterns of low physical activity (approximately less than 300 calories per 50-minute session, three times a week) occurred in 17%, and long-term patterns of high TV viewing (at least 4 hours daily) in 11%. The investigators compared these groups to those who had neither activity pattern in multivariate regression analyses that controlled for age, race, gender, education, smoking, alcohol use, body mass index, and hypertension.
At the end of their follow-up, people who sustained a low physical activity pattern but did not have high TV viewing were almost twice as likely to have declined on both the DSST and Stroop (odds ratios, 1.82 and 1.38, respectively). The RAVLT was not significantly affected.
Those with high TV viewing alone were also significantly more likely to show cognitive decline on the DSST and Stroop (OR, 1.34 and 1.61, respectively). Again, the RAVLT was not significantly affected.
The group was then trichotomized according to activity level. Both those in the high- and intermediate-activity groups enjoyed what Dr. Yaffe called “a modest protective effect” against dementia. The combination of low physical activity and lots of TV time, which occurred in 3% of patients in the subanalysis, more than doubled the odds for cognitive decline on the Stroop and DSST (OR, 2.45 and 2.38, respectively).
There are likely two mechanisms of protection in the high and intermediate activity groups, Dr. Yaffe said. One seems intuitive: Exercise reduces the risk of atherosclerosis, which occurs not only in coronary vessels but in the brain’s vasculature as well.
The other is more abstruse.
“We know from rodent models, which are now backed up by human imaging results, that physical exercise increases plasticity in the hippocampus, preserving volume. Physical activity seems to have a direct effect on the hippocampus.”
The National Heart, Lung, and Blood Institute sponsors the CARDIA study. Neither Dr. Yaffe nor Ms. Hoang had any relevant financial disclosures.
On Twitter @Alz_Gal
WASHINGTON – Couch-potato time in youth may reach far into a person’s future, doubling the risk of cognitive decline in older years.
Data extracted from a 25-year-long cardiovascular risk study show that individuals who get less than the recommended amount of exercise and also sit in front of a TV for hours were twice as likely to experience cognitive decline as were those who had one individual factor, Dr. Kristine Yaffe said at the Alzheimer’s Association International Conference 2015.
“This pattern of low physical activity and sedentary behavior is associated with worse cognitive function even in midlife,” said Dr. Yaffe of the University of California, San Francisco. “It sets the stage for what happens over the next 20-30 years.”
It’s an especially important message for young people, who are spending more and more time in front of electronic devices and simultaneously decreasing time for physical exercise, said Dr. Yaffe, who presented the data on behalf of her colleague, Tina Hoang of the Northern California Institute of Research and Education, San Francisco.
“We all need to understand that physical activity is not just important for our weight and heart, but also for our brain. This needs to be a public health issue,” Dr. Yaffe said.
She presented a subanalysis of the CARDIA study (Coronary Artery Risk Development in Young Adults). CARDIA examines the development and determinants of clinical and subclinical cardiovascular disease and its risk factors. It began in 1985 with about 5,000 subjects aged 18-30 years. They have been followed regularly since then.
The CARDIA subanalysis comprised 3,375 individuals who had undergone three cognitive tests at the end of their follow-up periods: the Stroop Test of color naming, the Digit Symbol Substitution Test (DSST), and the Rey Auditory Verbal Learning Test (RAVLT). At each visit, subjects completed a questionnaire that assessed physical activity and television viewing over time.
Long-term patterns of low physical activity (approximately less than 300 calories per 50-minute session, three times a week) occurred in 17%, and long-term patterns of high TV viewing (at least 4 hours daily) in 11%. The investigators compared these groups to those who had neither activity pattern in multivariate regression analyses that controlled for age, race, gender, education, smoking, alcohol use, body mass index, and hypertension.
At the end of their follow-up, people who sustained a low physical activity pattern but did not have high TV viewing were almost twice as likely to have declined on both the DSST and Stroop (odds ratios, 1.82 and 1.38, respectively). The RAVLT was not significantly affected.
Those with high TV viewing alone were also significantly more likely to show cognitive decline on the DSST and Stroop (OR, 1.34 and 1.61, respectively). Again, the RAVLT was not significantly affected.
The group was then trichotomized according to activity level. Both those in the high- and intermediate-activity groups enjoyed what Dr. Yaffe called “a modest protective effect” against dementia. The combination of low physical activity and lots of TV time, which occurred in 3% of patients in the subanalysis, more than doubled the odds for cognitive decline on the Stroop and DSST (OR, 2.45 and 2.38, respectively).
There are likely two mechanisms of protection in the high and intermediate activity groups, Dr. Yaffe said. One seems intuitive: Exercise reduces the risk of atherosclerosis, which occurs not only in coronary vessels but in the brain’s vasculature as well.
The other is more abstruse.
“We know from rodent models, which are now backed up by human imaging results, that physical exercise increases plasticity in the hippocampus, preserving volume. Physical activity seems to have a direct effect on the hippocampus.”
The National Heart, Lung, and Blood Institute sponsors the CARDIA study. Neither Dr. Yaffe nor Ms. Hoang had any relevant financial disclosures.
On Twitter @Alz_Gal
WASHINGTON – Couch-potato time in youth may reach far into a person’s future, doubling the risk of cognitive decline in older years.
Data extracted from a 25-year-long cardiovascular risk study show that individuals who get less than the recommended amount of exercise and also sit in front of a TV for hours were twice as likely to experience cognitive decline as were those who had one individual factor, Dr. Kristine Yaffe said at the Alzheimer’s Association International Conference 2015.
“This pattern of low physical activity and sedentary behavior is associated with worse cognitive function even in midlife,” said Dr. Yaffe of the University of California, San Francisco. “It sets the stage for what happens over the next 20-30 years.”
It’s an especially important message for young people, who are spending more and more time in front of electronic devices and simultaneously decreasing time for physical exercise, said Dr. Yaffe, who presented the data on behalf of her colleague, Tina Hoang of the Northern California Institute of Research and Education, San Francisco.
“We all need to understand that physical activity is not just important for our weight and heart, but also for our brain. This needs to be a public health issue,” Dr. Yaffe said.
She presented a subanalysis of the CARDIA study (Coronary Artery Risk Development in Young Adults). CARDIA examines the development and determinants of clinical and subclinical cardiovascular disease and its risk factors. It began in 1985 with about 5,000 subjects aged 18-30 years. They have been followed regularly since then.
The CARDIA subanalysis comprised 3,375 individuals who had undergone three cognitive tests at the end of their follow-up periods: the Stroop Test of color naming, the Digit Symbol Substitution Test (DSST), and the Rey Auditory Verbal Learning Test (RAVLT). At each visit, subjects completed a questionnaire that assessed physical activity and television viewing over time.
Long-term patterns of low physical activity (approximately less than 300 calories per 50-minute session, three times a week) occurred in 17%, and long-term patterns of high TV viewing (at least 4 hours daily) in 11%. The investigators compared these groups to those who had neither activity pattern in multivariate regression analyses that controlled for age, race, gender, education, smoking, alcohol use, body mass index, and hypertension.
At the end of their follow-up, people who sustained a low physical activity pattern but did not have high TV viewing were almost twice as likely to have declined on both the DSST and Stroop (odds ratios, 1.82 and 1.38, respectively). The RAVLT was not significantly affected.
Those with high TV viewing alone were also significantly more likely to show cognitive decline on the DSST and Stroop (OR, 1.34 and 1.61, respectively). Again, the RAVLT was not significantly affected.
The group was then trichotomized according to activity level. Both those in the high- and intermediate-activity groups enjoyed what Dr. Yaffe called “a modest protective effect” against dementia. The combination of low physical activity and lots of TV time, which occurred in 3% of patients in the subanalysis, more than doubled the odds for cognitive decline on the Stroop and DSST (OR, 2.45 and 2.38, respectively).
There are likely two mechanisms of protection in the high and intermediate activity groups, Dr. Yaffe said. One seems intuitive: Exercise reduces the risk of atherosclerosis, which occurs not only in coronary vessels but in the brain’s vasculature as well.
The other is more abstruse.
“We know from rodent models, which are now backed up by human imaging results, that physical exercise increases plasticity in the hippocampus, preserving volume. Physical activity seems to have a direct effect on the hippocampus.”
The National Heart, Lung, and Blood Institute sponsors the CARDIA study. Neither Dr. Yaffe nor Ms. Hoang had any relevant financial disclosures.
On Twitter @Alz_Gal
AT AAIC 2015
Key clinical point: Too little exercise and too much couch time in early adulthood significantly increases the risk of dementia when people reach their 50s and 60s.
Major finding: People with both low physical activity and high TV times in young adulthood had more than double the odds of poorer performance on two cognitive tests 25 years later.
Data source: CARDIA is a 25-year prospective cohort study of cardiovascular risk factors in people aged 18-30 years.
Disclosures: The National Heart, Lung, and Blood Institute sponsors the CARDIA study. Neither Dr. Yaffe nor Ms. Hoang had any financial disclosures.