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In healthy individuals, obesity has been linked to reduced cerebral blood flow and brain atrophy and to a higher risk of neurologic disorders, such as Alzheimer disease and vascular dementia, in patients with heart failure (HF), according to researchers from Kent State University in Ohio. Their study focused on the connection between HF, brain volume, and obesity. The researchers say it is time to consider obesity as an independent risk factor for structural brain changes in HF.
Their research supports the idea that common vascular risk factors, such as hypertension and diabetes, influence neurocognitive outcomes in HF through a negative impact on cerebral perfusion. The study is the first to examine the possible associations among body mass index (BMI), cerebral perfusion, and brain volume in the obese population.
The study participants (80 patients taking part in an ongoing study of neurocognitive outcomes in HF) were aged 50 to 85 years, with New York Heart Association class II, III, or IV HF. Exclusion criteria included a history of a significant neurologic disorder, such as dementia or stroke, severe head injury, severe psychiatric disorder, history of substance abuse, and renal failure. The participants underwent transcranial Doppler sonography and a brain MRI. The mean BMI was 29.89; 75% of the patients were overweight or obese.
Study findings suggested that increased BMI was associated with reduced white matter hyperintensities volume (P < .05). Body mass index also interacted with cerebral perfusion on total gray matter volume.
In discussing possible mechanisms, the researchers say their study and other work suggest that obesity and adiposity may introduce “unique pathophysiological mechanisms to produce brain changes in HF.” They note that obesity is associated with altered levels of the biomarkers leptin, ghrelin, and brain-derived neurotrophic factor, which play a role in regulating metabolism and weight. They also promote neuronal survival, neurogenesis, dendritic synaptic formations, and reduce apoptosis of neurons—all biologic processes that shape the cerebral structure. The researchers also cite that obesity can affect the brain through inflammatory processes.
However, the mechanisms remain unclear. The relationship between obesity and neurocognitive outcomes in HF is complex, they conclude, and likely involves other mechanisms beyond cerebral hemodynamics.
Source
Alosco ML, Brickman AM, Spitznagel MB, et al. BMC Obes. 2014;1:4.
doi: 10.1186/2052-9538-1-4.
In healthy individuals, obesity has been linked to reduced cerebral blood flow and brain atrophy and to a higher risk of neurologic disorders, such as Alzheimer disease and vascular dementia, in patients with heart failure (HF), according to researchers from Kent State University in Ohio. Their study focused on the connection between HF, brain volume, and obesity. The researchers say it is time to consider obesity as an independent risk factor for structural brain changes in HF.
Their research supports the idea that common vascular risk factors, such as hypertension and diabetes, influence neurocognitive outcomes in HF through a negative impact on cerebral perfusion. The study is the first to examine the possible associations among body mass index (BMI), cerebral perfusion, and brain volume in the obese population.
The study participants (80 patients taking part in an ongoing study of neurocognitive outcomes in HF) were aged 50 to 85 years, with New York Heart Association class II, III, or IV HF. Exclusion criteria included a history of a significant neurologic disorder, such as dementia or stroke, severe head injury, severe psychiatric disorder, history of substance abuse, and renal failure. The participants underwent transcranial Doppler sonography and a brain MRI. The mean BMI was 29.89; 75% of the patients were overweight or obese.
Study findings suggested that increased BMI was associated with reduced white matter hyperintensities volume (P < .05). Body mass index also interacted with cerebral perfusion on total gray matter volume.
In discussing possible mechanisms, the researchers say their study and other work suggest that obesity and adiposity may introduce “unique pathophysiological mechanisms to produce brain changes in HF.” They note that obesity is associated with altered levels of the biomarkers leptin, ghrelin, and brain-derived neurotrophic factor, which play a role in regulating metabolism and weight. They also promote neuronal survival, neurogenesis, dendritic synaptic formations, and reduce apoptosis of neurons—all biologic processes that shape the cerebral structure. The researchers also cite that obesity can affect the brain through inflammatory processes.
However, the mechanisms remain unclear. The relationship between obesity and neurocognitive outcomes in HF is complex, they conclude, and likely involves other mechanisms beyond cerebral hemodynamics.
Source
Alosco ML, Brickman AM, Spitznagel MB, et al. BMC Obes. 2014;1:4.
doi: 10.1186/2052-9538-1-4.
In healthy individuals, obesity has been linked to reduced cerebral blood flow and brain atrophy and to a higher risk of neurologic disorders, such as Alzheimer disease and vascular dementia, in patients with heart failure (HF), according to researchers from Kent State University in Ohio. Their study focused on the connection between HF, brain volume, and obesity. The researchers say it is time to consider obesity as an independent risk factor for structural brain changes in HF.
Their research supports the idea that common vascular risk factors, such as hypertension and diabetes, influence neurocognitive outcomes in HF through a negative impact on cerebral perfusion. The study is the first to examine the possible associations among body mass index (BMI), cerebral perfusion, and brain volume in the obese population.
The study participants (80 patients taking part in an ongoing study of neurocognitive outcomes in HF) were aged 50 to 85 years, with New York Heart Association class II, III, or IV HF. Exclusion criteria included a history of a significant neurologic disorder, such as dementia or stroke, severe head injury, severe psychiatric disorder, history of substance abuse, and renal failure. The participants underwent transcranial Doppler sonography and a brain MRI. The mean BMI was 29.89; 75% of the patients were overweight or obese.
Study findings suggested that increased BMI was associated with reduced white matter hyperintensities volume (P < .05). Body mass index also interacted with cerebral perfusion on total gray matter volume.
In discussing possible mechanisms, the researchers say their study and other work suggest that obesity and adiposity may introduce “unique pathophysiological mechanisms to produce brain changes in HF.” They note that obesity is associated with altered levels of the biomarkers leptin, ghrelin, and brain-derived neurotrophic factor, which play a role in regulating metabolism and weight. They also promote neuronal survival, neurogenesis, dendritic synaptic formations, and reduce apoptosis of neurons—all biologic processes that shape the cerebral structure. The researchers also cite that obesity can affect the brain through inflammatory processes.
However, the mechanisms remain unclear. The relationship between obesity and neurocognitive outcomes in HF is complex, they conclude, and likely involves other mechanisms beyond cerebral hemodynamics.
Source
Alosco ML, Brickman AM, Spitznagel MB, et al. BMC Obes. 2014;1:4.
doi: 10.1186/2052-9538-1-4.