Neuroimaging study reveals three distinct response types in brain areas that control hunger, food intake, and appetite in patients who had undergone weight loss surgery.
The brain regulates both eating for hunger and pleasure through serotonin-producing neurons in the midbrain, but the different types of feeding are wired by independent circuits that do not influence the other type of feeding.
Higher body fat leads to increased atrophy of the brain's gray matter and a greater risk of cognitive decline, researchers report.
A new study reveals adults with ADHD have an increased risk of developing nervous system, respiratory, musculoskeletal, and metabolic diseases. ADHD was also associated with a slightly increased risk of Parkinson's disease, dementia, and cardiovascular disease.
Consuming high GI foods, such as white bread and potatoes, following weight loss leads to people regaining weight and increases the risk of developing diabetes.
Researchers have identified a subpopulation of dopaminergic neurons in the caudal ventral tegmental area that appears to suppress food intake by triggering satiation in mice.
While there is an association between obesity during midlife and an increased risk of Alzheimer's disease, researchers say the link doesn't necessarily extend into later life. A new study revealed higher genetic risk for Alzheimer's and lower BMI, especially in older men, was linked to an increased risk of Alzheimer's disease and predicted the disease progression.
Obesity has been linked to severely restricted blood flow in the brain. Reduced blood flow in the brain, or cerebral hypoperfusion, can be an early indicator of vascular dementia and Alzheimer's disease.
Study sheds new light on how the brain regulates hunger. The findings may help with the development of new drugs to fight obesity.
Adding selenium to diet products helps prevent obesity and increases healthy lifespan in mouse models.
Mice that consumed high-fat diets not only became obese, they also displayed an increased risk of depression and anxiety symptoms. This was mediated by a defective brain circuit. When the disruptions were corrected either genetically or pharmaceutically, mice displayed fewer symptoms of depression and experienced weight loss.