Obesity and the Brain

Hypothalamus
It has been recently discovered that unlike inflammation in the in the peripheral tissues, inflammation in the brain due to high fat intake occurs as soon as 1-3 days. In this time following a large fat intake, neuron damage is identified, and inflammatory symptoms spring throughout the hypothalamus. While most alterations are initially reversible, continued fat intake cause permanent damage to many structures like the mediobasal hypothalamus.
While weight gain is delayed, brain damage occurs immediately, shedding light on emerging studies today that portray obesity as a brain disease. Acutely inflamed hypothalamus due to short term over-nutrition or chronic obesity can become dysfunctional. This brain structure, responsible for regulating diet and caloric intake, might disrupt the precise coupling between energy intake and energy expenditure, fostering overeating and further weight gain.
Hippocampus
Recent articles have revealed conditions stemming from obesity-related conditions such as diabetes, hypertension, and cardiovascular disease are proven to adversely influence hippocampal size. High-fat diets induce pro-apoptotic (inflammatory) signaling such as expression of caspase-3 and gliosis throughout structures of the hippocampus. This local signaling of inflammation and cell death ultimately leads to hippocampal tissue loss. The hippocampus, responsible for countless cognitive functions, becomes severely impaired. Studies have shown both obesity and a high BMI in midlife are strong indicators of hippocampal degeneration in late life. Furthermore, factors such as high blood glucose levels have been linked to 10% volume change of the hippocampus within 1 year, regardless of factors such as age, sex, alcohol, and smoking.
Cognitive Decline
Obesity is associated with cognitive decline across the human life span. Often, these cognitive impairments are evident during child or adolescence, where deficits are seen in executive functioning, attention, and decreased intelligence quotient. Many studies have explored the possibility that deficient executive functioning leads to increased appetite, due to a loss of cognitive control of actions such as unhealthy eating.
Even healthy obese people show cognitive deficits in learning, memory, and executive function in contrast to non-obese individuals, which reflects the impacts of obesity. Cognitive performance declines with decreased physical activity and aerobic exercise, which are often linked to increased weight. These cognitive declines occur not only at the rudimentary or elementary level. Scholastic performance at collegiate and graduate levels have decline in response to obesity.
Not all cognitive losses are irreversible, however. Weight loss may result in rapid improvement in some cognitive functions. Studies have revealed improved memory following subjects undergoing bariatric surgery. Weight loss influences many variables, such as blood pressure, arterial flow, sleep quality and nutrition composition which all ultimately contribute to cognitive inclines.
Early Life
Exposure to excessive nutrition during vulnerable pre- and postnatal periods can impair the brain cognitively and disrupt brain-governed feeding behavior. Environments of over-nutrition are mediated many functional alterations which can lead to obesity, dysmetabolism and cognitive disadvantages throughout life.
Although caloric restriction can later reduce body weight gain, early life hypothalamic disposition to hyperphagia is irreversible. Maintaining a healthy diet accompanied by exercise for pregnant mothers is crucial for lifetime eating habits, as this period where feeding behavior is imprinted into the nucleus of the hypothalamus.