Obesity is a diet-related chronic disease resulting from improper nutrition and an excess amount of body fat. It’s caused by genetic and environmental factors that are difficult to control. Doctors claim when the BMI (body mass index) is over thirty pounds, a person (adult or child) is considered obese. Obesity can increase the risk of developing related conditions such as diabetes, hypertension, sleep apnea, cancer, and heart attacks. Long-term medical treatments to decrease the frequency of accompanying diseases and death rates is required.
Obesity is detrimental to a person’s overall health. It can reduce a person’s life expectancy up to 9 years and cause chronic diseases. The extra weight or fat a person carries puts extra pressure on joints and limbs. In fact, “These extra pounds can lead to many problems, including arthritis. As the smooth surface called “cartilage” on the ends of bones becomes damaged or worn, you will start to feel pain and stiffness in the joint” (Kelly, p.1). Additionally, “People with severe obesity are more likely to have other diseases. These include type 2 diabetes, high blood pressure, sleep apnea, and many more.” (“The Impact of Obesity on Your Body and Health”). Other physical problems include obese women having a higher risk pregnancy compared to a healthy woman.
Despite this, the rate of obesity has gone up tremendously over the past decades due to accessible candies and cheap junk (fast) food. In fact, “The percentage of obese children has increased at a staggering rate of 18% since the 1970’s” (Yadav & Rane, 2015, p. 1329). Additionally, “the rate for adult obesity has hit an all-time high at 32.2% for men and 35.5% for women” (Yadav & Rane, 2015, p. 1329). To fully understand the severity of obesity, it’s important to comprehend how obesity effects cognition and the overall well-being of an individual.
Obesity and Cognition
Cognition encompasses several psychological functions such as perception, thought, language and memory. According to recent studies, it seems “a significant percentage of the detrimental effects of obesity on cognition are mainly mediated by obesity-induced activation of innate immunity which directly harms neurons” (Spyridaki, Avgoustinaki & Margioris, 2016, p. 170). Specifically, obesity causes low grade inflammation.
Low grade inflammation leads to substantial changes in neurocircuitry, neuroendocrine activity, neurotransmitter metabolism, activity and neurogenesis which result in the development of obesity related neuropsychiatric comorbidities. For example, obesity induced inflammation contributes to the development of insulin resistance. Insulin is a hormone produced by the pancreas that helps unlock the body’s cells so that sugar from the food we eat can be used by the cells for energy. Insulin resistance means that the cells aren’t unlocking completely causing a surplus of glucose in the bloodstream which results in type 2 diabetes. The surplus of sugar correlates with the decline of cognitive functions. Common cognitive repercussions include deterioration of memory and attention, increased impulsivity, poorer organizational and planning abilities.
Additionally, from an anatomical point of view, obesity is associated with the reduced volume of gray matter and enlargement of orbitofrontal white matter. Gray matter is made up of the cell bodies of nerve cells and processes the information in the brain. White matter is made up of the long filaments that extend from the cell bodies – the ‘telephone wires’ of the neuronal network, transmitting the electrical signals that carry the messages between neurons. Recently, a structural brain-scan study of intelligence has supported an association between general intelligence and the volume of gray matter tissue in specific regions of the brain. These structures are the same ones implicated in memory, attention, and language. In other words, obesity hinders cognitive function on all levels including intelligence. In fact, obesity was associated with lower performance on one of the two verbal memory tests utilized and was negatively associated with scores on visual retention. These “detrimental effects of obesity on components of cognition may be due to obesity-induced decreased brain blood flow and suppression of its metabolic rate particularly in the prefrontal cerebral cortex” (Spyridaki, Avgoustinaki & Margioris, 2016, p. 170).
Furthermore, poor cognition plays a role in causing obesity by adopting poor health habits such as dietary behavior and low physical activity. Studies show that the “intake of a high-fat diet that includes mostly omega-6 and SFAs is associated with worse performance on a cognitive task” (Freeman, Haley-Zitlin, Rosenberger & Granholm, 2014, p. 242-243). In fact, ‘the western diet’ is “a diet that contains large amounts of red meat, refined sugars, high fat foods, and refined grains” (Freeman, Haley-Zitlin, Rosenberger & Granholm, 2014, p. 241). It also contains large amounts of saturated (SFA) and trans fatty acids (TFA). This diet plays a major role in the increasing rates of obesity as well as diabetes and dementia.
Prospective studies suggest that obesity and increased consumption of high-fat diets increases the risk for development of dementia. Dementia is a progressive deterioration in two or more modalities of cognitive performance. It isn’t a single disease, but a general term to describe symptoms of impairment in memory, communication, and thinking. For example, Alzheimer’s disease is a type of dementia. It’s characterized by ‘plaques’ between the dying cells in the brain and ‘tangles’ within the cells due to protein abnormalities. The brain tissue in a person with Alzheimer’s has progressively fewer nerve cells and connections, and the total brain size shrinks. In severe cases, this will cause a person to lose awareness of recent experiences as well as of their surroundings, experience changes in physical abilities such as walking and swallowing, increased difficulty in communicating and become vulnerable to infections.
Recent studies show that those who’s dietary habits contain mostly SFAs and TFAs have an increased risk for Alzheimer’s disease. The reason for this is “diets high in fat and sugar influences the microbiota composition, which may lead to an imbalanced microbial population in the gut” (Solas, Milagro, Ramirez & Martinez, 2017, p. 87). The imbalance of the microbial population is called gut microbiota dysbiosis. This means that there is an overgrowth of small intestinal bacteria. Their studies show that “Gut microbiota can synthesize a range of neurotransmitters, induce the secretion of neurotrophic factors such as BDNF by intestinal smooth muscle cells, and mediate local and systemic inflammation” (Solas, Milagro, Ramirez & Martinez, 2017, p. 89). Due to this discovery, it’s assumed that “gut microbiota dysbiosis may be implicated in the pathophysiology of obesity and cognitive decline through its impact on local and systemic inflammation” (Solas, Milagro, Ramirez & Martinez, 2017, p. 89). To put it simply, obesity effects cognition because of poor dietary habits that cause the gut microbiota dysbiosis (which mainly effects cognition). Fortunately, cognitive decline from obesity can be avoided or reversed following weight loss by diet or surgery.
Obesity and Overall Well-Being
Obese individuals cope with discrimination against their weight and appearance daily. The negative portrayal of obese people in the media plays the largest role in this discrimination. In fact, “Obesity stigma, a form of discrimination, is responsible for a host of negative psychological effects on individual well-being.” (Oliver, Datta & Baldwin, 2017, p. 1). For example, obese individuals have an increased risk of depression, decreased self-esteem, elevated blood pressure, and dysregulations of stress response systems in the body.
The autonomic nervous system and hypothalamic-pituitary-adrenal (HPA) axis are the systems that respond to stress. The autonomic nervous system is comprised the sympathetic and parasympathetic nervous systems. In the sympathetic nervous system, the sympathetic-adrenal medullary (SAM) axis may activate the fight-or-flight response, which readies the body to either fight or run. When this system is dysregulated, there’s a decline insulin sensitivity, and it creates a vicious circle that may contribute to the development of hypertension, metabolic syndrome, cardiovascular and kidney disease. In contrast, the parasympathetic nervous system returns the body to homeostasis (state of stability or calmness). When this system is functioning abnormally, the body may never be in a stable state.
Additionally, the HPA axis regulates the release of cortisol. Cortisol, also known as the stress hormone, is responsible for anti-stress responses, immune functions, and blood glucose regulation. Studies show that exposure to obesity stigma, whether an individual was lean or obese, caused an increase in cortisol. High levels of cortisol can cause weight gain, anxiety, sleep disorders, increase in blood pressure and hormonal imbalances. Therefore, obesity stigma induced dysregulation of stress response systems causes multiple psychological and physiological issues.
Furthermore, a major effect of dysregulation in the stress systems is depression. Depression is a chronic inflammatory disease in the brain characterized by having a persistent depressed mood or loss of interest in activities, causing significant impairment in daily life. Unfortunately, depression can cause distorted thinking which leads to low self-esteem. It may also lead to social isolation, anxiety, insomnia, excessive hunger, and irritability. Consequently, people with depression are more likely to overeat, make poor food choices, and become sedentary which are factors leading to obesity. Additionally, “both depression and obesity are disorders of stress with dysregulation of the stress system” (Jantaratnotai, Mosikanon, Lee & McIntyre, 2017, p. 3). However, it hasn’t been proven yet how obesity and depression are connected.
Recent studies show that there’s a link between obesity and poor responses to antidepressants, which are medications used to treat or prevent depression. Currently, the cause of the relation is unknown, but the “leptin gene polymorphism is associated with resistance to response to various antidepressants” (Jantaratnotai, Mosikanon, Lee & McIntyre, 2017, p. 6). Leptin is a hormone that regulates food intake and body weight. It acts on specific receptors in the hypothalamus to inhibit appetite through both counteractive and stimulatory mechanisms. These mechanisms include counteracting the effects of a cannabinoid neurotransmitter called adandamide which stimulates appetite and promoting the synthesis of an appetite suppressant called α-melanocyte-stimulating hormone. Low levels of leptin have been found to be associated with depressive behaviors. In other words, leptin is the body’s natural antidepressant. The leptin gene has multiple variations, therefore, “there may be a common genetic pathway linking obesity and depression” (Jantaratnotai, Mosikanon, Lee & McIntyre, 2017, p. 6). Fortunately, studies show that treating obesity with weight loss improves depressive symptoms in those with mood disorders and treating depression with antidepressants improves weight control in obese patients.
Obesity is a diet-related chronic disease resulting from improper nutrition and an excess amount of body fat. Doctors claim when the BMI (body mass index) is over thirty pounds, a person (adult or child) is considered obese. It’s caused by genetic and environmental factors that are difficult to control. Obesity can increase the risk of developing related conditions such as diabetes, hypertension, sleep apnea, cancer, and heart attacks. To fully understand the severity of obesity, it’s important to comprehend how obesity effects cognition and the overall well-being of an individual.
Obesity causes low grade inflammation which leads to substantial changes in neurocircuitry, neuroendocrine activity, neurotransmitter metabolism, activity, and neurogenesis. One of the effects includes insulin resistance which leads to type 2 diabetes. Also, it’s associated with the reduced volume of gray matter and enlargement of orbitofrontal white matter. This hinders cognitive functions such as language, memory, and intelligence. The high-fat diet associated with obesity includes mostly omega-6 and SFAs. This decreases a person’s ability to perform a cognitive task and increases their risk for dementia. The reason for this is the diet causes an imbalance of gut microbiota which results in the inability to control inflammation. In other words, obesity effects cognition because of poor dietary habits that cause the gut microbiota dysbiosis (which mainly effects cognition). Fortunately, cognitive decline from obesity can be avoided or reversed following weight loss.
Lastly, obesity stigma, a form of discrimination, is responsible for most of the negative psychological effects on an individual’s well-being. In fact, most of obesity stigma stems from the media’s negative portrayal of obese individuals. The stress that comes from this discrimination can cause weight gain, anxiety, sleep disorders, increase in blood pressure, hormonal imbalances, and depression. Recently, depression and obesity have been genetically linked by a hormone called leptin. Low levels of leptin are associated with depressive behaviors. People with depression are more likely to overeat, make poor food choices, and become sedentary which are factors leading to obesity. Fortunately, treating obesity with weight loss improves depressive symptoms and treating depression with antidepressants improves weight control.