Neural Mechanisms in Controlling Eating Behaviour

Genetic research of obesity was partly successful in establishing obesity in model organisms – rodents where obesity occurs spontaneously together with other pathological aspects (insulin resistance, …). The main cause of monogenic obesity in these model organisms are common mutations always present in only one gene. Results of research on model organisms allowed us to understand biological mechanisms of calorie intake and regulation and maintenance of body weight. The most important insight into obesity was achieved in 1994 after discovery of ob gene encoding for leptin. In two years period, using screening method, candidate homologous genes, selected on genetic study basis on mice, another five genes were identified. Mutations on these genes were found to be the cause of autosomal recessive or dominant monogenic obesity. Products of these genes are leptin and its receptor, proopiomelanocortin (POMC) melanocortin receptor 4 (MC4R) and

Even despite electric shocks, they continued to eat until they became obese. When the researchers switched the obese rats’ diet to a healthy one, the rats refused to eat for almost two weeks. The rats that ate the fast food stopped responding to Leptin, a hormone that regulates hunger. As the rats became more obese, the amount of Leptin in their bodies indicated that the rats were on the brink of starvation; however, the rats continued to eat and become even more obese (Greviskes, 2013).

Conditions in the body have to be controlled with narrow limits. This is called homeostasis. These conditions include water content, ion content, body temperature and blood glucose concentration.

There has been research showing that serotonin, a brain chemical, influences a person's eating behavior. If there is a deficiency of the neurotransmitter serotonin this could cause cravings for sweets and other

Now, in 2015, the number of searches and available information increased from ~334,000 hits to ~32, 200, 00 hits. The idea that food has similar addictive characteristics as drugs that affect the brain is quite controversial. People tend to eat when they are depressed, happy, emotional, celebrating and many other situations because food is easily accessed and not illegal. Research regarding sugar having addictive qualities was conducted in 2010 by the University of Texas and the Oregon Research Institute. Equipped with Haagen-Dazs ice cream and a group of overweight women, the researchers measured the brains reward center activity when shown images of ice cream and when tasting an ice cream milk shake; six months down the road, the group reconvened and the women once again tasted the ice cream. The results were that the woman who had gained weight over the time gap had decreased activity in the striatum, an area of the brain that registers reward, thus needing more to reach a feel good level of satisfaction (Langreth & Stanford, 2011). "The significance of this finding is that these are the same regions of the brain that light up in drug addicts who are show images of drug paraphernalia or drugs" (Wormer & Davis, 2013).

Internally, the hunger we feel is conceived from the brain. It has once occurred to me that I did not realize lunch time passing because I was too busy working. This is clear proof that internal influence of hunger is by the brain and not the stomach (Hockenbury and Sandra 63). The brain part that regulates the hunger feeling is called hypothalamus. This segment of the brain is separated into the lateral and

The broken down food contains nutrients that activates the G-protein coupled receptors of enteroendocrine cells (Sam et al, 2012). On activation, it releases a number of gut hormones which passes the nutrient availability signal to the hypothalamic arcuate nucleus (ARC). This ARC is known to mediate intake of food and energy expenditure. (Peruzzo et al, 2000; Schaeffer et al, 2014; Sainsbury et al, 2010). Several circulating peptides: insulin and leptin are responsible for adiposity and energy deposits. ARC has two neural populations that act antagonist to each other. The medial part contains orexigenic neurons that regulate neuropeptide Y (NPY) and agouti-related protein (AgRP). The lateral part acts as an anorexigenic neurons expressing alpha-melanocyte-stimulating hormone (a-MSH) formed from pro-opiomelanocortin (POMC) and cocaine-amphetamine regulated transcript (CART) (Hahn et al, 1998; Elias et al,

Ramifications of obesity have been long recognized by health care professions, but there is no clinically recognized definition of food addiction. Mental health researchers at Yale University applied traditional criteria for substance abuse to eating and obesity and found striking similarities (Liebman, 2012). There remains considerable debate about classifying nonsubstance addictions, with some mental health professionals suggesting that these are behavioral disorders rather than disorders with neurobiological causes.

The University of Cincinnati (UC), hypothesized that that the body was developing extra leptin to fight the temptations of obesity. This is due to the fact that leptin is the protein that signals the brain to stop eating. The more leptin, the more signals that will tell the body to stop eating (Babcock,2017). They thought this was the case, however, in human preclinical trials, giving obese patients more leptin didn't work. They ate at the same rate, and still remained obese. The results of this study show that scientist need to rethink the ways of using leptin to treat obesity (University of Cincinnati Academic Health Center, 2015). There must be other options out there and it could be that researchers are focusing on the wrong

Overeating provides an interesting parallel to addictive behaviour. Much like habitual drug users, obese individuals commonly report experiencing craving and preoccupation with food (Herman and Polivy, 2008; Jastreboff, Sinha, Lacadie, Small, Sherwin & Potenza, 2013). The influence that food relevant cues (e.g. sight, smell, taste) have on food intake has also been well documented (for review see Herman & Polivy, 2008). . It is plausible that dopaminergic conditioning occurs in individuals who habitually overeat. Attempts to establish if attentional bias for food cues is a useful predictor of obesity risk have had mixed success. However there is a growing body of research that demonstrated that obese individuals allocate greater attentional

Leptin, which is a peptidic hormone (possessing two or more amino acids), essentially serves as a messenger between the brain and fat tissue, and has been noted to aid in the maintenance of body weight. In many animal models, which include rats and mice, obesity was found to be caused by mutations in the rodents' leptin and leptin receptors, where single mutations (mutations where changes occur to only one nucleotide base) occurred in the coding area or the 5' end of the non-coding region of the leptin gene. This sparked the interests of many scientists, as they began to wonder if mutations in leptin and its receptors may also be responsible for obesity in humans. At first, no evidence was found of this being true, but recently, new research suggests that particular forms of obesity in humans may be the result of mutations of the leptin gene. Early experiments of parabiosis had been done with mice, where two individuals were joined anatomically, and recognized that the lack of leptin was responsible for them having the complex, obese phenotype. Although the ob/ob mice could be treated with leptin, the db/db mice were not affected by the treatment of leptin, having researchers come to the conclusion that the incapability to respond to leptin is the cause of mutations in the leptin receptors.

The research report “Adult Picky Eating: Phenomenology, taste sensitivity, and psychosocial correlates,” was published in the international research journal, Appetite, by the University of Pennsylvania. The authors of the report wrote in a very conventional manner or in other words, adhered to this genre’s conventions. The intended audiences of this article are psychologists and scientists and we know this due to esoteric diction and the organization throughout the paper. Keywords and phrases such as “cognitive symptoms of disordered eating,” ARFID, psychopathology and references to DSM-V tell us this article is geared to more specifically psychologists. The article is written in the scientific method format and includes data written in scientific notation and key terms like chi square analyses, p-values, and the golden ratio symbol. Unintended audiences could be people interested in the study or anyone who may

Compulsive eating and other related eating disorders have a lot in common with drug addiction: both are based on reward processes, include compulsive elements (binge eating vs. binge drug intake), can be described as chronic diseases with high risk of relapse and both share a marked lack of sensitivity to behavioural and pharmacological therapies (for review see Wilson 1993). Among the different models existing for assessing eating disorders (West and York 1998, Tschöp and Heiman 2001, Corwin and Buda-Levin 2004), there is currently no single "gold standard" model or test battery for compulsive behaviour. Models evaluating the compulsive component of eating disorders in rodent by distinguishing between reward-related, energy-related and compulsion-related factors in eating control, may represent a valuable tool in the preclinical search for new pharmaco-therapeutic

Many people today eat when their emotionally such as because the person is bored, sad, anger or even happy. Obesity can be caused by things like stress or depression and can cause a number of different health implications. For example a person that is obese is more likely to have diabetes later in life and also suffer heart problems. Over 30% of today’s population seek treatment for weight problems and this is all caused through binge eating. Binge eating is when someone eats large amount of food while feeling they can’t control how much they are eating, people who seriously binge and a very obese develop a disorder call binge eating disorder. The people with this kind of eating disorder find it difficult to lose weight and also find it difficult to control how much they are eating. Many people may need serious help for example counselling or medication or even operation to

There are multiple ways to be guided to an eating disorder other than the media. “Eating behavior is a complex process controlled by the neuroendocrine system of which the Hypothalamus-pituitary-adrenal-axis (HPA axis) is a major component” (News Medical). Psychological research is very important to patients who have an eating disorder. Throughout the research in the paper, researchers have come to a conclusion that some of the qualities in the brain a person has a certain level