Neuroscientific Approach to Anorexia Nervosa
Anorexia nervosa (AN), usually referred to as merely anorexia is a predominant eating disorder that is more commonly in but not restricted to females in comparison to their male counterparts. Anorexia is split into two separate types within the disorder, restrictive and binge/purging. Restrictive Anorexia emphasizes constraints on food consumption supplemented with and not circumscribed to unwarranted exercise, obsessive rules in regard to food, and counting calories. Bingeing and Purging often times get characterized in a similar fashion to restrictive anorexia because of food restriction, yet binge eating is loss of control in the presence of food and a counteraction is performed through vomiting, laxative or diuretic use, or enemas to attenuate the feelings of guilt and fear. I am interested in this topic because of the sociocultural (specifically the media and cultural norms underlined by peers), familial, and psychological factors (e.g. low self-esteem, depression, anxiety), but also because of its overall bearing of one’s health long-term and increasing mortality, including suicide. There is a widespread notion that those who battle eating disorders of this type result from the reward pathway (mesolimbic dopamine pathway) not functioning properly. Truth be told, what interested me the most about the different types of anorexia is the media’s widespread source of influence and inability to see their fault in the matter. The problem isn’t the media’s at large, nor is it the girls who is a size 0. Bodies are individualistically manufactured in a unique fashion, yet the media pushes unrealistic expectations on people to be a precise size in order to be loved, seen, heard, or listened to, regardless of gender, sexual orientation, or age. The problem of profit for brands like Victoria’s Secret have been enhanced by the outcry of models diagnosed with eating disorders attesting to be both unethical, and stigmatizing that are too often overlooked. Neuroscientifical Approach to Anorexia Nervosa
As eating disorders progress, cognitive, emotional, and behavioral scarcities (specifically neurologically) appear heavily. The initiation of an eating disorder is characterized by both functional and rewarding feedback, but during the neurological analysis of patients studied who have AN or bulimia, hyperactivity and disturbed reward pathways are present (Scheurink et al. 2010). The disturbed pathways in the repressive disorder do not support the differentiation of salient stimuli because the neurocircuitry has been weakened due to inhibition, essentially inflicting starvation upon the brain. The ventral striatum, part of the basal ganglia, is an intersection for neural networks, specifically the subcortical structures such as the nucleus accumbens, and the olfactory tubercle that play crucial roles in the reward circuit and its functioning. It is often associated with input via the ventral-tegmental area (VTA). For the purpose of this paper, the ventral striatum and dorsal striatum will be referred to as one functioning system and will include the ventromedial caudate (learning and inhibitory control) and ventral putamen (learning and movement tracking) as well (Bischoff-Grethe et al., 2018). The ventral striatum is involved in reward processing and reinforcement therefore it is important because it activates when the brain forestalls learning or pleasure and mediates rewarding experiences.
Individuals who have eating disorders have associated structural differences in connectivity of certain pathways compared to healthy control counterparts. Anorexic individuals display greater connectivity in the ventral striatum than healthy control individuals, but they receive information from the anterior cingulate cortex (ACC; emotion and cognition), then relay it to the hypothalamus. Healthy individuals’ ventral striatal activity is motivated by the hypothalamus, which is in charge of homeostatic drives. This is a significant finding because it proves the difference in neurocircuitry. The communication via the ACC has the potential to be a reason that the drive to eat is absent and the ill reward process of individuals with eating disorders (Frank, Shott, Riederer, Pryor, 2016). The input of information derives in the opposite path toward the ACC rather than the hypothalamus, permitting the individuals brain to repulse the signals of hunger. The distorted communication of the ACC and ventral striatum explain why the “rewarding” compulsive behaviors exuded by eating disorder patients, such as self-starvation to inhibit weight gain do not reward but rather punish the healthy individuals (Frank et al., 2016; Keating, Tilbrook, Rossell, Enticott, Fitzgerald, 2012).
Normal
0
false
false
false
EN-US
X-NONE
X-NONE
/* Style Definitions */
table.MsoNormalTable
{mso-style-name:”Table Normal”;
mso-tstyle-rowband-size:0;
mso-tstyle-colband-size:0;
mso-style-noshow:yes;
mso-style-priority:99;
mso-style-parent:””;
mso-padding-alt:0in 5.4pt 0in 5.4pt;
mso-para-margin-top:0in;
mso-para-margin-right:0in;
mso-para-margin-bottom:8.0pt;
mso-para-margin-left:0in;
line-height:107%;
mso-pagination:widow-orphan;
font-size:11.0pt;
font-family:”Calibri”,sans-serif;
mso-ascii-font-family:Calibri;
mso-ascii-theme-font:minor-latin;
mso-hansi-font-family:Calibri;
mso-hansi-theme-font:minor-latin;
mso-bidi-font-family:”Times New Roman”;
mso-bidi-theme-font:minor-bidi;}
ORDER A PLAGIARISM-FREE PAPER HERE
Research has been aimed to answer the questions about self-starvation, functioning anorexic individuals, and what it is that is aiding in the advance of their disorder. There are simple homeostatic drives that humans seek to achieve equilibrium, including thirst or hunger. Hunger is signaled by low levels of glucose (glucoprivic hunger), or low levels of fatty acids (lipoprivic hunger). When the nutrients from glucose, or the fatty acids are minimal, the stomach releases ghrelin. Ghrelin is a hunger hormone that increases appetite (Atalayer, Gibson, Konopacka, Geliebter, 2012). Individuals with AN have high levels of the neuropeptide Y (NPY), high levels of ghrelin, and low levels of leptin, whereas individuals with bulimia have high ghrelin pre-meal, and low ghrelin post-meal (Kojima et al., 2004). Feeding is controlled by but not limited to taste, body signals, and nutrient and energy storage (Garrett, 2017) so it is puzzling to scholars the lengths the brain will reach to keep AN individual’s bodies functioning, even at a minimal level. Neuroscientifical Approach to Anorexia Nervosa
The idea that anorexic individuals withstand rejection of food and rewarding aspects of it intrigued the minds of many. In 2007, Wagner and colleagues built off previous studies to propose a study of the alteration of reward processing in anorexic individuals who had recovered compared to healthy individuals. Through guessing games, scanning procedures, and fMRI’s, results suggest within the striatum, the caudate of recovered AN individual’s is overactivated to become “strategic”, not hedonic, due to the absence of effective reward processing pathways. AN individual’s also struggle to interpret positive and negative feedback via the ventral striatum specifically unable to detect salience, in agreeance with previous studies in this area by Delgado. Delgado and colleagues concluded similarly individuals with AN can potentially have difficulty deciphering the differences between a reward or punishment, positive or negative (Delgado, Nystrom, Fissell, Noll, Fiez, 2000).
This characteristic of AN was significant as research continued, Fladung and colleagues found that women with AN display higher preference for underweight stimuli and react faster to overweight stimuli. The ventral striatal region was activated in disease-related stimuli, supporting theories that starvation dependence enables this disorder further. Dopamine 2 and 3 (D2 and D3) receptors within the ventral striatum were found to have increasing levels of binding, as well as altered striatal dopamine (DA) binding. The release of DA produces anxiety, which explains the fear of food by anorexic individuals (Fladung et al., 2010; Bailer et al., 2012).
Progression in research has proven the “neural signature” of AN to be ventral striatum insufficiency (Fladung, Schulze, Schöll, Bauer, Grön, 2013). 13 AN patients (10 restricting, 3 binge eating/purging) alongside 14 healthy controls had to estimate weight while in an MRI and results found that the ventral striatum signaling is linked to the disorder over time, and that AN individual’s depend on their disorder to starve. Alongside Fladung et al (2013) approaching AN as a disorder that involves dependence will further research if it is accompanied by the inability to correctly comprehend rewards.
A recent experimental study that explores the neural mechanisms of persistent AN was published in April of 2015, where 23 adults remitted from Anorexia (RAN) were compared to 17 healthy controls to evaluate if hunger enhances our sensitivity to expect an award, and answers why RAN individuals are not motivated by starvation as others are. Different tasks were given to target brain areas for immediate vs. delayed rewards. Results furthered previous research and provided evidence that hunger was an initiator for reward for healthy controls but not RAN individuals. The circuitry that was influenced heavily during reward salience was the ventral striatum, dorsal caudate, and ACC for immediate reward and the insula and ventrolateral prefrontal cortex for delayed reward. Because RAN individuals, and many AN individual are not influenced by the effect of hunger signals, they can easily decline food. An interesting approach that Wierenga and colleagues took that other researchers haven’t is the effect of the middle frontal gyrus (MFG) and its elevated response in RAN (Wierenga et al., 2015). The MFG is important for explicit learning and could be the cause of the inability to evaluate salience emotionally, cognitively, and behaviorally about the risks of this disorder. Neuroscientifical Approach to Anorexia Nervosa
Notwithstanding the evidence that there is a link between reward processing and the functioning of the ventral striatum, still lie many questions regarding reward motivation, salience, and structural connectivity in the brain. It is apparent that eating disorders are an issue in today’s world and that is not being overlooked. The field has heavily researched into pathways within the brain that are withholding dopamine, or working ineffectively, specifically the ventral striatum, dorsal striatum, MFG, and whether the VTA can be aided by leptin to lower hyperactivity. Anorexia, both restricting and purging, parallel addictive disorders socially, emotionally, physically, and behaviorally. The “high” that self-starvation causes is relative to an opiate high. I believe it should be treated as an addiction in many ways (i.e. eating recovery centers) but coupled with counseling to approach the mental and emotional side of the addiction. The current models are useful in approaching eating disorders in relation to neuroscience, but the dismissal of work put into research to have it overridden by dangerous ideas of what both men and women should look like is a societal issue we need to tackle ethically. With the image conscious era in America, many high-ranking individuals would rather donate to these causes than attack what the real issue is the unattainable perfection emitted by the society. Brand revenue is triumphing over taking care of people. When we as a society have elevated an outward body type over an inward feeling, the issue has sky rocketed.Neuroscientifical Approach to Anorexia Nervosa