The DSM-5 describes a group of disorders related to feeding and eating behavior. These disorders include binge-eating disorder (BED), bulimia nervosa (BN), anorexia nervosa (AN), and avoidant or restrictive food intake. These disorders are characterized by continuous abnormal eating behavior that leads to altered food consumption and eventually significant impairment of physical health and social functioning (American Psychiatry Association, 2013:329).
BED is a major eating disorder where a person frequently consumes abnormally big portions of food which leads to them eating uncontrollably. The DSM-5 diagnostic criteria for BED: is the reoccurrence of binge eating that must occur, on average at least once a week over a time period of 3 months (American Psychiatry Association, 2013:350-351). An episode of binge eating is defined as eating, in a discrete time period, an amount of food that is definitely larger than the average person would consume in a similar lapse of time under similar conditions (American Psychiatry Association, 2013:350-351). Binge eating is associated with an increase in distress and must include at least 3 of the following characteristics: eating much faster than normal; overeating until one feels uncomfortably full/bloated; overeating without the physical need to eat (hunger is not evident); eating by oneself due to the fear of embarrassment because of the amount of food one consumes in a single time period; the feeling of disgust with oneself; the feeling of guilt after binge eating or the feeling of depression (American Psychiatry Association, 2013:350-351).
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BN, which is commonly known as bulimia is a life-threatening eating disorder where the individual secretly purges after consuming an excessive amount of food in order to dispose of the extra calories consumed during the uncontrolled eating. In BN there are three essential characteristics: recurrent episodes of binge eating; recurrent inappropriate compensatory behaviors to prevent weight gain and self-evaluation that is excessively prejudiced by body shape and weight (American Psychiatry Association, 2013:345). Individuals with BN usually overeat in secret and they use various methods to induce vomiting after their binge session for diagnostic purposes, the binge eating must occur at least once a week for a period of at least three months (American Psychiatry Association, 2013:345).
AN, which is usually just referred to as anorexia, is a dangerous eating disorder associated with the person having an unusually low body weight, an extreme fear of putting on weight, and a very inaccurate perception of weight. AN comprises three vital characteristics: continuous energy intake limitation; extreme fear of putting on weight or becoming fat; persistent mannerisms that hinder weight gain and a disturbed perception of the way they see their weight and body shape (American Psychiatry Association, 2013:339). The individual has a body weight that is below the recommended BMI of a healthy individual (American Psychiatry Association, 2013:339).
Avoidant or Restrictive food intake (ARFI) is the last type of eating disorder that will be discussed in this review. ARFI was previously classified as a selective eating disorder. This disorder involves limitations in the amount and/or type of food that is consumed but it does not involve any fear or perceptions about body weight/shape or insecurities of size or weight gain. The main characteristic of ARFI is the avoidance or limitation of food consumption which is caused by the clinically significant failure to adhere to requirements for nutrition or inadequate energy intake by means of oral intake of food (American Psychiatry Association, 2013:334). One or more of the following essential elements must be present: significant weight loss; significant nutritional deficiency; an individual who becomes dependent on enteral feeding or oral nutritional supplements or a notable change in psychosocial functioning (American Psychiatry Association, 2013:334).
It is highly possible that these symptoms and characteristics are programmed in the limbic and cognitive circuits which have the function of regulating the neurological processes that are associated with cognitive control, appetite, and emotionality (Mishra et al., 2017:92).
Although the exact neurobiological mechanisms of the different eating disorders remain uncertain, human studies have shown that a dysregulation in the cortico-limbic systems in the brain is likely to be involved (Mishra et al., 2017:92). Eating disorders can be considered as a type of compulsion and this lends itself to the possibility to treat these disorders in the same way we treat obsessive-compulsive disorder (OCD). OCD results due to the over-powering effect that the overstimulation of the serotonin receptor has on the brain. OCD is treated by using a class of drugs that inhibits the uptake of the neurotransmitter serotonin. (Ackerman, 1992). A drug of note is Clomipramine, which successfully blocks the uptake of serotonin at synapses and affects noradrenaline uptake (Ackerman, 1992:50-51).
Studies that were recently conducted provide us with evidence that genetic factors could account for about 50-80% of the probability of developing eating disorders (ED) and this could lead to the neurobiological factors causing ED (Mishra et al., 2017:92). Other psychiatric disorders do not share the exclusive and multi-faceted appetitive symptomatology that is seen in ED and this could create the possibility that the ED reflect some irregularities in the appetitive pathways (Mishra et al., 2017:92).
The neurobiology of appetite consists of both the physiological and psychological drives of appetite. The physiological drive is the sense of hunger and is linked with the craving for food and various other physiological effects which results in the individual looking for an acceptable food supply. The psychological drive of appetite is the desire for food, usually a specific type and this is valuable as it helps the person decide the quality of food, he/she decides to eat (Mishra et al., 2017:92. The sense of satisfaction is achieved if the search for food is fruitful (Mishra et al., 2017:92). There are factors (metabolic and non-metabolic) that are involved in the commencement and upkeep of eating mannerisms (Mishra et al., 2017:92). Especially in the human race the non-metabolic factors (cues, reward, cognitive and emotions) play a vital role (Mishra et al., 2017:92) Homeostatic or hedonic are the terms given for the brain areas that regulate appetite (Mishra et al., 2017:92). If a person has not had any food intake for a long period of time, then the homeostatic processes would bring about the hunger awareness and if a person is not hungry but presented with a food stimulus may it be sight or smell or both, then the hunger awareness produces physical responses such as salivation (Mishra et al., 2017:92). The hypothalamus and brainstem form part of the homeostatic system that regulates food consumption which is based on caloric requirement and energy need (Mishra et al., 2017:92). These two areas integrate inputs from the cortical areas concerning the reward value of food which signifies that “hedonic” hunger is possibly neurally mediated thus the neural mechanisms in the hedonic system may supersede the homeostatic signs which contribute to ED (Mishra et al., 2017:92).
Homeostatic regulation involves the lateral nuclei of the hypothalamus which performs the function of the feeding center by starting the motor drives to set out on a quest for food (Mishra et al., 2017:93). The function of the satisfaction center is the ventromedial nuclei of the hypothalamus (Mishra et al., 2017:93). Hormones which control food intake and energy use, are released from the gastrointestinal tract (GIT) and adipose tissue and come together at points in the hypothalamus known as the arcuate nuclei (Mishra et al., 2017:93). Neural signals from the GIT provides the hypothalamus with sensory information about stomach filling, satisfaction from nutrients in the blood, GIT hormones, hormone signals related to the adipose tissue as well as signals from the cerebral cortex which all have some role in the feeding mannerisms (Mishra et al., 2017:93). The hypothalamic feeding and satisfaction centers contain high concentrations of receptors for a variety of neurotransmitters that control an individual’s feeding mannerisms (Mishra et al., 2017:95). “These neurotransmitters are broadly categorized as (1) orexigenic substances that stimulate feeding (example – Neuropeptide Y (NPY), Agouti-related protein (AGRP), Melatonin concentrating hormone (MCH), Orexin A & B, Endorphins, Galanin (Gal), glutamate & GABA, Ghrelin, Cortisol, endocannabinoids etc.) or (2) anorexigenic substances that inhibit feeding (Example – a-MSH, leptin, serotonin, CRH, norepinephrine, insulin, glucagon-like peptide (GLP), cholecystokinine (CCK), cocaine and amphetamine regulated transcript (CART), peptide YY (PYY)). Gastrointestinal Filling, CCK, PYY, GLP, Ghrelin, and various “oral factors” (chewing, salivation, swallowing, and tasting) are operative in the short-term regulation of food intake” (Mishra et al., 2017:95). There is a collaboration within the hypothalamus between temperature control and a food consumption regulation system which influences the homeostatic regulation of food consumption (Mishra et al., 2017:93). Due to the hormone known as leptin, which is secreted by adipocytes, the stimulation of various sites occurs in the hypothalamus which assists to reduce fat storage, reduce the manufacturing of orexigenics and increase the manufacturing of anorexigenics in the hypothalamus (Mishra et al., 2017:93).
Non-homeostatic regulation occurs when there is an exclusively cortical decision made about food intake without any hunger signal which is seen in homeostatic regulation. Hence, no hunger signal is evident, and the individual just wants to eat (Mishra et al., 2017:93). The external environment influences the degree of food consumption. The main components that regulate the appetite mannerisms of an individual are intrinsically intertwined structures and they are the amygdala/hippocampus, orbitofrontal cortex (OFC), insula, and striatum (Mishra et al., 2017:93). These structures incorporate not only the homeostatic data but also play an active role in learning what the individual likes, what they want and there is also a reward factor with regards to food by assigning attention, effort, and motivation for it (Mishra et al., 2017:93). The cognitive regulation of appetite is mediated by the modulatory regulation of the prefrontal cortex which overrides the appetite areas (Mishra et al., 2017:93).
There are various neurotransmitters that play a role in the standard feeding mannerisms (Mishra et al., 2017:93). The neurotransmitter serotonin (5-HT) has a hyperphagic effect which is most likely mediated by the post synaptic serotonin 2C receptors whilst the serotonin 1A and 1B receptors have contrasting effects on the food consumption mannerisms (Mishra et al., 2017:93). Another neurotransmitter known as Dopamine (DA), acts via the nucleus accumbens and is linked with reinforcing the effect in feeding (Mishra et al., 2017:93). Dopamine which is released in the hypothalamus has a linkage with the duration of food intake which therefore incorporates portion size (Mishra et al., 2017:93). Changes in the norepinephrine levels can result in an individual either eating more or reducing their food intake.
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