Download eating disorders research paper - This area is password protected

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Hyperkinesia wikipedia , lookup

Psychopharmacology wikipedia , lookup

Asperger syndrome wikipedia , lookup

Neuropsychopharmacology wikipedia , lookup

Phantosmia wikipedia , lookup

Neuropharmacology wikipedia , lookup

Transcript
Moore 1
Introduction
Eating disorders are medical illnesses that encompass both physiological and
psychological components in both their origin and outcome. Many adolescents suffer from these
disorders. In fact, eating disorders are the third most common chronic illnesses affecting
adolescents (1). In recent years, the age of onset has decreased with a significant percentage
developing under the age of 12. The most widely known and well-studied eating disorders are
anorexia nervosa and bulimia nervosa, but more adolescents are now being treated for atypical
eating disorders, as they do not meet the diagnostic criteria for either anorexia nervosa or bulimia
nervosa (2). Anorexia nervosa is primarily characterized by restraining oneself from food.
Although very few calories are consumed, some also engage in purging behaviors such as selfinduced vomiting and the use of diuretics, enemas, and laxatives. Bulimia nervosa is
characterized as either purging or non-purging. While the purging type will engage in typical
purging behaviors, such as those described previously, non-purging type bulimia nervosa
patients use other behaviors to compensate for the mass amount of calories that they consume,
such as excessive exercise or fasting. While the type and extremity of an eating disorder varies
by individual, they are all primarily characterized by three components: a disturbed body image,
an intense fear of weight gain, and an obsession to become thin (3).
It was long believed that eating disorders stemmed solely from psychological factors, as
they are often accompanied by depression, mood, or anxiety disorders (4). It is now understood
that biological factors do play a role in eating disorders, but the definite cause is still unknown.
In the past decade, several studies have explored potential biological mechanisms for various
types of eating disorders and discovered that many physiological factors may be involved, such
as dopamine, serotonin and oxytocin (5). While biological factors have shown to contribute to
Moore 2
the development of eating disorders, it is imperative to focus on all aspects of disordered eating
when analyzing these illnesses and developing treatments, as the accumulation of multiple
factors leads to their onset.
Risk Factors
There are several risk factors associated with developing an eating disorder, with some
populations experiencing greater risk than others. Athletes are considered a high-risk group,
especially young, female athletes as they have pressures placed upon them to be thin (3). Sports
such as swimming, dancing and gymnastics pose the greatest risk for young females, because
they rely on a lean physique for optimal performance. This type of sport usually requires tight
clothing and young girls may feel that they need to appear a certain way in this attire. When
comparing leanness-focused sports to non-leanness focused sports in a population of young
women, those in leanness-focused sports reported higher levels of body dissatisfaction and
disordered eating than those in non-leanness focused sports. In addition, elite athletes reported
the highest levels of body dissatisfaction and disordered eating as compared to competitive
athletes or those engaging in the sport recreationally. In fact, 60 percent of elite athletes reported
pressure from their coaches to be thin (6). Other risk factors are based on one’s personality and
behaviors, such as low self-esteem, high concern for one’s body, use of escape or avoidance
coping and a lack of perceived social support (7). Others include disease states that require
limiting food intake, family history of psychological or eating disorders, trauma during
childhood, and societal pressures to be thin (3).
Medical Consequences
Eating disorders perpetuate numerous medical consequences for adolescents that are
detrimental to their health, growth, and development. In extreme cases, eating disorders may
Moore 3
even be fatal. The mortality rate of anorexia nervosa is 12 times higher than the death rate of all
causes of death for females ages 15-24 (1). Medical consequences for adolescents include growth
retardation, pubertal delay or arrest, structural brain changes, and impaired acquisition of peak
bone mass, which can lead to osteoporosis in adulthood (3). When compared to obese females,
women with anorexia nervosa were at greater risk for hip fracture due to lower bone density (8).
It is still unknown whether many of these complications, such as structural brain changes, are
reversible, thus early detection and treatment of eating disorders is vital in adolescents (3).
Psychological and Social Components
Eating disorders have a strong social and psychological basis. The media has socially
constructed what men and women should look like through advertisements, movies, and
magazine covers. Children and adolescents are extremely susceptible to this information. In
recent years, numerous websites have launched that actually promote anorexia and other eating
disorders. These sites have been associated with a greater drive to be thin and higher levels of
perfectionism in adolescents (9). In a study conducted in pre-adolescent girls, total amount of
internet exposure was associated with four different measures of body image, including
internalization of the thin ideal, body surveillance, body esteem, and dieting behavior (10).
Social media and websites that encourage disturbed eating behavior put adolescents at greater
risk for eating disorders in today’s society.
Preadolescent body dissatisfaction has also been linked with dieting, reduced self-esteem,
obesity and disordered eating later in life (10). Other factors may influence pre-adolescent body
dissatisfaction aside form the media, including family and peers. Several studies have delineated
the effects that parents have on both body image and eating patterns. In females, negative
comments from parents about one’s body has been linked with internalization of those
Moore 4
comments, body dissatisfaction, a drive for thinness, and eventually, the development of an
eating disorder. In males, negative comments from parents regarding one’s body leads directly to
body dissatisfaction, a drive for thinness, and eventually eating disorder development. However,
this association is much stronger in females (11).
While most eating disorders do not develop until the pre-adolescent years, studies have
depicted abnormal eating behavior in children as young as pre-school, as they exhibit more
emotional eating patterns if their mother has experienced an eating disorder (12). The reasoning
behind this is unclear, but it may be due to the way that the mother presents food to the child or
the way that the mother behaves in the presence of food herself. Although the mother is
recovered, she may still engage in abnormal eating behaviors and may transmit these behaviors
to her children through observation. The father-daughter relationship has also been examined. A
“protectant and avoidant” parenting style has been associated with more food restraint,
depression, and more concern about eating, body shape, and appearance, when compared to a
“caring and benevolent” parenting style (13). Thus, the role of both the mother and father in an
adolescent’s life plays a pivotal role in their development of eating behaviors.
The effect that peers have on children and adolescents’ eating behaviors has also been
reported. More than 45 percent of overweight girls and boys report being teased about their
weight at least a few times a year. After five years, this teasing has been shown to induce bingeeating behaviors among boys and frequent dieting among girls (14).
Traumatic experiences during early childhood have also been associated with eating
disorders (3). In a study examining the effects of different types of trauma, individuals with
eating disorders had experienced more adversity during childhood and more repeated traumas
than individuals without eating disorders (15). Emotional abuse and emotional neglect were both
Moore 5
correlated with disordered eating in a population of male and female adolescents, which was
mediated through dysfunctional emotional regulation (16). Emotional regulation is the ability to
understand and cope with one’s emotions. With emotional maltreatment, adolescents’ feelings
may be invalidated or ignored, disrupting their ability to regulate their emotions.
Biological Components
An extensive body of research has been collected that demonstrates possible biological
mechanisms and implications for eating disorders. As food consumption is mediated through
certain brain pathways responsible for reward and motivation, such as the Nucleus Accumbens
(NAc), an abnormality in one or more of these pathways may contribute to the etiology of eating
disorders (17).
Binge eating, associated with both bulimia and the binge-purge anorexia type has been
documented to cause dysregulation in dopamine, opioids, acetylcholine (ACh) and serotonin.
When animals’ brains were examined through brain imaging, the ventral limbic circuit was
determined to be involved in the regulation of feeding behavior, which encompasses the
amygdalae, insula, anterior cingulated cortex, and the orbitofrontal cortex (17). Dopamine is
known to increase in the limbic system with weight loss or food restriction. Binging on a 10%
sucrose solution caused the release of dopamine in the NAc of rats, and this effect was increased
when rats were underweight. These effects also held true after the stomach had been completely
emptied, indicating the possible role in dopamine with binge-purging behavior. There was a
significant delay in the increase and peak of ACh as a meal progressed and satiety increased,
which is of notable mention as ACh normally increases with a peak at the end of a meal (18).
This effect may correspond with a delay in satiety, which could contribute as a mechanism
behind binge eating behavior.
Moore 6
It has also been proposed that opioids are involved in binge eating behavior. Rats given
the opportunity to binge eat on sucrose had a substantial increase in opioid receptor binding in
several brain regions, including the NAc (17). Bulimic patients had significantly less opioid
receptor binding in the insula than individuals without bulimia (19). Serotonin has also been
studied as a potential mechanism behind binge eating behavior, as there was decreased serotonin
transporter binding in obese binge eaters (17). Restriction of food also correlates with a decrease
in serotonin levels, explaining the possible effects of serotonin on food restricting behaviors in
eating disorders such as anorexia nervosa (20). In addition, extremely low fat diets in animals
have been shown to diminish serotonin activity, indicating a possible pharmaceutical treatment
for food restricting behaviors (21).
Other studies have shown that Neuropeptide Y (NPY) may be related to the pathology of
eating disorders. NPY is a peptide hormone that has been shown to increase food intake. When
anorexia nervosa patients, bulimia nervosa patients, and healthy controls were exposed to a high
carbohydrate meal, results revealed that NPY remained high in both anorexic and bulimic
patients following the meal, but decreased in healthy controls. This serves as an important
marker for disturbed eating behavior, as NPY should decrease after a meal as to ensure one does
not overeat. This may explain the binge eating behavior associated with eating disorders (22).
Oxytocin has been implicated as a hormone involved in satiety. When patients with
active anorexia nervosa, recovered anorexia nervosa or healthy controls were exposed to a
standardized meal, mean peripheral oxytocin levels were highest in anorexic patients,
intermediate in recovered anorexics, and lowest in controls. Oxytocin secretion was also
associated with leptin secretion in recovered anorexics and healthy controls, but not in anorexic
patients, suggesting a dysregulation in these hormones with active anorexia nervosa. Oxytocin
Moore 7
secretion was also associated with 9-22% of hypoactivation in the amygdala and insula, brain
regions associated with the regulation of food behavior. Researchers concluded that it might be
due to a defect in the insula, which is responsible for processing internal signals. Individuals with
a defect in this area would have difficulty distinguishing hunger from satiety (23). Thus,
abnormal activation in these brain regions aids in our understanding of their potential mechanism
in eating disorders.
Treatment for Adolescents
As eating disorders are complex medical illnesses, the most effective treatment focuses
on all aspects, including family, social, psychological, and biological factors (3). A team
approach is necessary, as one professional cannot treat an eating disorder patient alone. This
includes, but is not limited to a physician, nurse, therapist, and dietitian.
For anorexia nervosa, the main goals are nutrition rehabilitation, weight restoration,
improving eating behaviors, eliminating weight reduction behaviors, and improving the
psychological and emotional state of patients. The role of the dietitian is essential in this
treatment. One of the most helpful tools that a dietitian can provide is a meal plan that includes
foods that the patient feels are safe, as they often categorize foods as good or bad. Eventually,
foods they are less comfortable with may be added (3). This is a part of cognitive behavioral
therapy, a mode of treatment that challenges beliefs patients have about their food and weight
with more accurate perceptions (24).
With bulimia nervosa, treatment is similar to anorexia nervosa, but focuses more on
normalizing eating patterns and behaviors (3). Cognitive behavioral therapy is utilized as well
(24), as patients are often asked to record their food intake, behaviors and thoughts in a journal
and share these during therapy (3). These thoughts are then challenged by both the therapist and
Moore 8
patient. The therapist will discuss these thoughts with the patient, but eventually the goal is for
the patient to evaluate these thoughts on his or her own.
The most effective type of therapy for adolescents is Family Based Therapy (FBT). This
is a more focused treatment that includes the entire family instead of the child alone (24). FBT
engages the family and works to have the parents manage the eating disorder, whereas systemic
family therapy focuses less on engaging the family and more on the adolescent learning to
overcome the disorder on their own. While both types of treatment are often used and they may
be used in conjunction, FBT leads to faster weight gain, fewer days in the hospital, and lower
treatment costs (24). Thus, FBT is the primary method of treatment for adolescents with eating
disorders.
Conclusion
Eating disorders are complex biopsychosocial disorders that require extensive treatment
and care. Adolescents are at high risk for developing these disorders and they usually manifest
during the pre-adolescent years (3). It is vital that adolescents receive proper treatment as early
as possible as eating disorders have the highest morbidity and mortality rates than any other
psychiatric disorder (3, 24). While social and psychological factors play a major role in both the
development and aftermath of eating disorders, biological components have been discovered in
recent years. Dopamine, ACh, serotonin, opioids, NPY and oxytocin have all been examined for
their potential effects on eating disorders, and several studies have shown abnormalities that
delineate their contribution (17, 18, 19, 20, 21, 22, 23). As most of these studies have been
conducted in animal models, further studies need to be conducted in humans to determine
potential pharmaceutical treatments. It is also unknown at this time whether many of these
dysregulations cause eating disorders or are effected by them, as patients have not been studied
Moore 9
before and after the eating disorder manifests. Thus, more research is necessary to determine
which biological components have the greatest effects on the pathology of eating disorders. It is
still of the utmost importance to examine eating disorders from a multi-dimensional perspective,
as these disorders are deeply complex in nature and cannot be regarded as a single entity.