Académique Documents
Professionnel Documents
Culture Documents
Michelle Phan
Eating disorders are fairly rare in the general population. Not yet
documented as anorexia nervosa, cases of self-starvation date back to the
17th century (1). Anorexia Nervosa (AN) is the oldest documented eating
disorder (ED) (2) and was first recognized as a psychiatric illness in the late
19th century (3). Until the end of the 20th century, there was no knowledge of
the psychopathology of anorexic patients (1).
AN is described as an extreme psychiatric disorder illustrated by a deep fear
of becoming fat, refusal to maintain a minimally healthy body weight, and a
disturbed body image (4). According to the American Psychiatric Association
(6), the main component of AN is the restriction of caloric intake to
significantly lower body weight. Individuals with anorexia tend to have a
distorted body image and body concept; are obsessed with their body shape
and weight; are in denial of their low body weight; and are ignorant to the
health detriments of AN (6).
Anorexia mostly affects adolescent women with a female to male ratio
between 10:1 and 4:1. In the United States, anorexia has a lifetime
prevalence between 0.9% and 2.2% for women. It is estimated that the
prevalence of AN in young women is 0.3% (4). This disorder has an average
occurrence length of ten years. AN has high rates of morbidity and
comorbidity. Anorexia is typically comorbid with anxiety disorders that often
precede the ED. AN also has the highest mortality rate of any ED and
psychiatric illness with roughly 6% of anorexic women dying per decade of
having anorexia. The suicide rate of anorexic patients is 57 times higher than
in the general population and is one of the most common causes of death in
anorexic patients, along with acute starvation (7).
factors for those who develop AN. Those with occupations that have an
emphasis on weight or body shape; are valued for bodily appearance or for
physical performance; or are involved in food and weight management are
also more likely to develop this disorder (1).
Pathophysiology There are many medical complications that can occur
from the starvation, purging and/or over exercising associated with AN. The
serotonergic system have been found to be involved with the development of
AN. Several studies have shown that there are elevated levels of 5hydoxyindole acetic acid, the primary serotonin metabolite, in the
cerebrospinal fluid of anorexic individuals. These studies have also shown an
increase in frequency in abnormal serotonin receptor genes (12, 13, 14).
Neuroendocrine abnormalities and increased plasma cortisol have also been
found in those with AN. Endocrine changes makes an anorexic individual
have low serum insulin levels with an increase in glucagon concentration.
Endocrine changes also affect the sympathetic nervous system, gonadal
axis, adipose tissue hormones, thyroid, adrenal cortex, growth hormone,
vasopressin, inflammatory cytokines, hypothalamic control of hunger, and
bone density (9, 11).
The parietal lobe has also been found to be dysfunctional, potentially
affecting an anorexic individuals self-perception of body shape and weight.
Compared to men, the parietal lobe of women also tends to have decreased
volume and surface area, which can explain why females are more affected
than males. There are structural changes in the brain that directly occur from
the malnourishment of AN. There is gray and white matter loss; an increase
in cerebrospinal fluid volume; and enlarged sulci in the brains of anorexic
individuals (7).
The nutritional deficits may increase the chance of cardiac arrhythmias and
infection. There can be decreases in cardiac muscle mass, chamber size, and
cardiac output; with a prolapse in the mitral valve frequently detected (12).
Individuals with AN can also have bone mass loss, orthostatic hypotension,
severe bradycardia, loss of subcutaneous fat tissue, abnormal menstrual
function in females, decreased testosterone in males, hair loss, hypothermia,
and electrolyte imbalances. Many of these consequences may not be
reversible and can lead to more serious health conditions later on in life(15).
Clinical Manifestations The American Psychiatric Associations 5th edition
of the Diagnostic and Statistical Manual of Mental Disorders criteria for
anorexia indicates body weights that are significantly below expectations
considering age, height, sex, physical health, and developmental level. AN is
separated into two types by the current classification system: restricting type
and binge eating-purging type. The restricting type is the anorexic individual
that maintains a low body weight by extreme methods of food restriction and
in some, excessive exercise. The binge eating-purge type is the anorexic
individual who meets the weight criteria for anorexia but also binge eats and
purges (5, 7).
Symptoms and signs in anorexic individuals may be mild and temporary or
severe and long lasting. Physical signs and symptoms of anorexia may
include, but are not limited to extreme weight loss, emaciated appearance,
fatigue, insomnia, dizziness, fainting, thinning/loss of hair, dehydration,
constipation, irregular heart rhythms, osteoporosis, and/or low blood
pressure (1, 16). Behavioral symptoms and signs may include an absence of
emotion, refusal to eat, denial of hunger, fear of becoming fat, and/or
preoccupation with food (16). Malnourishment can lead to psychological
symptoms, such as depression, obsessional rituals, reduced alertness, social
withdrawal, and reduced concentration (5). Those with AN tend to have an
enhanced interest in cooking and nutrition. Despite the restriction of food
consumption, anorexic individuals are often very knowledgeable about the
nutritional components of food and use this knowledge to select low-energy
foods for consumption (11).
Medical Diagnosis In order to be diagnosed with anorexia nervosa, the
patient must meet the criteria in the Diagnostic and Statistical Manual of
Mental Disorders. The criteria includes the limitation of caloric intake
resulting in a considerably low body weight, fear of gaining weight with
behaviors that interfere with weight gain, and a disturbance in the
perception of the patients body image or denial of illness (5). If AN is
suspected, tests and exams will be conducted to help diagnose AN, rule out
underlying medical causes for the weight loss, and check for other
complications that may have ensued. A physical exam could include
assessment of the abdomen; measurement of heart rate, blood pressure,
and temperature; skin and nail health; heart and lung sounds; and height
and weight. Low body weight in adults is described, as a body mass index
(BMI) of less than or equal to 17 kg/m2 is considered significantly low. Age is
a crucial consideration in making a diagnosis because of the BMI range
during the time that AN is typical; in late childhood, adolescence, or early
adulthood (17). Lab tests may include a complete blood count; specialized
blood tests to check electrolytes, protein, and liver, kidney and thyroid
health; and a urinalysis. There may also be a psychological evaluation to
assess the patients thoughts, feelings, and eating habits. X-rays may be
conducted to check bone density and examine potential stress fractures or
broken bones. X-rays may also be used to check for cardiothoracic issues,
electrocardiograms may be used to look for irregularities in the heart (1, 14,
17). A 19 year old, college sophomore female patient has been diagnosed
with anorexia. Her physical exam could show a low BMI, while her
psychological evaluation has the potential of pinpointing the onset of AN to
her going away to college or using anorexia as a weight-management
technique. College students with anorexia typically become unusually lean,
but still talk about feeling overweight (18).
Treatment and Effects Many patients with anorexia do not know or deny
that they have anorexia, presenting a challenge in treating AN. Patients
typically undergo treatment only when their condition is serious. There are
inpatient and outpatient treatments; course of action should be arranged
with a team of medical providers. Hospitalization may be required and
nutritional supplementation would be provided in those cases. Evidence-
based treatment options are very limited but there are several treatment
plans for AN that focus on weight restoration, behavior change, and
pathopsychological reduction. Some studies have shown that psychotherapy,
such as cognitive behavioral therapy (CBT) and family therapy, is successful
in reducing the risk of relapse in adult patients. CBT helps the patient
restructure their thoughts and actions to healthier ones (6). There are no
medications approved for treatment of AN, but psychiatric medications can
help treat other mental disorders that the patient may have. There have
been weak studies that show that the use of selective serotonin reuptake
inhibitors (SSRIs) can help prevent relapse in recovered patients. SSRIs are
ineffective in restoring weight and reducing symptoms of AN. Olanzapine has
also shown to help produce weight gain and relieve anxiety (8, 15). There are
different treatment options within residential treatment facilities that
typically produce long-term positive outcomes (5).
With the college patient, if she seeks treatment early enough, she can
potentially recover completely. College students typically do not receive
treatment until the later stages of their disorder. At this point, the patient
would most likely be at risk of having a serious medical condition, if she does
not already have one. If she were to seek treatment, she would most likely
undergo CBT to negate the distorted views she may have about herself. She
would have to be committed to the treatment for it to be successful. She
may seek help from counselors and support groups so that she does not
relapse (6, 5).
References:
1. Halmi KA, editor. Psychobiology and treatment of anorexia nervosa and
bulimia nervosa. 1st ed. DC: American Psychiatric Press; 1992.
2. Heaner MK, Walsh BT. A history of the identification of the characteristic
eating disturbances of Bulimia Nervosa, Binge Eating Disorder and
Anorexia Nervosa. Appet 2013;01.005.
3. Gull WW. Anorexia nervosa (apepsia hysterica, anorexia hysterica). Trans
Clin Soc Lond 1874; 7, 2228.
4. Chakraborty K, Basu D. Management of anorexia and bulimia nervosa: An
evidence-based review. Indian J Psychiatry 2010; 52(2):174-186.
5. American Psychiatric Association: Diagnostic and statistical manual of
mental disorders, fifth edition. Arlington, VA, American Psychiatric
Association, 2013. Web. [access date: 31 Mar 2015].
dsm.psychiatryonline.org
6. Oudijn MS, Storosum JG, Nelis E, Denys D. Is deep brain stimulation a
treatment option for anorexia nervosa. BMC Psychiatry 2013; 13: 277.
7. Bohon C. Anorexia Nervosa. Reference Module in Biomedical Sciences.
Elsevier; 2014.
8. Bulik CM, Sullivan PF, Tozzi F, Furberg H, Lichtenstein P, Pedersen NL.
Arch Gen Psychiatry 2006 Mar; 63(3):305-12.
9. Walsh BT. The enigmatic persistence of anorexia nervosa. Am J Psychiatry
2013 May 1; 170(5): 477-484.
10. Jacobi C, Hayward C, de Zwaan M, Kraemer HC, Agras WS. Psychol Bull
2004 Jan; 130(1):19-65.
11. Encyclopedia of Human Nutrition. Waltham (MA): Academic Press; c2013
[cited 2015 Mar 31].
12. Kaye WH, Gwirtsman HE, George DT, Jimerson DC, Ebert MH. CSF 5-HIAA
concentrations in anorexia nervosa: Reduced values in underweight
subjects normalize after weight gain. Biological Psychiatry 1988; 23(1):
102105.
13. Kipman A, Bruins-Slot L, Boni C, Hanoun N, Ades J, Blot P, et al. 5-HT (2A)
gene promoter polymorphism as a modifying rather than a vulnerability
factor in anorexia nervosa. European Psychiatry 2002; 17(4): 227229.
14. Madison J, Marcil W, Petty F. Reference module in biomedical sciences.
Elsevier; 2014.
15. Treasure J, Claudino AM, Zucker N. Eating disorders. Lancet.
2010;375:583-593.
16. Mayo Clinic. Anorexia nervosa. (2014) (cited March 2015). Available
from: http://www.mayoclinic.org/diseases-conditions/anorexia
17. Hebebrand J, Himmelmann GW, Wewetzer C, Gutenbrunner C, Heseker
H, Remschmidt H, et al. Body weight in acute anorexia nervosa and at
follow-up assessed with percentiles for the body mass index: implications
of a low body weight at referral. Int J Eat Disord 1996; 19:347357
18. Sullivan PF. Am J Psych 1995;152(7).