Anorexia nervosa is an eating disorder characterized by immoderate food restriction and irrational fear of gaining

weight, as well as a distorted body self-perception. It typically involves excessive weight loss and is usually found
more in females than in males.
[1]
Due to the fear of gaining weight, people with this disorder restrict the amount of food
they consume. This restriction of food intake causes metabolic and hormonal disorders.
[2]
Outside of medical
literature, the terms anorexia nervosa and anorexia are often used interchangeably; however, anorexia is simply a
medical term for lack of appetite, and people with anorexia nervosa do not in fact, lose their appetites.
[3]
Patients
suffering from anorexia nervosa may experience dizziness, headaches, drowsiness and a lack of energy.
Anorexia nervosa is characterized by low body weight, inappropriate eating habits, obsession with having a thin figure,
and the fear of gaining weight. It is often coupled with a distorted self image
[4][5]
which may be maintained by
various cognitive biases
[6]
that alter how the affected individual evaluates and thinks about her or his body, food and
eating.
[7]
Those suffering from anorexia often view themselves as "too fat" even if they are already
underweight.
[8]
They may practice repetitive weighing, measuring, and mirror gazing, alongside other obsessive
actions to make sure they are still thin, a common practice known as "body checking".
[9]

Anorexia nervosa most often has its onset in adolescence and is more prevalent among adolescent females than
adolescent males.
[10]
However, more recent studies show the onset age has decreased from an average of 13 to 17
years of age to 9 to 12.
[11]
While it can affect men and women of any age, race,
and socioeconomic and cultural background,
[12]
anorexia nervosa occurs in ten times more females than males
People with anorexia nervosa continue to feel hunger, but they deny themselves all but very small quantities of
food.
[7]
The average caloric intake of a person with anorexia nervosa is 600800 calories per day, but extreme cases
of complete self-starvation are known. It is a serious mental illness with a high incidence of comorbidity and similarly
high mortality rates to serious psychiatric disorders.
[8]
People suffering from anorexia have extremely high levels
of ghrelin (the hunger hormone that signals a physiological desire for food) in their blood. The high levels of ghrelin
suggests that their bodies are trying to desperately switch the hunger aspect on; however, that hunger call is being
suppressed, ignored, or overridden. Nevertheless, one small single-blind study found that intravenous administration
of ghrelin to anorexia nervosa patients increased food intake by 1236% over the trial period.
[14]
Anorexia nervosa is an eating disorder characterized by attempts to lose weight, sometimes to the point of starvation.
A person with anorexia nervosa may exhibit a number of signs and symptoms, the type and severity of which may
vary in each case and may be present but not readily apparent. Anorexia nervosa, and the
associated malnutrition that results from self-imposed starvation, can cause severe complications in every
major organ system in the body.
[19][20][21]

Hypokalaemia, a drop in the level of potassium in the blood, is a sign of anorexia nervosa. A significant drop in
potassium can cause abnormal heart rhythms, constipation, fatigue, muscle damage and paralysis.
Between 50% and 75% of individuals with an eating disorder experience depression. In addition, one in every four
individuals who are diagnosed with anorexia nervosa also exhibit obsessive-compulsive disorder.
[22]

Symptoms for a typical patient include:
Refusal to maintain a normal body mass index for their age
[23]

Amenorrhea, the absence of three consecutive menstrual cycles
[23]

Fearful of even the slightest weight gain and takes all precautionary measures to avoid weight gain and becoming
overweight
[23]

Obvious, rapid, dramatic weight loss
Lanugo: soft, fine hair growing on the face and body
[24]
One theory is that this is related to hypothyroidism as a
similar hypertrichosis occurs in hypothyroidism.
[25]

Obsession with calories and fat content of food
Preoccupation with food, recipes, or cooking; may cook elaborate dinners for others, but not eat the food
themselves
[26]

Dieting despite being thin or dangerously underweight
Rituals: cuts food into tiny pieces; refuses to eat around others; hides or discards food
Purging: uses laxatives, diet pills, ipecac syrup, or water pills; may engage in self-induced vomiting; may run to
the bathroom after eating in order to vomit and quickly get rid of thecalories
[27][28]
(see also bulimia nervosa).
May engage in frequent, strenuous exercise
[29]

Perception of self to be overweight despite being told by others they are too thin and, in most cases, underweight.
Becomes intolerant to cold and frequently complains of being cold from loss of insulating body fat or poor
circulation resulting from extremely low blood pressure; body temperature lowers (hypothermia) in effort to
conserve energy
[30]

Depression: may frequently be in a sad, lethargic state
[31]

Solitude: may avoid friends and family; becomes withdrawn and secretive
Cheeks may become swollen because of enlargement of the salivary glands caused by excessive vomiting
[32]

Swollen joints
[33]

Abdominal distension
Bad breath (from vomiting or starvation-induced ketosis)
Hair loss or thinning
[34]

Fatigue
[35]

Rapid mood swings
Alcoholism
Tendencies to drug addictions
[36]

Causes
Studies have hypothesized the continuance of disordered eating patterns may be epiphenomena of starvation. The
results of the Minnesota Starvation Experiment showed normal controls exhibit many of the behavioral patterns of
anorexia nervosa (AN) when subjected to starvation. This may be due to the numerous changes in
the neuroendocrine system, which results in a self-perpetuating cycle.
[64][65][66][67]
Studies have suggested the initial
weight loss such as dieting may be the triggering factor in developing AN in some cases, possibly because of an
already inherent predisposition toward AN. One study reported cases of AN resulting from unintended weight loss that
resulted from varied causes, such as a parasitic infection, medication side effects, and surgery. The weight loss itself
was the triggering factor.
[68][69]
Even though anorexia does not affect males in comparison to females, studies have
shown that males with a female twin have a higher chance of getting anorexia. Therefore anorexia may be linked to
parental exposure to female hormones.
[70]

[edit]Biological
Obstetric complications: various prenatal and perinatal complications may factor into the development of anorexia
nervosa, such as maternal anemia, diabetes mellitus, preeclampsia,placental infarction,
and neonatal cardiac abnormalities. Neonatal complications may also have an influence on harm avoidance, one
of the personality traits associated with the development of AN.
[71][72]

Genetics: anorexia nervosa is believed to be highly heritable, with estimated inheritance rates ranging from 56%
to 84%.
[73][74][75]
Association studies have been performed, studying 128 different polymorphisms related to
43 genes including genes involved in regulation of eating behavior, motivation and reward mechanics, personality
traits and emotion. Consistent associations have been identified for polymorphisms associated with agouti-related
peptide, brain derived neurotrophic factor, catechol-o-methyl transferase, SK3 and opioid receptor delta-1.
[76]
In
one study, variations in the norepinephrine transporter gene promoter were associated with restrictive anorexia
nervosa, but not binge-purge anorexia.
[77]
Recent studies have advanced the theory that the sex difference in
incidence and the common onset at the age of puberty may reflect an abnormal response of the brain to anorexic
(feeding suppressing) effects of the female sex hormone, estrogen.
[78]
This viewpoint has been recently supported
by a report that abnormal forms of the estrogen receptor are more common in women with anorexia nervosa of
the restricting type.
[79]

epigenetics: Epigenetic mechanisms: are means by which genetic mutations are caused by environmental
effects that alter gene expression via methods such as DNA methylation, these are independent of and do
not alter the underlying DNA sequence. They are heritable, as was shown in the verkalix study, but also
may occur throughout the lifespan, and are potentially reversible. Dysregulation
of dopaminergic neurotransmission and Atrial natriuretic peptide homeostasis resulting from epigenetic
mechanisms has been implicated in various eating disorders.
[80]
"We conclude that epigenetic mechanisms
may contribute to the known alterations of ANP homeostasis in women with eating disorders."
[80][81]



Dysregulation of the dopamine andserotonin pathways has been implicated in the etiology, pathogenesis andpathophysiology of anorexia
nervosa.
[82][83][84][85]

serotonin dysregulation;
[86]
particularly high levels in those areas in the brain with the 5HT
1A
receptor a system
particularly linked to anxiety,mood and impulse control. Starvation has been hypothesized to be a response to
these effects, as it is known to lower tryptophan and steroid hormone metabolism, which might reduce serotonin
levels at these critical sites and ward off anxiety. Other studies of the 5HT
2A
serotonin receptor (linked to
regulation of feeding, mood, and anxiety), suggest that serotonin activity is decreased at these sites. There is
evidence that both personality characteristics associated with AN, and disturbances to the serotonin system are
still apparent after patients have recovered from anorexia.
[87]

Brain-derived neurotrophic factor (BDNF) is a protein that regulates neuronal development and neuroplasticity, it
also plays a role in learning,memory and in the hypothalamic pathway that controls eating behavior and
energy homeostasis. BDNF amplifies neurotransmitter responses and promotes synaptic communication in
the enteric nervous system. Low levels of BDNF are found in patients with AN and some comorbid disorders such
as major depression.
[88][89]
Exercise increases levels of BDNF
[90]

leptin and ghrelin; leptin is a hormone produced primarily by the fat cells in white adipose tissue of the body it has
an inhibitory (anorexigenic) effect on appetite, by inducing a feeling of satiety. Ghrelin is an appetite inducing
(orexigenic) hormone produced in the stomach and the upper portion of the small intestine. Circulating levels of
both hormones are an important factor in weight control. While often associated with obesity both have been
implicated in the pathophysiology of anorexia nervosa and bulimia nervosa.
[91]

cerebral blood flow (CBF); neuroimaging studies have shown reduced CBF in the temporal lobes of anorectic
patients, which may be a predisposing factor in the onset of AN.
[92]

autoimmune system; Autoantibodies against neuropeptides such as melanocortin have been shown to affect
personality traits associated with eating disorders such as those that influence appetite and stress responses.
[93]

Infections: Some people are hypothesized to have developed anorexia abruptly as a reaction to a streptococcus
or mycoplasma infection. PANS is an acronym for Pediatric acute-onset neuropsychiatric syndrome, a hypothesis
describing children who have abrupt, dramatic onset of obsessive-compulsive disorder (OCD) or anorexia
nervosa coincident with the presence of two or more neuropsychiatric symptoms.
[94]

Nutritional deficiencies
Zinc deficiency may play a role in anorexia. It is not thought responsible for causation of the initial illness but
there is evidence that it may be an accelerating factor that deepens the pathology of the anorexia. A 1994
randomized, double-blind, placebo-controlled trial showed that zinc (14 mg per day) doubled the rate of body
mass increase compared to patients receiving the placebo.
[95]

[edit]Environmental
Sociocultural studies have highlighted the role of cultural factors, such as the promotion of thinness as the ideal
female form in Western industrialized nations, particularly through the media. There is a necessary connection
between anorexia nervosa and culture and whether culture is a cause, a trigger, or merely a kind of social address or
envelope which determines in which segments of society or in which cultures anorexia nervosa will appear. The strong
thesis of this connection is that culture acts as a cause by providing a blueprint for anorexia nervosa. A moderate
thesis is that a specific cultural factors trigger the illness which is determined by many factors including family
interactions, individual psychology, or biological predisposition. Culture change can trigger the emergence of anorexia
in adolescent girls from immigrant families living in highly industrialized Western Societies.
[96]
A recent epidemiological
study of 989,871 Swedish residents indicated that gender, ethnicity and socio-economic status were large influences
on the chance of developing anorexia, with those with non-European parents among the least likely to be diagnosed
with the condition, and those in wealthy, white families being most at risk.
[97]
People in professions where there is a
particular social pressure to be thin (such as models and dancers) were much more likely to develop anorexia during
the course of their career,
[98]
and further research has suggested that those with anorexia have much higher contact
with cultural sources that promote weight-loss.
[99]

Anorexia nervosa is more likely to occur in a person's pubertal years, especially for girls.
[100]
Female students are 10
times more likely to suffer from anorexia nervosa than male students. According to a survey of 1799 Japanese female
high school students, "85% who were a normal weight wanted to be thinner and 45% who were 1020% underweight
wanted to be thinner."
[101]
Teenage girls concerned about their weight and who believe that slimness is more attractive
among peers trend to weight-control behaviors. Teen girls are learning from each other to consume low-caloric, low-
fat foods and diet pills. This results in lack of nutrition and a greater chance of developing anorexia nervosa.
[102]

It has also been noted that anorexia nervosa is more likely to occur in populations in which obesity is more prevalent.
It has been suggested that anorexia nervosa results from a sexually selected evolutionary drive to appear youthful in
populations in which size becomes the primary indicator of age.
[103]

There is also evidence to suggest that patients who have anorexia nervosa can be characterised
by alexithymia
[104]
and also a deficit in certain emotional functions. A research study showed that this was the case in
both adult and adolescent anorexia nervosa patients.
[105]

There is a high rate of reported child sexual abuse experiences in clinical groups of who have been diagnosed with
anorexia. The connection between eating disorders and abuse has been convincingly evidenced by a number of
studies, including one published in Epidemiology (and strengthened by blind hypothesis survey), which showed in a
comparison of women with no history of eating disorders, women with a history of eating disorders were twice as likely
to have reported childhood sexual abuse.
[106]
While the joint effect of both physical and sexual abuse resulted in a
nearly 4-fold risk of eating disorders that met DSM-IV criteria.
[106]
It is thought that links between childhood abuse and
sexual abuse are complex, such as by influencing psychologic processes that increase a woman's susceptibility to the
development of an eating disorder, or perhaps by producing changes in psychobiologic process and neurotransmitting
function, associated with eating behaviour.
[106]

Recent efforts have been made to dispel some of the myths around anorexia nervosa and eating disorders, such as
the misconception that families, in particular mothers, are responsible for their daughter developing an eating
disorder.
[107]

[edit]Media effects
Media are among the principal social agents in many societies around the world. Television, magazines, newspapers,
radio, cinema, advertising, the Internet, and other so-called "new media" or "new technologies" are the principal
factors behind body dissatisfaction, concerns about weight, and disordered eating behaviour. Mass media
interventions frequently offer a distorted vision of the world, and it may be difficult for children and adolescents to
distinguish whether what they see is real or not, so that they are more vulnerable to the messages transmitted. Field,
Cheung, et al.'s survey of 548 preadolescent and adolescent girls found that 69% acknowledged that images in
magazines had influenced their conception of the ideal body, while 47% reported that they wanted to lose weight after
seeing such images.
[108]
There was also the survey by Utter et al. who studied 4,746 adolescent boys and girls
demonstrating the tendency of magazine articles and advertisements to activate weight concerns and weight
management behaviour. He discovered that girls who frequently read fashion and glamour magazines and girls who
frequently read articles about diets and issues related to weight loss were seven times more likely to practice a range
of unhealthy weight control behaviours and six times more likely to engage in extremely unhealthy weight control
behaviours (e.g., taking diet pills, vomiting, using laxatives, and using diuretics)
[108]
from magazines, websites that
stress the message of thinness as the ideal have surfaced the internet and has managed to embed itself as an
increasing source of influence. The possibility that pro-anorexia websites may reinforce restrictive eating and exercise
behaviours is an area of concern. Pro-anorexia websites contain images and writing that support the pursuit of an
ideal thin body image. Research has shown that these websites stress thinness as the ideal choice for women and in
some websites ideal images of muscularity and thinness for men
[109]
It has also been shown that women who had
viewed these websites at least once had a decrease in self-esteem and reports also show an increased likelihood of
future engagement in many negative behaviours related to food, exercise, and weight.
[109]
Evidence of the value of
thinness in majority U.S culture is found in Hollywood's elite and the media promotion of waif models in fashion and
celebrity circles (e.g. Nicole Richie, Mary Kate Olsen, and Kate Moss Lady Gaga
[110]
).
[edit]Relationship to autism
Since Gillberg's (1983 & 1985)
[112][113]
and others' initial suggestion of relationship between anorexia nervosa
and autism,
[114][115]
a large-scalelongitudinal study into teenage-onset anorexia nervosa conducted in Sweden
confirmed that 23% of people with a long-standing eating disorder are on the autism
spectrum.
[116][117][118][119][120][121][122]
Those on autism spectrum tend to have a worse outcome,
[123]
but may benefit from
the combined use of behavioural and pharmacological therapies tailored to ameliorate autism rather than anorexia
nervosa per se.
[124][125]
Other studies, most notably research conducted at the Maudsley Hospital, UK, furthermore
suggest that autistic traits are common in people with anorexia nervosa; shared traits include, e.g., poor executive
function, autism quotient score, central coherence, theory of mind, cognitive-behavioural flexibility, emotion regulation
and understanding facial expressions.
[126][127][128][129][130][131]

Zucker et al. (2007) proposed that conditions on the autism spectrum make up the cognitive
endophenotype underlying anorexia nervosa and appealed for increased interdisciplinary collaboration (see figure to
right).
[111]
A pilot study into the effectiveness cognitive behaviour therapy, which based its treatment protocol on the
hypothesised relationship between anorexia nervosa and an underlying autistic like condition, reduced perfectionism
and rigidity in 17 out of 19 participants.
Diagnosis
[edit]Medical
The initial diagnosis should be made by a competent medical professional. There are multiple medical conditions,
such as viral or bacterial infections, hormonal imbalances, neurodegenerative diseases and brain tumors which may
mimic psychiatric disorders including anorexia nervosa. According to an in depth study conducted by psychiatrist
Richard Hall as published in the Archives of General Psychiatry:
Medical illness often presents with psychiatric symptoms.
It is difficult to distinguish physical disorders from functional psychiatric disorders on the basis of psychiatric
symptoms alone.
Detailed physical examination and laboratory screening are indicated as a routine procedure in the initial
evaluation of psychiatric patients.
Most patients are unaware of the medical illness that is causative of their psychiatric symptoms.
The conditions of patients with medically induced symptoms are often initially misdiagnosed as a functional
psychosis.
[133][134]

Complete Blood Count (CBC): a test of the white blood cells. red blood cells and platelets used to assess the
presence of various disorders such as leukocytosis, leukopenia, thrombocytosisand anemia which may result
from malnutrition.
[135]

urinalysis: a variety of tests performed on the urine used in the diagnosis of medical disorders, to test for
substance abuse, and as an indicator of overall health
[136]

ELISA: Various subtypes of ELISA used to test for antibodies to various viruses and bacteria such as Borrelia
burgdoferi (Lyme Disease)
[137]

Western Blot Analysis: Used to confirm the preliminary results of the ELISA
[138]

Chem-20: Chem-20 also known as SMA-20 a group of twenty separate chemical tests performed on blood serum.
Tests include cholesterol, protein and electrolytes such as potassium,chlorine and sodium and tests specific
to liver and kidney function.
[139]

glucose tolerance test: Oral glucose tolerance test (OGTT) used to assess the body's ability to metabolize
glucose. Can be useful in detecting various disorders such as diabetes, aninsulinoma, Cushing's
Syndrome, hypoglycemia and polycystic ovary syndrome
[140][141]

Secritin-CCK Test: Used to assess function of pancreas and gall bladder
[142][143]

Serum cholinesterase test: a test of liver enzymes (acetylcholinesterase and pseudocholinesterase) useful as a
test of liver function and to assess the effects of malnutrition
[144]

Liver Function Test: A series of tests used to assess liver function some of the tests are also used in the
assessment of malnutrition, protein deficiency, kidney function, bleeding disorders, Crohn's Disease
[145]

Lh response to GnRH: Luteinizing hormone (Lh) response to gonadotropin-releasing hormone (GnRH): Tests the
pituitary glands' response to GnRh a hormone produced in the hypothalumus. Central hypogonadism is often
seen in anorexia nervosa cases.
[146]

Creatine Kinase Test (CK-Test): measures the circulating blood levels of creatine kinase an enzyme found in the
heart (CK-MB), brain (CK-BB) and skeletal muscle (CK-MM).
[147][148]

Blood urea nitrogen (BUN) test: urea nitrogen is the byproduct of protein metabolism first formed in the liver then
removed from the body by the kidneys. The BUN test is used primarily to testkidney function. A low BUN level
may indicate the effects of malnutrition.
[149]

BUN-to-creatinine ratio: A BUN to creatinine ratio is used to predict various conditions. High BUN/creatinine ratio
can occur in severe hydration, acute kidney failure, congestive heart failure, intestinal bleeding. A low
BUN/creatinine can indicate a low protein diet, celiac disease rhabdomyolysis, cirrhosis of the liver.
[150][151][152]

electrocardiogram (EKG or ECG): measures electrical activity of heart can be used to detect various disorders
such as hyperkalemia
[153]

electroencephalogram (EEG): measures the electrical activity of the brain. Can be used to detect abnormalities
such as those associated with pituitary tumors
[154][155]

Upper GI Series: test used to assess gastrointestinal problems of the middle and upper intestinal tract
[156]

Thyroid Screen TSH, t4, t3 :test used to assess thyroid functioning by checking levels of thyroid-stimulating
hormone (TSH), thyroxine (T4), and triiodothyronine (T3)
[157]

Parathyroid hormone (PTH) test: tests the functioning of the parathyroid by measuring the amount of (PTH) in the
blood. Test is used to diagnose parahypothyroidism. PTH also controls the levels of calcium and phosphorus in
the blood (homeostasis).
[158]

barium enema: an x-ray examination of the lower gastrointestinal tract
[159]

neuroimaging; via the use of various techniques such as PET scan, fMRI, MRI and SPECT imaging should be
included in the diagnostic procedure for any eating disorder to detect cases in which a lesion, tumor or other
organic condition has been either the sole causative or contributory factor in an eating disorder.
Treatment
There is no conclusive evidence that any particular treatment for anorexia nervosa work better than others, however,
there is enough evidence to suggest that early intervention and treatment are more effective.
[196]
Treatment for
anorexia nervosa tries to address three main areas.
Restoring the person to a healthy weight;
Treating the psychological disorders related to the illness;
Reducing or eliminating behaviours or thoughts that originally led to the disordered eating.
[197]

Although restoring the person's weight is the primary task at hand, optimal treatment also includes and monitors
behavioral change in the individual as well.
[23]
Not all anorexia nervosa patients recover completely. About 20% of the
patients develop anorexia nervosa as a chronic disorder.
[198]
If anorexia nervosa is not treated, serious complications
such as heart conditions and kidney failure can initiate and eventually lead to death. "As many as 6 percent of people
with the disorder die from causes related to it."
[199]

[edit]Dietary
Diet is the most essential factor to work on in patients with anorexia nervosa, and must be tailored to each patient's
needs. Initial meal plans may be low in calories, about 1200, in order to build comfort in eating, and then food amount
can gradually be increased. Food variety is important when establishing meal plans as well as foods that are higher in
energy density. Other more specific dietary treatments are listed below.
[200]

Zinc supplementation has been shown in various studies to be beneficial in the treatment of AN even in patients
not suffering from zinc deficiency, by helping to increase weight gain.
[201][202][203]
Patients with anorexia nervosa
have a high likelihood of being zinc deficient, and this probability increases if they are vegetarians. Vegetarianism
is adapted by many patients with eating disorders because it is widely acclaimed as healthy and easy to manage
calorie intake.
[204]
Sufficient Zinc must be available during recovery, and normal zinc levels were seen in the Notre
Dame study to increase weight gain at a faster rate. Zinc supplementation can also help reduce reproductive
issues for patients with anorexia nervosa. Leptin, a hormone regulating hunger and metabolism, levels decrease
from zinc deficiency and even more with patients due to the reduction in size of adipose tissue. Reproductive
tissues have recently been discovered to contain leptin receptors, thus a decrease in leptin concentration would
lead to a lower rate of fertility. Unfortunately, despite the connection to weight gain and reproduction, zinc
supplementation seems to be largely under-appreciated and many do not consider zinc deficiency as an
important factor in regard to anorexia nervosa.
[205]

Calories Patients must be fed adequate calories at a measured pace for improvement of their condition to occur.
The best level for calorie intake is to start by providing 1200 to 1500 calories daily and increasing this amount by
500 each day. This process should continue until the level of 4000 calories (for male patients) or 3500 calories
(for female patients) This system should also decrease effects such as apathy, lethargy, and food-related
obsessions.
[206]

Essential fatty acids:The omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA)
have been shown to benefit various neuropsychiatric disorders. There was reported rapid improvement in a case
of severe AN treated with ethyl-eicosapentaenoic acid (E-EPA) and micronutrients.
[207]
DHA and EPA
supplementation has been shown to be a benefit in many of the comorbid disorders of AN including: attention
deficit/hyperactivity disorder (ADHD), autism, major depressive disorder (MDD),
[208]
bipolar disorder, and
borderline personality disorder. Accelerated cognitive decline and mild cognitive impairment (MCI) correlate with
lowered tissue levels of DHA/EPA, and supplementation has improved cognitive function.
[209][210]

Nutrition counseling
[211][212]

Medical Nutrition Therapy;(MNT) also referred to as Nutrition Therapy is the development and provision of a
nutritional treatment or therapy based on a detailed assessment of a person's medical history, psychosocial
history, physical examination, and dietary history.
[213][214][215]

[edit]Medication
Olanzapine: has been shown to be effective in treating certain aspects of AN including to help raise the body
mass index and reduce obsessionality, including obsessional thoughts about food.
[216][217]
However, its primary
usefulness is that it is one of the most potent appetite stimulants known, and causes the body to preferentially
store fat.
[edit]Therapy
Cognitive behavioral therapy (CBT) CBT is an evidence based approach which in studies to date has shown to be
useful in adolescents and adults with anorexia nervosa.
[218][219][220]
Components of using CBT with adults and
adolescents with anorexia nervosa have been outlined by several professionals as:
the therapist focuses on using cognitive restructuring to modify distorted beliefs and attitudes about the
meaning of weight, shape and appearance
[221]

specific behavioral techniques addressing the normalization of eating patterns and weight restorations,
examples of this include the use of a food diary, meal plans, and incremental weight gain
[221]

cognitive techniques such as restructuring, problem solving, and identification and expression of affect
[221]

When using CBT with adolescents and children with AN, several professionals have expressed concerns
about the minimum age and level of cognition necessary for implementing cognitive behavioral
techniques.
[221]
Modified versions and elements of CBT can be implemented with children and
adolescents with AN. Such modifications may include the use of behavioral experiments to disconfirm
distorted beliefs and absolutistic thinking in children and adolescents.
[221]

Acceptance and commitment therapy: A type of CBT, has shown promise in the treatment of AN" participants
experienced clinically significant improvement on at least some measures; no participants worsened or lost
weight even at 1-year follow-up."
[222]

Cognitive Remediation Therapy (CRT): is a cognitive rehabilitation therapy developed at King's College in
London designed to improve neurocognitive abilities such as attention, working memory, cognitive
flexibility and planning, and executive functioning which leads to improved social functioning.
Neuropsychological studies have shown that patients with AN have difficulties in cognitive flexibility. In
studies conducted at Kings College
[223]
and in Poland with adolescents CRT was proven to be beneficial in
treating anorexia nervosa,
[223]
in the United States clinical trials are still being conducted by the National
Institute of Mental Health
[224]
on adolescents age 1017 and Stanford University in subjects over 16 as a
conjunctive therapy with Cognitive behavioral therapy.
[225]

Family therapy: Family therapy has been reported to be more successful than individual therapy in most
treatment trials.
[23]
There are various forms of family-based therapy (FBT) that have been proven to work in
the treatment of adolescent AN including "conjoint family therapy" (CFT), in which the parents and child are
seen together by the same therapist, "separated family therapy" (SFT) in which parents and child attend
therapy separately with different therapists. "Eisler's cohort show that, irrespective of the type of FBT, 75% of
patients have a good outcome, 15% an intermediate outcome ...".
[226][227]
Proponents of Family therapy for
adolescents with AN assert that it is important to include parents in the adolescent's treatment.
[228]

Several components of Family therapy for patients with AN are:
the family is seen as a resource for the adolescent
[221]

anorexia nervosa is reframed in benign, non blaming terms
[221]

directives are provided to parents so that they may take charge of their child or adolescent's eating
routine
[221]

a structured behavioral weight gain program is implemented
[221]

after weight gain, control over eating is gradually returned to the child or adolescent
[221]

as the child or adolescent begins to eat and gain weight, the therapeutic focus broadens to include family
interaction problems, growth and autonomy issues and parent child conflicts
[221]

Maudsley Family Therapy: A 4 to 5 year follow up study of the Maudsley approach, a manualized model,
showed full recovery at rates up to 90%.
[229]
Although this model may work well for parents and children,
critics claim that it has the potential in an intimate relationship to create power struggles and may disrupt
equal partnerships.
[230]

[edit]Alternative medicine
Yoga: In preliminary studies individualized yoga treatment has shown positive results for use as an
adjunctive therapy to standard care. The treatment was shown to reduce eating disorder symptoms,
including food preoccupation, which decreased immediately after each session. Scores on the Eating
Disorder Examination decreased consistently over the course of treatment.
[

Some symptoms of vitamin D toxicity are a result of hypercalcemia (an elevated level ofcalcium in the
blood) caused by increased intestinal calcium absorption. Vitamin D toxicity is known to be a cause
of high blood pressure. Gastrointestinal symptoms of vitamin D toxicity can include anorexia, nausea,
and vomiting.

Vitamin D deficiency is a nutritional disorder characterized in adults by softening of the bones. In children it manifests
as rickets and in adults as osteomalacia.

Vitamin D is an essential nutrient that increases serum calcium levels by facilitating calcium absorption and mobilizing
calcium from bone. It also absorbs calcium and phosphorous from the diet. Without vitamin D, these minerals are not
absorbed in sufficient quantities. Because calcium and phosphorous are important in forming and maintaining healthy
bones and teeth, a deficiency in vitamin D has a profound effect on these structures.

Vitamin D deficiency is a relatively rare condition since it is found in many foods such as fortified milk, margarine,
eggs, liver, fish, and fish oils. The body can also make vitamin D when the skin is exposed to sunlight. A lack of
vitamin D in the diet is usually only seen in strict vegetarians (vegans) who avoid all animal products including dairy
products and eggs. Individuals who avoid exposure to sunlight or wear protective sunscreen may limit the body's
ability to make vitamin D, thereby increasing the need to rely on dietary sources. Another cause of vitamin D
deficiency is an inability of the body to absorb the vitamin during digestion (malabsorption) or an inability to process
the vitamin once it is absorbed. These individuals may experience a deficiency despite a healthy, balanced diet and
normal sun exposure. Certain medications used to treat seizures can also cause vitamin D deficiency. The
recommended daily allowance (RDA) for vitamin D is 400 IU.
Risk: The risk of developing osteomalacia is higher in those who are housebound, institutionalized, elderly, poor, or required by
custom to be completely covered when outdoors. Those with dark skin are also at increased risk. Certain diseases of the kidney,
pancreas, liver, intestines, or stomach may also increase the risk of vitamin D deficiency. Alcoholics, individuals with eating
disorders such as anorexia nervosa or bulimia nervosa, and those who follow diets that severely limit certain foods (fad diets) have
a greater risk of developing vitamin D deficiency. Individuals who abuse laxatives are also at increased risk.
Incidence and Prevalence: The overall incidence of osteomalacia is 1 in every 1,000 individuals. Pregnancy and breastfeeding
increase a woman's need for vitamin D and therefore increase the risk of deficiency. Women are affected slightly more often than
men.