ArticlePDF Available

Abstract and Figures

There is a commonly held view that eating disorders are lifestyle choice. Eating disorders are actually serious and often fatal illnesses, obsessions with food, body weight, and shape may also signal an eating disorders. Common eating disorders include anorexia nervosa, bulimia nervosa, night-eating syndrome, eating disorders not otherwise specified and binge-eating disorders. Eating disorders occur in men and women, young and old, rich and poor and from all cultural backgrounds; they result in about 7000 death a year as of 2010, making them the mental illnesses with the highest mortality rate. The chance for recovery increases the earlier they are detected, therefore, it is important to be aware of some of the warning signs of an eating disorder. In this review, different types of eating disorder, their side effects, complications and treatments are discussed.
Content may be subject to copyright.
Overview on eating disorders
Wissam Zam1, Reham Saijari1, Ziad Sijari2
1 Department of Analytical and Food Chemistry, Faculty of Pharmacy, Al-Andalus University for Medical Sciences, Syrian Arab
Republic - E-mail:; 2 Department of Periodontology and Implantology, Dental school, University of
Turin, Italy
Summary. ere is a commonly held view that eating disorders are lifestyle choice. Eating disorders are actu-
ally serious and often fatal illnesses, obsessions with food, body weight, and shape may also signal an eating
disorders. Common eating disorders include anorexia nervosa, bulimia nervosa, night-eating syndrome, eat-
ing disorders not otherwise specified and binge-eating disorders. Eating disorders occur in men and women,
young and old, rich and poor and from all cultural backgrounds; they result in about 7000 death a year as of
2010, making them the mental illnesses with the highest mortality rate. e chance for recovery increases
the earlier they are detected, therefore, it is important to be aware of some of the warning signs of an eating
disorder. In this review, different types of eating disorder, their side effects, complications and treatments are
Key words: eating disorders, types, side effects, complications, treatments
Progress in Nutrition 2018; Vol. 20, Supplement 2: 29-35 DOI: 10.23751/pn.v20i2-S.6970 © Mattioli 1885
Whether it is the effect of the media, family or friends,
the number of eating disorders has significantly increased
and they are becoming more and more prevalent. ere are
five classifications of eating disorders: anorexia, bulimia,
binge eating disorder (BED), eating disorders not other-
wise specified (EDNOS) and night eating syndrome (1).
Over seven million girls and women and one million boys
and men will suffer from an eating disorder in their lifetime.
Up to 3.7% of females will be diagnosed with anorexia ner-
vosa and an estimated 4.2% will have bulimia nervosa (2).
e majority of adolescent patients seen in referral centers
fit into a third category (EDNOS) and does not fit strict
criteria for either anorexia or bulimia (3). Nineteen percent
of college-aged females are bulimic; many go undiagnosed
until much later. At the other end of the spectrum, 1% to
5% of the population falls into the category of binge eat-
ing disorder, not yet an approved psychiatric diagnosis (4).
Anorexics are more likely to be female (90%-95%); 80%
of bulimics are female and 60% of BEDs are female (5).
Eating disorders begin early, with 10% being diagnosed in
children less than 10 years of age. One third of patients
are diagnosed as preteens and adolescents up to age 15. In
total, 86% of patients are diagnosed with eating disorders
before the age of 20 (6).
Etiology of Eating Disorders
e eating disorders have traditionally been viewed as
sociocultural in origin. However, recently it was found that
genetics tend to have a strong influence on these disorders
(7). Current research demonstrates that eating disorder
symptoms may be as common or more common among
certain ethnic groups (Asians, blacks, and Hispanics) when
compared with whites (8). ere was no difference found
in dieting and restraint scores between Asian, Latino, and
white adolescent girls and boys (9) and no difference in
binging or BED in obese patients who sought to lose
weight with bariatric surgery (10). However, an analysis of
18 studies (1987-2001) concluded that African-American
women were less likely than white women to have an eat-
ing disorder (11). As well, a study in school age girls dem-
W. Zam, R. Saijari, Z. Sijari
onstrated that Native American girls had higher rates of
restricting/purging and dieting than white or nonwhite/
non-Native American populations (12).
Types of Eating Disorders
1. Anorexia nervosa (AN)
Anorexia nervosa is a highly distinctive serious
mental disorder. It can affect individuals of all ages,
sexes, sexual orientations, races, and ethnic origins;
however, adolescent girls and young adult women are
particularly at risk (13, 14). e disorder involves the
fear of gaining weight, having a distorted body im-
age, a refusal to maintain normal weight, and the use
of extreme measures to keep the weight off. Anorexia
is typically diagnosed after a person is 25-30 percent
below the normal weight for three months or more (15).
Additionally, cognitive and emotional functioning are
markedly disturbed in people with this disorder (16).
Typically, two sub-types of anorexia are identified.
First, restricting-type anorexics (R-AN) lose weight
purely by dieting and exercising without binge eating
or purging. Second, binge-eating/purging-type anorex-
ics (BP-AN) also restrict their food intake and exercise
to lose weight, but periodically engage in binge eating
and/or purging (17).
Anorexia is often associated with denial of illness
and resistance to treatment. Consequently it is difficult
to engage individuals with AN in treatment, including
nutritional restoration, and weight normalization (18).
e physical signs and effects of anorexia are presented
in figure 1.
2. Bulimia nervosa (BN)
Bulimia nervosa is a serious, potentially life-threat-
ening eating disorder. It is characterized by a cycle of
bingeing and compensatory behaviors such as self-in-
duced vomiting designed to undo or compensate for
the effects of binge eating (19). Patients diagnosed with
bulimia nervosa follow closely with patients diagnosed
with binge-purge anorexia (1). Bulimia is diagnosed if
the binge-purge cycle occurs at least two times a week.
e act of purging can cause severe damage to the es-
ophagus and teeth and it can also cause the gag reflex to
be less sensitive (1).
Non-Purging type of bulimia is also diagnosed and
is characterized by using other inappropriate methods
of compensation for binge episodes, such as excessive
exercising or fasting. In these cases, the typical forms of
purging, such as self-induced vomiting, are not regularly
utilized (20). e physical signs and effects of bulimia
nervosa are presented in figure 2.
Figure 1. Physical signs and effects of anorexia nervosa Figure 2. Physical signs and effects of bulimia nervosa
Overview on eating disorders 31
3. Binge-eating disorders (BED)
According to the Diagnostic and Statistical Manual
of Mental Disorders (DSM), 5th edition, binge-eating
disorder is defined by several criteria (21). Individuals
must report consuming an amount of food that is defi-
nitely larger than what most people would eat in a simi-
lar period of time under similar circumstances in addi-
tion to experiencing a loss of control over one’s eating
behavior during this time (21). In addition, at least three
of the following characteristics must also be present:
summing food much more rapidly than normal; eating
food until uncomfortably full; consuming large amounts
of food when not feeling physically hungry; consum-
ing food alone to avoid embarrassment; or feeling dis-
gusted, depressed, or guilty after the eating event (22).
e diagnosis also requires that a significant amount of
distress be associated with the binge episodes, which
must occur at least once per week for 3 months or more.
Lastly, the disorder must not be accompanied by any
regular compensatory behavior, nor should the binge
eating occur solely during an episode of bulimia nervosa
or anorexia nervosa (22). e physical signs and effects
of binge-eating disorder are presented in figure 3.
4. Eating disorders not otherwise specified (EDNOS)
Eating disorders not otherwise specified is much
used by clinicians yet largely ignored by researchers. It
is the category for disorders that do not meet the crite-
ria for any other specific eating disorder and accounts
for about 50% of eating disorders (23, 24). Although
patients with EDNOS do not meet the diagnostic cri-
teria for either AN or BN, if the disordered behaviors
continue, they may progress to frank AN or BN. For
example, some patients may have met all criteria for
AN with the exception of missing three consecutive
menstrual periods, or they may be of normal weight
and purge without bingeing. Although patients may not
present with medical complications, they often present
with medical concerns and treatment modality depend
on the severity of impairment and the symptoms (24).
Fairburn and Bohn described two subtypes as
particularly common for EDNOS. e first are in-
stances where the individual’s presentation closely re-
sembles AN or BN nervosa, but he or she just fails to
meet the diagnostic thresholds. e second subtype are
cases in which the clinical features of AN and BN are
combined in ways other than in the two recognized
syndromes (25).
5. Night-eating syndrome (NES)
e other prominent form of disordered eat-
ing related to overweight and obesity is NES. NES
was first described by Stunkard et al. among a group
of individuals with obesity seeking weight loss treat-
ment (26). ey reported that those with the syndrome
consumed a large majority of their caloric intake (25%
or more) at a time when individuals without obesity
would not be eating. In addition, the patients expe-
rienced insomnia and morning anorexia. Attention
to NES was neglected until the late 1990’s, when the
focus of eating-related research shifted in response to
the growing prevalence of obesity in the United States
(27). Since this time, the definition of NES has varied.
For example, in later years, Stunkard’s definition was
expanded to include nocturnal ingestions (28).
NES is characterized by recurrent episodes of
night eating, which is described as either excessive
food consumption in the evening (after dinnertime,
i.e., evening hyperphagia) or eating after awaken-
ing from sleep (i.e., nocturnal ingestions). NES is
also characterized by at least three of the following
symptoms: morning anorexia, the presence of a strong
urge to eat between dinner and sleep and/or during
Figure 3. Physical signs and effects of binge eating disorder
W. Zam, R. Saijari, Z. Sijari
the night, sleep onset and/or maintenance insomnia,
frequently depressed mood or mood worsening in
the evening, and a belief that one cannot get back to
sleep without eating (28, 29). In order to be diagnosed
with NES, individuals must be aware of and be able
to recall the eating episodes. ese symptoms must
also cause significant distress and/or impairment in
functioning and not be better explained by external
factors or another disorder, such as a sleeping disor-
der or other disordered eating pattern (30). NES is
classified in the Diagnostic and Statistical Manual of
Mental Disorders, Fifth Edition (DSM5) as an “other
specified feeding or eating disorder.”
Side effects of eating disorders
1. Osteoporosis
Anorexics are at increased risk of osteoporosis
due to lowered intake, being under- weight, and de-
creased estrogen related to amenorrhea. Calcium sup-
plementation in pubertal girls may increase peak bone
mass (31). Calcium supplementation may increase
the beneficial effects of physical activity on bone (32).
Deficiency of vitamin D in young people can affect
their ability to reach peak bone mass (33). Special risks
in eating disorder patients for osteoporosis include the
Anorexic girls (aged 13-23 years) who also suer
from depression may be at higher risk for osteo-
porosis than those without depression; the rea-
son for this finding is not known (34).
. Amenorrhea in anorexic women and young girls
may indicate the onset of estrogen deficiency,
which can have a negative effect on bone density
and peak bone mass.
Under-nutrition can aect bone density through
deficiency of anabolic hormones such as insulin
like growth factor I; in addition, low weight is
also a risk factor for lowered bone mass (35).
Data indicate that osteoporosis could be con-
sidered a risk factor for periodontal disease pro-
gression, especially in subjects with preexisting
periodontitis (36).
2. Taste receptors damaged
For all four taste stimuli (sweet, salty, sour, and
bitter), intensities on the palate have been found to be
lower in bulimic subject than in control subject (37),
reduced taste sensitivity affected only the palate and
not the whole mouth. Specifically, taste receptors lo-
cated on the palate may become damaged because
vomit is directed toward the roof of the mouth during
purging (37, 38).
3. Oral Health
e association between oral pathology and eat-
ing disorders is most clearly established in cases with
frequent self-induced vomiting, regardless of whether
the diagnosis is anorexia or bulimia, and is charac-
terized by dental erosion on palatal surfaces. Dental
caries and dry mouth secondary to salivary gland
dysfunction also occur (39). Gingival inflammatory
changes due to vitamin C deficiency/scurvy are also
observed (40).
4. Others
ere were other side effects as well, including
decreased concentration and other cognitive changes;
physical changes that included decreased need for
sleep; gastrointestinal problems; dizziness; headaches;
noise and light sensitivity; weakness; fluid retention;
cold intolerance; and difficulties with hearing and
sight. ere was a 40% slowing of basal metabolic rate,
low body temperature, decrease in heart rate, and res-
piration (41).
Complications of eating disorders
No rehabilitation works 100% every time and a
risk of relapse is always present. Re-feeding is one of
the most prevalent complications characterized by the
inability of the body to cope with the extreme change
in metabolic function. e main signs of the re-feeding
syndrome are (42):
Hypophosphatemia, hypokalemia and hy-
Heart failure
Salt and water retention
Depletion of vitamins such as B1, B6
Overview on eating disorders 33
ese symptoms are caused by the change in me-
tabolism in the body from fat to carbohydrates. When
an anorexic patient starves themselves they are using
stored fat as the primary source of energy. But when
they start eating again their bodies can switch from
using stored fat as energy to using carbohydrates from
food again. is change will lead to insulin being re-
leased from the pancreas to aid in the uptake of glu-
cose. When the insulin is released cells will start to
increase the amount of glucose, phosphate, potassium,
magnesium and water that they take in (43).
To avoid re-feeding syndrome, levels of phospho-
rus, magnesium, potassium and calcium should be de-
termined for the first 5 days and every other day for
several weeks; electrocardiogram should be also per-
formed (18). If indicated, during the first days of re-
feeding, large amounts of multi-vitamins and minerals,
in particular potassium, thiamine, phosphate and mag-
nesium, should be provided. Again, strict monitoring
is needed to prevent vitamin A and D toxicity in case
of excessive supplements (44).
Types of treatment on eating disorders
1. Pharmacological treatments
Medications are generally useful for patients with
bulimia nervosa and BED. Common forms of phar-
macotherapy include antidepressants, antiepileptic
medications, anti-obesity, and stimulant medications
(45). For bulimia nervosa, antidepressant medications
are the primary pharmacologic treatment (46). e ev-
idence for the use of fluoxetine in the treatment of bu-
limia nervosa comes in the form of various case reports,
systematic studies, and double-blind, randomized pla-
cebo controlled trials (47). Tricyclic antidepressants
and monoamine oxidase inhibitors are also found to
be effective were also found to be more effective than
placebo in decreasing the binging and vomiting in
patients with bulimia nervosa (48). Ondansetron at
24mg/day is also reported to reduce binge eating and
self-induced vomiting in a small placebo-controlled
study of 29 patients with bulimia nervosa (49).
For BED, lisdexamfetamine is reported to be
generally well tolerated and effective, and is the first
medication to be indicated by the FDA for treatment
of BED (46). e anticonvulsant topiramate adminis-
tered at a dose of 25 to 600mg daily is found to signifi-
cantly reduce binge frequency and weight (50).
For anorexia nervosa, there is limited evidence
supporting benefits of medications and different treat-
ments were used for treating the accompanying symp-
toms. Olanzapine appears to demonstrate some ben-
efit for weight gain and transdermal administration of
hormonal agents is also being explored for improving
bone health in anorexia nervosa (46).
2. Family-based treatment (FBT)
Although early models of family therapy for AN
focused on addressing problematic aspects of the fam-
ily that were believed to contribute to the development
and maintenance of AN (51, 52), more recent models
have focused on reducing blame and utilizing the fam-
ily as a resource for recovery (53). In FBT, parents play
a central role in restoring their child’s health, and sib-
lings are encouraged to provide emotional support to
their ill sibling. e FBT should happen in the home
during parental meal and needs the support of both
parents. If parents do not have a shared understanding
of how to undertake these tasks, they may uninten-
tionally undermine each other (54).
3. Inpatient
Inpatient treatment is usually for very seriously ill
patient who are usually the ones with cardiac or severe
psychological issues that might need special medical
attention throughout their treatment. ese patients
are fed by nasogastric feeding in order to reduce the
risk of re-feeding syndrome and insulin spikes that can
cause serious problems (55). Patients have also shown
that they have less abdominal distention, nausea, and
bloating (55). By being fed this way, doctors are able
to add in more necessary fat to the diet without the
patient objecting leading to a decreased hospital stay.
4. Outpatient
e standard nutritional treatment for outpatient
is progressive bolus oral feeding (55). is is when the
patient has a nutritionist set up a plan for what they
need to eat to meet their goal caloric intake as well as
nutritional needs. But some patients have had diges-
tive issues such as nausea, bloating and pain from re-
W. Zam, R. Saijari, Z. Sijari
turning to normal eating too quickly (55). e biggest
consequence of this form of treatment is that it can
lead to re-feeding syndrome and refusal to eat alto-
gether. Many patients will struggle with the idea of
eating solid food again especially enough to meet the
caloric intake goal needed to make them healthy.
Eating disorders affect not only the diagnosed pa-
tients, but the families surrounding them. ey can be
triggered by society trends, genetics, and family and can
develop during any stage in life, classified as a medi-
cal illness. Although these conditions are treatable, the
symptoms and consequences can be detrimental and
deadly if not addressed. ey commonly coexist with
other condition, such as anxiety disorder, substance
abuse, or depression. Eating disorders can lead to
heart and kidney problems and even death. Treatment
involves monitoring, talk therapy, nutritional coun-
seling, and sometimes medicines. People with eating
disorder suffer of osteoarthritis, Kidney failure, high
blood pressure, diarrhea, dizziness, etc. ere are many
complications that can arise with treatment such as re-
feeding syndrome and hypophosphatemia, which can
lead to patient distress or fatality. Eating disorders are
a lifelong battle even after treatment is completed.
1. Weiten W. Psychology themes & variations. 8th Ed. Las Vegas,
NV: University of Nevada W. 2011, 570p.
2. American Psychiatric Association Work Group on Eating
Disorders. Practice guideline for the treatment of patients with
eating disorders (revision). Amer J Psych. 2000; 157(Suppl. 1):
3. Merikangas KR, He J, Burstein M, et al. Lifetime prevalence of
mental disorders in U.S. adolescents: Results from the National
Comorbidity Study-Adolescent Supplement (NCS-A). J Am
Acad Child Adolesc Psychiatry. 2010; 49(10): 980-989.
4. Smink FRE, van Hoeken D, Hoek HW. Epidemiology of
Eating Disorders: Incidence, Prevalence and Mortality Rates.
Curr Psychiatry Rep. 2012; 14(4): 406–414.
5. Wade T, Keski-Rahkonen A, Hudson J. Epidemiology of eat-
ing disorders. In: Tsuang M, Tohen M. Textbook in Psychiatric
Epidemiology (3rd ed). New York: Wiley, 2011, 660p.
6. Stice E, Marti CN, Shaw H, Jaconis M. An 8-year longitu-
dinal study of the natural history of threshold, sub-threshold,
and partial eating disorders from a community sample of
adolescents. Journal of Abnormal Psychology. 2010; 118(3):
7. Wade B. e Genetics of Eating Disorders. Psychiatry
(Edgmont). 2004; 1(3): 18-25.
8. Shaw H, Ramirez L, Trost A, et al. Body image and eating
disturbances across ethnic groups: More similarities than dif-
ferences. Psych of Addic Behav. 2004; (18): 12-18.
9. Cachelin FM, Weiss JW, Garbanati JA. Dieting and its rela-
tionship to smoking, acculturation, and family environment
in Asian and Hispanic adolescents. Eating Disorders. 2004;
(11): 51-61.
10. Sanchez-Johnson L, Dymek M, Alverdy J, Le Grange D.
Binge eating and eating-related cognitions and behavior in
ethnically diverse obese women. Obesity Research. 2003;
(11): 1002-1009.
11. O’Neill SK. African American women and eating distur-
bances: A meta-analysis. Journal of Black Psychology. 2003;
(29): 3-16.
12. Lynch WC, Eppers KD, Sherrod JR. Eating attitudes of
Native American and white female adolescents: a comparison
of BMI-and age-matched groups. Ethnicity & Health. 2004;
(9): 253-266.
13. Zipfel S, Mack I, Baur LA, et al. Impact of exercise on energy
metabolism in anorexia nervosa. J Eat Disord 2013; (1): 37.
14. American Psychiatric Association. Diagnostic and statisti-
cal manual of mental disorders: DSM-5. Washington, DC:
American Psychiatric Association. 2013, 947p.
15. American Dietetic. Position of the American dietetic associa-
tion: Nutrition intervention in the treatment of anorexia ner-
vosa, bulimia nervosa, and other eating disorders. Journal of
the American Dietetic Association. 2007; 106(12): 2073-82.
16. Zipfel S, Giel K, Bulik C, Hay P, Schmidt U. Anorexia ner-
vosa: aetiology, assessment, and treatment. Lancet psychiatry,
2015; 2(12): 1099-111.
17. Kelly AC, Carter JC. Eating disorder subtypes differ in their
rates of psychosocial improvement over treatment. J Eat
Disord. 2014; 2: 2.
18. American Psychiatric Association: Treatment of patients with
eating disorders, 3rd ed. Am J Psychiatry. 2006; 163: 4-54.
19. Favaro A, Caregaro L, Tenconi E, Bosello R, Santonastaso P.
Time trends in age at onset of anorexia nervosa and bulimia
nervosa. Journal of Clinical Psychiatry. 2009; 70(12): 1715-21.
20. Ramacciotti CE, Coli E, Paoli R, et al. e relationship be-
tween binge eating disorder and non-purging bulimia ner-
vosa. Eat Weight Disord. 2005; 10(1): 8-12.
21. American Psychiatric Association. Diagnostic and Statistical
Manual of Mental Disorders. 5th ed. DSM-5. Washington
DC. 2013, 991p.
22. Stice E, Bohon C. Eating Disorders. In: Child and Adolescent
Psychopathology, 2nd Edition, Beauchaine , Linshaw S,
1st ed. New York: Wiley, 2012, 912.
23. Martha M, Levine P, Levine RL. Psychiatric Medication. In:
Treatment of Eating Disorders, 2010.
24. Spear BA. Eating Disorders. In: Handbook of Clinical
Nutrition, (4 Ed), 2006.
Overview on eating disorders 35
25. Fairburn CG, Bohn K. Eating disorder NOS (EDNOS): an
example of the troublesome “not otherwise specified” (NOS)
category in DSM-IV. Behav Res er. 2005; 43(6): 691–701.
26. Stunkard J, Grace WJ, Wolff HG. e night eating syndrome:
a pattern of food intake among certain obese patients. Am. J.
Med; 1955 (19): 78–86.
27. Birketvedt GS, Florholmen J, Sundsfjord J, et al. Behavioral
and neuroendocrine characteristics of the night-eating syn-
drome. JAMA. 1999; 282(7): 657-63.
28. Allison C, Lundgren D, O’reardon J, et al. Proposed diag-
nostic criteria for night eating syndrome. Int. J. Eat. Disord.
2010; (43): 241-247.
29. De Zwaan M, Marschollek M, Allison KC. e night eat-
ing syndrome (NES) in bariatric surgery patients. Eur. Eat.
Disord. Rev. 2015; (23): 426-434.
30. Howell MJ, Schenck CH, Crow SJ. A review of nighttime
eating disorders. Sleep Med Rev. 2009; 13(1): 23-34.
31. Dodiuk-Gad RP, Rozen GS, Rennert G, et al. Sustained ef-
fect of short-term calcium supplementation on bone mass in
adoles- cent girls with low calcium intake. Am J Clin Nutr.
2005; (81): 175-188.
32. Hemayattalab R. Effects of physical training and calcium
intake on bone mineral density of students with mental re-
tardation. Research in Developmental Disabilities. 2010; 31:
33. Calvo MS, Whiting SJ, Barton CN. Vitamin D intake: a
global perspective of current status. J Nutr. 2005; (135): 310-
34. Konstantynowicz J, Kadziela-Olech H, Kaczmarski M, et al.
J Clin Endocrinol Metab, 2005; (90): 5382-5.
35. Miller KK. Mechanisms by which nutritional disorders cause
reduced bone mass in adults. J Womens Health (Larchmt).
2003; (12): 145-150.
36. Esfahanian V, Shamami MS, Shamami MS. Relationship be-
tween Osteoporosis and Periodontal Disease: Review of the
Literature. J Dent (Tehran). 2012; 9(4): 256–264.
37. Garcia-Burgos D, Maglieri S, Vögele C, Munsch S. How
Does Food Taste in Anorexia and Bulimia Nervosa? A
Protocol for a Quasi-Experimental, Cross-Sectional Design
to Investigate Taste Aversion or Increased Hedonic Valence
of Food in Eating Disorders. Front Psychol. 2018; 9: 264.
38. Grabenhorst F, Rolls ET, Bilderbeck A. How cognition
modulates affective responses to taste and flavor: top-down
influences on the orbitofrontal and pregenual cingulate corti-
ces. Cereb. Cortex. 2008; 18, 1549–1559.
39. Frydrych AM, Davies GR, McDermott BM. Eating disor-
ders and oral health: a review of the literature. Aust Dental J.
2005; 50: 6-15.
40. Omori K, Hanayama Y, Naruishi K, et al. Overgrowth caused
by vitamin C deficiency associated with metabolic syndrome
and severe periodontal infection: a case report. Clin Case
Rep. 2014; 2(6): 286-95.
41. Latner JD, Wilson GT. Binge eating and satiety in bulimia
nervosa and binge eating disorder: effects of macronutrient
intake. Int J Eat Disord. 2004; 36(4): 402-15.
42. Gentile G, Lessa C, Cattaneo M. Metabolic and nutritional
needs to normalize body mass index by doubling the admis-
sion body weight in severe anorexia nervosa. Clinical Medi-
cine Insights: Case Reports. 2013; (6): 51-56.
43. Crook A, Hally V, Panteli V. e importance of the re-feed-
ing syndrome. Nutrition. 2001; 17(78): 632-637.
44. NICE: Core interventions in the treatment and management
of anorexia nervosa, bulimia nervosa and related eating disor-
ders (Clinical Guideline 9). London: National Collaborating
Centre for Medical Health; 2004.
45. Reas L, Grilo M. Pharmacological treatment of binge eating
disorder: up to date review and synthesis. Expert Opin. Phar-
macother. 2015; (16): 1463-1478.
46. Davis H, Attia E. Pharmacotherapy of eating disorders. Curr
Opin Psychiatry. 2017; 30(6): 452-457.
47. Zhu AJ, Walsh BT. Pharmacologic treatment of eating disor-
ders. Can J Psychiatry 2002; 47: 227-34.
48. Bacaltchuk J, Hay P. Antidepressants versus placebo for peo-
ple with bulimia nervosa. Cochrane Database Syst Rev. 2003;
(4): CD003391.
49. Faris PL, Kim SW, Meller WH, et al. Effect of decreasing
afferent vagal activity with ondansetron on symptoms of bu-
limia nervosa: a randomised, double-blind trial. Lancet. 2000;
355(9206): 792-7.
50. McElroy SL, Arnold LM, Shapira NA, et al. Topiramate in
the treatment of binge eating disorder associated with obe-
sity: a randomized, placebo-controlled trial. Am J Psychiatry.
2003; 160(2): 255-61.
51. Minuchin S, Rosman L, Baker L. Psychosomatic families:
Anorexia nervosa in context. Cambridge, MA: Harvard Uni-
versity Press.1978, 351p.
52. Stanton M, Welsh R. Systemic inking in Couple and Fam-
ily Psychology Research and Practice. Couple and Family
Psychology: Research and Practice 2012; 1 (1): 14 –30.
53. Eisler I, Dodge L, Wallis A. What’s new is old and what’s old
is new: e origins and evolution of eating disorders family
therapy. In: Loeb KL, Le Grange D, Lock J. Family therapy
for adolescent eating and weight disorders: New applications
New York, NY: Routledge/Taylor & Francis. 2015, 454.
54. Dimitropoulos G, Freeman E, Lock J, Le Grange D. Clini-
cian perspective on parental empowerment in family-based
treatment for adolescent anorexia nervosa. Journal of Family
erapy. 2017; 39(4): 537-562.
55. Agostino H, Erdstein J, Di Meglio G. Shifting paradigms:
Continuous nasogastric feeding with high caloric intakes in
anorexia nervosa. Journal of Adolescent Health. 2013; 53(5):
Wissam Zam
Department of Analytical and Food Chemistry,
Faculty of Pharmacy, Al-Andalus University for
Medical Sciences, Syrian Arab Republic
... [2] ED is a general term for several diseases such as anorexia nervosa, bulimia nervosa, and binge eating. [3] Individuals with ED have significantly lower health-related quality of life than individuals without ED. In the United States, it is estimated that 3.3 million healthy life years are lost yearly as a result of ED. [4,5] In Saudi Arabia, a study done in 2018 reported that 35% of female university students in Taif were at risk of ED. [6] This is considered extremely high compared with such western countries as the United States, where ED risk was reported as 11.6% and 5.7% among female and male university students, respectively. ...
Full-text available
Abstract: BACKGROUND: In Saudi Arabia, there is not much research on the risk of eating disorders and the influence of sociocultural factors on increasing the risk among university students. The objective of this study was to assess the prevalence of the risk of eating disorder (EDs) in King Abdulaziz University students, the influence of sociocultural factors, and any differences between males and females. MATERIALS AND METHODS: A cross-sectional study was conducted on 763 university students in Jeddah, Saudi Arabia. The data were collected in 3 months from February 2021 to April 2021. A self-administered Eating Attitude Test-26 scale was used to assess the risk of eating disorder among the students. The sociocultural attitude toward appearance questionnaire was used to measure the internalization of thinness, masculinity, and family, peer, and media attitude toward appearance. To test for statistical significance, t-test was used for continuous variables, whereas Ch-square test was performed for categorical variables. Logistic regression analysis were performed to determine factors associated with ED risk; all tests were performed at 0.05 significance level. RESULTS: The prevalence of the risk of eating disorder among the students was observed as 34%. The sociocultural attitude toward appearance was significantly higher among at risk of eating disorder students. The multiple logistic regression analysis showed that females are twice more likely to be at risk for eating disorder than males (2.25) with 95% confidence interval (1.50,3.39). Peer influence was significantly higher among males than females; however, females were significantly more influenced by the media than males. CONCLUSION: The prevalence of eating disorder risk in Saudi university students in Jeddah was observed as alarming and highly influenced by sociocultural factors; therefore, screening university students for eating disorder is very necessary. In addition, there should be media and health promotion campaigns on eating disorder and body image issues. Keywords: Body mass index, eating disorder risk, Saudi Arabia, sociocultural factors, university students
Full-text available
Introducción Antecedentes: La anorexia nerviosa (AN) y la bulimia nerviosa (BN) son enfermedades mentales graves y crónicas que afectan a un alto porcentaje de la población. Un número creciente de estudios han informado de alteraciones neuropsicológicas en esta población, que aparentemente contribuyen a la aparición y progresión del trastorno, y que repercuten en la eficacia del tratamiento y la recuperación. Metodología: El objetivo de esta Revisión Narrativa es resumir los hallazgos relativos al perfil neuropsicológico de las mujeres con AN y BN en diferentes fases de tratamiento. Resultados: La evidencia disponible sugiere que las mujeres con AN y BN presentan un perfil de déficits de cognición ejecutiva y social. Estos resultados son consistentes con la evidencia de los hallazgos de neuroimagen de alteraciones cerebrales estructurales en las áreas frontales y en los circuitos frontales-subcorticales. Conclusiones: El conocimiento de los perfiles neuropsicológicos de las mujeres con AN y BN ofrece información clave para entender la presentación clínica de esta población y los retos en la adherencia y beneficio del tratamiento. Los estudios futuros deberían explorar la eficacia de las intervenciones dirigidas a las deficiencias neuropsicológicas y cómo contribuyen al tratamiento habitual.
Full-text available
Background: Despite on-going efforts to better understand dysregulated eating, the olfactory-gustatory deficits and food preferences in eating disorders (ED), and the mechanisms underlying the perception of and responses to food properties in anorexia nervosa (AN) and bulimia nervosa (BN) remain largely unknown; both during the course of the illness and compared to healthy populations. It is, therefore, necessary to systematically investigate the gustatory perception and hedonics of taste in patients with AN and BN. To this end, we will examine whether aversions to the taste of high-calorie food is related to the suppression of energy intake in restricting-type AN, and whether an increased hedonic valence of sweet, caloric-dense foods may be part of the mechanisms triggering binge-eating episodes in BN. In addition, the role of cognitions influencing these mechanisms will be examined. Method: In study 1, four mixtures of sweet-fat stimuli will be presented in a sensory two-alternative forced-choice test involving signal detection analysis. In study 2, a full-scale taste reactivity test will be carried out, including psychophysiological and behavioral measures to assess subtle and covert hedonic changes. We will compare the responses of currently-ill AN and BN patients to those who have recovered from AN and BN, and also to those of healthy normal-weight and underweight individuals without any eating disorder pathology. Discussion: If taste response profiles are differentially linked to ED types, then future studies should investigate whether taste responsiveness represents a useful diagnostic measure in the prevention, assessment and treatment of EDs. The expected results on cognitive mechanisms in the top-down processes of food hedonics will complement current models and contribute to the refinement of interventions to change cognitive aspects of taste aversions, to establish functional food preferences and to better manage food cravings associated with binge-eating episodes. No trial registration was required for this protocol, which was approved by the Swiss ethics committee (CER-VD, n° 2016-02150) and the Ethics Review Panel of the University of Luxembourg.
Full-text available
It has been suggested that vitamin C deficiency/scurvy is associated with gingival inflammatory changes; however, the disorder is very infrequently encountered in the modern era. Here, we report a case of extensive gingival overgrowth caused by vitamin C deficiency associated with metabolic syndrome and severe periodontal infection.
Full-text available
Background Individuals with Anorexia Nervosa (AN) are renowned for their poor short- and long-term treatment outcomes. To gain more insight into the reasons for these poor outcomes, the present study compared patients with AN-R (restrictive subtype), AN-BP (binge-purge subtype), bulimia nervosa (BN), and eating disorder not otherwise specified (EDNOS) over 12 weeks of specialized eating disorders treatment. Eighty-nine patients completed the Eating Disorder Examination- Questionnaire (EDE-Q) and various measures of psychosocial functioning at baseline, and again after weeks 3, 6, 9, and 12 of treatment. Results Multilevel modeling revealed that, over the 12 weeks, patients with AN-BP and AN-R had slower improvements in global eating disorder pathology, shape concerns, and self-compassion than those with EDNOS and BN. Patients with AN-BP had slower improvements in shame, social safeness (i.e., feelings of warmth in one’s relationships), and received social support compared to those with AN-R, BN, and EDNOS. Conclusions These findings support the need for more effective and comprehensive clinical interventions for patients with AN and especially AN-BP. Results also highlight not-yet studied processes that might contribute to the poor outcomes AN patients often face during and after treatment.
Full-text available
Excessive physical activity is one of the most paradoxical features of anorexia nervosa (AN). However, there is individual variation in the degree of physical activity found in AN-patients. As a result, marked differences in energy expenditure may be expected. Furthermore, exercise has a positive impact on a variety of psychological disorders and the psychopathology may be different in AN displaying high exercise levels versus AN displaying low exercise levels. We analyzed the energy metabolism and psychological data in low-level exercise and high-level exercise AN-patients compared with healthy, age matched controls. REE was decreased in AN-patients compared with controls but not when adjusted for body surface area or lean body mass. No differences in TDEE between AN- patients and controls were observed. Subgroup analyses showed that the percentage of high-level AN- exercisers was higher compared with controls. This subgroup had increased resting EE, total daily EE and scored higher on depression and the EDI-item "Drive for thinness" compared with low-level AN-exercisers. We identified a significant subgroup of high-level AN-exercisers (66%) with consecutive increased energy requirements. An easy way for clinicians to assess the amount of exercise before and in the course of treatment is a single question in the established Eating Disorder Inventory-SC (EDI-SC).
Purpose of review: Medications are commonly prescribed in the treatment of eating disorders. In this review, we discuss relevant medications used for the treatment of bulimia nervosa, binge eating disorder (BED), and anorexia nervosa. We focus on recent research developments, where applicable, in addition to discussing important findings from older studies to provide a complete synopsis of the current evidence base for eating disorder treatment using pharmacologic agents. Recent findings: Medications are generally useful for patients with bulimia nervosa and BED. For bulimia nervosa, antidepressant medications are the primary pharmacologic treatment and limited new research has been completed. For BED, lisdexamfetamine is reported to be generally well tolerated and effective, and is the first medication to be indicated by the US Food and Drug Administration for treatment of BED. For anorexia nervosa, there is limited evidence supporting benefits of medications. Second-generation antipsychotics, particularly olanzapine, appear to demonstrate some benefit for weight gain in anorexia nervosa, although are not advised as a stand-alone treatment. Transdermal administration of hormonal agents is also being explored for improving bone health in anorexia nervosa. Summary: Although pharmacotherapy has established utility in bulimia nervosa and BED, further research on medications for the treatment of eating disorders, particularly anorexia nervosa, is necessary.
Anorexia nervosa is an important cause of physical and psychosocial morbidity. Recent years have brought advances in understanding of the underlying psychobiology that contributes to illness onset and maintenance. Genetic factors influence risk, psychosocial and interpersonal factors can trigger onset, and changes in neural networks can sustain the illness. Substantial advances in treatment, particularly for adolescent patients with anorexia nervosa, point to the benefits of specialised family-based interventions. Adults with anorexia nervosa too have a realistic chance of achieving recovery or at least substantial improvement, but no specific approach has shown clear superiority, suggesting a combination of re-nourishment and anorexia nervosa-specific psychotherapy is most effective. To successfully fight this enigmatic illness, we have to enhance understanding of the underlying biological and psychosocial mechanisms, improve strategies for prevention and early intervention, and better target our treatments through improved understanding of specific disease mechanisms.
The night eating syndrome (NES) has been included into the Diagnostic and Statistical Manual of Mental Disorders 5 as an example of an 'other-specified feeding or eating disorder'. The prevalence of NES has found to be higher in obese populations than in the general population and seems to rise with increasing body mass index. Recent studies suggest a prevalence of 2%-20% in bariatric surgery samples. Given that the core feature of this eating disorder may involve a shift in the circadian pattern of eating that disrupts sleep, and not the ingestion of objectively large amounts of food, it is a pattern that can continue after bariatric surgery. Nonetheless, symptoms of NES appear to decrease after weight loss surgery, and there is no evidence that pre-surgery NES negatively impacts weight loss following surgery. Prospective and longitudinal studies of the course of night eating symptoms are warranted using clear criteria and standardized assessment instruments. Copyright © 2015 John Wiley & Sons, Ltd and Eating Disorders Association.
This qualitative study explored which core principles of family-based treatment (FBT) for adolescents with anorexia nervosa (AN) are perceived as most necessary for FBT to be effective in clinical practice. Paediatric interdisciplinary teams were recruited to discuss the delivery of FBT in eating disorder programmes in Ontario, Canada (N = 6). Thematic analysis was used to analyze the data generated from focus groups. Three major themes emerged: (i) parental empowerment (PE) is the most salient principle of FBT; (ii) various adolescent, parental and family factors are viewed as interfering with or enhancing PE; (iii) a variety of clinical interventions are utilized by clinicians to cultivate and increase PE. PE is identified as essential for adolescents with AN to successfully recover. Greater focus on addressing barriers to empowering parents is needed throughout FBT. Future studies should include measurements of PE to ascertain effects on treatment outcomes. Training and supervision protocols focused on promoting PE are recommended.Practitioner pointsPE is the most salient principle of FBT.Strategies to enhance PE in phase 1 are imperative if there has been a long illness duration or parents experience mental health issues/burnout.Special clinical attention to individual factors is recommended: comorbid diagnoses, affect dysregulation and enduring eating disorder symptoms.Efforts to enhance parental involvement throughout the treatment is paramount to supporting adolescents to recover from AN.