British Journal of Obstetrics and Gynaecology
June 2000, Vol107, pp. 707-713
RE VIEW
The reproductive endocrine consequences of
anorexia nervosa
Introduction
Anorexia nervosa is a complex psychosomatic eating
disorder primarily affecting adolescent girls and young
women. It is not only a psychiatric illness, as it often has
serious gynaecological and medical ramifications. In
Western cultures the prevalence of anorexia nervosa is
estimated to be approximately 0.5% among young
women. Between 90% and 95% of patients with this dis-
order are female, typically white and middle to upper
middle socioeconomic status. The age of onset may
range from eight years to the mid-thirties, with peaks
occurring between the ages of 13 and 14 years and
between the ages of 17 and 18 years'".
According to the Diagnostic and Statistical Manual of
Mental Disorders6anorexia nervosa is distinguished by
a refusal to maintain the minimal normal weight for age
and height (i.e. loss of weight of > 15% weight for
height), an intense fear of gaining weight or becoming
fat while being underweight, a disturbance in the way in
which one's weight or shape is perceived, and amenor-
rhoea for at least three consecutive menstrual cycles in
postmenarchal female~l-~.
This is not a disorder exclusive to white western cul-
tures. Smaller numbers of anorexics have been reported
among non-western ethnic populations. Most of these
cases highlight family pathology, inter-generational
conflicts and confusion over racial identity as predomi-
nant risk factors. However, with an increase in the
degree of identification with Western culture through
global media and communications and changes in
dietary habits, the prevalence and incidence of anorexia
nervosa is increasing on a worldwide scale7.
7 3 ~ types
0 of anorexic patients have been defined in
the diagnostic criteria for this disease. The restricting
types are quite controlled of their behaviour. These indi-
viduals do not engage in regular binge eating or purging;
instead, they engage in other behaviours, such as fasting
and excessive exercise. There is a preoccupation with
food, and its avoidance becomes an obsession to the
exclusion of other activities. The second type of
anorexic patient is referred to as bulimic anorexic.
These individuals tend to be more distressed, depressed,
overtly angry and impulsive. Binge eating and purging
are regular behaviours, as well as self-induced vomiting,
Q RCOG 2000 British Journal of Obstetricsand Gynaecology
the misuse of laxatives, diuretics, diet pills, enemas or
even thyroid medications. There is a continuum
between these types with some moving from one to the
other either during the course of the illness or during the
process of recovery13.
Anorexia nervosa is not a modern ailment. There have
been records of self-induced weight loss over the last
few hundred years, with the first modem account occur-
ring in the late 19th c e n w . It has probably become
more prevalent in Western society due to: 1. the abun-
dance of food, and 2. to the present cultural image of
thinness and success being inseparable. Not surpris-
ingly, disturbed eating behaviours may begin as a mech-
anism of control in a young woman's life in response to
the desirability of slenderness advertised by the media
and fashion industry. Anorexia nervosa has also been
described as a defence against puberty, with vulnerable
adolescents adopting flight responses when under pres-
sure from a range of maturational problems*. Other indi-
vidual risk factors include stressful life situations,
genetic vulnerability, a family history of a psychiatric
disorder, prominence of depressive disorders, perkc-
tionism, obsessive behaviour and previous history of
sexual abuse. Some individuals may be predisposed to
anorexia because of their occupations, including balleri-
nas, athletes, models, flight attendants, gymnasts and
long distance r ~ n n e r s ' ~ ~ . ~ . ~ .
Most patients with anorexia nervosa present with
denial of symptoms and are brought to medical attention
through an external source, usually a family member or
teacher. The symptoms include primary or secondary
amenorrhoea, obvious weight loss, cold intolerance,
bloating, constipation or diarrhoea, fatigue, fainting,
easy bruising, frequent fractures, nerve compression,
scalp hair loss, dry skin and early satiety24
Few organ systems escape the progressive deterioration
that is seen in this disorder. There is no other psychiatric
illness which manifests as many medical complications,
which are primarily a direct result of starvation. Most
are usually reversible after feeding and weight gain.
However, some consequences are life threatening.
Cardiovascular complications may account for some
of the mortality associated with anorexia nervosa. These
include congestive heart failure, arrhythmias, and
707
708 REVIEW

emetic-induced myocardial damagelo. Electrocardio- strenuous exercise and the commencementof eating dis-
graph abnormalities usually return to normal after the ordered weight controlled practices are probably the
patient begins to eat and regain weight. Haematological influences causing the menstrual disturbance^'^.
abnormalities include mild forms of anaemia, leukope- Another theory postulated by Levine et al." is that
nia, neutropenia and thrombocytopenia; these also usu- there may be a weight-related set point for maintenance
ally return to normal following weight gain. Chronic of menses, and that some anorexic patients may have
dehydration as a result of vomiting or laxative abuse higher individual critical weights at which point menses
may cause irreversible damage to renal tubules. How- cease. Therefore it would be possible for amenorrhoea
ever, most other renal complications resolve with rehy- to occur at a normal body weight in some women.
dration and refeeding. There are also dental Secondary sexual characteristics are also affected as a
consequencesfrom regular vomiting with the most com- result of food deprivation. For example, mature breasts
mon repercussion being the erosion of dental enamel, and pelvic contours lose their female conformation,
which can lead to tooth destruction. Gastrointestinal, while axillary and pubic hair become coarse and pig-
dermatological, and neurobiological complications are mented or even depleted1.5*10*'3.
also observed upon physical examination and are also There are conflicting studies about the importance of
primarily reversible with nutritional rehabilitation5. amenorrhoea in the diagnosis of anorexia nervosa.
Numerous endocrine abnormalities are also associ- Selzer et ~ 1 . assessed
' ~ the relation between amenor-
ated with anorexia nervosa as secondary effects of star- rhoea and symptoms of eating disorders and concluded
vation. The principal complication is amenorrhoea. that amenorrhoea should be viewed as a possible marker
Hypercortisolism and hypothyroidism have been of disordered eating in general. At the other end of the
described in such patients, perhaps as a protective mech- spectrum, Garfinkel et aLZ0concluded from a Canadian
anism to conserve energy". Growth hormone concentra- study that the criterion of amenorrhoea in the diagnosis
tions are often increased as a result of starvation, while of anorexia nervosa excluded a group of women whose
IGF-1 concentrations are quite low. It appears that there psychopathology included disturbances in eating and
is marked irregularity in the release of growth hormone, weight. Presently these women are diagnosed under the
which results in growth hormone resistance and category of 'eating disorders otherwise specified', and
decreased secretion of IGF-1l2. Insulin and blood sugar perhaps this group is at a level that reflects a phase for
concentrations are decreased, but prolactin concentra- some anorexic patients. In 1994 it became mandatory
tions remain normal. There is also a disturbance in the that the diagnosis of anorexia nervosa must include the
ability to concentrate urine suggesting a problem with presence of amenor~hoea~*'~.
vasopressin secretion5. In biological terms it is very reasonable that repro-
ductive function is shut down in response to a
depleted nutrient supply. Thus, the prompt reduction
Menstrual disturbances
in reproductive potential during periods of reduced
Menarche is quite a late event in the process of pubertal availability of food seems to be important for the sur-
development and can be disturbed by a combination of vival of the individual female as well as the human
physical, psychological and nutritional stre~ses'~.'~.species. Examples of this can be found naturally in the
Weight loss of between 10%and 15% of normal weight seasonal infertility of nomadic populations, such as
for height retards pubertal development and delays the desert-dwelling Kung peoples14.
menarche (primary amenorrhoea). Sexual maturation is There are also other menstrual abnormalities, apart
delayed in pre-pubertal anorexic patients. The growth from amenorrhoea, ranging from a prolonged follicu-
spurt may be affected with maximum height potential lar phase to an inadequate luteal phasez1 in post-
not being reached thereby resulting in short stature15. menarchal patients.
There may also be impaired breast development. Gener-
ally, these developmental delays are reversible,
although in severe cases they may be irreversible16.
Endocrine mechanisms of amenorrhoea
Secondary amenorrhoea is the absence of menstrual Amenorrhoea in anorexia nervosa is a result of hypotha-
periods for six or more cycles in a post-menarchal lamic dysfunction. Principal endocrine abnormalities
female. In the majority of women a weight loss of are low concentrations of gonadotrophins and hypo-
between 10% and 15% of normal weight for height e s t r o g e n i ~ m ' ~caused
* ' ~ . ~ ~by inhibition of gonadotrophin-
causes this disruption. Weight and body fat are instru- releasing hormone p u l ~ a t i l i t y ~a ~blunted
, ~ ~ , response of
mental but not deciding factors in the maintenance of luteinising hormone to gonadotrophin-releasing hor-
menstrual cycles. In up to 20% of anorexic patients monez4and diminished pulsatile release of luteinising
amenorrhoea may precede weight loss. It has been hormone2, loss of feedback effect of oestrogenZ5,and
hypothesised that a combination of psychological stress, multifollicular changes in the ovary resulting in the

0 RCOG 2000 Br J Obsret Gynaecol 107,707-713


failure of follicle selection and dominance15.In the pre-
menarchal patients there is a delay in pubertal develop-
ment due to the continuation of these pre-pubertal
secretory patterns.
Menstrual cycles can be induced in these patients
with the use of pulsatile gonadotrophin-releasing hor-
mone injected subcutaneously at 60-90 minute inter-
vals, thus imitating the natural in vivo pattern of
gonadotrophin-releasing hormone pulsesz6.This obser-
vation suggests that the pituitary and the ovary remain
fully capable of functioning during the active disorder
and that the hypogonadism witnessed in such patients is
of hypothalamic origin. It is not clear which mecha-
nisms are involved in the instigation of this hypotha-
lamic dysfunction.
There has been conflicting evidence about the possi-
bility that luteinising hormone pulsatility can be
restored in anorexics by endorphin antagonists. This
would indicate the action of an inhibitory opioid path-
way, such that with the elevation of endorphin concen-
trations there is inhibition and/or alteration of
gonadotrophin-releasing hormone pulse secretion,
which affects luteinising hormone pulsatility. Bara-
nowska et observed the restoration of luteinising
hormone pulsatility in anorexic patients after the admin-
istration of naloxone, an opioid antagonist. Similar
results of opioid-mediated inhibition of hypothalamic
function were also observed in experiments with fasting
ratsz8.However Giusti et aLZ9observed no correction of
luteinising hormone pulsatility after the administration
of another opioid antagonist, naltrexone. Dopamine is
also known to inhibit luteinising hormone secretion.
However, there was no significant rise in luteinising
hormone concentrations in anorexic patients after doses
of a dopamine receptor blocker, meto~lopramide~~.
Investigations concerning whether the serotoninergic
system may participate in control of luteinising hor-
mone secretion concluded that serotonin either stimu-
lates gonadotrophin-releasing hormone release from the
hypothalamus or increases the response of the pituitary
to gonadotrophin-releasing hormone, which thereby
results in an increase in the amplitude of the luteinising
hormone pulse3'. In anorexic patients the levels of the
major serotonin metabolite, 5-hydroxyindoleacetic acid
are low but have been observed to increase above nor-
mal after recovery. It has been suggested that this distur-
bance of serotonin activity is another risk factor for
developing anorexia n e r v o ~ a ~ ~ , ~ ~ .
There have been other reasons given for the cause of
amenorrhoea. One suggestion is that glycosylation of
gonadotrophin isoforms may affect gonadotrophin
bioactivity. Anorexic patients display an altered glyco-
sylation pattern of their gonadotrophin isoforms and
perhaps this alteration has an effect on the quality and
biological activity of gonadotrophin secretion34.
0 RCOG 2000 Br J Obstet Gynaecol 107,707-7 13
REVIEW 709
Another suggestion is that leptin may play a role in
the regulation of the hypothalamic-pituitary-ovarian
axis during starvation. With food restriction there is a
rapid decline in leptin concentrationsprior to weight loss.
This low leptin concentration seems to be the trigger that
initiates the physiological responses to starvation,includ-
ing cessation of menstrual function and reproduction.
Leptin receptors are present in the hypothalamus and
ovary. However, the actual mechanism of the trigger is
unknown. Leptin concentrations increase significantly
upon refeeding and correlate linearly with total body fat
and body mass It also seems that the regula-
tion of leptin secretion during starvation is associated
with factors other than body weight. Mehler et ~ 1 . ~ '
observed that despite similar body mass index, anorexic
patients using purgatives had elevated leptin levels
when compared with restricting anorexics. This may be
due to increased glucocorticoid stimulation of leptin3'.
Other factors may include insulin, growth hormone,
IGF-1 and proinflammatory cytokines.
Osteoporosis
The hypoestrogenic state observed in anorexia ner-
vosa, a direct result of the effects of hypothalamic
amenorrhoea, is further exaggerated by changes in
oestrogen metabolism. There are two forms of oestro-
gen metabolism that are affected by loss of body fat.
The first is aromatisation of androgens to oestrogens,
which occurs in adipose tissue. Because of the loss of
body fat, there is a severe lack of adipose tissue, lead-
ing to a decrease in ammatisation. The second is a shift
in oestrogen metabolism from the active form of
oestradiol towards catecholoestrogen, which has no
intrinsic oestrogenic activity. This shift is also a direct
consequence of weight and fat loss. Catecholoestrogen
competes with catecholamine for the enzyme, chol-o-
methyltransferase. This competition may cause an
increase in dopamine secretion. Dopamine is a known
inhibitor of gonadotrophin-releasing hormone pulsatil-
ity, which ultimately will also have a negative effect on
oestrogen produ~tion~.'~,'~.
There are numerous consequences to this hypoestro-
genic state. The breasts and uterus, organs which pro-
duce a trophic response to oestrogen, decrease in size
and volume. The most serious complication is osteo-
porosis, a disease characterised by low bone mass lead-
ing to an increased occurrence of fractures with minimal
stress. It may not be fully r e ~ e r s i b l e ~ ~ .
Adolescence is the critical time for bone mineral
accretion as more than half of the bone calcium in an
individual is normally laid down during these years,
with bone development continuing into the next decade
of life. After the third decade, skeletal mass begins to
decrease and is accelerated after the menopause, when
710 REVIEW
the rate of bone loss exceeds that of bone formation.
Failure to attain sufficient bone density during the ado-
lescent years results in osteopoenia which refers to a
bone density of between 1 and 2.5 standard deviations
below the average for young adults of the same sex and
is a risk factor for osteoporosis. There are other factors
that contribute to peak bone density, including genetic
factors, exercise, body weight and n u t r i t i ~ n ~Both ~ . ~ ~ . includes early diagnosis, recommendations for decreas-
decreased bone formation and increased bone resorp-
tion occur in anorexia nervosa, and these may not be
fully reversible.
The age of onset and the duration of anorexia nervosa
and amenorrhoea correlate significantly in most studies
with bone d e n ~ i t y ~Younger
~ v ~ ~ . patients with prolonged
amenorrhoea have more severe and long lasting bone
defects as they do not reach their maximum peak bone
mass43.In order to prevent further bone loss in anorexic
patients it is most important to direct treatment towards
the resumption of menses, weight gain and adequate
nutrition. Young women with this disease may lose as
much as 2% to 6% of bone mass each year of their disor-
der. Previous studies indicated that bone density
increases with recovery44. However, more recent
research, including results from long term follow up
studies of recovered anorexics, have shown that losses
in bone density may not be fully reversible even when
there is resumption of menses and weight gain4042. resolution of existing emotional issues. Many studies
Anorexia nervosa can no longer be regarded as having
no long term detrimental effects.
Strenuous exercise is one of the major factors in the
maintenance and development of normal bone mass.
There have been conflicting reports as to the benefit of
exercise in anorexics in relation to bone loss. Even
though physical activity provides some protection
from bone loss the amount of exercise must be moni-
tored so as not to participate in further weight
addition, the absence of normal plasma concentrations
of oestradiol may limit the positive effects exercise has
upon bone density40.
Most recent studies have also reported (once again in
contradiction to previous experiments*) that oestrogen
replacement has little independent effect in the correc-
tion or prevention of osteopoenia in anorexia ner-
vosa40~41. Some suggestions as to why this is so include
the possibility that the natural cycle of oestrogen may be
important in bone recovery. Also, there may be factors
other than oestrogen deficiency that also promote
osteopoenia. These factors include hypercortisolism,
decreased calcium and phosphate intake, decreased
muscle mass, progesterone (which promotes bone for-
mation) deficiency and low concentrations of IGF- 1
(which stimulates type 1 collagen b i o s y n t h e ~ i s ) ~ ~ ~ * *using
The female athletic triad is a syndrome that occurs in
young active girls and women. The components of the
triad are interrelated and include the development of
eating disorders, amenorrhoea and osteoporosis.Females
training in sports that emphasise appearance and a low
body weight for athletic performance are at highest risk.
The repercussions of the triad include a decrease in
physical performance along with subsequent serious
health complications, resulting from disordered eating
and osteoporosis. The most appropriate prevention
ing the intensity, duration or frequency of exercise along
with nutritional coun~elling~~.
Fertility
During the active stage of anorexia nervosa, infertility is
expected. This is due to a combination of anovulation
and a rejection of sexual activity. Restricting anorexics,
when they are at a low body weight, are predominantly
sexually passive. This may be due to their low self-
esteem but may also be due to reduced libido resulting
from low concentrations of circulating sex hormones.
On the other hand, bulimic anorexics are known to be
more sexually assertive and therefore are less likely to
remain at a low body weight45.
Resumption of menses depends on restoration of the
hypothalamic-pituitary-ovarian axis. This requires
nutritional rehabilitation with weight gain, as well as
have concluded that on attaining 90% of the predicted
weight for height, most anorexic patients will resume
menses within six months to one y e p 9 . The percent-
age of women who continue to have amenorrhoea
despite weight gain varies considerably in different
studies, from 13%17 to 30%47.Persistence of amenor-
rhoea despite weight gain may be due to continuation of
abnormal eating practices, as well as underlying psy-
In chological issues. Other factors associated with resump-
tion of menses include the duration of disorder. The
longer the duration of the active illness the greater the
likelihood of persistent amenorrhoea. Existence of an
anxiety disorder has also been established in one study
to be associated with a greater probability of persistent
lack of menses4*.Obviously, women who have persis-
tent amenorrhoea will remain infertile. However it has
been concluded from the majority of studies that these
patients do not desire pregnancy. Most women who
have recovered from anorexia nervosa and who resume
menstruating and have a normal eating behaviour are
successful in conceiving and have a satisfactory fertil-
ity outcome. It is possible for women who remain
amenorrhoeic to conceive via ovulation induction
using pulsatile gonadotrophin-releasing hormone or
~ . gonadotrophins.
Observations from women attending infertility clinics
have shown that high proportions have a hidden eating
~ , ~ ~ .et d s O
d i ~ o r d e r ~Stewart reported that 17% of the
0 RCOG 2000 Br J Obstet Gynaecol 107,707-713

66 patients in their study were diagnosed with an eating
disorder and 8% were confirmed to be anorexic.
Amongst the infertile women with amenorrhoea or
oligomenorrhoea, 58% had an eating disorder. None of
these patients volunteered information about their eat-
ing patterns, harbouring fears that this had caused their
infertility. However, most of these women conceived
naturally after practising normal eating behaviour and
reaching the predicted ideal body weight. Therefore it
has been recommended that prior to any other infertility
investigation, a routine questionnaire on the history of
nutritional intake, eating behaviour and examination of
body weight is essential.
Pregnancy and parenting
Pregnancy is very unusual in women with active
anorexia nervosa. If pregnancy occurs, it usually is
detected at an advanced stage. The suggestive early
signs of pregnancy are identical to some of the symp-
toms of anorexia nervosa (for example, delay in men-
strual cycle, vomiting and fatigue). Conception may
occur in the first ovulatory cycle, after a period of amen-
orrhoea. This is more frequent in anorexic women in the
recovery phase of their disorder.
The effect of pregnancy on anorexia nervosa itself
varies. In some women there may be symptomatic
improvement. In one study, 70% of women who
reported abnormal eating patterns six months before
conception acknowledged an improvement in their
symptoms directly as a consequence of their preg-
nancy5*.In general, women who have been treated and
recovered from anorexia nervosa tend to have uncom-
plicated pregnancies especially when they have support
systems in place53. However, if the symptoms of
anorexia nervosa persist or become worse during preg-
nancy then there is more likely to be an increase in
psychological and physiological problems. These
include poor weight gain, growth retarded babies,
more fetal abnormalities, more miscarriages, more
caesarean deliveries, greater perinatal mortality, diffi-
culties in postpartum adjustment and breastfeeding
problems. Several studies have targeted the importance
of the nutritional condition of the mother in relation to
the perinatal result. A significant correlation has been
observed between the lack of weight gain of the
mother and low birthweight of the child. These low
birthweight babies may have long term developmental
difficulties including impaired intellectual ability. In
addition, the perinatal mortality rate of babies born to
anorexic mothers was observed to be six times that of
the general population5s55.
Hyperemesis gravidarum is a rare life-threatening
syndrome, defined as intense vomiting in the first
trimester of pregnancy. This results in weight loss and
0 RCOG 2000 Br J Obstet Gynuecol 107,707-7 13
REVIEW 711
metabolic disturbances, often requiring hospitalisation.
Hyperemesis gravidarum may be caused by an array of
psychological, social and physiological problems.
However, all aspects of this syndrome are inadequately
understood, with the exception that hyperemesis gravi-
darum may be connected to the worsening of anorexia
nervosa during pregnancy. Therefore, it is vital for the
health of the mother and baby that diagnosis of this
syndrome in a pregnant anorexic is rapid and that
treatment is thorough56.
The postpartum period for all women is a vulnerable
time due to rapid hormonal changes, sleep deprivation,
and the stress of coping with a newborn. During this
time, some women may revert to unhealthy eating prac-
tices as a direct response to feeling out of control.
Another cause for concern in relation to anorexic ner-
vosa is parenting. The problems that e anorexic
d
mother faces with her food, weight and bo y image can
compromise her ability to take care of her child ade-
quately and thereby threaten her childs health. There
have been reports of decreased rates of breastfeeding,
poor nutrition and stunting of growth in the children of
anorexic mothers. As well as negative emotions being
displayed during meal times, the conflict that exists
between the mothers concern about her own body
image, the fear of her child becoming obese and provid-
ing a role model for normal eating behaviour during
family meals are
If a history of anorexia nervosa is acknowledged prior
to conception, the woman should be counselled to delay
pregnancy until the active disorder is treated and under
control. If, however, the anorexic patient is already
pregnant then it is vital that she receives intensive pre-
natal care in order to monitor prenatal nutrition and fetal
development to minimise any medical complications.
Perinatal care and regular observations of the child
should continue after birth until the anorexic mother is
truly in remission.
Anorexia nervosa in males
Anorexia nervosa is considered rare among males, repre-
senting approximately 10%of reported cases. This enor-
mous gender discrepancy is observed for all the eating
disorders. However, in the last decade there has been a
steady increase in the proportion of male patients from
5% to There are significant similarities in the aeti-
ology and clinical presentation of this disorder in both
sexes, including the strong association with underlying
psychiatric disorders such as depression. Nevertheless,
certain features are more prevalent in male patients,
including a later age of onset (late adolescence to early
adulthood), a past history of premorbid obesity, a high
rate of co-morbid substance abuse, mood disorder, sex-
ual identity concerns and excessive exercising61A5.
712 REVIEW
Medical complications and hospital admissions in
male anorexics have been reported to be high in propor-
tion to the small number of patients. This could be due
to a delay in diagnosis. Medical abnormalities include
anaemia, hypotension, short stature and structural brain
changes. The endocrinological problems include
delayed puberty, osteoporosis, significantly lower
testosterone concentrations and other endocrine distur-
bances similar to those observed in female anorex-
i c ~ ~ ~ *There
" , ~ ~ has
. been little research into male
anorexia nervosa and its reproductive consequences.
Tkeatment and outcome of anorexia nervosa
The treatment of anorexia nervosa is a long term pro-
cess. A multi-disciplinary team approach has been the
most successful method leading to recovery. This
approach involves psychotherapy, medical care, and
eating behaviour modification. The first goal for the
multi-disciplinary team may be to keep the patient
alive. Many patients will require hospitalisation at
some time during recovery but most treatment will
occur as an outpatient. Long term psychotherapy aims
to develop strategies for coping that are an improve-
ment to the current eating behaviours and directing the
patient towards a healthy nutritional cognitive state6*.
Nutritional management aims at establishing normal
eating behaviour and encouraging a normal attitude
towards food and hungef19. Family therapy has also
been identified as an important factor in the complete
management for anorexics.
Most long term follow up studies of these patients
indicate that approximately 70% have at least a good to
moderate improvement, while 20%-30% remain chron-
ically ill with no improvement. The mortality rate is
approximately 5%-lo%,the main cause being suicide.
Even though many of the acute symptoms of the disor-
der may disappear with recovery, most patients will con-
tinue to suffer from continuing abnormal eating
practices, depression, social anxiety, obsessive-compul-
sive behaviour, perfectionism and excessive attention
to food and weight7'.
Conclusion
Anorexia nervosa is a debilitating eating disorder with
many serious and potentially life-threatening conse-
quences. Thus, diagnosis and immediate medical, nutri-
tional and psychiatric treatment is crucial in preventing
long term complications.It is widely acknowledged that
the prognosis for patients with anorexia nervosa wors-
ens with the duration of the illness and the intensity of
the weight loss, especially with regard to osteoporosis.
Luckily, most of the medical complications are biologi-
cal adaptations to the condition of starvation and are
therefore reversible with nutritional rehabilitation. This
is also the consensus with the reproductive changes. It is
accepted that the majority of physically and emotionally
recovered anorexics will be able to conceive naturally
upon resumption of their menses. It is also possible to
induce ovulation in the women who have persistent
amenorrhoea, but this is not recommended unless the
patient has undergone a full recovery. Anorexia nervosa
is more than just an eating disorder. It is an illness that
overwhelms both the mind and the body.
*Mandy G. Katz & **BeverleyVollenhoven
*Monash Institute of Reproduction and Development &
**Department of Obstetrics and Gynaecology, Monash
Universio, Monash Medical Centre, Victoria,Australia
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