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5 Comorbid Eating Disorders 119
patients. However, it is essential to remember that autonomic nervous
system function is typically abnormal in eating disorder patients, which
may cause and contribute to an abnormal gut microbiome [10–13]. By
far the most common and bothersome gut complication associated with
eating disorders is constipation. Prucalopride® is a relatively new treat-
ment for colonic hypofunction that is often beneficial. It stimulates the
nervous system of the colon before its effects reach the bowel, thereby,
strengthening the bowel muscle and promoting normal peristalsis [14].
As detailed below, the most common comorbid psychological disor-
ders associated with an eating disorder diagnosis include anxiety disorders
such as panic disorder (or panic symptoms), major depressive disorder,
obsessive-compulsive disorder, post-traumatic stress disorder, disorders of
impulse control such as kleptomania, self-injurious behaviour, substance
use disorder, and family systems disorders [15–35]. Additionally, some
studies suggest that personality disorders, such as borderline personality
disorder, are more common in eating disorder patients, but the research
evidence supporting the assertion is weak. That is, all the disorders that
prevent or hinder eating disorder recovery, such as borderline personality
disorder, diabetes mellitus, and substance use, are only prevalent due to
the long duration of their effects [36, 37].
5.3 Eating Disorders and Anxiety and Mood
Disorders
Mostpatients with eating disordersexperience symptoms of anxiety and/or
depression, and some present with marked fluctuations in mood that may
lead to the often false diagnosis of bipolar affective disorder [17, 23, 27,
31–33, 38–45].
Given the high comorbidity between eating disorders and affective dis-
orders, how can one distinguish between a primary mood disorder diag-
nosis and the symptoms of an eating disorder? The answer is—it can be
very difficult and only time will prove if you are right or wrong, although
in my clinical experience major depressive disorder is underdiagnosed in
eating disorder patients, because of the symptom overlap. However, the
120 C. L. Birmingham
likelihood of an independent mood disorder is increased if: the mood dis-
order pre-existed the eating disorder; the course of the mood disorder is
different and separate from the eating disorder trajectory; there are strong
vegetative symptoms; or there is a strong family history of a mood dis-
order. Of course, there can be an independent mood disorder as well as
mood symptoms that are due to the eating disorder. It is important to
appreciate that depression often worsens after the patient has shown some
physical recovery and neuropsychological improvement, as they become
more aware of their life challenges.
In contrast, bipolar affective disorder may be over-diagnosed in eating
disorder patients, relative to the published co-prevalence estimates for the
disorders, which is probably no more than 3% [16, 17, 46, 47]. Clinically,
many eating disorder patients experience a roller-coaster course of the
disorder interms of thesymptoms they experienceand their consequences.
In contrast, sedating medications that are prescribed for bipolar affective
disorder can reduce a patient’s resistance to weight gain or other treatments.
Taken together, the observation/s may be taken as diagnostic evidence of
an affectivedisorder,when the eating diagnosis can parsimoniously explain
the patient’s behaviour.
Irrespective of the specific diagnosis, theresponse to treatment is impor-
tant. Malnutritiondecreases the responseto antidepressants, whereasover-
sedation can result in patient compliance that may be misinterpreted as
clinical improvement. Consider medicating the mood symptoms if the
patient is recovering from their eating disorder but their mood is wors-
ening, without a detectable social or psychological cause. Consider a trial
of antidepressants such as Fluoxetine® gradually increasing from 10 to
60 mg over time. If this is ineffective, the addition of a small dose of
bupropion® may help. In addition, continue to watch for panic attacks,
phobias, symptoms of depression including lack of energy, lack of interest,
suicidality, and early morning awakening as indicators of major depres-
sive disorder. Watch for: marked changes in mood that don’t parallel the
patient’s clinical course; rapid thinking and speaking; and, dangerous or
outlandish behaviour, as possible indicators of bipolar affective disorder.
However, medication toxicity, medication withdrawal, and recreational
drug and alcohol use can also cause these symptoms.
5 Comorbid Eating Disorders 121
Regarding the treatment of anxiety in eating disorder patients, it can
be reduced by compassionate competent psychiatric (or psychological)
care. As detailed at the end of the chapter, it can also be managed using
body-warming strategies. Further, it may be managed by engaging the
patient in a new activity. In my clinical practice, I have seen that knitting
can markedly reduce anxiety in patients. It busies the patient’s cerebral
hemispheres, similar to the effects of eye movement desensitization and
reprogramming (EMDR) [48]. Knitting also costs little, can occur in
groups, at appointments, and at rest, and it produces something tangible.
Teaching knitting to other patients and making presents for others can
also increase the patient’s self-esteem. Additionally, the knitted product
can be used to warm the patient, as outlined below.
5.4 Can Comorbid Psychiatric Disorders
Prevent Recovery from Eating
Disorders?
Major depressive disorder(MDD), obsessive-compulsivedisorder (OCD),
and post-traumatic stress disorder (PTSD) are the most common comor-
bid disorders that have been reported to prevent recovery from anorexia
nervosa [28, 35]. Pertinently, weight recovery is always necessary for the
recovery from anorexia nervosa. As a consequence, some consideration
may need to be given to the treatment of comorbid psychiatric disorders.
Thus, in terms of scheduling the therapy, MDD and OCD should be
treated at the same time as anorexia nervosa or beforehand, whereas the
treatment of PTSD should be delayed until weight restoration has been
achieved.Treatment of the PTSD usually contributes toan increase inanx-
iety and therapy may be difficult when the cognitive state of the patient is
diminished, due to low weight. Thus, early treatment of the PTSD could
prevent recovery of the eating disorder and should therefore await weight
restoration [49].
Attention disorders are reported to commonly prevent recovery from
binge eating disorder and bulimia nervosa. Lisdexamfetamine® is used to
treat attention deficit disorder and it is now also used in some countries
122 C. L. Birmingham
to treat binge eating disorder and bulimia nervosa [50–52]; and clinically,
it appears to work in patients with an attention disorder and an eating
disorder. However, the danger in using Lisdexamfetamine® is that it is an
amphetamine that could be used to induce weight loss, decrease appetite,
and increase energy levels, and it can also be addictive [53–55]. Therefore,
patients should be prescribed the lowest effective dose and be monitored
regularly, including blood pressure, h eart rate, and BMI or body fat.
Several otherdisorders are reportedto commonly prevent recovery from
eating disorders, but they are only mentioned here in brief, including dia-
betes mellitus, substance abuse, hyper- and hypothyroidism, and ongoing
family or couple dysfunction [23, 56, 57]. All of the disorders and issues
should be treated concurrently with the eating disorder, and in family-
centred or younger patients, traditional systems family therapy is essential.
5.5 Anorexia Nervosa, Body Temperature,
Hyperactivity, and Clinical Outcomes
Patients with anorexia nervosa have low total body fat, meaning they have
less insulation to keep themselves warm. Sick euthyroid syndrome, a body
adaptation that prevents death by reducing the need for energy, occurs in
people with low body fat which is associated with a reduced metabolic rate
[58]. I have personally observed that patients with anorexia nervosa are
unaware that they are hypothermic or hyperthermic. Hypothermia and
fever may be unrecognized by the patient with anorexia nervosa [59, 60].
As a consequence, their body temperature will change with ambient tem-
perature more so than in normal-weight individuals. If they come in from
the cold (and particularly the wet), their core body temperature (BT),
which is best captured clinically by taking the temperature of a freshly
voided urine specimen, will be 2–3 °C lower than normal. However, in
contrast to normal-weight people, who would be shivering, these patients
typically do not. Similarly, if the patient has been in a very hot environ-
ment, their core BT may be 2–3 degrees above normal and yet they will
not typically feel “hot”.
Interestingly, the incidence of anorexia nervosa in people who spend
their whole life in a warm climate is reported to be considerably lower
5 Comorbid Eating Disorders 123
than its incidence in cooler climates [61], although as yet, the rea-
sons underpinning its greater prevalence in cold climates are unknown.
However, it could in part be due to the fact that anorexia nervosa patients
typically have a low BT (e.g. 35.5–37 °C), which may cause them to
feel cold. Patients who are chronically cold may report feeling better if
they: drink warm or hot beverages, use a sauna, put their body next to a
heater (this can cause hyperpigmentation of the skin, erythema ab igne),
holiday in very warm climates or go to therapy centres in very warm
climates. Often, the patients don’t know why the warming makes them
feel better—but it does because they are warming themselves up, that is,
increasing their BT. That is, due to the effects of low body fat and body
weight, anorexia nervosa patients typically have low BT, but paradoxi-
cally, they may have a reduced sensitivity to thermal stimuli. However,
as a result of the hypothermia, patients tend to compensate by increasing
their activity levels (i.e. hyperactivity), which transiently increases their
BT, helping them to feel warm [62].
As discussed in detail in Chapter 7, physical activity is associated with a
transient increase in BT [63] which is paralleled by an increasein heart rate
[64], energy expenditure, and the production of body heat. Spontaneous
physical activity (SPA; i.e. unplanned biologically driven behaviour such
as fidgeting, foot-tapping, restless behaviour, and activities-of-daily-living,
e.g. talking, maintenance of posture), which is commonly observed in
anorexia nervosa patients,also transiently increases BT [65]. SPAis known
to be inversely correlated with body weight and weight gain [66]; such
that lean people tend to engage in a lot of SPA [67]; and they are more
active, restless, and spend less time sitting or lying in bed than overweight
people [68]. Physiologically, non-exercise-activity-thermogenesis (NEAT) is
the energy that is expended during SPA. It is thought to protect lean
individuals from gaining weight during a caloric challenge by increasing
activity after overfeeding and decreasing it with underfeeding [69], and it
is increased with exercise [70, 71].
However, in anorexia nervosa patients, marked hyperactivity often
occurs inresponse to the low BT. About one-third of patients with anorexia
nervosa show markedly increased NEAT and as a result they will tend to
constantly burn-off extra calories by fidgeting, foot and leg movements,
and a general inability to sit still [72–74]. Affected patients are easy to
124 C. L. Birmingham
identify—as they need to eat a lot more calories to gain weight, although
SPA could be measured using triaxial accelerometry if verification of high
SPA is required. In contrast, patients without elevated NEAT may be able
to gain weight on a diet of 1500–2000 kcal/day, whereas patients with
elevated NEAT may require 3000–4500 kcal/day to gain weight.
Finally, in regard to BT, anorexia nervosa patients often fail to mount a
detectable fever response during bacterial infection. In an analysis of 311
consecutive hospital admissions of anorexia nervosa patients, those with
bacterial infection showed a reduced fever response, were often difficult
to diagnose due to few signs and symptoms, and as a result, the diagnosis
was sometimes delayed. The risk of infection increased with advancing
patient age [59]. Thus, due to the effects of hypothermia in anorexia ner-
vosa patients, they show a reduced fever response and signs and symptoms
of infection, which can significantly delay the infection diagnosis, thus,
increasing the complication rate for bacterial infection; with similar results
reported in another study [75]. Results suggest that the low BT in anorexia
nervosa patients can have consequences for the clinical course of the ill-
ness, and if infection is suspected, an early full blood count and possibly
bacteriologic cultures might be considered.
5.6 Body Warming to Treat Anorexia
Nervosa, Hyperactivity, and Exercise
Addiction
Body warming strategies are known to effectively treat patients with
anorexia nervosa, and in part, the therapy is thought to lead to clinical
improvement via a reduced propensity to be hyperactive. Emilio Gutierrez
identified warming as a treatment for anorexia nervosa after reading the
first clinical report describing anorexia nervosa [76–81]. William Gull,
who first reported anorexia nervosa, was physician to Queen Victoria,
and a surgeon and psychiatrist. He owned psychiatric hospitals (sanito-
ria) in which he treated psychiatric patients by warming or cooling them.
The psychiatric patients he identified as suffering from anorexia nervosa
showed a marked benefit from the warming.
5 Comorbid Eating Disorders 125
Emilio Gutierrez first used saunas to treat patients withanorexia nervosa
and observed an improvement in the patients. Emilio, Peter Beumont,
and I then reported on the benefits of a trial of warming in hospitalized
anorexia nervosa patients. As detailed below, researchers at the Karolinska
Institute have since reported similar findings, including in patients with
bulimia nervosa. As detailed below, warming treatment has been shown
to increase the speed and chances of recovery from anorexia nervosa.
For example, in an RCT of 1428 eating disorders patients (i.e. anorexia
nervosa, bulimia nervosa, eating disorder not otherwise specified) in 6
clinics, a therapy package, comprised of the mandometer (i.e. portable
computer feedback technology), ambient warming, and restricted physical
activity [82] led to reduced physical activity in patients. Remission was
achieved in an estimated 75% of patients after a median of 12.5 months
of therapy, and it was associated with a reduced relapse rate at 5 years.
However, in a small study, Birminghamand colleagues [79] found that the
therapy (heating vest set to medium heat for 3 hours/day for 21 days) was
not associated with weight recovery in anorexia nervosa patients, relative
to control patients who wore an unheated vest, but it was associated with
lower anxiety levels and improved compliance. Further, a small study [83]
showed that ambient heating (i.e. warm environment, intermittent use
of a thermal waistcoat or sauna baths in an infrared enclosure) led to a
reduction in anxiety and depression in anorexia nervosa patients, which
antedated the body weight recovery, as well as reduced their hyperactivity;
but the study had no control group. Nevertheless, another larger study
[84] recently showed that ambient warming exerted anxiolytic effects on
anorexia nervosa patients; in particular, postprandial anxiety was reduced
in patients who rested for 30 minutes immediately after lunch in a room
heated to 32 °C, relative to higher pre-meal anxiety levels.
Thus, body warming strategies appear to significantly improve the
clinical course of eating disorders including anorexia nervosa, including
the patient’s weight, hyperactivity, and affective symptoms (e.g. anxiety,
depression). However, the provision of body warming strategies can be
a little difficult in practice, outside the clinical setting, although patients
often report that moving to a warm climate for a period of time or going
to a treatment centre in a warm climate is helpful. The simplest and
most inexpensive treatment approach is to use an electric warming pad
126 C. L. Birmingham
set at medium heat for one hour three times a day, applied to the thighs,
abdomen or back. The strategy is most effective if it is used at mealtimes as
the warming increases bowel activity and thereby reduces feelings of full-
ness andconstipation. Another method of bodywarming is a dry (infrared)
sauna set at a temperature between 30 and 35 °C for 10 minutes once a
day. Finally, maintaining the heat in the patient’s apartment or home at
30–35 °C can be used in eating disorder outpatients. Warming strategies
should be used during the weight gain stage of recovery, to reduce feelings
of anxiety in patients at any stage, and to reduce over-exercise or to treat
exercise addiction. Even the cheetah stops running when its internal tem-
perature rises too high. Similarly, humans tend to exercise less if they are
already very warm.
Several practical matters need to be observed when using body warming
for eating disorder patients: Do not suggest the use of heat that is “hot” as
this will be perceived as a stressor by the body. If an electric warming pad
is used, caution against warming a single area of the body as hyperpig-
mentation of the skin will occur after weeks or months of locally applied
heat. Do not use hot water bottles or hot rocks as these will generally be
too hot at the outset and quickly become too cool. In contrast, heating an
apartment or house may be unacceptable to the other cohabitants.
Nevertheless, it is unclear exactly how the warming therapy approach
works. It might work by effectively decreasing SPA and the associated
NEAT or it could be the result of increased parasympathetic tone (as
measured by heart rate variability or change in heart rate variability)
or a change in brain receptor activity or perhaps a combination of all
of these [9]. Irrespective of the mechanism/s, it is evident that body
warming has beneficial effects in improving physical and mental health
outcomes in eating disorder patients.
5.7 Other Medical Treatments for Anorexia
Nervosa
Rita Bakan reported on the appearance of anorexia nervosa-like symptoms
and signs in African people who were zinc deficient in the 1970–1980s
5 Comorbid Eating Disorders 127
[85–88]. She asked Elliot Goldner and I to help her test the hypothe-
sis that zinc deficiency can play a causal role in anorexia nervosa. In our
studies [87, 88], we reported that the diets of anorexia nervosa patients
were typically low in zinc, the taste abnormalities often seen in zinc defi-
ciency existed in anorexia nervosa, and case reports and case series from
around the world supported the clinical benefits of zinc supplementation
in anorexia nervosa patients [89]. Finally, we carried out a randomized,
double-blinded, placebo-controlled trial in inpatients with anorexia ner-
vosa. Patients who received zinc supplementation gained BMI faster than
those not receiving the supplementation [90, 91]. Since that time, the
role of zinc in malnutrition has become better recognized, and it is also
appreciated that recovery may be faster in anorexia nervosa patients who
receive zinc supplementation.
Clinically, zinc deficiency can occur rapidly in the brain as the brain
has no store of zinc. In dogs, eating preferences can change after only a
few days of a zinc-deficient diet. Zinc is typically bound with fibre, and
in the elderly, human zinc deficiency can be caused by a high-fibre diet
due to its rapid transit through the gut [92, 93]. Zinc and copper are
absorbed through the same pathways in the proximal small bowel so it is
possible that copper supplementation could contribute to zinc deficiency
[94]. The major source of zinc in the Western diet is cow’s milk—a food
that is often avoided by eating disorder patients. Thus, eating disorder
patients should be treated with oral zinc if they avoid milk products or
have symptoms of zinc deficiency such as dry skin, skin that heals slowly
or inadequately or dysgeusia (i.e. abnormal taste sensation).
Dysgeusias are common in eating disorder patients, but they tend not
to report it unless they are specifically asked about it. Alternately, they
may not notice a change in their taste. A recent patient of mine with zinc
deficiency denied any change in taste but said that if she puts spice on
her food, she has to use a great deal of it to be able to taste it, which is
clearly abnormal. Clinically, you should ask the patient if they need more
spice or other condiments to experience the taste or if they have a metallic
taste in the mouth or experience less taste than is usual from food. Unless
you provide such an example, you may miss the diagnosis of dysgeusia.
Taste-testing kits are unreliable in my experience and serum zinc does not
tend to reflect brain zinc levels in patients. In patients with suspected zinc
128 C. L. Birmingham
deficiency, give 50 mg of elemental zinc as zinc citrate for the first 90 days
and then 14 mg of elemental zinc thereafter unless their intake of zinc is
normalized (e.g. drink normal quantities of milk products or eat lots of
red meat).
Finally, many different brain regions have been reported to function
abnormally in anorexia nervosa patients including the amygdala, insula,
frontal lobe, precuneus, and occipital lobe [95]. Our clinical practice h as
been utilizing LORETA imaging for many years now to assess the elec-
trical function of the brain at rest and during stimulation. Additionally,
it can facilitate operant conditioning of specific brain regions and fre-
quency bands in patients [96]. EEG measures the electrical activity on
the surface of the scalp, which reflects the electrical activity of the brain.
Low-resolution electromagnetic tomography (LORETA) was developed
by the KEY Institute in Switzerland in 1990. LORETA mathematically
calculates a 3-dimensional image of the brain from the output of a stan-
dard digital 19 lead. The data can be compared to known data on the
networks and symptom regions of the brain to examine for comorbid
conditions (e.g. attention disorders, major depressive disorder, anxiety,
post-traumatic disorder, and concussion).
LORETA neurofeedback uses operant conditioning procedures to
reduce abnormal brain activity in eating disorder patients. In our clinic,
operant conditioning is used to reward the subject when they success-
fully change a certain response; specifically, a change in the patient’s brain
waves (i.e. biofeedback). However, more broadly, biofeedback can focus
on changes in any physiological index (e.g. heart r ate, respiratory rate). For
example, if a patient with anorexia nervosa shows elevated activity in the
amygdala, insula, precuneus or anterior cingulate, they can be rewarded
if the activity in those areas diminishes. Rewards in this context typi-
cally include music playing, lines approaching normal, a coloured light
appearing, or video games playing.
The amygdala, which is part of the limbic system, is responsible for
detecting emotional valence in the stimulus array, including fear-inducing
stimuli. More broadly, it is responsible for the perception of emotions
including fear/anxiety, anger and sadness,is involved incontrolling aggres-
sion, and it plays a role in sexual activity and libido [97]. In contrast, the