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Lecture

PHSI 208 Lecture Notes - Opioid, Cortisol, Serotonin Receptor Agonist


Department
Physiology
Course Code
PHSI 208
Professor
Neil Hibbert

Page:
of 3
Bulimia Nervosa
Ms Bs beh is BN. Bulimia from a Greek word means ox hunger.
This disorder involves episodes of rapid consumption of a large amount of food, followed by
compensatory beh such as vomiting, fasting or excessive exercise to prevent weight gain
The DSM defines a binge as eating an excessive amount of food within less than two hours.
BN is not diagnosed if the binging and purging occur only in the context of AN and its
extreme weight loss; the diagnosis in such as case is AN binge eating purging subtype
Binges typically occur in secret may be triggered by stress and the negative emotions it
arouses and continue until the person is uncomfortably full.
Stressors that involve negative social interactions may be particularly potent elicitors of
binges.
Bulimics have high levels of interpersonal sensitivity, as reflected in large increases in self-
criticism following negative social interactions.
Further binge episodes tend to be preceded by poorer than average social experiences, self
concepts and moods
Also reported that the binge episodes are followed by deterioration in self concept, mood state
and social perception
The person who is engaged in a binge often feels a loss of control over the amount of food
being consumed. Foods that can be rapidly consumed, esp sweets such as ice cream or cake
are usually part of a binge. Although research suggests that patients with BN sometimes
ingest an enormous quantity of food during a binge.
Binges are not always as large as the DSM implies and there may be wide variation in the
caloric content consumed by individuals with BN during binges. Patients are usually ashamed
of their binges and try to conceal them. They report that they lose control during a binge even
to the point of experiencing something akin to a dissociative state perhaps losing awareness of
what they are doing of feeling that it is not really they who are binging
After the binge is over disgust, feelings of discomfort and fear of weight gain lead to the 2nd
step of BN—[urging to undo the caloric effects of the binge. As seen with Ms. B purging can
involve induced vomiting and excessive exercise. The use of laxatives and diuretics is
common even though this odes not actually result in weight loss
The DSM diagnoses of BN requires that the episodes of binging and purging occur at least
twice a week for three months
Suggesting that there is a continuum of severity rather than a sharp distinction
Like patients with AN patients with BN are afraid of gaining weight and their self esteem
depends heavily on maintaining normal weight.
Observed that a morbid fear of fat is an essential diagnostic criterion for BN cuz 1) it covers
what clinicians and researchers view as the core psychopathology of BN 2) it makes the
diagnosis more restrictive and 3) it makes the syndrome more closely resemble the related
disorder or AN
as with anorexia two subtypes of BN are distinguished: a purging type and a non purging type
in which the compensatory beh are fasting or excessive exercise. And recent evidence does
not strongly support the validity of this distinction
BN typically begins in late adolescence or early adulthood. About 90% of cases are women
and prevalence among women is thought to be about 1 to 2% of the population.
Find tat lifetime rates for females are approx 1.1% of the population for BN and 0.5% of the
population for AN
Suggests that bulimia is more common than anorexia among adolescents
One study found that by age 18 80% of young women in BC with normal height and weight
indicate that they would like to weight less.
Another study of more than 1,800 females from Ottawa, Hamilton, and T,O between the ages
of 12 and 18 found that 27% has disordered eating attitudes and beh and approx 1 in 7
participants engaged in binge eating with associated loss of control
Comparisons across time suggest that the frequency of BN may be increasing.
Cohort effect- with rates being higher among ppl born after 1960 who alsp tend to have
younger ages of onset
BN patients are somewhat overweight before the onset of the disorder and that the binge
eating often starts during an episode of dieting.
Long term follow up of BN patients reveal that about 70% recover although about 10%
remain fully symptomatic
BN is associated with numerous other diagnoses, notably depression, personality disorders
( esp borderline person disorder) anxiety dis, substance abuse and conduct disorder
Suicide rates are much higher among ppl with BN than in the general population. A twin
study had found that bulimia and depression are genetically related
Somewhat curiously BN has been associated with stealing. Patients with bulimia who steal
tend also to be illicit drug users and promiscuous. This combination of beh may reflect
impulsivity or lack of self control, characteristics that may be relevant to the beh of binge
eating
Like anorexia bulimia is associated with several psychical side effects. Frequent purging can
cause potassium depletion. Heavy use of laxatives includes diarrhoea which can also lead to
changes in electrolytes and cause irregularities in the heart beat. Recurrent vomiting may lead
to dental enamel as stomach acids eat away at the teeth, making them ragged. The salivary
glands may become swollen. However mortality appears to be much less common in BN than
in AN
Binge Eating Disorder
DSM-IV-TR includes binge eating disorder (BED) as a diagnosis in need of further study
rather than a formal diagnosis. This disorder includes recurrent binges (2 x per week for at
least 6 months), lack of control during the binging episode, and distress about binging as well
as other characteritcs such as rapid eating and eaing alone.
It is distinguished from AN by the absence of weight loss from BN by the absence of
compensatory beh (purging, fasting or excessive exercise)
Binge eating disorder appears to be more prevalent than either AN or BN
One advantage of including BED as a diagnosis is that it would apply to many patients who
are now given the vague diagnosis of eating disorder not otherwise specified since they do not
meet criteria for anorexia or bulimia
BED has several features that support its validity. It occurs more often in women than in men
and is associated with obesisty and a history of dieting.
Its linked with impaired work and social functioning, depression, low self esteem, substance
abuse and dissatisfaction with body shape
Risk factors for developing BED include childhood obesity, critical comments regarding
being overweight, low self concept, depression, and childhood physical or sexual abuse
Recent data also indicate that the average life time duration of BED (14.4 yrs) may be greater
than the duration of AN (5.9 yrs) or BN (5.8 yrs)
Reported that only about half of the women with an apparent binge eating disorder reported
feeling “out of control”
Do not view binge easting disorder as a discrete diagnostic category seeing it instead as a less
severe version of BN.
Found few differences between patients with binge eating disorder and the non purging form
of BN but the preponderance of evidence seems to support the distinction between these
disorders
ETIOLOGY OF EATING DISORDERS
A single factor is unlikely to cause an eating disorder
including genetics, the role of the brain, socio-cultural pressures to be thin, the role of the
family and the role of the environment
table 9.1 pg 257 and table 9.2 pg 261
Biological Factors
Genetics
both AN and BN run in families. 1st degree relatives of young women with AN are about 4 x
more likely than average to have the disorder themselves
twin studies of eating disorders also suggest a genetic influence. Most studies of both anorexia
and bulimia report higher identical than fraternal concordance rates
a strong genetic component was found with a herabtability estimate of 56%
research has also shown that key features of the eating disorders such as dissatisfaction with
ones body and a strong desire to be thin appear to be heritable
eating disorders and the brain
the hypothalamus is a key brain centre in regulating hunger and eating. Research on animals
with lesions to the lateral hypothalamus indicates that they lose weight and have no appetite
thus its not surprising that the hypothamlus has been proposed to play a role in anorexia. The
paraventicular nucleus has also been implicated.
The level of some hormones regulated by the hypothalamus such as cortisol are indeed
abnormal in patients with anorexia; rather than causing the disorder however these hormonal
abnormalities occur as a reulst of self starvation and levels return to normal following weight
gain
Animals appear to have no hunger and become indifferent to food, whereas patients with
anorexia continue to starve themselves despite being hungry and having an interest in food.
Nor does the hypothalamic model account for body images disturbances or fear of becoming
fat.
A dysfunctional hypothalamus thus does not seem a high likely factor in anorexia nervosa
Endogenous opiods- are substances produced by the body that reduce pain sensations,
enhance mood and suppress appetite at least among those with low body weight.
Opiods are released during starvation and have been viewed as playing a role in both anorexia
and bulimia.
Starvation among patients with anorexia may increase the levels of endogenous opiods
resulting in positively reinforcing euphoric state
The excessive exercise seen among some patients with eating disorders would increase opiods
and thus be reinforcing
Hypothesized that bulimia is medicated by low levels of endogenous opiods which are though
to promote craving; a euphoric state is then produced by the ingestion of food thus reinforcing
binging
Some data support the theory that endogenous opiods do play a role in eating disorder at least
in bulimia
Found low levels of the endogenous opiod beta endorphin in patienst with bulimia; they also
observed that the more severe cases of bulimia had the lowest levels of beta endorphin
Patients with bulimia have decreased regional mu-opiod receptor binding in the insular cortex
and this is inversely correlated with fasting beh
Animal research has shown that serotonin promotes satiety (Feeling full) therefore it could be
that the binges patients with bulimia result from a serotonin deficit which would cause them
not to feel satisfied as they eat
Have identified low levels of serotonin metabolites in patients with bulimia and serotonin
metabolites have been linked with the negative mood and self concept changes that precipitate
binge episodes.
Patients with bulimia also show smaller responses to serotonin agonists (Chemicals that
combine with receptors to initiate a reaction) again suggesting an under active serotonin
system
When patients who had recovered from BN had their serotonin levels reduced they showed an
increase in cognitions related to eating disorders such as feeling fat.
These data all suggest that a serotonin deficit may well be related to BN
This work focuses principally on brain mechanisms, relevant to hunger, eating and satiety and
does little to account for other key features of both disorders particularly the intense fear or
becoming fat