Anorexia Nervosa

Anorexia nervosa is a chronic disorder characterized by self-induced

weight loss, negative perception of body image, and physiological
changes that result from nutritional depletion. Patients with anorexia
nervosa have a fixation on weight control and often insist on having a
bowel movement every day despite inadequate food intake. They often
abuse laxatives, which worsens the fluid and electrolyte imbalances and
nutrient deficiencies. The disorder is found predominantly in young, single
females, and it may be inherited. Abnormal patterns of menstruation,
amenorrhea (absence of menstruation), and a lowered basal metabolic
rate reflect the depressant effects of starvation. Individuals may become
emaciated and may ultimately die of starvation or one of its
complications. Also associated with the disorder are osteoporosis,
depression, and brain abnormalities coupled with impaired mental
performance. Treatment consists of psychotherapy and dietary regulation.

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Emotional Eating
In addition to keeping us alive, eating serves countless psychological,
social, and cultural purposes. We eat to celebrate, punish, comfort, defy,
and deny. Eating in response to emotional drives, such as feeling stressed,
bored, or tired, is called emotional eating. Emotional eating is so
common that, within limits, it is considered well within the range of normal
behavior. Who hasn’t at one time or another headed for the refrigerator
after a bad day? Problems arise when emotional eating becomes so
excessive that it interferes with health. Physical health problems include
obesity and associated disorders such as hypertension and heart disease.
Psychological health problems include poor self esteem, an inability to
cope effectively with feelings of stress, and in extreme cases, eating
disorders such as anorexia nervosa, bulimia, and obesity. Eating provides
comfort and solace, numbing pain and “feeding the hungry heart.” Eating
may provide a biochemical “fix” as well. Emotional eaters typically
overeat carbohydrate foods (sweets and starches), which may raise brain
serotonin levels and lead to feelings of
relaxation. Food becomes a way to self-medicate when negative emotion
arise.

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Obesity, Eating Disorders

Several regulatory circuits are considered to be responsible for
regulating body weight, each governed by the hypothalamus, for
example, by its ventromedial nucleus as the “satiety center” and by the
lateral hypothalamus as the “eating center”. The regulatory cycle that is
probably decisive in the long term is the lipostatic mechanism: the body’s
fat mass is recognized on the basis of a substance that is secreted by the
fat cells (probably leptin, see below), and a feedback loop keeps this fat
mass constant during changes in appetite and physical activity (A). Thus
fat, even if surgically removed, is rapidly replaced. Obesity (adiposity,
excess weight) is a risk factor for hypertension, type 2 diabetes mellitus,
hyperlipidemia, atherosclerosis as well as renal stones and gallstones.
More than 40% excess weight is associated with a twofold risk of
premature death. Obesity is partly of (poly)genetic, partly of
environmental origin. Its causes are little known. Two defective genes
have been discovered, one in two male mouse strains with extreme
obesity and one in type 2 diabetes. If the ob[esity]-gene is defective, the
16-kDa protein leptin, coded by the obgene, is absent from plasma.
Injection of leptin
into mice with homozygotic ob mutation counteracts the symptoms of the
gene defect. Its administration to normal mice leads to weight loss. But if
the db-gene has mutated, the leptin receptor in the hypothalamus (in
the arcuate nucleus, among other sites) is defective. While high
concentrations of leptin circulate in plasma, the hypothalamus does not
respond to them. Some obese persons also have a defective leptin gene,
but in most others the plasma leptin concentration is high. In this case the
feedback chain after leptin must have been interrupted somewhere (A,
red X). Various possible defects have been postulated:  Leptin can no
longer overcome the blood– brain barrier (? defective transcytosis). The
inhibitory effect of leptin on the secretion of neuropeptide Y (NPY) in the
hypothalamus, which stimulates food intake and reduces energy
consumption, is abnormal.  Leptin does not cause the release in the
hypothalamus of -melanocortin (melanocytestimulating hormone [-
MSH]), which acts there via MCR-4 receptors and has the opposite effect
of NPY. Quite recently a homozygotic leptin receptor defect was found in
three very obese sisters. As they had never gone through puberty and the
secretion of both somatotropin hormone and thyrotropin-releasing
hormone had been reduced, it seems that leptin also plays a part in other
endocrine regulatory cycles. In 90% of cases of eating disorders it is
young women who are affected, bulimia nervosa (bouts of overeating
followed by self-induced vomiting and/or purgative abuse) being more
common than anorexia nervosa (self-induced weight loss through very
restrictive
diet). These eating disorders are characterized by a distorted body self-
image (the patients feel “too fat” even though they have a normal or
below normal weight) and an abnormal attitude toward eating (association
between the sense of one’s own worth and body weight). There is a
genetic disposition (50% concordance
in monozygotic twins), without the primary genetic defect being known.
Psychological factors, such as disturbed family interaction
(overprotectiveness, avoidance of conflict, rigidity) and sexual-pubertal
conflicts as well as socio-cultural influences (ideals of beauty, social
expectations) are probably significant. The disorder in anorexia nervosa
(B) ranges from eating a very restrictive diet to
complete refusal to eat, and often includes purgative abuse. This results in
marked weight loss, even cachexia, which may require drip feeding. It
leads to severe autonomic–hormonal disorders, for example, increased
cortisol and diminished gonadotropin release (amenorrhea; loss of libido,
and impotence inmales), and even hypothermia, bradycardia, hair loss,
etc. If the condition takes a prolonged course,
the mortality rate can be up to 20%. Bulimia is characterized by eating
binges followed by self-induced vomiting; a reasonably normal body
weight may be maintained.

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