Anorexia nervosa
It is a physical and mental illness , which affects
adults and children .
Causes
Biological factors : help natural sedatives
secreted by the body to reduce the feeling of a sense of hunger in patients
with loss of anorexia nervosa , some studies have shown an imbalance in the
functions of neurotransmitters , particularly serotonin , as well as adrenaline
and dopamine which are important in regulating appetite through
Alheiboethelamos . As well as disruption of thyroid function and hormones in
general . It also showed a lot of studies of radiological scans and expansion
in the presence of voids that contain cerebrospinal fluid , which may go back
to normal as soon as overweight .
Social factors : find people with the loss of
anorexia nervosa encourages their behavior socially where the standards of
beauty shall be taken by slim and exercise style is excellent for life
Ktkulaidhm for a celebrity of physical, especially when characterized by
thinness , as well as some professions that require the thinnest like
supermodels and exhibitors fashion , the hosts of Aviation , players Ballet
some of the sports that do not bear the increase in weight . load, research
also indicates that family atmosphere for these patients is characterized by unfavorable
atmosphere and aggressive patient suffers from a significant degree of
isolationism and lack of a sense of empathy among its members
.
Psychological factors : combines a lot of
therapists for these cases that patients suffer from the inability to
independence from the mother in particular, tends others to interpret their
behavior as a conscious attempt to destroy their bodies inhabited the effects
of authoritarian mother .
Coupled with lack of appetite and weakness of the
bones that become brittle and dangerously skinny . The reason for this is to
lose weight and lack of nutrients such as Alcalaseyoum , was driving a decline
in bone mineral density to increase the risk of fracture and crush . People
with this disease suffer from many medical problems such as
:
Low temperature ( declining to less than 35
degrees).
Swelling of the feet and slow heartbeat
.
Low blood pressure, and change the hair, as
some patients resort to the use of laxatives frequently , leading to a change
in the pH of the blood.
Disorders of the heart and its small size ,
particularly in the late stages of the disease may be the cause of these
disorders low potassium in the blood , which may be dangerous to the patient.
Appetite is the desire to eat food, felt as hunger.
Appetite exists in all higher life-forms, and serves to regulate adequate
energy intake to maintain metabolic needs. It is regulated by a close interplay
between the digestive tract, adipose tissue and the brain. Appetite has a
relationship with every individual's behavior. Appetitive and consummatory
behaviours are the only processes that involve energy intake, whereas all other
behaviours affect the release of energy. When stressed, appetite levels may
increase and result in an increase of food intake. Decreased desire to eat is
termed anorexia, while polyphagia (or "hyperphagia") is increased
eating. Dysregulation of appetite contributes to anorexia nervosa, bulimia
nervosa, cachexia, overeating, and binge eating disorder.
Contents
1 Physiological
factors
2
Regulation
2.1 Effector
2.2 Sensor
3
Role in disease
4
Pharmacology
5
See also
6
References
Physiological factors
Cannon and Washburn (1912) proposed that eating begins
when we have an empty stomach. They suggest that the walls of an empty stomach
rub against each other to produce what are commonly called "hunger
pangs". Some skeptics called Cannon's explanation of hunger "the
rumble theory". However, observations of surgical patients indicated that
there was more to the onset of eating than hunger pangs. Removal of the stomach
did not abolish hunger pangs, and these patients reported the same feelings of
hunger and satiety that they had experienced before surgery (Inglefinger,
1944). (The patients had had their stomachs removed because of cancer or large
ulcers, and their esophagi had been attached directly to their small
intestines). Although the patients ate small, frequent meals because they had
no stomachs to hold food, their reports of feelings of hunger and their total
food intake were essentially normal. Depletion of the body's store of nutrients
is a more likely cause of hunger. The primary fuels for the cells of our body
are glucose (a simple sugar) and fatty acids (compounds produced by the
breakdown of fats). If the digestive system contains food, these nutrients are
absorbed in the blood and nourish our cells. But the digestive tract is
sometimes empty; in fact, it is empty when we wake up every morning. There must
be a reservoir that stores nutrients to keep the cells of the body nourished
when the gut is empty. Indeed, there are two reservoirs: a short-term reservoir
and a long-term reservoir. The short-term reservoir stores carbohydrates and
the long-term reservoir stores fat. A number of variables have been found to
relate to appetite sensation in individuals. The most influential of these is
gender and age, with females experiencing greater appetite satisfaction than
males and a decrease in appetite with age. Although BMI was not found to
influence appetite, smokers and women ovulating experienced a lower appetite
than their counterparts.[1]
Regulation
The regulation of appetite (the appestat) has been the
subject of much research in the last decade. Breakthroughs included the discovery,
in 1994, of leptin, a hormone produced by the adipose tissue that appeared to
provide negative feedback. Leptin is a peptide hormone that affects homeostasis
and immune responses.[2] Lowering food intake can lower leptin levels in the
body, while increasing the intake of food can raise leptin levels. Later
studies showed that appetite regulation is an immensely complex process
involving the gastrointestinal tract, many hormones, and both the central and
autonomic nervous systems.[2] The circulating gut hormones that regulate many
pathways in the body result in appetite stimulation.[3]
Effector
The hypothalamus, a part of the brain, is the main
regulatory organ for the human appetite. The neurons that regulate appetite
appear to be mainly serotonergic, although neuropeptide Y (NPY) and
Agouti-related peptide (AGRP) also play a vital role. Hypothalamocortical and
hypothalamolimbic projections contribute to the awareness of hunger, and the
somatic processes controlled by the hypothalamus include vagal tone (the
activity of the parasympathetic autonomic nervous system), stimulation of the
thyroid (thyroxine regulates the metabolic rate), the
hypothalamic-pituitary-adrenal axis and a large number of other mechanisms.
Opioid receptor-related processes in the nucleus accumbens and ventral pallidum
effect the palatability of foods.[4]
The nucleus accumbens (NAc) is the area of the brain
that coordinates neurotransmitter, opioid and endocannabinoids signals to
control feeding behaviour. The few important signalling molecules inside the
NAc shell modulates the motivation to eat and the affective reactions for food.
These molecules include the DA, Ach, oipoids and cannabinoids and their action
receptors inside the brain, DA, muscarinic and MOR and CB1 receptors
respectively.[5]
Sensor
The hypothalamus senses external stimuli mainly
through a number of hormones such as leptin, ghrelin, PYY 3-36, orexin and
cholecystokinin; all modify the hypothalamic response. They are produced by the
digestive tract and by adipose tissue (leptin). Systemic mediators, such as
tumor necrosis factor-alpha (TNFα), interleukins 1 and 6 and
corticotropin-releasing hormone (CRH) influence appetite negatively; this
mechanism explains why ill people often eat less.
In addition, the biological clock (which is regulated
by the hypothalamus) stimulates hunger. Processes from other cerebral loci,
such as from the limbic system and the cerebral cortex, project on the
hypothalamus and modify appetite. This explains why in clinical depression and
stress, energy intake can change quite drastically.
Role in disease
A limited or excessive appetite is not necessarily
pathological. Abnormal appetite could be defined as eating habits causing
malnutrition and related conditions such as obesity and its related problems.
Both genetic and environmental factors may regulate
appetite, and abnormalities in either may lead to abnormal appetite. Poor
appetite (anorexia) can have numerous causes, but may be a result of physical
(infectious, autoimmune or malignant disease) or psychological (stress, mental
disorders) factors. Likewise, hyperphagia (excessive eating) may be a result of
hormonal imbalances, mental disorders (e.g. depression) and others. Dyspepsia,
also known as indigestion, can also affect appetite as one of its symptoms is
feeling "overly full" soon after beginning a meal.[6]
Abnormal appetite may also be linked to genetics on a
chromosomal scale. In the 1950s, the discovery of the Prader Willi Syndrome, a
type of obesity, displayed a causation at a gene locus. Additionally, anorexia
nervosa and bulimia nervosa are more commonly found in females than males -
thus hinting a possibility of a linkage to the X-chromosome.[7]
Dysregulation of appetite lies at the root of anorexia
nervosa, bulimia nervosa and binge eating disorder. Anorexia nervosa is an
eating condition categorized by a penetrating fear of being fat and severe
limit of food consumption. Furthermore, they might do excessive exercise.
Individuals that have anorexia have high levels of ghrelin, a hormone that
stimulates appetite, so the body is trying to cause hunger, but it is being
suppressed by the person.[8] Binge eating disorder (commonly referred to as
BED,) is described as eating excessively (or uncontrollably) between periodic
time intervals. The risk for BED can be present in children and most commonly
manifests during adulthood. Studies suggest that the heritability of BED in
adults is approximately 50%.[9] Likewise to bulimia, several people may be
involved in purging and binging. They might puke after food intake or take
purgatives. However, the person may still believe they are overweight.[10]
Various hereditary forms of obesity have been traced
to defects in hypothalamic signalling (such as the leptin receptor and the MC-4
receptor), or are still awaiting characterisation – Prader-Willi syndrome – in
addition, decreased response to satiety may promote development of obesity.[11]
Other than genetically-stimulated appetite
abnormalities, there are physiological ones that do not require genes for
activation. For example, ghrelin and leptin are released from the stomach and
pancreas, respectively, into the blood stream at the signal of the
hypothalamus. Ghrelin stimulates feelings of hunger, whereas leptin stimulates
feelings of satisfaction from food.[12] Any changes in normal production levels
of these two hormones will lead to obesity. Looking at leptin, the more cells
present in a body, the more adipose tissues there are, and thus, the more
leptin would be produced. This overproduction of leptin will cause the
hypothalamus to become resistant to leptin and so, although the pancreas is
producing leptin, the body will not understand that it should stop eating.[13]
This will produce a perpetual cycle for those that are obese.
Pharmacology
Mechanisms controlling appetite are a potential target
for weight loss drugs. Appetite control mechanisms seem to strongly counteract
under eating, whereas, they appear weak to control over-eating. Early
anorectics were fenfluramine and phentermine. A more recent addition is
sibutramine which increases serotonin and noradrenaline levels in the central
nervous system, but had to be withdrawn from the market when it was shown to
have an adverse cardiovascular risk profile. Similarly, the appetite
suppressant rimonabant (a cannabinoid receptor antagonist) had to be withdrawn
when it was linked with worsening depression and increased risk of suicide.
Recent reports on recombinant PYY 3-36 suggest that this agent may contribute
to weight loss by suppressing appetite.
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