Physiological basis of hunger

1. PHYSIOLOGICAL BASIS OF
HUNGER
Module 1

2. GLOSSARY
appetite: the integrated response to the sight, smell, thought, or taste of food that
initiates or delays eating.
hunger: the painful sensation caused by a lack of food that initiates food-seeking
behavior
hypothalamus: a brain center that controls activities such as maintenance of water
balance, regulation of body temperature, and control of appetite.
satiation: the feeling of satisfaction; and fullness that occurs during a meal and stop
eating. Satiation determines how much food is consumed during a meal.

3. satiety: the feeling of fullness and satisfaction that occurs after a meal and
inhibits eating until the next meal. Satiety determines how much time passes
between meals.
binge-eating disorder: an eating disorder with criteria similar to those of
bulimia nervosa, excluding purging or other compensatory behaviors.
Bulimia nervosa: an eating disorder characterized by repeated episodes of
binge eating usually followed by self induced vomiting, misuse of laxatives or
diuretics, fasting, or excessive exercise.

4. Physiology of appetite and hunger Regulation of food intake
Ingestion of food is determined by the intrinsic desire of the person for food,
this is called hunger
hunger is the physiological response to a need for food caused by nerve
signals and chemical messengers originating and acting in the brain, primarily
in the hypothalamus.
• Hormones of hypothalamus promotes thoughts of eating
• The type of food the person preferred is determined by appetite

5. • When there are no food for many hours, the stomach undergo intense rhythmic
contraction called hunger contractions
• These contraction cause a tight feeling in the stomach and cause pain known as hunger
pangs
• Hungry person also become more tense and restless and often has a strange feeling in his
entire body
• After a meal Satiety is developed; this means the feeling of fullness and satisfaction that
occurs after a meal and inhibits eating until the next meal. Satiety determines how much
time passes between meals
• The feeling of satiety continues to suppress hunger and allows a person to not eat again
for a while.

6. During the course of a meal, as food enters the GI tract and hunger diminishes, satiation
develops "stop eating, ".
As receptors in the stomach stretch and hormones such as cholecystokinin become active,
the person begins to feel full. The response: satiation occurs and the person stops eating

8. Factors influences hunger
1-Physiological influences of hunger
Empty stomach
Gastric contractions
• Absence of nutrients in small intestine GI
• Hormones such as Ghrelin that produced by fundus of the human stomach and
cells of the pancreas and Leptin release from adipose tissue

9. Endorphins (the brain's pleasure chemicals)
Endorphins are neurotransmitters produced by pituitary gland and hypothalamus
Enhancing the desire for food by the smell,sight, or taste of foods,
Dopamine is classified as a catecholamine (a class of molecules that serve as neurotransmitters
and hormones).

10. 2-Sensory influences
• Seek food and start me
Thought, sight, smell, sound, taste of food
Endorphins

11. 3-Cognitive influences
Keep eating
• Presence of others, social stimulation
Perception of hunger, awareness of fullness
• Favorite foods, foods with special meanings
• Time of day
• Abundance of available food

12. 4-Postingestive influences (after food enters the digestive tract)
• Satiation: End meal
• Food in stomach activates stretch receptors
Nutrients in small intestine draw out hormones (for example, fat draw out
cholecystokinin, which slows gastric emptying)
cholecystokinin, receptor regulates satiety and the release of beta-endorphin and
dopamine.

13. 5-Postabsorptive influences (after nutrients enter the blood)
. Satiety: Several hours later
• Nutrients in the blood signal the brain (via nerves and hormones) about their
availability, use, and storage
As nutrients decrease, satiety diminishes
Hunger develops

14. Neural Centers for regulation of food intake hypothalamus.
• Most hormones are secreted from the glands that produce them under the influence
of stimulating hormones from the hypothalamus.
• The hypothalamus is a part of the brain involved in the control of involuntary
activity in the body; contains many centers of neural control such as temperature,
hunger, appetite and thirst
These hormones in turn are activated by releasing hormones from the pituitary
gland.

15. Lateral hypothalamus & Ventromedial nuclei of the hypothalamus
Hunger and satiety centers; hypothalamus gland responsible of the hunger and satiety
• Lateral hypothalamus stimulation cases a person . to eat greedily or hungrily (hunger or
feeding center neurotransmitters Endorphins )
• Ventromedial nuclei of the hypothalamus causes the sensation of food rejection or complete
satiety (satiety center neurotransmitters )
•Destructive lesions or trauma of the Lateral hypothalamus causes complete lack of desire for
food
• While destructive lesions of the Ventromedial nuclei of the hypothalamus cause; voracious
and the person continued eating until it become extremely obese (overactive)

17. Factors that regulate food intake
Regulation of food intake can be divided into;
● 1-nutritional regulation (metabolic regulation);
concerned with the maintenance of normal quantities of nutrient stores in the body
• Factors that control the degree of activity of feeding center of the hypothalamus are;

18. A) Decrease in blood glucose concentration is associated with the development of
hunger (the glucostatic regulation theory of hunger and feeding regulation)
B) the effect of blood amino acid concentration on feeding; increase concentration
of amino acid in the blood reduces feeding activity
C) effect of fat metabolism on feeding (long term feeding); as the quantity of
adipose tissue increases the rate of feeding decrease this is caused by a negative
feedback regulation
D) body temperature and food intake interrelationship; cold person tends to
overeat

19. • When exposed to heat tends to under eat
This relationship is due to interaction within the hypothalamus between the temperature
regulation system (hypothalamic thermostat) and the food regulating system (Lateral
hypothalamus & Ventromedial nuclei of the hypothalamus)
• The temp of the body is regulated by nervous feedback mechanisms these mechanisms
operate through temperature regulating centers in the hypothalamus
● 2-alimentray regulation, non-metabolic regulation;
Habit, Gastrointestinal filling

20. Neural Centers That Influence the Mechanical Process of Feeding.
Another aspect of feeding is the mechanical act of the feeding process itself. If
the brain is sectioned below the hypothalamus but above the mesen-cephalon, the
animal can still perform the basic mechanical features of the feeding process. It
can salivate, lick its lips,chew food, and swallow. Therefore, the actual
mechanics of feeding are controlled by centers in the brain stem. The function of
the other centers in feeding, then, is to control the quantity of food intake and to
excite these centers of feeding mechanics to activity.

21. Neural centers higher than the hypothalamus also play important roles in the control of
feeding, particularly in the control of appetite.
These centers include the amygdala and the prefrontal cortex, which are closely
coupled with the hypothalamus. that portions of the amygdala are a major part of the
olfactory nervous system.
Destructive lesions in the amygdala have demonstrated that some of its areas increase
feeding, whereas others inhibit feeding. In addition, stimulation of some areas of the
amygdala elicits the mechanical act of feeding.
An important effect of destruction of the amygdala on both sides of the brain is a
“psychic blindness” in the choice of foods. In other words, the animal loses or at least
partially loses the appetite control that determines the Type and quality of food it eats.

22. Hormonal control of feeding, appetite and hunger
• Hormones that play an important role in controlling feeding pattern;
Short-term signals, consisting of:
● gastric hormone ghrelin (hunger signal),
● duodenal peptide cholecystokinin (CCK; meal-related satiety signal).
Medium-term signals, consisting of:
● colonically synthesized hormone PYY3–36 which suppresses interprandial appetite,
● plasma concentrations of nutrients.
–
•

23. Long-term signals, consisting of:
● adipose tissue hormone leptin, which works to keep the level of fat in the
body constant,
● pancreatic hormone insulin, which not only regulates blood glucose but
which acts with leptin to regulate long-term body weight
● energy signals.

24. Short-term signals Medium-term
signals
Long-term
signals
Stimulator Ghrelin (a) energy
signals
Anti-stimulators CCK PYY3–36 (a) leptin
Vagal afferents
relaying
mechanical
distention
Plasma nutrients'
concentrations
(b) insulin
(c) energy
signals

25. Short-term signals
Gastrointestinal Filling Inhibits Feeding. When the gastrointestinal tract becomes
distended, especially the stomach and the duodenum, stretch inhibitory signals are
transmitted mainly by way of the vagi to suppress the feeding center, thereby
reducing the desire for food Gastrointestinal Hormonal Factors Suppress Feeding.
Cholecystokinin (CCK), released mainly in response to fat and proteins entering the
duodenum, enters the blood and acts as a hormone to influence several
gastrointestinal functions such as gallbladder contraction, gastric emptying, gut
motility, and gastric acid secretion.

26. However, CCK also activates receptors on local sensory nerves in the duodenum,
sending messages to the brain via the vagus nerve that contribute to satiation and meal
cessation. The effect of CCK is short-lived and chronic administration of CCK by
itself has no major effect on body weight. Therefore, CCK functions mainly to
prevent overeating during meals but may not play a major role in the frequency of
meals or the total energy consumed

27. Peptide YY (PYY) is secreted from the entire gastrointestinal tract, but
especially from the ileum and colon. Food intake stimulates release of PYY,
with blood concen-trations rising to peak levels 1 to 2 hours after ingesting a
meal.
These peak levels of PYY are influenced by the number of calories ingested and
the composition of the food, with higher levels of PYY observed after meals
with
a high fat content.
Although injections of PYY into mice have been shown to decrease food intake
for 12 hours or more, the importance of this gastrointestinal hormone in
regulating appetite in humans is still unclear.

28. the presence of food in the intestines stimulates them to secrete glucagon-like
peptide (GLP), which in turn enhances glu-cose-dependent insulin production
and secretion from the pancreas.
Glucagon-like peptide and insulin both tend to suppress appetite. Thus, eating a
meal stimulates the release of several gastrointestinal hormones that may induce
satiety and reduce further intake of food

29. Ghrelin—a Gastrointestinal Hormone—Increases Feeding. Ghrelin is a hormone
released mainly by the oxyntic cells of the stomach but also, to a much less extent,
by the intestine. Blood levels of ghrelin rise during fasting, peak just before eating,
and then fall rapidly after
a meal, suggesting a possible role in stimulating feeding. Also, administration of
ghrelin increases food intake in experimental animals, further supporting the
possibility that it may be an orexigenic hormone.

30. Intermediate and Long-Term Regulation
of Food Intake
An animal that has been starved for a long time and is then presented with
unlimited food eats a far greater quantity than does an animal that has been on a
regular diet.
Conversely, an animal that has been force-fed for several weeks eats very little
when allowed to eat according to its own desires. Thus, the feeding control
mechanism of the body is geared to the nutritional status of the body.

31. Importance of Having Both Long- and Short-Term
Regulatory Systems for Feeding
The long-term regulatory system for feeding, which includes all the nutritional energy
feedback mechanisms, helps maintain constant stores of nutrients in the tissues,
preventing them from becoming too low or too high.
The short-term regulatory stimuli serve two other purposes.
First, they tend to make the person eat smaller quantities at each eating session, thus
allowing food to pass through the gastrointestinal tract at a steadier pace so that its
digestive and absorptive mechanisms can work at optimal rates rather than becoming
periodically overburdened. Second, they help prevent the person from eating amounts
at each meal that would be too much for the metabolic storage systems once all the
food has been absorbed.

32. Effect of Blood Concentrations of Glucose, Amino Acids, and Lipids on Hunger
and Feeding
It has long been known that a decrease in blood glucose concentration causes hunger,
which has led to the so-called glucostatic theory of hunger and feeding regulation.
Similar studies have demonstrated the same effect for blood amino acid concentration
and blood concentration of breakdown products of lipids such as the keto acids and
some fatty acids, leading to the aminostatic and lipostatic theories of regulation.
That is, when the availability of any of the three major types of food decreases, the
desire for feeding is increased, eventually returning the blood metabolite
concentrations back toward normal.

33. Neurophysiological studies of function in specific areas of the brain also support the
glucostatic, aminostatic, and lipostatic theories, by the following observations:
(1) A rise in blood glucose level increases the rate of firing of glucoreceptor neurons
in the satiety center in the ventro-medial and paraventricular nuclei of the
hypothalamus.
(2) The same increase in blood glucose level simultaneously decreases the firing of
glucosensitive neurons in the hunger center of the lateral hypothalamus. In addition,
some amino acids and lipid substances affect the rates of firing of these same neurons
or other closely associated neurons.

34. Temperature Regulation and Food Intake
When an animal is exposed to cold, it tends to increase feeding; when it is exposed
to heat, it tends to decrease its caloric intake. This is caused by interaction within the
hypothalamus between the temperature-regulating system and the food intake
regulating system. This is important because increased food intake in a cold animal
(1) increases its metabolic rate and
(2) provides increased fat for insulation, both of which tend to correct the cold state.

35. leptin (identified in 1994), Leptin release from adipose tissue is enhanced by insulin
• Obese persons are found with high circulating leptin levels but without response to
leptin in the arcuate nucleus
• Neurons are nerve cells that receive and send electrical signals over long distances
within the body
Acts on hypothalamus to decrease food intake and increase energy consumption
• Abnormalities in leptin signaling appear to be correlated to overeating and obesity

36. ghrelin (identified in 1999), called "hunger hormone," is produced in the stomach and
brain, induces food intake, and operates through a brain region that controls cravings
for food and other energy sources
ghrelin is peptide hormone secreted by gastric mucosa, on an empty stomach and
during fasting this hormones increase, and level fall rapidly after meal
• work together with leptin to balance the states of hunger and satiety

37. Insulin release from pancreatic islets cells follows intake of both carbohydrates and
proteins.
• Insulin increase appetite by inhibiting stimulatory neurons and by activating releasing
neurons.
• Resistance to insulin is very often associated with obesity and the loss of insulin's
regulation of metabolism as seen in diabetes type 2.
• Insulin increase appetite by inhibiting stimulatory neurons and by activating releasing
neurons.
• Resistance to insulin is very often associated with obesity and the loss of insulin's
regulation of metabolism as seen in diabetes type 2.

38. orexin, Also called Hypocretins
neurotransmitter hormones that increase food intake,
Synthesized in neurons located in the lateral Hypothalamus
orexin are inhibited by leptin and activated by Ghrelin and Hypoglycemia

39. Cholecystokinin
is a peptide hormone of the gastrointestinal system
responsible for stimulating the digestion of fat and protein.
Cholecystokinin, officially called pancreozymin, is
synthesized and secreted by enteroendocrine cells in the
duodenum, the first segment of the small intestine. Its
presence causes the release of digestive enzymes and bile
from the pancreas and gallbladder, respectively, and also
acts as a hunger suppressant.
CCK plays important physiological roles both
as a neuropeptide in the central nervous system and as a
peptide hormone in the gut. It participates in a number of
processes such as digestion, satiety and anxiety.

40. As a peptide hormone, CCK mediates satiety by acting on the CCK
receptors distributed widely throughout the central nervous system. The mechanism for
hunger suppression is thought to be a decrease in the rate of gastric emptying. CCK
also has stimulatory effects on the vagus nerve, effects that can be inhibited by
capsaicin.The stimulatory effects of CCK oppose those of ghrelin, which has been
shown to inhibit the vagus nerve.
The effects of CCK vary between individuals. For example, in rats, CCK
administration significantly reduces hunger in adult males, but is slightly less effective
in younger subjects, and even slightly less effective in females. The hunger-
suppressive effects of CCK also are reduced in obese rats.

41. Peptide yy
After PYY is released in your bloodstream, PYY binds to receptors, or cells that
receive signals, in the brain. It also functions by slowing down the movement of food
in the digestive tract.
Your body produces PYY when there is food in the digestive tract, especially food
that contains fat and protein. Eating high calorie foods causes your body to produce
more PYY than eating low calorie foods. PYY levels are the highest two hours after
eating but eventually PPY decreases. Most people have low levels of PYY after not
eating for a long period of time.

42. Although it is uncommon, very
high levels of PYY will decrease your
appetite. High PYY levels are often
associated with conditions that may lead
to weight loss such as eating disorders,
inflammatory bowel disease and certain
cancers. Low PYY levels mean that you
may experience an increase in appetite.
Lower PYY levels may contribute to
weight gain, however it is not believed to
be the main cause of obesity. It is very
rare to have a genetic or endocrine
disorder of PYY.

43. Glucagon-like peptide 1 (GLP-1)
is a 30-amino acid peptide hormone produced in the intestinal epithelial endocrine L-
cells by differential processing of proglucagon, the gene which is expressed in these
cells. The current knowledge regarding regulation of proglucagon gene expression in
the gut and in the brain and mechanisms responsible for the posttranslational
processing are reviewed. GLP-1 is released in response to meal intake, and the stimuli
and molecular mechanisms involved are discussed. GLP-1 is extremely rapidly
metabolized and inactivated by the enzyme dipeptidyl peptidase IV even before the
hormone has left the gut, raising the possibility that the actions of GLP-1 are
transmitted via sensory neurons in the intestine and the liver expressing the GLP-1
receptor.

44. Because of this, it is important to distinguish between measurements of the intact hormone
(responsible for endocrine actions) or the sum of the intact hormone and its metabolites,
reflecting the total L-cell secretion and therefore also the possible neural actions. The main
actions of GLP-1 are to stimulate insulin secretion (i.e., to act as an incretin hormone) and
to inhibit glucagon secretion, thereby contributing to limit postprandial glucose excursions.
It also inhibits gastrointestinal motility and secretion and thus acts as an enterogastrone and
part of the “ileal brake” mechanism. GLP-1 also appears to be a physiological regulator of
appetite and food intake. Because of these actions, GLP-1 or GLP-1 receptor agonists are
currently being evaluated for the therapy of type 2 diabetes. Decreased secretion of GLP-1
may contribute to the development of obesity, and exaggerated secretion may be
responsible for postprandial reactive hypoglycemia.

45. Obesity
Obesity can be defined as an excess of body fat. A
surrogate marker for body fat content is the body
mass index (BMI), which is calculated as:
BMI = Weight in kg/Height in m2
In clinical terms, a BMI between 25 and 29.9kg/m2
is called overweight, and a BMI greater than 30
kg/m2 is called obese. BMI is not a direct estimate
of adiposity and does not take into account the fact
that some individuals have a high BMI due to a large
muscle mass. A better way to define obesity is to
actually measure the percentage of total body fat.

46. Obesity is usually defined as 25 % or greater total body fat in men and 35 % or greater
in women. Although percentage of body fat can be estimated with various methods,
such as measuring skin-fold thickness, bioelectrical imped-ance, or underwater
weighing, these methods are rarely used in clinical practice, where BMI is commonly
used to assess
obesity.
Obesity Results from Greater Energy Intake Than Energy Expenditure. When
greater quantities of energy (in the form of food) enter the body than are expended, the
body weight increases, and most of the excess energy is stored as fat. Therefore,
excessive adiposity (obesity) is caused by energy intake in excess of energy output.
For each 9.3 Calories of excess energy that enter the body, approximately 1 gram of fat
is stored.Fat is stored mainly in adipocytes in subcutaneous tissue
and in the intraperitoneal cavity, although the liver and other tissues of the body often
accumulate significant amounts of lipids in obese persons.

47. CAUSES OF OBESITY
Decreased Physical Activity and Abnormal Feeding Regulation as Causes of
Obesity
The causes of obesity are complex. Although genes play an important role in
programming the powerful physiological mechanisms that regulate food intake and
energy metabolism, lifestyle and environmental factors may play the dominant role in
many obese people. The rapid increase in the prevalence of obesity in the past 20 to 30
years emphasizes the important role of lifestyle and environmental factors because
genetic changes could not have occurred so rapidly.

48. Edentary Lifestyle Is a Major Cause of Obesity
Regular physical activity and physical training are known to increase
muscle mass and decrease body fat mass, whereas inadequate physical activity is typically
associated with decreased muscle mass and increased adiposity. For example, studies
have shown a close association between sedentary behaviors, such as prolonged television
watching, and obesity.About 25 to 30 percent of the energy used each day by the average
person goes into muscular activity, and in a laborer, as much as 60 to 70 percent is used in
this way. In obese people, increased physical activity usually increases energy
expenditure more than food intake, resulting in significant weight loss. Even a single
episode of strenuous exercise may increase basal energy expenditure for several hours
after the physical activity is stopped. Because muscular activity is by far the most
important means by which energy is expended in the body, increased physical activity is
often an effective
means of reducing fat stores.

49. Abnormal Feeding Behavior Is an Important Cause of Obesity
Although powerful physiological mechanisms regulate food intake, there are also
important environmental and psychological factors that can cause abnormal feeding
behavior, excessive energy intake, and obesity.Environmental, Social, and
Psychological Factors Contribute to Abnormal Feeding. As discussed previously, the
importance of environmental factors is evident from the rapid increase in the
prevalence of obesity in most industrialized countries, which has coincided with an
abundance of high-energy foods (especially fatty foods) and sedentary
lifestyles.Psychological factors may contribute to obesity in some people. For
example, people often gain large amounts of weight during or after stressful
situations, such as the death of a parent, a severe illness, or even mental depression. It
seems that eating can be a means of releasing tension.

50. Childhood Overnutrition as a Possible Cause of Obesity
One factor that may contribute to obesity is the prevalent idea that healthy eating
habits require three meals a day and that each meal must be filling. Many young
children are forced into this habit by overly solicitous parents, and the children
continue to practice it throughout life.The rate of formation of new fat cells is
especially rapid in the first few years of life, and the greater the rate of fat storage, the
greater the number of fat cells. The number of fat cells in obese children is often as
much as three times that in normal children. Therefore, it has been suggested that
over-nutrition of children especially in infancy and, to a lesser extent, during the later
years of childhood can lead to a life-time of obesity.

51. Neurogenic Abnormalities as a Cause of Obesity
We previously pointed out that lesions in the ventromedial nuclei of the
hypothalamus cause an animal to eat excessively and become obese. People with
hypophysial tumors that encroach on the hypothalamus often develop progressive
obesity, demonstrating that obesity in human beings, too, can result from damage to
the hypothalamus.Although hypothalamic damage is almost never found in obese
people, it is possible that the functional organization of the hypothalamic or other
neurogenic feeding centers in obese individuals is different from that in nonobese
persons.

52. Also, there may be abnormalities of neurotransmitters or receptor mechanisms in
the neural pathways of the hypothalamus that control feeding. In support of this
theory, an obese person who has reduced to normal weight by strict dietary
measures usually develops intense hunger that is demonstrably far greater than that
of a normal person. This indicates that the “set-point” of an obese person’s feeding
control system is at a much higher level of nutrient storage than that of a nonobese
person.

53. Genetic Factors as a Cause of Obesity
Obesity definitely runs in families. Yet it has been difficult to determine the
precise role of genetics in contributing to obesity because family members
generally share many of the same eating
habits and physical activity patterns. Current evidence, how-ever, suggests that
20 to 25 percent of cases of obesity may be caused by genetic factors.Genes can
contribute to obesity by causing abnormalities of
(1) one or more of the pathways that regulate the feeding centers
(2) energy expenditure and fat storage.

54. Three of the monogenic (single-gene) causes of obesity are
(1) mutations of MCR-4, the most common monogenic form of obesity
discovered thus far;
(2) congenital leptin deficiencycaused by mutations of the leptin gene, which
are very rare;
(3) mutations of the leptin receptor, also very rare. All these monogenic forms
of obesity account for only a very small percentage of obesity. It is likely that
many gene variations interact with environmental factors to influence the
amount and distribution of body fat.

55. Treatment of Obesity
Treatment of obesity depends on decreasing energy input below energy
expenditure and creating a sustained negative energy balance until the desired weight
loss is achieved. In other words, this means either reducing energy intake or increasing
energy expenditure.

56. Diet
To decrease energy intake, most reducing diets are designed to contain large quantities
of “bulk,” which is generally made up of non-nutritive cellulose substances. This bulk
distends the stomach and thereby partially appeases hunger. In experimental animals,
such a procedure simply makes the animal increase its food intake even more, but
human beings can often fool themselves because their food intake is sometimes
controlled as much by habit as by hunger. As pointed out later in connection with
starvation, it is important to prevent vitamin deficiencies during the dieting period.

57. Drugs
Various drugs for decreasing the degree of hunger have been used in the treatment of
obesity. The most widely used drugs are amphetamines , which directly inhibit the
feeding centers in the brain. One drug for treating obesity is sibutramine, a
sympathomimetic
that reduces food intake and increases energy expenditure. The danger in using these
drugs is that they simultaneously overexcite the sympathetic nervous system and
raise the blood pressure. Also, a person soon adapts to the drug, so weight reduction
is usually no greater than 5 to 10 percent.Another group of drugs works by altering
lipid metabolism. For example, orlistat, a lipase inhibitor, reduces the intestinal
digestion of fat. This causes a portion of the ingested fat to be lost in the feces and
therefore reduces energy absorption. However, fecal fat loss may cause unpleasant
gastrointestinal side effects, as well as loss of fat-soluble vitamins in the feces.

58. Exercise
Significant weight loss can be achieved in many obese persons with increased
physical activity. The more exercise one gets, the greater the daily energy
expenditure and the more rapidly the obesity disappears. Therefore, forced exercise
is often an essential part of treatment. The current clinical guidelines for the
treatment of obesity recommend that the first step be lifestyle modifications that
include increased
physical activity combined with a reduction in caloric intake. For morbidly obese
patients with BMIs greater than 40, or for patients with BMIs greater than 35 and
conditions such as hypertension or type II diabetes that predispose them to other
serious diseases,various surgical procedures can be used to decrease the fat mass of
the body or to decrease the amount of food that can be eaten at each meal.

59. Surgery
Two of the most common surgical procedures used in the United States to treat
morbid obesity are gastric bypass surgery and gastric banding surgery. Gastric
bypass surgery involves construction of a small pouch in the proximal part of the
stomach that is then connected to the jejunum with a section of small bowel of
varying lengths; the pouch is separated from the remaining part of the stomach with
staples. Gastric banding surgery involves placing an adjustable band around the
stomach near its upper end; this also creates a small stomach pouch that restricts the
amount of food that can be eaten at each meal. Although these surgical procedures
generally produce substantial weight loss in obese patients, they are major
operations, and their long-term effects on overall health and mortality are still
uncertain.

60. Eating disorder
• Both men and women are susceptible to eating disorders, although a greater percent
of eating disorders are found in women.
The three most common eating disorders found are:
● 1-Anorexia Nervosa
● 2-Bulimia
● 3-Inantion
● 4-Cachexia
● 5-Picca

61. Warning Signs of an Eating Disorder
Preoccupation (worry) with food and weight
Repeatedly expressed concerns about being fat Increasing criticism of one's body
● Frequent eating alone
● Use of laxatives
● Trips to the bathroom during or following meals
● Continuous drinking of diet soda or water
● Compulsive, excessive exercise
● Complaining of always being cold

62. Anorexia nervosa
• Anorexia nervosa: an eating disordercharacterized
by a refusal to maintain a minimally normal body
weight and a distortion in perception of body
shape and weight
( BMI < 17.5)
Excessive concern with weight or weight gain

63. Health Complications from Anorexia
• Anorexia poses life-threatening complications including:
malnutrition
Abnormal Heart Rhythms
low blood pressure
Dehydration
electrolyte imbalance
• amenorrhea (interruption of the menstrual cycle)
osteoporosis (decreased bone mass)
sleep disorder

64. Signs and Symptoms of Anorexia
• Excessive weight loss
Always thinking about food, calories, and body weight
Wearing layered clothing
• Mood swings or depression
Inappropriate use of laxatives, or diuretics in order to lose weight
Avoiding activities that involve food

65. Bulimia
• Bulimia is one such eating disorder that describes a cycle of binging and purging.
• Bulimia can begin when restrictive diets fail, or the feeling of hunger associated with
reduced calorie intake leads to reduce eating.
• Like the person with anorexia nervosa, the person with bulimia nervosa spends much
time thinking about body weight and food
• Bulimia are multi-factorial, with psycho developmental, socio-cultural, and
genetic contribution factors

66. Bulimia is of Two types:
1-Purging type: The person regularly engages in self-induced vomiting or the misuse
of laxatives, diuretics.
2-Nonpurging type: The person uses other compensatory behaviors, such as fasting or
excessive exercise, but does not regularly engage in self-induced vomiting or the
misuse of laxatives, diuretics,

67. Signs and Symptoms of Bulimia
• Excessive weight loss
Visiting the bathroom after meals
• Depression
• Excessive dieting, followed by binge eating
Always criticizing one's body

68. Inanition
is the opposite of obesity and is characterized by extreme weight loss. It can be
caused by inadequate availability of food or by pathophysiological conditions
that greatly decrease the desire for food, including psychogenic disturbances,
hypothalamic abnormalities, and factors released from peripheral tissues. In
many instances, especially in those with serious diseases such as cancer, the
reduced desire for food may be associated with increased energy expenditure,
causing serious weight loss.

69. Cachexia
is a metabolic disorder of increased energy
expenditure leading to weight loss greater than
that caused by reduced food intake alone.
Anorexia and cachexia often occur together in
many types of cancer or in the “wasting
syndrome” observed in patients with acquired
immunodeficiency syndrome (AIDS) and
chronic inflammatory disorders. Almost all
types of cancer cause both anorexia and
cachexia, and more than half of cancer patients
develop anorexia-cachexia syndrome during the
course of their disease.

70. Picca
Pica is a eating disorder characterized by an appetite
for substances that are largely non-nutritive.The
substance may be biological such as hair or feces ,
natural such as ice or dirt , and otherwise chemical or
manmade. The term originates from the Latin word
pica , from the concept that magpies will eat almost
anything.

71. According to Diagnostic and Statistical Manual of Mental Disorders, 5th Edition
(DSM-5) criteria, for these actions to be considered pica, they must persist for more
than one month at an age when eating such objects is considered developmentally
inappropriate, not part of culturally sanctioned practice, and sufficiently severe to
warrant clinical attention. Pica may lead to intoxication in children, which can result
in an impairment of both physical and mental development. In addition, it may
cause surgical emergencies to address intestinal obstructions, as well as more subtle
symptoms such as nutritional deficiencies and parasitosis.Pica has been linked to
other mental and emotional disorders. Stressors such as emotional trauma, maternal
deprivation, family issues, parental neglect, pregnancy, and a disorganized family
structure[failed verification] are strongly linked to pica as a form of comfort

72. Pica is the consumption of substances with no significant nutritional value such
as soap, drywall, or paint. Subtypes are characterized by the substance eaten:
● Acuphagia (sharp objects)
● Amylophagia (purified starch, as from corn)
● Cautopyreiophagia (burnt matches)
● Coniophagia (dust)
● Coprophagia (feces)
● Emetophagia (vomit)
● Geomelophagia (raw potatoes)
● Geophagia (earth, soil, clay, chalk)
● Hyalophagia (glass)

73. ● Lithophagia (stones)
● Metallophagia (metal)
● Mucophagia (mucus)
● Pagophagia (ice)
● Plumbophagia (lead)
● Trichophagia (hair, wool, and other fibers)
● Urophagia (urine)
● Hematophagia (vampirism) (blood)
● Xylophagia (wood, or derivates such as paper)

74. ANNIE VADAKKAN