Hunger, eating & health

Hunger, Eating & Health

Ayoma, Karla Caressa
Bajana, Sheema
Galdo, Geneva
Tecson, Louis Marie

Digestion
- is the mechanical and chemical breaking
down of food into smaller components, to a
form that can be absorbed, for instance, into a
blood stream. Digestion is a form of
catabolism; a break-down of macro food
molecules to smaller ones.

Steps in Digestion
Teeth- Digestion starts here. It’s job is to start
tearing and crushing the food down into small
enough pieces so that it can fit down our
throats.
Saliva- This helps soften the food in the mouth
so that it is easier to swallow. Saliva is also the
first of several chemicals that start to break
down foods into simpler forms.

• Tongue- The tongue is a muscle that works with
the food and saliva to form a "ball" that can be
swallowed.
• Esophagus- The esophagus is simply a
transportation tube from the mouth to the
stomach. When we swallow, what we are really
doing is closing a trap door in our throat called
the epiglottis. This sends food down the
esophagus and prevents food from going down
the trachea (or windpipe) and into our lungs.

• Stomach- The first stop after the esophagus is the
stomach. Once the food gets to the stomach, it
uses chemicals to try to make the food tinier
• Liver/Gall Bladder- At this point, our food is hit
with more chemicals. The liver makes a chemical
called bile but bile is not stored in the liver.
Instead it is stored in the gall bladder. When the
gall bladder mixes bile with our food, it does an
important job: breaking down the fat (from milk,
butter, cheeses) into tiny droplets. This fat will
supply us with much energy later.

• Large Intestine- Whatever the body cannot put to
use is sent to the large intestine. Many plants, for
example, contain cellulose which cannot be
digested. The big job of the large intestine is to
remove water. Water has been necessary up until
now but it is no longer needed and in the large
intestine water is sent into the blood stream .
Food spends about 12 hours in the large intestine
where it become feces and later leaves the body
through the anal opening.

• Pancreas- The pancreas also adds a digestive
chemical as the food leaves the stomach. This
digestive juice works on breaking down the
carbohydrates (from breads, potatoes, etc.) and
the proteins (from meats, cereals, peanut butter).
• Small Intestine- The small intestine is a tube that
is about 22 feet long! This is where the real
digestion takes place. As the food passes through,
it is mixed with the new chemicals and soon our
"food" is now digested small enough to be put to
use by the body.

Energy Storage in the Body
Energy is delivered to the body in three forms
– Lipids (fats)
– Glucose (simple sugar)
– Amino Acids (breakdown product of proteins)
Energy is stored in three forms:
- fats
- glycogen
- proteins

Metabolism
– Is the totality of an organism’s chemical reactions
– Arises from interactions between molecules

Energy Metabolism
- the chemical changes by which energy is
made available for an organism’s use

Three Phases of Energy
• Cephalic Phase – preparatory phase; Often
begins with the sight, smell or thought of food
and ends when the food is being absorbed in the
bloodstream.
• Absorptive Phase – energy absorbed in the blood
stream from the meal is meeting the body’s
energy needs.
• Fasting Phase – unstored energy form the
previous meal has been used and the body is
withdrawing energy from it’s reserves

Three components of the set point
systems
1. Set point mechanism – defines the set point
2. Detector mechanism – detect deviation form
the set point
3. Effector mechanism – acts to eliminate the
deviations

• All set-point systems are negative feedback
systems

Theories of Hunger and Eating

Set point Assumption
People attribute hunger to the presence of
energy deficit and they view eating as the
means by which the resources of the body are
returned to their optimal level

• Glucostatic Theory– we become hungry when
our blood glucose levels drop significantly below
their set point and that we become satiated
when eating returns our blood glucose levels to
their set point.
• Lipostatic Theory – every person has a set-point
for body fat, and deviations from this set point
procedure compensatory adjustments in the level
of eating that return level of body fat to their set
point.

Problems with Set-Point Theories of
Hunger and Eating
1. Inconsistent with basic eating-related
evolutionary pressures
2. Major predictions of the set-point theories of
hunger and eating have not been confirmed.
3. Set-point theories of hunger and eating are
deficient because they fail to recognize the
major influences on hunger and eating of
such important factors as taste, learning, and
social influences.

Factors that determine what we eat

Learned taste preference and aversion
Prefer tastes that are followed by an infusion of
calories, and they learn to avoid tastes that are
followed by illness

Learning to eat vitamins and minerals
Dietary deficiencies influence diet selection

Positive-Incentive Perspective
- Humans and animals are not normally driven
to eat by internal energy deficits but are
drawn to eat by the anticipated pleasure of
eating

* the anticipated pleasure of behavior is called
positive-incentive value

Factors that influence when we eat

Premeal Hunger
provide compelling support for hunger

Pavlovian Conditioning of Hunger
hunger is cause by expectation of food, not
by energy deficit

Factors that influence how much we
eat
Satiety Signals
Food in the gut and glucose entering the blood
can induce satiety signals, which inhibit
subsequent consumption.
Sham eating
satiety signals are not necessary to terminate a
meal.
Serving size and satiety
the larger the servings, the more we tend to eat

Social Influences and Satiety
depends on whether we are eating alone or with
others
Sensory-Specific Satiety
the number of different tastes available at each
meal has a major effect on meal size.
Appetizer Effect and Satiety
small amounts of food consumed before meal
actually increase hunger rather than reducing it

Role of Blood Glucose Levels in
Hunger and Satiety
• It is a simple matter to construct a situation in
which drops in blood glucose levels do not
precede eating
• The usual premeal decrease in blood glucose
seem to be a response to the intention to start
eating, not the other way around
• If an expected meal is not served, blood
glucose levels soon return to their previous
homeostatic level

• The glucose levels in the extra-cellular fluids
that surrounds CNS neurons stay relatively
constant, even when blood glucose levels drop
• Injections of insulin do not reliably induce
eating unless the injections are sufficiently
great to reduce blood glucose levels by 50%
and large premeal infusions of glucose do not
suppress eating

Myth of Hypothalamic Hunger and
Satiety Centers
Two different regions of the hypothalamus:

Satiety by the Ventromedial Hypothalamus
Large bilateral electrolytic lesions to the
ventromedial hypothalamus produce
hyperphagia (excessive eating) and extreme
obesity in rats.

VMH Syndrome has 2 different phases

Dynamic Phase
Begins as soon as the subject regains
consciousness after operation, characterized
by several weeks of grossly excessive eating
and rapid weight gain.
Static Phase
After dynamic phase, consumption gradually
declines to a level that is sufficient to maintain
a stable level of obesity

Feeding by the Lateral Hypothalamus
Produce aphagia – a complete cessation of
eating. It is the feeding center.

2 important features of LH syndrome
found that aphagi was accompanied by
adipsia – a complete cessation of drinking &
LH-lesioned rats partially recover if they are
kept alive by tube feeding.

Reinterpretation of the Effects of VHM
and LH Lesions
• The VHM-lesioned animals become obese
because they overeat, hoewever, the evidence
suggests the converse – that they overeat
because they become obese
• LH Lesions produce a wide range of severe
motor disturbances and a general lack of
sensory input of which food and drink are but
two examples.

Role of Gastrointestinal Tract in Satiety
• The role of gastrointestinal tract in hunger and
satiety quickly waned with the discovery that
human patients whose stomachs had been
surgically removed and whose esophagus had
been hooked up directly to their duodenums
continued to report feelings of hunger and
satiety and continued to maintain their
normal body weights by eating more meals of
smaller size.

Hunger and Satiety Peptides
• Circulating gut peptides provide the brain with
information about the quantity and nature of
food in the gastrointestinal tract and that this
information plays a role in satiety.
• Peptides can function as satiety signals
• Satiety peptides (peptides that decrease
appetite)

Serotonin and Satiety
• Serotonin agonists consistently reduced rat’s food
intake.
• Serotonin agonists have been shown to reduce
hunger, eating, and body weight under variety of
conditions
• Satiety-inducing effects of serotonin have three
major characteristics:
– Overcome the powerful attraction of highly palatable
cafeteria diets
– Reduce the amount of food that is consumed
– Associated with a shift in food preferences away form
fatty foods

Body Weight Regulations: Set Points
VS. Settling Points
Variability of Body Weight
Set point theories of body weight regulation
suggest that the best method of maintaining a
constant body weights is to eat each time
there is a motivation to eat because the main
function of hunger is to defend the set point
Set Points and Health
each person’s set point Is optimal for that
person’s health – or at least not incompatible
with good health

Regulation of Body Weight by Changes
in the Efficiency of Energy Utilization

How much a person eats plays a role in his or
her body weight. The body controls its fat
levels, to a large degree, by changing the
efficiency with which it uses energy.

Set Points and Settling Points in
Weight Control
• Settling Point – the level at which the various
factors that influence body weight achieve an
equilibrium.
• Settling-point model – provides loose kind of
homeostatic regulation. Body weight remains
stable as long as there are no long term
changes in the factors that influence it.

Statistics
• A survey by the National Statistics
Coordination Board (NSCB) as of 2008 showed
that 26.6% of Filipino adults are overweight,
higher than 16.6% in 1993.
• Of the number, 5.2% are obese.
• Among children aged 5 to 10 years old, 6.6%
are overweight against only 5.8% during the
last survey in 2003.

• The rise comes despite a reported drop in Filipinos'
food intake to 861 grams per day in 2008 from 803
grams in 1993, said Candido Astrologo Jr. of the NSCB
during a seminar for health journalists in Quezon City
recently.
• However, Astrologo said the question that should be
asked is not how much food Filipinos eat, but what
kind.
• He said households' nutrition habits are changing.
According to him, consumption of meat and poultry
has been on the rise, contributing to obesity.

Human Obesity: Causes, Treatments,
and Mechanisms
• QUESTION: Are obese people more
susceptible to health problems even if their
blood pressure and blood cholesterol levels
are within the healthy range?

Human Obesity: Causes, Treatments,
and Mechanisms
• ANSWER: Yes.
• A recent study of over 17,000 people found
that those who are obese have a significantly
higher risk of mortality even if their blood
pressure and blood cholesterol levels are
normal.

Why is there an epidemic of Obesity?
• Inconsistent food supplies were one of the
main threats to survival. As a result, the fittest
individuals were those who preferred high-
calorie foods, ate to capacity when food was
available, stored as many excess calories as
efficiently as possible. Individuals who did not
have these characteristics were unlikely to
survive a food shortage, and so these
characteristics were passed on to future
generations.

Why is there an epidemic of Obesity?
• The development of numerous cultural
practices and beliefs that promote
consumption has augmented the effects of
evolution.

Why do some people become obese
while others do not?
• Those who are obese are those whose energy
intake has grossly exceeded their energy
output; those who are slim are those whose
energy intake has not grossly exceeded their
energy output. This serves to emphasize that
two kinds of individual differences play a role
in obesity: those that lead to differences in
energy input and those that lead to
differences in energy output.

Factors that lead some people to eat
more than others who have
comparable access to food
• Some people consume more energy because
they have strong preferences for the taste of
high-calorie foods
• Some consume more because they were
raised in families and/or cultures that
promote excessive eating

Factors that lead some people to eat
more than others who have
comparable access to food
• Some consume more because they have
particularly large cephalic-phase responses to
the sight or smell.

• Differences in basal metabolic rate
• Ability to react to fat increases by diet-induced
thermogenesis
• NEAT – nonexercise activity thermogenesis
*generated by activities such as fidgeting
and the maintenance of posture and
muscle tone

Why are weight-loss programs
typically ineffective?
Most weight-loss programs are unsuccessful in
the sense that, as predicted by the settling-point
model, most of the lost weight is regained once
the dieter stops following the program.

• The key to permanent weight loss is a permanent
lifestyle change.
• Any healthy person who consistently eats a
nutritional low-calorie diet will have no problems
with obesity.
• Exercise has many health-promoting effects;
however, despite the general belief that exercise
is the most effective method of losing weight,
several studies have shown that it often
contributes little to weight loss.

• About 80% of the energy you expend is used
to maintain the resting physiological processes
of your body and to digest your food.

Leptin and the Regulation of Body Fat

Fat is more than a passive storehouse of energy;
it actively releases a peptide hormone called
leptin.

Obese Mice and the Discovery of
Leptin
• In 1950, a spontaneous genetic mutation
occurred in the mouse colony being maintained
in the Jackson Laboratory at Bar Harbor, Maine.
• The mutant mice were homozygous for the gene
(ob), and they were grossly obese, weighing up to
three times as much as typical mice.
• These mutant mice are commonly referred to as
ob/ob mice.

Obese Mice and the Discovery of
Leptin
• Ob/ob mice eat more than control mice; they
convert calories to fat more efficiently; and
they use their calories more efficiently.
• It was hypothesized by Coleman that ob/ob
mice lack a critical hormone that normally
inhibits fat production and maintenance.

Hypothesis
• Perhaps leptin is a negative feedback signal
that is normally released from fat stores to
decrease appetite and increase fat
metabolism. Could leptin be administered to
obese humans to reverse the current
epidemic of the problem?

Leptin as a Treatment for Human
Obesity
• The early studies of leptin seemed to confirm
the hypothesis that it could function as an
effective treatment for obesity.
• Receptors for leptin were found in the brain,
and injecting it into ob/ob mice reduced both
their eating and their body fat.

Leptin as a Treatment for Human
Obesity
• However, when research on leptin turned
from obese mice to obese humans, the
program ran into two major snags.
• First, obese humans--- unlike ob/ob mice---
were found to have high, rather than low,
levels of leptin.
• Second, injections of leptin did not reduce
either the eating or the body fat of obese
humans.

This is what kids
with a leptin
deficiency looks
like.

Leptin, Insulin and the Arcuate
Melancortin System
• Leptin was not the first peptide hormone to
be discovered that seems to function as a
negative feedback signal in the regulation of
body fat.
• More than 25 years ago, Woods and
colleagues suggested that the pancreatic
peptide hormone insulin serves such a
function.

Melancortin System
• The suggestion that insulin serves as a
negative feedback signal for body fat
regulation was viewed with skepticism.
• How could the level of insulin on the body,
which goes up and then comes back down to
normal following each meal, provide the brain
with information about gradually changing
levels of body fat?

Melanocortin System
• It turns out that insulin does not readily
penetrate the blood-brain barrier, and its
levels in the brain were found to stay relatively
stable.
• Brain levels of insulin were found to be
positively correlated with levels of body fat.

Why are there two fat feedback
signals?
• Leptin levels are more closely correlated to
subcutaneous fat (fat stored under the skin)
• Insulin levels are more closely correlated to
visceral fat (fat stored around the internal
organs of the body cavity)
Each fat signal provides different information.
Visceral fat is more common in males and poses
the greater threat to health.

• Arcuate nucleus – location for receptors for
both peptide hormones
• Located in two classes of neurons:
1) Neurons that release neuropeptide Y (the gut
hunger peptide)
2) Neurons that release melanocortins (class of
peptides that includes the gut satiety peptide
*alpha melanocyte stimulating hormone*)

Serotonergic Drugs and the Treatment
of Obesity
• Serotonin agonists have been shown to
reduce food consumption in both human and
nonhuman subjects, they have considerable
potential in the treatment of obesity.
• Serotonin agonists produce long-term satiety
signals based on fat stores.
• They seem to increase short-term satiety
signals associated with consumption of a
meal.

Anorexia and Bulimia Nervosa
Anorexia Nervosa
- a disorder of under consumption
-it is a very serious condition because it can
lead to death
- there is a particular high rate of suicide
among anorexics.

Anorexic food behavior Signs and
Symptoms
• Dieting despite being thin
• Obsession with calories, fat grams, and
nutrition
• Pretending to eat or lying about eating
• Preoccupation with food
• Strange or secretive food rituals

Anorexic appearance and body image
signs and symptoms
• Dramatic weight loss
• Feeling fat, despite being underweight
• Fixation on body image
• Harshly critical of appearance
• Denial that you’re too thin

Purging signs and symptoms
• Using diet pills, laxatives, or diuretics
• Throwing up after eating
• Compulsive exercising

Major risk factors for anorexia nervosa
• Body dissatisfaction
• Strict dieting
• Low self-esteem
• Difficulty expressing feelings
• Perfectionism
• Troubled family relationship
• History of physical or sexual abuse
• Family history of eating disorders

Tips for helping a person with anorexia
• Think of yourself as an “outsider.”
• Be a role model
• Take care of yourself
• Don’t act like a food police
• Avoid threats, scare tactics, angry outbursts,
and put-downs

Bulimia Nervosa
- a disorder characterized by periodic
bingening ( eating huge amounts of food in a
short period of time )
- followed by efforts to immediately eliminate
the consumed calories form the body by
voluntary purging; excessive use of laxatives,
enemas or diuretics; or by extreme exercise

Binge eating signs and symptoms
• Lack of control over eating
• Secrecy surrounding eating
• Eating unusually large amounts of food
• Disappearance of food
• Alternating between overeating and fasting

Purging signs and symptoms
• Going to the bathroom after meals
• Using laxatives, diuretics, or enemas
• Smell of vomit
• Excessive exercising

Physical signs and symptoms
• Calluses or scars on the knuckles or hands
• Puffy “chipmunk” cheeks
• Discolored teeth
• No underweight
• Frequent fluctuations in weight

Relation between Anorexia and
Bulimia Nervosa
• Anorexics often require treatment for reduced
metabolism, bradycardia (slow heart rate),
hypotension (low blood pressure), hypothermia
(low body temperature), and anemia (deficiency
of red blood cells)
• In contrast, bulimics often require treatment for
irritation and inflammation of the esophagus,
vitamin and mineral deficiencies, electrolyte
imbalance, dehydration, and acid reflux.

Bulimia Nervosa
Both anorexia and bulimia nervosa begin with
an obsession about body image and slimness
and extreme efforts to lose weight. Both
anorexics and bulimics attempt to lose weight
by strict dieting, but bulimics are less capable of
controlling their appetites and thus enter into a
cycle of starvation, bingeing, and purging.

Bulimia Nervosa
Both have a distorted body image, seeing
themselves as much fatter and less attractive
that they are in reality.
Both show the same pattern of distribution in
the population. Although their overall incidence
in the population is low, estimates for American
adults are 0.6% and 1.0% for anorexia and
bulimia, respectively.

Bulimia Nervosa
Both conditions occur more commonly among
educated females in affluent cultural groups,
Both anorexia and bulimia are highly correlated
with OCD and depression.
Neither disorder responds well to existing
therapies. Short-term improvements are
common, but relapse is usual.

STATISTICS
• It is estimated that 8 million Americans have an
eating disorder – seven million women and one
million men
• One in 200 American women suffers from
anorexia
• Two to three in 100 American women suffers
from bulimia
• Nearly half of all Americans personally know
someone with an eating disorder (Note: One in
five Americans suffers from mental illnesses.)
• An estimated 10 – 15% of people with anorexia
or bulimia are males

Steps to Anorexia and bulimia nervosa
recovery
• Admit you have a problem
• Talk to someone
• Stay away from people, places, and activities
that trigger your obsession with being thin
• Seek professional help

ACCESS TO TREATMENT

• Only 1 in 10 people with eating disorders
receive treatment
• About 80% of the girls/women who have
accessed care for their eating disorders do not
get the intensity of treatment they need to
stay in recovery – they are often sent home
weeks earlier than the recommended stay

• Treatment of an eating disorder in the US ranges
from $500 per day to $2,000 per day. The average
cost for a month of inpatient treatment is
$30,000. It is estimated that individuals with
eating disorders need anywhere from 3 – 6
months of inpatient care. Health insurance
companies for several reasons do not typically
cover the cost of treating eating disorders
• The cost of outpatient treatment, including
therapy and medical monitoring, can extend to
$100,000 or more

ADOLESCENTS
• Anorexia is the 3rd most common chronic
illness among adolescents
• 95% of those who have eating disorders are
between the ages of 12 and 25
• 50% of girls between the ages of 11 and 13
see themselves as overweight
• 80% of 13-year-olds have attempted to lose
weight

Some celebrities that suffer from
Anorexia and Bulimia Nervosa

In 2006, the troubled
actress admitted to
suffering from
bulimia in an interview
with Vanity Fair. She
didn't go into much
detail, as people with
bulimia find it difficult to
talk about their illness...

Fresh from waging war
against the Disney Channel
for making a joke about
eating disorders in one of its
shows, Demi came out with
a blog on Seventeen
magazine's website entitled
"My Battle With Eating
Disorders," in which she talks
about her own struggles with
the disease and offers sound
advice to others who are
going through it as well.

Diana, Princess of Wales, literally
married her Prince at the age of
20 and 750 million people
worldwide watched the event.
Unfortunately, the pressures of
constantly being in the public eye
put a strain on Diana that led her
to depression and bulimia as a
way of coping. Diana claimed in
an interview that sometimes she
would binge and then vomit
daily, depending on the pressures
that she was dealing with. She
called it her “escape mechanism”
and dealt with it for many years
before she finally was able to
overcome her bulimia.

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