3. WHAT IS HUNGER?
• It is a feeling of discomfort or weakness caused by lack of
food, coupled with the desire to eat.
• Having a strong desire or craving for.
4. How the digestive system
influence food selection?
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•
•
•
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Digestion begins in the mouth.
Swallowed food travels down the
esophagus to the stomach.
The stomach stores food for a
time, and then a round sphincter
muscle opens at the end of the
stomach to release food to the
small intestine.
The small intestine has enzymes
that digest proteins, fats, and
carbohydrates.
The large intestine absorbs water
and minerals and lubricates the
remaining materials to pass as
feces.
5. Biological explanation for
hunger
• Hunger drive is triggered by the lowering of the sugar level of
the blood, but our eating is controlled by the hypothalamus.
• After the glucose supply has been replenished, ventromedial
nucleus turns off the hunger drive.
• If the body needs sugar, the person will be motivated to take
plenty of sugar, which is called the innate wisdom of the
body.
6. Enzymes and consumption of
dairy products
• Newborn mammals survive at first on mother’s milk. As they
grow older, they stop nursing for several reasons: The milk
dries up, the mother pushes them away, and they begin to try
other foods.
• LACTASE – an intestinal enzyme which is necessary for
metabolizing lactose.
• LACTOSE – a sugar in milk.
• From then on, milk consumption causes stomach cramps and
gas.
• Many adults have enough lactase levels to consume milk and
other dairy products throughout life.
• Worldwide, however, most adults cannot comfortably tolerate
large amounts of milk products.
7. Other influences on food
selection
• For a carnivore (meat eater), selecting a satisfactory diet is
relatively simple.
• herbivores (plant eaters) and omnivores (those that eat both
meat and plants) must distinguish between edible and
inedible substances and find enough vitamins and minerals
• One way to do so is to learn from the experiences of others.
• First, you would select sweet foods, avoid bitter ones, and eat
salty or sour foods in moderation. Most sweets are
nutritious, and bitter substances are harmful.
• Second, you would prefer anything that tasted familiar.
familiar foods are safe, and new foods may not be.
• Third, you would learn the consequences of eating each food
you try.
8. Other influences on food
selection
• This phenomenon is known as conditioned taste aversion. It
is a strong phenomenon that occurs reliably after just a single
pairing of food with illness, even if the illness came hours after
the food.
9. • Factors controlling hunger include distension of the stomach
and intestines, secretion of CCK by the duodenum, and the
availability of glucose and other nutrients to the cells.
• Appetite depends partly on the availability of glucose and
other nutrients to the cells. The hormone insulin increases the
entry of glucose to the cells, including cells that store
nutrients for future use. Glucagon mobilizes stored fuel and
converts it to glucose in the blood. Thus, the combined
influence of insulin and glucagon determines how much
glucose is available at any time.
10. BRAIN MECHANISMS
• Hunger depends on the contents of your stomach and
intestines, the availability of glucose to the cells, and your
body’s fat supplies, as well as your health and body
temperature.
• many kinds of information impinge onto two kinds of cells in
the arcuate nucleus of the hypothalamus, which is regarded as
the “master area” for control of appetite.
• Axons extend from the arcuate nucleus to other areas of the
hypothalamus.
11. • Much of the output from the arcuate nucleus goes to the
paraventricular nucleus of the hypothalamus.
• It inhibits the lateral hypothalamus, an area important for
eating. So the paraventricular nucleus is important for satiety.
• Axons from the satiety-sensitive cells of the arcuate nucleus
deliver an excitatory message to the paraventricular
nucleus, which is a type of chemical called a melanocortin.
• Melanocortin receptors in the paraventricular nucleus are
important for limiting food intake, and deficiencies of this
receptor lead to overeating.
12. Arcuate Nucleus & Paraventricular
Hypothalamus
• The arcuate nucleus of the hypothalamus has one set of
neurons sensitive to hunger signals and a second set sensitive
to satiety signals.
• The hunger-sensitive cells receive input from the taste
pathway.
• Another input to the hunger-sensitive cells comes from axons
releasing the neurotransmitter ghrelin.
• The stomach releases ghrelin during a period of food
deprivation, where it triggers stomach contractions.
• It also acts on the hypothalamus to decrease appetite and acts
on the hippocampus to enhance learning.
13. Lateral Hypothalamus
• The lateral hypothalamus controls insulin secretion, alters
taste responsiveness, and facilitates feeding in other ways.
• The lateral hypothalamus contributes to feeding in several
ways:
• Axons from the lateral hypothalamus to the NTS (nucleus
of the tractus solitarius), part of the taste pathway, alter
the taste sensation and the salivation response to the
tastes.
• Axons from the lateral hypothalamus extend into several
parts of the cerebral cortex, facilitating ingestion and
swallowing and causing cortical cells to increase their
response to the taste, smell, or sight of food
14. Lateral Hypothalamus
• The lateral hypothalamus increases the pituitary gland’s
secretion of hormones that increase insulin secretion.
• The lateral hypothalamus sends axons to the spinal
cord, controlling autonomic responses such as
digestive
secretions.
16. ventromedial hypothalamus
• Neuroscientists have known since the 1940s that a large lesion
centered on the ventromedial hypothalamus (VMH) leads to
overeating and weight gain.
• damage limited to the ventromedial hypothalamus does not
consistently increase eating or body weight.
• To produce a large effect, the lesion must extend outside the
ventromedial nucleus to invade nearby axons, especially the
ventral noradrenergic bundle.
17. Multiple controls of hunger
• Eating is controlled by many brain areas that monitor
blood, glucose, stomach distension, duodenal contents, body
weight, fat cells, hormones, and more.
• However, the complexity of the system also provides a kind of
security: If one part of the system makes a mistake, another
part can counteract it.
• Perhaps we should be even more impressed by how many
people eat more or less appropriately.
• The regulation of eating succeeds not in spite of its complexity
but because of it.
Notas do Editor
Its function is to break food into smaller molecules that the cells can use. Digestion begins in the mouth, where enzymes in the saliva break down carbohydrates. Swallowed food travels down the esophagus to the stomach, where it mixes with hydrochloric acid and enzymes that digest proteins.The stomach stores food for a time, and then a round sphincter muscle opens at the end of the stomach to release food to the small intestine.The small intestine has enzymes that digest proteins, fats, and carbohydrates. It is also the site for absorbing digested materials into the bloodstream.The blood carries those chemicals to body cells that either use them or store them for later use. The large intestine absorbs water and minerals and lubricates the remaining materials to pass as feces.
*When the supply of glucose in the blood runs low, a center in the lateral region of the hypothalamus is activated and it signals us to eat to replenish our glucose supply.
Most mammals stop their “pagdedede” to their mothers because of lack of lactase. When this lactase emptied, there will be stomach cramps. The declining of lactase level may be the evolution mechanism that says, “stop na”* Most human beings, after all, are Asians, and nearly all thepeople in China and surrounding countries lack the gene thatenables adults to metabolize lactose (Flatz, 1987). They eatcheese and yogurt, which are easier to digest than milk, andmoderate quantities of other dairy products, but they developcramps or gas pains if they consume too much.
*One way to do so is tolearn from the experiences of others. For example, juvenilerats tend to imitate the food selections of their elders (Galef,1992). Similarly, children acquire their culture’s food preferences,especially the spices, even if they do not like every foodtheir parents enjoy (Rozin, 1990).If you try something new and then become ill,even hours later, your brain blames the illness on the food,and it won’t taste good to you the next time (Rozin & Kalat,1971; Rozin & Zellner, 1985).
*One way to do so is tolearn from the experiences of others. For example, juvenilerats tend to imitate the food selections of their elders (Galef,1992). Similarly, children acquire their culture’s food preferences,especially the spices, even if they do not like every foodtheir parents enjoy (Rozin, 1990).If you try something new and then become ill,even hours later, your brain blames the illness on the food,and it won’t taste good to you the next time (Rozin & Kalat,1971; Rozin & Zellner, 1985).
An animalwith damage in this area refuses food and water, averting itshead as if the food were distasteful. Th e animal may starve todeath unless it is force-fed, but if kept alive, it gradually recoversmuch of its ability to eat
An animalwith damage in this area refuses food and water, averting itshead as if the food were distasteful. Th e animal may starve todeath unless it is force-fed, but if kept alive, it gradually recoversmuch of its ability to eat
Axons from the lateral hypothalamusmodify activity in several other brainareas, changing the response to taste,facilitating ingestion and swallowing,and increasing food-seeking behaviors.Also (not shown), the lateral hypothalamuscontrols stomach secretions.
Rats with damage in and around the ventromedial hypothalamusshow an increased appetite compared to undamagedrats of the same weight (B. M. King, 2006; Peters, Sensenig, &Reich, 1973). Recall that rats with damage to the paraventricularnucleus eat large meals. In contrast, those with damagein the ventromedial area eat normal-sized meals, but they eatmore frequently (Hoebel & Hernandez, 1993). One reason isthat they have increased stomach motility and secretions, andtheir stomachs empty faster than normal. Th e faster the stomachempties, the sooner the animal is ready for its next meal.Another reason for their frequent meals is that the damageincreases insulin production (B. M. King, Smith, & Frohman,1984), and therefore, much of each meal is stored as fat. If animalswith this kind of damage are prevented from overeating,they gain weight anyway! According to Mark Friedman andEdward Stricker (1976), the problem is not that the rat getsfat from overeating. Rather, the rat overeats because it is storingso much fat. Th e high insulin levels keep moving blood