PSYCH 3M03 Lecture 5: Chapter 5 Thirst, Hunger and Elimination
18 Jun 2018
School
Department
Course
Professor
Thirst
Obviously, water is important for us and all mammals.
-
Joints in our body ae heavily composed of water.
Our bodies are approximately 66% water.
○
-
Major struggle for many people around the world, but it's a huge motivator.
People will risk diseases, danger and exhaustion to access water.
○
People have wars over bodies of water.
○
-
When people are deprived of water, their entire lives become about water.
-
Example of homeostasis
-
Physiological processes:
Extracellular thirst
○
Cellular thirst
○
-
Extracellular Thirst (Hypovolemic)
Accounts for 1/3 of total water in body.
-
Water outside cells (blood, CSF, body cavities).
-
Induced by perspiration, blood loss, diarrhea, heavy menstrual bleeding.
-
Blood volume and blood pressure decrease.
-
Requires replacement of electrolytes and water.
-
Extracellular Thirst Mechanisms
Drop in blood pressure.
1.
Activation of baroreceptors in kidneys.
Baroreceptors respond to blood pressure.
-
2.
Release of renin from kidneys into blood stream.
@ the same time, angiotensinogen (a peptide hormone) is released by the
liver.
-
3.
Renin converts angiotensinogen to angiotensin in blood.
4.
Angiotensin causes vasoconstriction and production of aldosterone (adrenal
gland) and vasopressin (anti-diuretic hormone) from pituitary.
5.
Aldosterone leads to increased sodium reabsorption by kidneys.
6.
Vasopressin leads to increased water reabsorption.
7.
How does angiotensin (a peptide hormone) interact wit the hypothalamus and
pituitary to stimulate the production of vasopressin?
Subfornical organ
Located outside the blood-brain barrier.
§
Contains osmoreceptors and also responds to angiotensin.
§
Neurons in the subfornical organ project to the hypothalamus.
§
Neurons responsive to salt ion concentrations (extracellular thirst).
§
-
If you inject, rats with angiotensin , you'll increase drinking behaviour.
Also happens when you inject it near the pituitary gland.
§
-
-
Cellular Thirst (Osmotic/Sodium)
Accounts for 2/3 of water in body.
-
Water inside cells.
-
Induced by excess salt consumption or severe thirst.
-
Excess salt consumption or severe thirst leads to increased extracellular sodium.
-
Osmotic force draws water out of cells.
Salt changes osmolarity, therefore thirst.
-
Causes cell to shrink.
-
-
Need to increase extracellular water.
Often occurs after extracellular thirst.
-
-
The Ventricular System
Osmoreceptors around hypothalamus near the third ventricle.
-
Textbook Figure 4-9
-
What If You Stopped Drinking Water?
Drinks
Evolutionarily, we seek out liquids in order to quench our thirst.
-
Pops, juice, energy drinks, etc. - many things available that aren't water and are
actually full of salt.
-
Prandial Drinking
Prandial drinking: water intake associated with food intake.
-
Food intake leads to fluid entering digestive tract and often elevated sodium
intake.
-
Because we need to balance out the salts, we take in water.
-
Interestingly, we drink almost the exact amount of water needed to balance out
the salt.
-
Cessation of Drinking
Occurs before extracellular or cellular fluids rebalanced.
We stop drinking before they're back in balance.
-
Because we know exactly how much we need to drink.
-
-
Species-specific mechanism:
Dogs drink a lot water very rapidly.
-
Rats drink slower and more frequently.
-
Humans drink ~ 75% of water they need in about 5 mins, for next 30 mins,
they sip.
-
-
Cessation derives from receptors in mouth, esophagus, and stomach, as well as
swallowing reflex.
-
Obesity and Starvation
Famine more common than abundance throughout evolutionary history.
-
Humans adapted to environments where starvation can be imminent.
-
Therefore, our bodies reserved fat even though we no longer need to.
-
Feeding and Fasting
Feeding (absorptive) phase
Insulin release from pancreas
-
Glucose from blood moves into cells, glucose becomes glycogen.
-
Glucose is stored as energy in cells.
-
Parasympathetic innervations.
-
-
Fasting Phase
Levels of blood sugar decrease.
-
Glucagon released from insulin.
Glycogen stores from cells metabolized to glucose and released into
blood.
§
-
Liberates stored energy.
-
Sympathetic innervations.
-
-
Stomach Distension
Stomach pangs and growling associated with reports of strong hunger.
-
Increased stomach contractions when hungry.
-
Full stomach associated with less appetite.
-
Walter Canon Experiment
Participants report how hungry they are.
-
Balloon down throat & inflate.
-
Look at if stomach is contracting.
-
More stomach contractions when hungry -- pangs
-
If you leave balloon inflate, feeling full after a while -- feelings of fullness,
less appetite.
-
-
Ghrelin
Secreted by epithelial cells lining empty stomach, as well as intestines and
pancreas.
-
Levels in blood rise during fasting.
-
Signals hunger and stimulates feeding.
-
Basically, when you haven't eaten, Ghrelin is released to tell you that you're
hungry.
-
Cholecystokinin (CCK)
Released when food reaches the intestines (duodenum).
-
Stimulates processing/digestion of fats and proteins (lipids and peptide).
-
Injecting CCK reduces feeding and food seeking behaviour.
Suppresses appetite.
-
-
We aren't totally sure how it works.
-
CCK induces anxiety responses when injected in animals.
-
Could be involved in exploratory/novel food seeking behaviour.
-
CCK too large to get to the brain.
Receptors in many areas, influence on hypothalamus directly and through
vagus nerve.
-
-
Glucostatic Factors
Glucose is the "currency" of energy throughout body and brain.
-
Low intracellular glucose = hunger
No evidence that the opposites true.
-
-
Low blood glucose = hunger
-
High blood glucose = no hunger, satiety
-
Hunger and feeding correlate with low blood sugar.
-
Glucose Receptors
Brain cells respond to glucose, but we can't find glucose receptors in brain.
-
Liver receptors are critical.
Receptive to blood glucose.
-
-
Hepatic portal vein has receptors detecting levels of glucose.
Glucose here reduces appetite.
-
-
Liver information delivered to the hypothalamus via the vagus nerve.
-
Glucose levels in the blood are very important for short-term hunger regulation.
-
Glucose
Blood glucose
Levels detected by hepatic portal vein
-
Information sent to hypothalamus via the vagus nerve
-
Involved in hunger regulation
-
NOT used as an energy sources
-
-
Intracellular Glucose
Used as a source of energy.
-
Cells capable of signaling in response to low intracellular glucose.
-
Involved in hunger regulation.
-
-
Inject insulin
Blood glucose decreases
-
Intracellular glucose increases
-
Then .. Intracellular goes down
-
Hunger
-
-
Diabetes
Although hepatic portal vein plays important role, it can't stop hunger.
-
Because no glucose is produced, glucose can't get into the cells.
-
-
Question: Which of the following best describes the functions of intracellular and
blood glucose?
Intracellular glucose is involved in hunger regulation, whereas blood glucose is
used as energy.
A)
Both intracellular glucose and blood glucose are used as energy, but only blood
glucose is involved in hunger regulation.
B)
Both intracellular glucose and blood glucose are involved in hunger regulation,
but only intracellular glucose can be used as energy.
C)
Lipostatic Factors
Homeostatic mechanism, long-term regulation.
-
Lipo-sensor detecting fats allowing mass to return to set point???????????
-
"Lipo-sensors" were not found for decades, but now evidence suggests role of
leptin.
-
Homeostatic mechanism, long-term regulation.
-
Food deprived animals eat to compensate.
-
Overfed animals reduce subsequent feeding.
-
Leptin
Secreted by adipose tissue (fat).
-
Decreases food intake.
More leptin = decreased food seeking behaviour.
-
-
Increases metabolism.
Helps get fat down to homeostatic levels.
-
-
Involved in long-term regulation of body weight and fat stores.
-
Leptin and OB Mice:
OB mice lack leptin production.
-
Obese
-
Often diabetic (because increased use of pancreas)
-
Low metabolism
-
Reversible with leptin injections.
-
Inject with leptin from birth and they'll never become obese in the first
place.
-
-
Brain Physiology
We can stimulate different brain regions to see which behaviours start.
-
We can lesion different brain regions to see which behaviours stop.
-
Lesion the ventromedial hypothalamus (VMH) = hyperphagia (over eating)
-
Lesion the lateral hypothalamus (LH) = aphagia (failure to eat)
-
Opposite effects observed when these areas are electrically stimulated.
-
Neuropeptide Y
NPY neurons are found in arcuate nucleus of hypothalamus located at the base
of the third ventricle.
-
Hunger inducing factor - stimulates feeding behaviour.
-
NPY less active in well-fed state.
-
NPY active during hunger.
-
Injecting NPY into hypothalamus of rats leads to ravenous and frantic eating
behaviours.
-
Obesity can be associated with excessive NPY.
-
Chronic stress and a high fat, high sugar diet are associated with excess NPY in
studies of mice and monkeys.
-
Chemical interactions
Leptin inhibits NPY secreting neurons - decreases food intake.
-
Ghrelin activates NPY secreting neurons - increases food intake.
-
-
Chemical Before Eating Cookie After Eating Cookie
Insulin Low High
Glucagon High Low
Ghrelin High Low
CCK Low High
Blood Glucose Low High
Leptin ?? ??
Neuropeptide Y High Low
** can't tell about leptin because it's a long-term regulator and these are short term
effects.
Psychological Factors
Odour and sight of food induces appetite.
-
Social influences on feeding behaviour.
Food we eat reflects culture and where we grew up.
-
We are likely to enjoy food our parents like.
-
Sometimes we eat certain things with certain people.
-
Herman et al (2003):
3 types of cookies
§
Participants get lists with fake names and their levels of hunger and
are asked to then indicate their own level of hunger (0-10).
§
Two conditions: (1) fake participants say they're really hungry, (2)
fake participants say they're not hungry.
§
Results:
Perceptions of your own hunger effected by others.□
Fake Ss hunger score related to Ss hunger score.□
When allowed to actually eat the cookies, people eat equal
amounts of cookies in both conditions.
□
So it's not that your physical hunger is changing, but just your
perception.
□
§
-
deCastro (1994):
People asked to record what they ate, who they were with, how
much and for how long.
§
Results:
When with family, ate more food faster.□
When with friends, ate more food slower.□
§
-
-
Innate Appetites
Humans have innate appetites for sweetness (glucose) and saltiness (sodium).
-
Other innate appetites are under consideration, but limited evidence available.
-
Sweetness
Appetite for sweets observable in many species, such as ants, wasps, dogs,
horses, monkeys, rats, mice, etc.
-
Sweet foods provide rapid energy with little metabolic costs.
-
Evolutionarily, sugars are fast/easily digestible.
-
Sweetness receptors on tongue.
-
Newborns and anencephalic infants.
New infants will prefer (smile at) sucrose water over regular water or
even standard formula.
-
Anencephalic infants have no forebrain, but they still show the same
preference for sucrose water.
-
This suggests that our preference for sweetness is ancient and in an older
part of the brain (maybe the brainstem?)
-
-
Saltiness
Tongue can directly sense saltiness.
-
Herbivores will travel great distances for salt.
-
Carnivores usually obtain sufficient dietary salt.
-
Omnivores vary depending on the environment.
-
Salt deprivation needed for many things (e.g., enzymatic metabolism).
-
Salt deprivation will cause animals to drink very high salinity solutions.
-
Adrenalectomized (no aldosterone) rats increase they're consumption of salt.
Because adrenal gland not producing aldosterone, no salt regulation.
-
-
Humans and Sodium
Humans ingest far more sodium than is required.
-
Health Canada reports adults should ideally be ingesting 1500mg of sodium
daily, and no more than 2300mg.
-
Health Canada reports adults actually consume around 3400mg of sodium daily.
-
We eat much more salt then required, almost double the suggested.
-
Avoidance
Avoidance to certain foods argued as innate appetites.
-
Learning to avoid sickening foods is rapid and single-trial, and does not follow
conventional laws of learning (radiation or LiCl).
-
Rats will avoid food when sick an hour later.
-
Only works for taste/smell cues, not auditory or visual - can be trained to long
delays.
-
Dietary Neophobia
They avoid foods they never experienced ever.
-
-
It only takes a little bit of bad shit to make small mammals sick.
-
Elimination
Urination
-
Defecation
-
Vomiting
-
Disgust
Viewed as a primitive/primary emotion.
-
Stereotyped expression across cultures.
-
Early emergence in infancy.
-
Odors of decay, feces, death are found universally repulsive.
-
Believed it was evolved to protect us and allow us to avoid contact with gross
things that could likely make us sick.
There's usually a reason why we're disgusted by something, it's not just a
social thing.
-
-
Area Postrema
Sits right outside blood-brain barrier.
-
Detects levels of toxins in the blood stream.
When detected, it induces vomiting behaviour.
-
-
Controls vomiting reflex in response to toxins in food.
-
Strong release of vasopressin from the posterior pituitary can induce vomiting.
-
Chapter 5: Thirst, Hunger and Elimination
Tuesday, January 30, 2018
4:50 PM
Thirst
Obviously, water is important for us and all mammals.
-
Joints in our body ae heavily composed of water.
Our bodies are approximately 66% water.
○
-
Major struggle for many people around the world, but it's a huge motivator.
People will risk diseases, danger and exhaustion to access water.
○
People have wars over bodies of water.
○
-
When people are deprived of water, their entire lives become about water.
-
Example of homeostasis
-
Physiological processes:
Extracellular thirst
○
Cellular thirst
○
-
Extracellular Thirst (Hypovolemic)
Accounts for 1/3 of total water in body.
-
Water outside cells (blood, CSF, body cavities).
-
Induced by perspiration, blood loss, diarrhea, heavy menstrual bleeding.
-
Blood volume and blood pressure decrease.
-
Requires replacement of electrolytes and water.
-
Extracellular Thirst Mechanisms
Drop in blood pressure.1.
Activation of baroreceptors in kidneys.
Baroreceptors respond to blood pressure.
-
2.
Release of renin from kidneys into blood stream.
@ the same time, angiotensinogen (a peptide hormone) is released by the
liver.
-
3.
Renin converts angiotensinogen to angiotensin in blood. 4.
Angiotensin causes vasoconstriction and production of aldosterone (adrenal
gland) and vasopressin (anti-diuretic hormone) from pituitary.
5.
Aldosterone leads to increased sodium reabsorption by kidneys.6.
Vasopressin leads to increased water reabsorption.
7.
How does angiotensin (a peptide hormone) interact wit the hypothalamus and
pituitary to stimulate the production of vasopressin?
Subfornical organ
Located outside the blood-brain barrier.
§
Contains osmoreceptors and also responds to angiotensin.
§
Neurons in the subfornical organ project to the hypothalamus.
§
Neurons responsive to salt ion concentrations (extracellular thirst).
§
-
If you inject, rats with angiotensin , you'll increase drinking behaviour.
Also happens when you inject it near the pituitary gland.
§
-
-
Cellular Thirst (Osmotic/Sodium)
Accounts for 2/3 of water in body.
-
Water inside cells.
-
Induced by excess salt consumption or severe thirst.
-
Excess salt consumption or severe thirst leads to increased extracellular sodium.
-
Osmotic force draws water out of cells.
Salt changes osmolarity, therefore thirst.
-
Causes cell to shrink.
-
-
Need to increase extracellular water.
Often occurs after extracellular thirst.
-
-
The Ventricular System
Osmoreceptors around hypothalamus near the third ventricle.
-
Textbook Figure 4-9
-
What If You Stopped Drinking Water?
Drinks
Evolutionarily, we seek out liquids in order to quench our thirst.
-
Pops, juice, energy drinks, etc. - many things available that aren't water and are
actually full of salt.
-
Prandial Drinking
Prandial drinking: water intake associated with food intake.
-
Food intake leads to fluid entering digestive tract and often elevated sodium
intake.
-
Because we need to balance out the salts, we take in water.
-
Interestingly, we drink almost the exact amount of water needed to balance out
the salt.
-
Cessation of Drinking
Occurs before extracellular or cellular fluids rebalanced.
We stop drinking before they're back in balance.
-
Because we know exactly how much we need to drink.
-
-
Species-specific mechanism:
Dogs drink a lot water very rapidly.
-
Rats drink slower and more frequently.
-
Humans drink ~ 75% of water they need in about 5 mins, for next 30 mins,
they sip.
-
-
Cessation derives from receptors in mouth, esophagus, and stomach, as well as
swallowing reflex.
-
Obesity and Starvation
Famine more common than abundance throughout evolutionary history.
-
Humans adapted to environments where starvation can be imminent.
-
Therefore, our bodies reserved fat even though we no longer need to.
-
Feeding and Fasting
Feeding (absorptive) phase
Insulin release from pancreas
-
Glucose from blood moves into cells, glucose becomes glycogen.
-
Glucose is stored as energy in cells.
-
Parasympathetic innervations.
-
-
Fasting Phase
Levels of blood sugar decrease.
-
Glucagon released from insulin.
Glycogen stores from cells metabolized to glucose and released into
blood.
§
-
Liberates stored energy.
-
Sympathetic innervations.
-
-
Stomach Distension
Stomach pangs and growling associated with reports of strong hunger.
-
Increased stomach contractions when hungry.
-
Full stomach associated with less appetite.
-
Walter Canon Experiment
Participants report how hungry they are.
-
Balloon down throat & inflate.
-
Look at if stomach is contracting.
-
More stomach contractions when hungry -- pangs
-
If you leave balloon inflate, feeling full after a while -- feelings of fullness,
less appetite.
-
-
Ghrelin
Secreted by epithelial cells lining empty stomach, as well as intestines and
pancreas.
-
Levels in blood rise during fasting.
-
Signals hunger and stimulates feeding.
-
Basically, when you haven't eaten, Ghrelin is released to tell you that you're
hungry.
-
Cholecystokinin (CCK)
Released when food reaches the intestines (duodenum).
-
Stimulates processing/digestion of fats and proteins (lipids and peptide).
-
Injecting CCK reduces feeding and food seeking behaviour.
Suppresses appetite.
-
-
We aren't totally sure how it works.
-
CCK induces anxiety responses when injected in animals.
-
Could be involved in exploratory/novel food seeking behaviour.
-
CCK too large to get to the brain.
Receptors in many areas, influence on hypothalamus directly and through
vagus nerve.
-
-
Glucostatic Factors
Glucose is the "currency" of energy throughout body and brain.
-
Low intracellular glucose = hunger
No evidence that the opposites true.
-
-
Low blood glucose = hunger
-
High blood glucose = no hunger, satiety
-
Hunger and feeding correlate with low blood sugar.
-
Glucose Receptors
Brain cells respond to glucose, but we can't find glucose receptors in brain.
-
Liver receptors are critical.
Receptive to blood glucose.
-
-
Hepatic portal vein has receptors detecting levels of glucose.
Glucose here reduces appetite.
-
-
Liver information delivered to the hypothalamus via the vagus nerve.
-
Glucose levels in the blood are very important for short-term hunger regulation.
-
Glucose
Blood glucose
Levels detected by hepatic portal vein
-
Information sent to hypothalamus via the vagus nerve
-
Involved in hunger regulation
-
NOT used as an energy sources
-
-
Intracellular Glucose
Used as a source of energy.
-
Cells capable of signaling in response to low intracellular glucose.
-
Involved in hunger regulation.
-
-
Inject insulin
Blood glucose decreases
-
Intracellular glucose increases
-
Then .. Intracellular goes down
-
Hunger
-
-
Diabetes
Although hepatic portal vein plays important role, it can't stop hunger.
-
Because no glucose is produced, glucose can't get into the cells.
-
-
Question: Which of the following best describes the functions of intracellular and
blood glucose?
Intracellular glucose is involved in hunger regulation, whereas blood glucose is
used as energy.
A)
Both intracellular glucose and blood glucose are used as energy, but only blood
glucose is involved in hunger regulation.
B)
Both intracellular glucose and blood glucose are involved in hunger regulation,
but only intracellular glucose can be used as energy.
C)
Lipostatic Factors
Homeostatic mechanism, long-term regulation.
-
Lipo-sensor detecting fats allowing mass to return to set point???????????
-
"Lipo-sensors" were not found for decades, but now evidence suggests role of
leptin.
-
Homeostatic mechanism, long-term regulation.
-
Food deprived animals eat to compensate.
-
Overfed animals reduce subsequent feeding.
-
Leptin
Secreted by adipose tissue (fat).
-
Decreases food intake.
More leptin = decreased food seeking behaviour.
-
-
Increases metabolism.
Helps get fat down to homeostatic levels.
-
-
Involved in long-term regulation of body weight and fat stores.
-
Leptin and OB Mice:
OB mice lack leptin production.
-
Obese
-
Often diabetic (because increased use of pancreas)
-
Low metabolism
-
Reversible with leptin injections.
-
Inject with leptin from birth and they'll never become obese in the first
place.
-
-
Brain Physiology
We can stimulate different brain regions to see which behaviours start.
-
We can lesion different brain regions to see which behaviours stop.
-
Lesion the ventromedial hypothalamus (VMH) = hyperphagia (over eating)
-
Lesion the lateral hypothalamus (LH) = aphagia (failure to eat)
-
Opposite effects observed when these areas are electrically stimulated.
-
Neuropeptide Y
NPY neurons are found in arcuate nucleus of hypothalamus located at the base
of the third ventricle.
-
Hunger inducing factor - stimulates feeding behaviour.
-
NPY less active in well-fed state.
-
NPY active during hunger.
-
Injecting NPY into hypothalamus of rats leads to ravenous and frantic eating
behaviours.
-
Obesity can be associated with excessive NPY.
-
Chronic stress and a high fat, high sugar diet are associated with excess NPY in
studies of mice and monkeys.
-
Chemical interactions
Leptin inhibits NPY secreting neurons - decreases food intake.
-
Ghrelin activates NPY secreting neurons - increases food intake.
-
-
Chemical Before Eating Cookie After Eating Cookie
Insulin Low High
Glucagon High Low
Ghrelin High Low
CCK Low High
Blood Glucose Low High
Leptin ?? ??
Neuropeptide Y High Low
** can't tell about leptin because it's a long-term regulator and these are short term
effects.
Psychological Factors
Odour and sight of food induces appetite.
-
Social influences on feeding behaviour.
Food we eat reflects culture and where we grew up.
-
We are likely to enjoy food our parents like.
-
Sometimes we eat certain things with certain people.
-
Herman et al (2003):
3 types of cookies
§
Participants get lists with fake names and their levels of hunger and
are asked to then indicate their own level of hunger (0-10).
§
Two conditions: (1) fake participants say they're really hungry, (2)
fake participants say they're not hungry.
§
Results:
Perceptions of your own hunger effected by others.□
Fake Ss hunger score related to Ss hunger score.□
When allowed to actually eat the cookies, people eat equal
amounts of cookies in both conditions.
□
So it's not that your physical hunger is changing, but just your
perception.
□
§
-
deCastro (1994):
People asked to record what they ate, who they were with, how
much and for how long.
§
Results:
When with family, ate more food faster.□
When with friends, ate more food slower.□
§
-
-
Innate Appetites
Humans have innate appetites for sweetness (glucose) and saltiness (sodium).
-
Other innate appetites are under consideration, but limited evidence available.
-
Sweetness
Appetite for sweets observable in many species, such as ants, wasps, dogs,
horses, monkeys, rats, mice, etc.
-
Sweet foods provide rapid energy with little metabolic costs.
-
Evolutionarily, sugars are fast/easily digestible.
-
Sweetness receptors on tongue.
-
Newborns and anencephalic infants.
New infants will prefer (smile at) sucrose water over regular water or
even standard formula.
-
Anencephalic infants have no forebrain, but they still show the same
preference for sucrose water.
-
This suggests that our preference for sweetness is ancient and in an older
part of the brain (maybe the brainstem?)
-
-
Saltiness
Tongue can directly sense saltiness.
-
Herbivores will travel great distances for salt.
-
Carnivores usually obtain sufficient dietary salt.
-
Omnivores vary depending on the environment.
-
Salt deprivation needed for many things (e.g., enzymatic metabolism).
-
Salt deprivation will cause animals to drink very high salinity solutions.
-
Adrenalectomized (no aldosterone) rats increase they're consumption of salt.
Because adrenal gland not producing aldosterone, no salt regulation.
-
-
Humans and Sodium
Humans ingest far more sodium than is required.
-
Health Canada reports adults should ideally be ingesting 1500mg of sodium
daily, and no more than 2300mg.
-
Health Canada reports adults actually consume around 3400mg of sodium daily.
-
We eat much more salt then required, almost double the suggested.
-
Avoidance
Avoidance to certain foods argued as innate appetites.
-
Learning to avoid sickening foods is rapid and single-trial, and does not follow
conventional laws of learning (radiation or LiCl).
-
Rats will avoid food when sick an hour later.
-
Only works for taste/smell cues, not auditory or visual - can be trained to long
delays.
-
Dietary Neophobia
They avoid foods they never experienced ever.
-
-
It only takes a little bit of bad shit to make small mammals sick.
-
Elimination
Urination
-
Defecation
-
Vomiting
-
Disgust
Viewed as a primitive/primary emotion.
-
Stereotyped expression across cultures.
-
Early emergence in infancy.
-
Odors of decay, feces, death are found universally repulsive.
-
Believed it was evolved to protect us and allow us to avoid contact with gross
things that could likely make us sick.
There's usually a reason why we're disgusted by something, it's not just a
social thing.
-
-
Area Postrema
Sits right outside blood-brain barrier.
-
Detects levels of toxins in the blood stream.
When detected, it induces vomiting behaviour.
-
-
Controls vomiting reflex in response to toxins in food.
-
Strong release of vasopressin from the posterior pituitary can induce vomiting.
-
Chapter 5: Thirst, Hunger and Elimination
Tuesday, January 30, 2018 4:50 PM
Thirst
Obviously, water is important for us and all mammals.
-
Joints in our body ae heavily composed of water.
Our bodies are approximately 66% water.
○
-
Major struggle for many people around the world, but it's a huge motivator.
People will risk diseases, danger and exhaustion to access water.
○
People have wars over bodies of water.
○
-
When people are deprived of water, their entire lives become about water.
-
Example of homeostasis
-
Physiological processes:
Extracellular thirst
○
Cellular thirst
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Extracellular Thirst (Hypovolemic)
Accounts for 1/3 of total water in body.
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Water outside cells (blood, CSF, body cavities).
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Induced by perspiration, blood loss, diarrhea, heavy menstrual bleeding.
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Blood volume and blood pressure decrease.
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Requires replacement of electrolytes and water.
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Extracellular Thirst Mechanisms
Drop in blood pressure.1.
Activation of baroreceptors in kidneys.
Baroreceptors respond to blood pressure.
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2.
Release of renin from kidneys into blood stream.
@ the same time, angiotensinogen (a peptide hormone) is released by the
liver.
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3.
Renin converts angiotensinogen to angiotensin in blood. 4.
Angiotensin causes vasoconstriction and production of aldosterone (adrenal
gland) and vasopressin (anti-diuretic hormone) from pituitary.
5.
Aldosterone leads to increased sodium reabsorption by kidneys.6.
Vasopressin leads to increased water reabsorption.7.
How does angiotensin (a peptide hormone) interact wit the hypothalamus and
pituitary to stimulate the production of vasopressin?
Subfornical organ
Located outside the blood-brain barrier.
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Contains osmoreceptors and also responds to angiotensin.
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Neurons in the subfornical organ project to the hypothalamus.
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Neurons responsive to salt ion concentrations (extracellular thirst).
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If you inject, rats with angiotensin , you'll increase drinking behaviour.
Also happens when you inject it near the pituitary gland.
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Cellular Thirst (Osmotic/Sodium)
Accounts for 2/3 of water in body.
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Water inside cells.
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Induced by excess salt consumption or severe thirst.
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Excess salt consumption or severe thirst leads to increased extracellular sodium.
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Osmotic force draws water out of cells.
Salt changes osmolarity, therefore thirst.
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Causes cell to shrink.
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Need to increase extracellular water.
Often occurs after extracellular thirst.
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The Ventricular System
Osmoreceptors around hypothalamus near the third ventricle.
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Textbook Figure 4-9
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What If You Stopped Drinking Water?
Drinks
Evolutionarily, we seek out liquids in order to quench our thirst.
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Pops, juice, energy drinks, etc. - many things available that aren't water and are
actually full of salt.
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Prandial Drinking
Prandial drinking: water intake associated with food intake.
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Food intake leads to fluid entering digestive tract and often elevated sodium
intake.
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Because we need to balance out the salts, we take in water.
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Interestingly, we drink almost the exact amount of water needed to balance out
the salt.
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Cessation of Drinking
Occurs before extracellular or cellular fluids rebalanced.
We stop drinking before they're back in balance.
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Because we know exactly how much we need to drink.
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Species-specific mechanism:
Dogs drink a lot water very rapidly.
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Rats drink slower and more frequently.
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Humans drink ~ 75% of water they need in about 5 mins, for next 30 mins,
they sip.
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Cessation derives from receptors in mouth, esophagus, and stomach, as well as
swallowing reflex.
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Obesity and Starvation
Famine more common than abundance throughout evolutionary history.
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Humans adapted to environments where starvation can be imminent.
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Therefore, our bodies reserved fat even though we no longer need to.
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Feeding and Fasting
Feeding (absorptive) phase
Insulin release from pancreas
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Glucose from blood moves into cells, glucose becomes glycogen.
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Glucose is stored as energy in cells.
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Parasympathetic innervations.
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Fasting Phase
Levels of blood sugar decrease.
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Glucagon released from insulin.
Glycogen stores from cells metabolized to glucose and released into
blood.
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Liberates stored energy.
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Sympathetic innervations.
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Stomach Distension
Stomach pangs and growling associated with reports of strong hunger.
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Increased stomach contractions when hungry.
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Full stomach associated with less appetite.
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Walter Canon Experiment
Participants report how hungry they are.
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Balloon down throat & inflate.
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Look at if stomach is contracting.
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More stomach contractions when hungry -- pangs
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If you leave balloon inflate, feeling full after a while -- feelings of fullness,
less appetite.
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Ghrelin
Secreted by epithelial cells lining empty stomach, as well as intestines and
pancreas.
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Levels in blood rise during fasting.
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Signals hunger and stimulates feeding.
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Basically, when you haven't eaten, Ghrelin is released to tell you that you're
hungry.
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Cholecystokinin (CCK)
Released when food reaches the intestines (duodenum).
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Stimulates processing/digestion of fats and proteins (lipids and peptide).
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Injecting CCK reduces feeding and food seeking behaviour.
Suppresses appetite.
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We aren't totally sure how it works.
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CCK induces anxiety responses when injected in animals.
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Could be involved in exploratory/novel food seeking behaviour.
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CCK too large to get to the brain.
Receptors in many areas, influence on hypothalamus directly and through
vagus nerve.
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Glucostatic Factors
Glucose is the "currency" of energy throughout body and brain.
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Low intracellular glucose = hunger
No evidence that the opposites true.
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Low blood glucose = hunger
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High blood glucose = no hunger, satiety
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Hunger and feeding correlate with low blood sugar.
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Glucose Receptors
Brain cells respond to glucose, but we can't find glucose receptors in brain.
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Liver receptors are critical.
Receptive to blood glucose.
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Hepatic portal vein has receptors detecting levels of glucose.
Glucose here reduces appetite.
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Liver information delivered to the hypothalamus via the vagus nerve.
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Glucose levels in the blood are very important for short-term hunger regulation.
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Glucose
Blood glucose
Levels detected by hepatic portal vein
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Information sent to hypothalamus via the vagus nerve
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Involved in hunger regulation
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NOT used as an energy sources
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Intracellular Glucose
Used as a source of energy.
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Cells capable of signaling in response to low intracellular glucose.
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Involved in hunger regulation.
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Inject insulin
Blood glucose decreases
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Intracellular glucose increases
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Then .. Intracellular goes down
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Hunger
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Diabetes
Although hepatic portal vein plays important role, it can't stop hunger.
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Because no glucose is produced, glucose can't get into the cells.
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Question: Which of the following best describes the functions of intracellular and
blood glucose?
Intracellular glucose is involved in hunger regulation, whereas blood glucose is
used as energy.
A)
Both intracellular glucose and blood glucose are used as energy, but only blood
glucose is involved in hunger regulation.
B)
Both intracellular glucose and blood glucose are involved in hunger regulation,
but only intracellular glucose can be used as energy.
C)
Lipostatic Factors
Homeostatic mechanism, long-term regulation.
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Lipo-sensor detecting fats allowing mass to return to set point???????????
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"Lipo-sensors" were not found for decades, but now evidence suggests role of
leptin.
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Homeostatic mechanism, long-term regulation.
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Food deprived animals eat to compensate.
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Overfed animals reduce subsequent feeding.
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Leptin
Secreted by adipose tissue (fat).
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Decreases food intake.
More leptin = decreased food seeking behaviour.
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Increases metabolism.
Helps get fat down to homeostatic levels.
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Involved in long-term regulation of body weight and fat stores.
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Leptin and OB Mice:
OB mice lack leptin production.
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Obese
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Often diabetic (because increased use of pancreas)
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Low metabolism
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Reversible with leptin injections.
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Inject with leptin from birth and they'll never become obese in the first
place.
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Brain Physiology
We can stimulate different brain regions to see which behaviours start.
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We can lesion different brain regions to see which behaviours stop.
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Lesion the ventromedial hypothalamus (VMH) = hyperphagia (over eating)
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Lesion the lateral hypothalamus (LH) = aphagia (failure to eat)
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Opposite effects observed when these areas are electrically stimulated.
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Neuropeptide Y
NPY neurons are found in arcuate nucleus of hypothalamus located at the base
of the third ventricle.
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Hunger inducing factor - stimulates feeding behaviour.
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NPY less active in well-fed state.
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NPY active during hunger.
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Injecting NPY into hypothalamus of rats leads to ravenous and frantic eating
behaviours.
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Obesity can be associated with excessive NPY.
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Chronic stress and a high fat, high sugar diet are associated with excess NPY in
studies of mice and monkeys.
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Chemical interactions
Leptin inhibits NPY secreting neurons - decreases food intake.
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Ghrelin activates NPY secreting neurons - increases food intake.
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Chemical Before Eating Cookie After Eating Cookie
Insulin Low High
Glucagon High Low
Ghrelin High Low
CCK Low High
Blood Glucose Low High
Leptin ?? ??
Neuropeptide Y High Low
** can't tell about leptin because it's a long-term regulator and these are short term
effects.
Psychological Factors
Odour and sight of food induces appetite.
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Social influences on feeding behaviour.
Food we eat reflects culture and where we grew up.
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We are likely to enjoy food our parents like.
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Sometimes we eat certain things with certain people.
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Herman et al (2003):
3 types of cookies
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Participants get lists with fake names and their levels of hunger and
are asked to then indicate their own level of hunger (0-10).
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Two conditions: (1) fake participants say they're really hungry, (2)
fake participants say they're not hungry.
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Results:
Perceptions of your own hunger effected by others.□
Fake Ss hunger score related to Ss hunger score.□
When allowed to actually eat the cookies, people eat equal
amounts of cookies in both conditions.
□
So it's not that your physical hunger is changing, but just your
perception.
□
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deCastro (1994):
People asked to record what they ate, who they were with, how
much and for how long.
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Results:
When with family, ate more food faster.□
When with friends, ate more food slower.□
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Innate Appetites
Humans have innate appetites for sweetness (glucose) and saltiness (sodium).
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Other innate appetites are under consideration, but limited evidence available.
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Sweetness
Appetite for sweets observable in many species, such as ants, wasps, dogs,
horses, monkeys, rats, mice, etc.
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Sweet foods provide rapid energy with little metabolic costs.
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Evolutionarily, sugars are fast/easily digestible.
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Sweetness receptors on tongue.
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Newborns and anencephalic infants.
New infants will prefer (smile at) sucrose water over regular water or
even standard formula.
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Anencephalic infants have no forebrain, but they still show the same
preference for sucrose water.
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This suggests that our preference for sweetness is ancient and in an older
part of the brain (maybe the brainstem?)
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Saltiness
Tongue can directly sense saltiness.
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Herbivores will travel great distances for salt.
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Carnivores usually obtain sufficient dietary salt.
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Omnivores vary depending on the environment.
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Salt deprivation needed for many things (e.g., enzymatic metabolism).
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Salt deprivation will cause animals to drink very high salinity solutions.
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Adrenalectomized (no aldosterone) rats increase they're consumption of salt.
Because adrenal gland not producing aldosterone, no salt regulation.
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Humans and Sodium
Humans ingest far more sodium than is required.
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Health Canada reports adults should ideally be ingesting 1500mg of sodium
daily, and no more than 2300mg.
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Health Canada reports adults actually consume around 3400mg of sodium daily.
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We eat much more salt then required, almost double the suggested.
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Avoidance
Avoidance to certain foods argued as innate appetites.
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Learning to avoid sickening foods is rapid and single-trial, and does not follow
conventional laws of learning (radiation or LiCl).
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Rats will avoid food when sick an hour later.
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Only works for taste/smell cues, not auditory or visual - can be trained to long
delays.
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Dietary Neophobia
They avoid foods they never experienced ever.
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It only takes a little bit of bad shit to make small mammals sick.
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Elimination
Urination
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Defecation
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Vomiting
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Disgust
Viewed as a primitive/primary emotion.
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Stereotyped expression across cultures.
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Early emergence in infancy.
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Odors of decay, feces, death are found universally repulsive.
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Believed it was evolved to protect us and allow us to avoid contact with gross
things that could likely make us sick.
There's usually a reason why we're disgusted by something, it's not just a
social thing.
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Area Postrema
Sits right outside blood-brain barrier.
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Detects levels of toxins in the blood stream.
When detected, it induces vomiting behaviour.
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Controls vomiting reflex in response to toxins in food.
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Strong release of vasopressin from the posterior pituitary can induce vomiting.
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Chapter 5: Thirst, Hunger and Elimination
Tuesday, January 30, 2018 4:50 PM
Document Summary
Obviously, water is important for us and all mammals. Joints in our body ae heavily composed of water. Major struggle for many people around the world, but it"s a huge motivator. People will risk diseases, danger and exhaustion to access water. When people are deprived of water, their entire lives become about water. Accounts for 1/3 of total water in body. Induced by perspiration, blood loss, diarrhea, heavy menstrual bleeding. Release of renin from kidneys into blood stream. @ the same time, angiotensinogen (a peptide hormone) is released by the liver. Angiotensin causes vasoconstriction and production of aldosterone (adrenal gland) and vasopressin (anti-diuretic hormone) from pituitary. Aldosterone leads to increased sodium reabsorption by kidneys. Neurons in the subfornical organ project to the hypothalamus. Neurons responsive to salt ion concentrations (extracellular thirst). If you inject, rats with angiotensin , you"ll increase drinking behaviour. Also happens when you inject it near the pituitary gland. Induced by excess salt consumption or severe thirst.
