Physiology of eating

Dr. Pradeep Kumar R. Associate Professor Dept. of Zoology

Govt. College for Women Thiruvananthapuram

EATING INTRODUCTION
Process of taking food into our body Energy
Nutrients Body repair
Immune response
Synthesis of steroid hormones and vit D Growth

Latmdhy
pothalamù nucleus
(hungef cente Venttonædial hypothdamusr)(saticty ccntct)
 Fat cells No leptin We
empty signal to eat!
hypothalamus

Fat cells Leptin signal sent We don't eat

full to hypothalamus (no om nom
nom

PYY- Peptide YY/ Peptide tyrosine tyrosine, Cholecystokinin

Hypothalamus Food
intake

• o e Energy
Leptin expended
o ” e
Fat tissue

PYY- Peptide YY/ Peptide tyrosine tyrosine, Cholecystokinin

Arcuate nucleus: (ARC) A collection of neurons (nerve cells) at the base of the hypothalamus on
either side of the third cerebroventricle,. It is the most
important site in the hypothalamic integration of energy balance. Distinct clusters of neurons in the
ARC produce orexigenic peptides such as neuropeptide Y (NPY)
arcuate neurons contain a substance called neuropeptide Y (NPY) and influence hunger.
When activated, these neurons can produce remarkable increases in eating that result in obesity.
These neurons may be regulated by glucose, insulin, and the
hormone leptin.

pro-opiomelanocortin
cocaine and amphetamine regulated transcript

The Nucleus Tractus Solitarius (NTS) is the principal visceral sensory nucleus in thebrain and
comprises neurochemically and biophysically distinct neurons located in the dorsomedial medulla
oblongata.

Orexigenic signal -AgRP- agouti-related protein, NPY-neuropeptide Y, GABA- gamma- amino-butyric

acid
Anorexigenic signal -POMC - pro-opiomelanocortin, CART, cocaine and amphetamine regulated
transcript

Orexin- overrides satiety messages

Arcuate nucleus- paraventricular nucleus- lateral hypothalamus (LH) LH- insulin secretion, taste
responsiveness, facilitates feeding Damage to this area- distasteful- starve to death
1.LH- Axons to NTS (Nucleus Tractus Solitarius )- part of taste pathway- alters-taste sensation ,
salivation – food taste better
2.Areas of brain – cerebral cortex- facilitating ingestion and swallowing – cortical cells- responsiveness
to taste, smell or sight of food
3.Pituitary gland- increase insulin secretion
4.Axons to spinal cord- ANS- digestive secretion

Centrally projecting neurons of the arcuate nucleus

Among the centrally-projecting neurons, two different sub-populations are distinguished, each
characterized by the neurotransmitters they produce

1.POMC/CART neurons: involved in the generation of an anorexigenic signal.

A.POMC stands for pro-opiomelanocortin, a precursor peptide that is converted by prohormone
convertases to yield as many as 10 different active peptide. Amongst these are α- and β-MSH
(melanocortins) but also β- endorphorine.
B.CART, cocaine and amphetamine regulated transcript It is a precursor peptide that is converted by
prohormone convertase into at least two active peptides.

MSH, melanocyte-stimulating hormone, was discovered as a peptide hormone that induces the
production of melanin (pigment) by melanocytes in skin and hair. Later it was shown to exist as a
family of hormones including ACTH, α-, β- and γ-MSH and collectively they are referred to as
melanocortins. It is the alpha form that plays an important role in pigmentation
Alpha-melanocyte-stimulating hormone (α-MSH) is a 13-amino-acid peptide derived from
proopiomelanocortin (POMC)
MSH regulates food intake and energy homeostasis by acting on melanocortin-3 receptors (MC3R)
and melanocortin-4 receptors (MC4R). MC3Rs are distributed throughout the hypothalamus and
limbic structures, while MCR4s are more extensively expressed in the amygdala, thalamus, cortex,
striatum, hippocampus, hypothalamus, notably, the ARC, the PVN, the LHA (lateral hypothalamic
area), the VMN (ventromedial hypothalamic nucleus), and the brainstem
Axons- satiety cells of arcuate nucleus- αMSH- malanoreceptors-PVN-limit food intake.
Deficiency of receptors- overeating

2.AgRP/Npy/GABA neurons: involved in the generation of an orexigenic signal.

1.AgRP stands for agouti-related protein.
AgRP acts as an antagonist of the melanocortin receptor-3 and -4 and thus blocks the action of the
above mentioned α-MSH in the arcuate nucleus.
2.Npy, neuropeptide Y- short peptide that was first isolated from the hypothalamus and resembling
PYY (peptide tyrosine tyrosine) produced by the digestive tract (member of the family of tyrosine
peptides). Neuropeptide Y is synthesized in neurons situated in the far ventromedial aspect of the
hypothalamic arcuate nucleus. Within the hypothalamus, NPY-expressing fibers project from the
arcuate nucleus to the paraventricular nucleus, where the peptide is released .Thus, the
administration of NPY to the hypothalamic paraventricular nucleus results in a robust and sustained
increase of food intake in rodents.
3.GABA, gamma-amino-butyric acid- an amino-acid-derived neurotransmitter in brain. It binds to an
ion-channel receptor and leads to hyperpolarization of the neuronal membrane. γ-aminobutyric acid
(GABA), a major inhibitory neurotransmitter, plays a critical role in feeding behaviour regulation
Input from hunger sensitive neurons of arcuate nucleus-inhibit PVN and satiety sensitive cells of
arcuate nucleus by GABA and NPY andAgRP.

Peripheral factors

Ghrelin - Appetite-inducing peptide hormone - 28 amino-acids.

entero-endocrine cells -fundus region -stomach. Stretching of the wall may turn off hormone release.
Ghrelin levels in blood were found to be at their peak just before and at their lowest just after a meal .
Ghrelin - generally low in obese persons Ghrelin is also detected in the hypothalamus.
inhibiting the activity of the vagus nerve - reducing the discharge of neurotransmitters in the brain.
Ghrelin receptors (GHSR) are present on afferent neurons of the vagus nerve.
In the arcuate nucleus, ghrelin stimulates appetite by increasing the activity of orexigenic neurons
(the Npy/AgRP/GABA containing neurons)
Leptin- is a peptide hormone - 167 amino acids. Its receptors are found in brain areas.
In addition to adipose tissue, it is also detected, placenta, ovaries, skeletal muscle, stomach),
mammary epithelial cell etc.
Leptin- inhibits appetite by decreasing the activity of orexigenic neurons (Npy/AgRP/GABA containing
neurons) and increasing the activity of the anorexigenic neurons (POMC/CART containing neurons) in
the hypothalamus (see figure 13). Both populations express the leptin receptor.
Insulin - is a peptide hormone of 51 amino acids.
intestinal absorption -raises blood glucose levels above a steady 70-100 mg/dl. Increased uptake of
glucose in β-cells of the pancreas-release insulin Anabolic effect; it assures removal of glucose from
the blood and stimulates its conversion into glycogen.
Glycogen reaches its saturation point (not more than 300 grams in an adult) istorage of glucose -
adipose tissue in the form of triglycerides .

CCK- Cholecystokinin- Cholecystokinin is a peptide hormone of 95 amino acids, secreted from mucosal
epithelial cells of the small intestine (duodenum)
It plays a key role in facilitating digestion within the small intestine. It stimulates production and
release of digestive enzymes from the pancreas and bile from the gallbladder. Closes sphincter muscle
between stomach and duodenum and decreases gastric emptying

Stimulate vagus nerve , send message to hypothalamus Release – shorter CCK-

EATING DISORDERS

OBESITY

Obesity is a medical condition in which excess body fat has accumulated to the extent that it may
have a negative effect on health, leading to reduced life expectancy and increased health problems.
Body Mass Index (BMI) where m and h are the person’s weight and height respectively. BMI is usually
expressed in kilograms per square metre, resulting when weight is measured in kilograms and height
in metres.

18.50–24.99- normal weight , 25.00–29.99- overweight , 30.00–34.99- class I obesity, 35 or 40

kg/m2 - severe obesity.

Effects of Obesity

1.causes various diseases such as osteoarthritis, obstructive sleep apnea etc

2.Type 2 diabetes, cancer, cardiovascular disease, non-alcoholic fatty liver disease high blood
pressure, high blood cholesterol, and high triglyceride levels Increases in body fat alter the body's
response to insulin, potentially leading to insulin resistance.
3.Increased fat also creates a proinflammatory state and a prothrombotic state.
4.Obesity increases the chances heart disease and certain types of cancer . As a result, obesity has
been found to reduce life expectancy.
5.Obesity can lead to social stigmatization and disadvantages in employment .

Causes
1.Excessive food energy intake
2.Lack of physical activity
3.Genetic susceptibility- a few cases are caused primarily by genes .
4.Insufficient sleep
5.Decreased rates of smoking, because smoking suppresses appetite
6.Increased use of medications that can cause weight gain
7.Pregnancy at a later age
8.Natural selection for higher BMI
9.Assortative mating leading to increased concentration of obesity risk factors
10.Consumption of sweetened drinks such as soft drinks, fruit drinks, iced tea, and energy and vitamin
water drinks
11.A sedentary lifestyle plays a significant role in obesity
12.Increasing use of mechanized transportation and a greater prevalence of labor-
saving technology in the home.
13.Malnutrition in early life

TREATMENT

1.Dieting and physical exercising

2.A suitable Diet programs may produce weight loss- All types of low-carbohydrate and low-fat diets
appear equally beneficial.
3.Anti-obesity drugs may be taken to reduce appetite or decrease fat absorption -orlistat , lorcaserin
3. Gastric balloon may assist with weight loss, or surgery - bariatric surgery
4.Intensive behavioral counseling
5.Lifestyle changes.
Anorexia nervosa

Anorexia -as a reduction in food intake caused an abnormal loss of the appetite for food.
Anorexia can be caused by cancer, AIDS, a mental disorder (i.e., anorexia nervosa), or other diseases.

Anorexia nervosa is an abnormal psychic state in which a person loses all desire for
food and even becomes nauseated by food; as a result, severe inanition occurs.

Anorexia nervosa (AN), characterized by lack of maintenance of a healthy body weight, an obsessive
fear of gaining weight or refusal to do so, and an unrealistic perception, or non-recognition of the
seriousness, of current low body weight.

Anorexia can cause menstruation to stop, and often leads to bone loss, loss of skin integrity, etc.

It greatly stresses the heart, increasing the risk of heart attacks and related heart problems. The risk
of death is greatly increased in individuals with this disease. It may not just be a vanity, social, or
media issue, but it could also be related to biological and or genetic components.

Cachexia is a “wasting” disorder- metabolic disorder of increased energy expenditure leading to

weight loss and muscle wasting greater than that caused by reduced food intake alone.
Almost all types of cancer cause both anorexia and cachexia, and anorexia- cachexia syndrome
develops in more than half of persons with cancer during the course of their disease. Also in late
stages of serious diseases like AIDS, COPD, kidney disease, and congestive heart failure (CHF).

Cancer and cancer treatments may affect taste, smell, appetite, and even the ability particularly in
oral cancers, to eat enough food or absorb the nutrients from food.
This can cause malnutrition
Several inflammatory cytokines-tumor necrosis factor-α, interleukin-6, interleukin-1β, and a
proteolysis inducing factor, have been shown to cause anorexia.
Most of these inflammatory cytokines appear to mediate anorexia by activation of the melanocortin
system in the hypothalamus
Increased peripheral tryptophan leading to increased central serotonin; or alterations of release of
peripheral hormones that alter feeding, e.g. peptide tyrosine tyrosine and ghrelin.
Central effects include depression and pain, decreasing the desire to eat.

Medicine may be needed to counteract these side effects by targeting the following:
To help increase appetite. To help digest food.
To help the muscles of the stomach and intestines contract (to keep food moving along).
To prevent or treat nausea and vomiting.
To prevent or treat diarrhea.
To prevent or treat constipation.
To prevent and treat mouth problems (such as dry mouth, infection, acute
oral pain, and sores).
To prevent and treat general pain in other areas of the body.

FOOD CRAVING
A food craving is an intense desire for a specific food. This desire can seem uncontrollable, and the
person’s hunger may not be satisfied until they get that particular food.
Some experts believe food cravings last only about 3-5 minutes. Every person experiences cravings
differently. Cravings are often for junk foods and processed foods high in sugar, salt, and fat.

Causes
1.Nutrient defeciencies- body craves certain foods because it lacks certain nutrients.
2.Bad Eating Habits
3.An imbalance of hormones, such as leptin and serotonin,
some endocrinologic conditions, including diabetes, hyperthyroidism, and Graves' disease
4.Due to endorphins that are released into the body after someone has eaten,
which mirrors an addiction.
5.Emotions may also be involved in producing a food craving, especially if a person eats for comfort.

6.Pregnant women experience especially strong cravings, which may be due to

hormonal changes that can disrupt their taste and smell receptors.

Craving can be selective or non-selective.

Selective cravings are cravings for specific foods, which may be a person’s favorite chocolate bar, a
specific burger from their favorite restaurant, or a bag of potato chips.
Non-selective hunger is the desire to eat anything. It may be the result of real hunger and hunger
pangs, but it can also be a sign of thirst. Drinking water may help with intense non- selective cravings.

Ways to reduce unwanted food cravings Reducing stress levels Drinking plenty of water Getting
enough sleep
Eating enough protein
Changing the scenery
Avoiding hunger

Bulimia nervosa (BN), characterized by recurrent binge eating followed by compensatory behaviors
such as purging (self-induced vomiting, excessive use of laxatives/diuretics, or excessive exercise).
Fasting and over-exercising may also be used as a method of purging following a binge. This involves
vomiting, exercise or use of laxatives.People with binge eating disorder eating large amounts of food
to cope with feelings. Food is often eaten without attention to hunger or fullness. Vomiting and
laxative abuse can lead to swollen glands, vitamin and mineral imbalance and wearing down of tooth
enamel. There also can be long-lasting problems with digestion and the heart

Binge Eating Disorder (BED), characterized by binge eating at least 2-3 times a week without
compensatory behavior. This type of eating disorder is more common than either bulimia or anorexia.
The disorder can develop within individuals of a wide range of ages and socioeconomic class This
disorder brings an increased risk for a heart attack, high blood pressure, high cholesterol, kidney
disease, arthritis, bone loss and
stroke.
Polyphagia or hyperphagia refers to excessive hunger or increased appetite. In medicine, polyphagia
(sometimes known as hyperphagia) is a medical sign meaning excessive hunger and abnormally large
intake of solids by mouth. It can be caused by disorders such as diabetes, Kleine–Levin syndrome (a
malfunction in the hypothalamus), the genetic disorders Prader–Willi syndrome, and Bardet–Biedl
syndrome. Causes-Anxiety,Depression,Certain drugs Diabetes mellitus
,Hyperthyroidism ,Hypoglycemia ,Premenstrual syndrome Graves' disease.

Aphagia is the inability or refusal to swallow. ." It is related to dysphagia which is difficulty swallowing
(and odynophagia, painful swallowing. Aphagia may be temporary or long-term, depending on the
affected organ. It is an extreme, life- threatening case of dysphagia. Depending on the cause,
untreated dysphagia may develop into aphagia.
a.Passive aphagia: An animal with passive aphagia will not respond to food if it is
presented. However, if food is inserted into the mouth, the animal will chew.
b.Active aphagia: Active aphagia is a complete rejection of food. The animal will physically push food
away or move its head from it.
c.Mixed aphagia: When presented with food, the animal initially does not react positively or
negatively. However, when food is placed in the mouth, the animal demonstrates active aphagia,
spitting out the food and refusing to eat thereafter

Specifc hunger/ Specific appetite

Animals including man require a qualitative regulation of food intake. Carbohydrates, proteins, lipids,
vitamins, and minerals are required in right proportion to maintain a balanced diet. When the
physiological conditions are changed, food preferences occur in feeding. A craving for a particular
food or nutrient, especially one in which the body is deficient or a drive to eat foods with specific
flavors or other characteristics at specific physiological conditions is specific hunger. The Specific
Hungers Theory was first proposed by Curt Richter in the 1940s. The brain controls our feelings of
hunger and also determines the types of nutrients we should be eat. Following protein starvation,
brain circuit promotes protein feeding and also simultaneously suppresses sugar intake. In an
experiment, rats are fed with a diet deficient in vitamin B, which caused illness. When they are
presented with original diet and a vitamin B rich diet; rats chose vitamin B rich diet.
Eg:- specific hunger during pregnancy and lactation, salt appetite/sodium appetite, specific hunger for
salt- salty snacks taste good etc.

Lateral hypothalamic syndrome

Lateral hypothalamic area provides a link between neural systems that regulate homeostasis including
food intake, water intake, salt intake, and sexual behavior. Lesions in lateral hypothalamus produce a
complex set of symptoms. Experiments were conducted in mice proving role of the region in
controlling feeding. In rats, lesions in lateral hypothalamus resulted in sudden and continued refusal
to eat and animal starved to death. The aphagia is accompanied by adipsia. When they were tube fed,
the animals recovered at different stages. It may be due to the recovery of a few undamaged cells.
These symptoms also indicate that hunger and thirst mechanisms overlap anatomically.

Hypothalamic hyperphagia/ VMH lesion syndrome

Ventromedial nucleus of hypothalamus (VMH) has been designated as the satiety center. Its
stimulation causes cessation of eating in the animals. When VMH area in rat is lesioned, the animal
doubles or triples their normal food intake within a few days and continued the eating. Their body
weight increased 2-3 times the normal weight. Then their food intake dropped to the normal level.
The lesions exerted an inhibitory influence of satiety and shut off mechanism for hunger has been
destroyed. This proved the presence of satiety centre in hypothalamus and its role in feeding
behavior.

ORBITOFRONTAL CORTEX
(OFC)

The orbitofrontal cortex is the area of the prefrontal cortex that sits just above the orbits.
It is thus found at the very front of the brain, and has extensive connections with sensory areas as
well as limbic system structures involved in emotion and memory.
OFC - plays an important role in representing taste, flavor, and food reward.

Food selection -a computation of the expected relative reward value of available food items.
Receives well-processed sensory input from multiple sensory modalities-
gustatory, olfactory, somatosensory, and visual modalities.
OFC - as secondary olfactory and gustatory cortex, because of its importance for chemosensory
processing- computation of perceived pleasantness
Cells in the OFC respond to the taste, smell, touch, and sight of food, and some of these cells
demonstrate multimodal response characteristics in that they fire in response to both the sight and
taste (flavor) of specific food items.
OFC integrates multiple sensory inputs and computes reward value to
guide feeding behavior.
SEX
2 forms of individuals in many species - female / male.
-determined by chromosomes, hormones & genitalia
mating behaviours
basic drive -essential to survival of species

Dynamics of Sexual Behaviour

varies from species to species
reproductively motivated- mating or copulation
non-reproductively motivated- interspecific sexuality, sexual arousal from objects or places, sex with
dead animals, homosexual sexual behaviour, etc.

Monogamy:
one partner- long-lasting pairs
Lifetime-pigeons
one mating season - emperor penguins
cooperate in raising offspring
Polygamy:
>1 mate
Polygyny: 1 male - >1 female mates (lion, mice)
Polyandry: 1 female - >1male (Angler fish)
Polygynandry/ Promiscuity : multiple males - multiple females (chimpanzees & bonobos)

Mating Patterns - Breeding Period

corals & sea urchins - specific breeding periods (offspring born / hatch at optimum environmental
condition)
Estrus- lower animals - periods of ovulation- sex urge maximum & female “in heat”
Human female receptive to some degree most of the time

Patterns & Frequency of Sexual Behaviour

Elephants - two year period
laboratory rats - several times a day
Human - vary

External Control of Sexual Behaviour

Light-day length- away from the Equator-onset of a favourable period for reproduction
equatorial regions-rain
female must be receptive & male must be responsive
receptivity of female - internal factors
responsiveness of male - external cues

“Coolidge effect”
Social factors
tendency of a male to be more responsive with a variety of sexual partners
occurs among most higher species
-sheep

EXTERNAL CUES
lower animals -specific
chief clues
visual,
auditory
olfactory –
combination used

Visual clues
Appearance of many higher vertebrates changes with onset of reproductive activity
prenuptial moult -male birds -nuptial plumage, differs from other times of the year /nonreproductive
individual
hindquarters of female baboons - bright red in colour
less common in the lower animals but do occur in many fishes, crabs, and cephalopods (e.g., squids
and octopuses).
 changes in behaviour: aggressive behaviour between males - grouse females

Eastern Cattle Egret

Auditory clues
sound signals can travel around barriers- widespread - frogs, insects, & birds
encodes several pieces of information- reveal caller’s species, sex, &, in some cases, whether or not
it is mated
frog - number of other males located nearby
sounds produced by wings of mosquitoes attract females - species specific- artificial sound
generators to eradicate certain mosquitoes
also serve to repel other males- territorial song of many songbirds

Olfactory clues
chemical means- urine, feces, & scent markings - mammals -breeding territories & sexual state
mammals - female sexually receptiveness - smelling urine
substance in the urine of male mice- induces & accelerates estrous cycle
female gypsy moth attract males 1000s m downwind -minute quantities sex pheromone each second
1 female silkworm moth -1.5 μg of bombykol- activate >1,000,000,000 males
sex attractant of barnacles-causes individuals to aggregate

Electric discharge
Fishes
Mormyridae of Africa (elephant fish)
Gymnotidae of South America (electric eels)

EXTERNAL CUES FOR HUMAN SEXUAL BEHAVIOUR

very broad social norms

many far from conventional norms
external cues - what we see, touch, hear, smell, or even think
no single, invariable external cue or group of cues for sexual behaviour in humans.

BRAIN
translates nerve impulses from skin into pleasurable sensations controls nerves & muscles used
during sexual behavior regulates release of hormones-physiological origin of sexual desire
cerebral cortex-origin of sexual thoughts & fantasies limbic system (amygdala, hippocampus,
cingulate gyrus & septal area)- emotions & feelings originate

HYPOTHALAMUS  most important - for sexual functioning nerve-cell bodies - receives input from
limbic system destruction areas complete elimination of sexual behavior Produce releasing factors
 anterior pituitary FSH (follicle stimulating hormone) & LH (luteinizing hormone) HYPOTHALAMUS

production of sperm

FSH

development of egg

Male
production

LH /

Female

testosterone

ICSH ovulation

damaged hypothalamus  decline in LH & FSH  ovaries or testes atrophy  declined estrogen &
testosterone levels  diminished sexual behaviour
Replacement therapy (estrogen & testosterone) restores sexual behaviour

Hormones on Hypothalamus
neural cells sensitive to sex hormones
Injection to different areas  different sexual behaviours
structural differences between male & female hypothalamus
A nucleus in medial preoptic area larger in male rats
In humans nuclei in pre-optic suprachaismatic & anterior regions of hypothalamus differ

Ventro medial hypothalamus

(V

MhasHoe)strogen & progesterone receptors

crucial for receptiveness & lordosis

Female Rats- Oestrogen increases
size of dendritic trees
number of progesterone receptors  proteins – lordosis (posture - some female mammals during
mating)

spinal cord sense- mounting male  lordosis

Ventromedian Hypothalamus (VMH)

Periaqueductal grey region of mid brain

Medullary reticular formation

Reticulospinal tract  Spinal cord -

Mounting male  lordosis

•hypothalamic medial preoptic area

•Rats - copulatory behaviour (mounting)

mPOA

medial forebrain bundle

ventral midbrain

basal ganglia

mounting behaviours

Cerebrum- caudate, putamen, & globus pallidus Midbrain- substantia

Diencephalon- subthalamic nucleus

Hypothalamus
deep sexual identity - psychological attitude to sex
anterior hypothalamus - male sexual behavior
Interstitial nucleus of anterior hypothalamus - dimorphic - smaller in women & gay men
Feed back
Receive information directly from genital regions
Paraventricular nucleus- activated during copulation & orgasm- produces oxytocin, vasopressin,
enkephalins, & dopamine
Oxytocin - reward system
A aMlmoYndGshDapAedLA
in medial temporal lobes
connections with cortical & subcortical structures
part of structures - emotion processing
projects to structures fundamental for sex- hypothalamus
regulation of autonomic responses & cognitive functions
stimulation  orgasmic like pleasure sensations
gender related differences- activation increased in men

CORTICAL AREAS
Evolution sexual behavior complex
substantial role - subcortical structures
cerebral cortex -make sexual behavior adaptive & shaped on social and cultural influences
areas -conscious processing
prefrontal cortex,
orbitofrontal cortices,
cingulate cortex
insula

Complex cognitive behaviors, personality expression, decision making & moderate correct social
behaviour
shape thoughts & actions- internal goals
integrate & elaborate stimuli in executive function –
differentiate conflicting thoughts; good & bad, better & best, same & different
future consequences of current activities
prediction of outcomes
expectation based on actions
social "control" (suppress urges 
socially unacceptable outcomes)

sexual inhibition- inhibit activation of excitatory mechanisms -shift attention & behavior to
nonsexual stimuli or situations
Hypersexuality- patients with OFC lesions
OFC - pleasant body representation & euphoric feelings
Connected to subcortical structures - reward system
Cognitive filtering of sex

•most conspicuous part of limbic system,

•surrounds corpus callosum
•divided into anterior, middle, & subgenual regions
• ACC activation- response to erotic stimuli- process sexual stimuli in divergent contexts,
enhancing decision making - outputs to motor related areas & periaqueductal gray
•middle cingulate cortex activity elicited during arousal
• subgenual cingulate cortex activity negatively correlate with arousal
• increased cingulate cortex activation - males during erection & in females during orgasm
• key relay structure between subcortical limbic structures & associative cortices
Sexual behavior complexity-conscious modulation
insular cortex is a hub of the salience network- process sensorial stimuli & relay to other cortical
areas- facilitating attention & working memory
sex related task - co activation of insula & ACC
conveys integrated information to
brainstem structures- regulate autonomic responses
motor related area responses to sexual stimuli
anterior insula active - desire phase
posterior insula active - arousal phase
Disorders in genital arousal - insula lesions

in the basal forebrain

cognitive processing of motivation, aversion, reward & reinforcement learning
induction of slow-wave sleep
medium spiny neurons (MSNs) receive inputs from prefrontal cortex, hippocampus, amygdala, &
thalamus.
affect
(1)copulatory behavior through MPOA- copulation
(2)motor outputs as a part of basal ganglia
(3)emotional/motivated & autonomic responses via its direct projection to lateral hypothalamus

ventral midbrain
multisynaptic pathway spinal cord - reflexes of copulation
brain stem nuclei- paragigantocellular nucleus in pons
 spinal cord - inhibit penial erection reflex circuit
mPOA inhibits “inhibitory nucleus”

The Performance Circuit

Sexual behaviour- chain of events
each element - controlled by specific neural component in a complex circuit
Motivation (urge to engage in sexual behaviour) - rooted in the hypothalamic-pituitary-gonad circuit
performance - rooted in spinal cord cortex circuit
Damage to spinal cord or the cortex, can disrupt sexual behaviour - urge still be there, but the ability
to perform is gone

The Performance Circuit

male dog brain detached from spinal cord shows erection & intense ejaculatory response when its
penis is directly stimulated
Normal intact dogs, will not ejaculate to direct genital stimulation unless a receptive female is
present
So brain normally acts to inhibit reflex circuits & the environmental cues act to remove the inhibitory
effect

The Performance Circuit

stimulation of medial forebrain bundle 
isolated ejaculation
anterior dorsolateral hypothalamus  erection
hypothalamus  full sequence of copulatory behaviour
Damage to the different regions of brain  drastic difference in the sexual behaviour of male
experimental animals; lesser impact presented by females

sexual response in man

consists of responses & sensations that involve the entire body

Four phases- excitation, plateau, orgasm & resolution

ROLE of nervous system in sexual

response of man
Central NS: Brain & spinal cord
Brain- interpret what sensations are to be perceived as sexual & issuing appropriate "orders"
Spinal cord - transmission cable & mediate certain reflex actions.
Peripheral NS: Cerebrospinal nerves
Afferent cerebrospinal nerves - go to the spinal cord, carry sensory messages to the brain.
Efferent cerebrospinal nerves - come from the spinal cord) carry commands from the brain to
activate muscles.
Autonomic NS: regulate & maintain body processes necessary to life (heart rate, breathing, digestion
& temperature control); controls sexual involuntary responses

Nervous System During Sexual Intercourse

Integration of
Local Level
Spinal Level
Central Level

Local Level: Touch & mechanical stimulation of external genitalia in man & woman by means of
pressure, touch & attrition

Nervous System During Sexual Intercourse

Spinal Level:
excitation of several kinds of sensorial receptors in skin, mucosa & subcutaneous tissue  travels
through sensory nerves of lower abdomen to sacral spinal cord & lumbar spinal cord neurons (part of
reflex circuit) ejaculation
reflexes  autonomic reflexes (sympathetic & parasympathetic)  selective afflux of blood to
reproductive organs, secretion of glands & contraction of smooth muscles in the sexual organs
occur independent of the higher portions of the nervous systems
in tetraplegic individuals- spinal cords sectioned by accident at higher levels erection & ejaculation
can be achieved

Intercourse
Central Level
sensorial impulses from genitalia travel up to brain, to the (sensory cortex & limbic system) & elicit
conscious perception & pleasurable reactions
Sensory cortex and limbic system, in addition to its signalling functions, excite hypothalamus & other
structures  stimulate autonomic nervous system  spinal cord reflexes accompanying coitus more
stimulated (self-sustaining "loop“)
hypothalamus excite hypophysis- release hormones -ovary & testis stimulated - release gonadal
hormones into blood
hormones, such as oxytocin, FSH & LH will act peripherically to modulate & render local circuits at
the sexual organs more sensitive to the nervous stimuli

Intercourse
Integration of the Levels
Interplay between the local, spinal & central levels essential to the development of the normal
sexual response in humans
But, brain (central) mechanisms more important than in other animals
Sexual excitation can be aroused by central mechanisms
alone-hearing, seeing or even smelling, so-called erotic stimuli (mostly learned & of cultural origin)
evoke sexual excitation through the sensory systems, limbic system, hypothalamus & autonomous
nervous system

Brain
No specific "sex area" : hypothalamus & limbic system most concerned
nerve impulses from skin  pleasurable sensations
controls nerves & muscles used during sex
regulates release of hormones- physiological origin of sexual desire
cerebral cortex- origin of sexual thoughts & fantasie
limbic system (amygdala, hippocampus, cingulate gyrus & septal area)- emotions & feelings originate
lab animals - destruction of certain areas hypothalamus 
complete elimination of sexual behaviour

Endocrine
system
one of the body’s two major coordinating systems
works by transmitting - hormones produced by endocrine gland (ductless)

Hormones & Sexual behaviour

most animal species brain controls & regulates sexual behaviour primarily by means of hormones
higher animals (monkeys & humans) - sexual behaviour more closely related to nervous system than
to hormonal levels
However, hormones seems to affect arousability by altering threshold for erotic stimulation

Sex Hormones
divided roughly into two groups
Androgens:
most prominent, testosterone
predominate in males (chiefly produced from testes)
Estrogens:
most prominent, estradiol
predominate in females (chiefly produced from ovaries)
both group secreted from adrenal cortex also both women & men have both estrogen &
testosterone (different quantities)

Hypophysis / pituitary
Master endocrine gland many of its hormones targets other endocrine glands
releases a number of hormones for a particular gland,
 which picks up the hormone from the blood stream
 produces its own hormone
controlled by chemical factors produced by neuroendocine cells in the brain

Hypothalamus
located in brain directly above hypophysis, is known to exert control over it by means of
neural connections
hormone like substances - releasing factors

HYPOTHALAMUS  most important - for sexual

functioning
nerve-cell bodies - receives input from limbic system
destruction areas
complete elimination of sexual behavior
Produce releasing factors  anterior pituitary FSH (follicle stimulating

production of sperm

FSH

development of egg

Male
production

LH /

Female

testosterone

ICSH ovulation

damaged hypothalamus  decline in LH & FSH  ovaries or testes atrophy  declined estrogen &
testosterone levels  diminished sexual behaviour
Replacement therapy (estrogen & testosterone) restores sexual behaviour

Sex Hormones
affect arousability by altering threshold for erotic stimulation
They act:
centrally - by determining amount of change in arousal produced by a given stimulus
peripherally - by determining amount of receptor response to a stimulus

Feedback control of production of gonadal hormones

hypothalamus secretes gonadotropin releasing factor (GnRH)
GnRH reaches pituitary through hypothalamo hypophyseal portal system & stimulates it to secrete
gonadotrophic hormone (GTH)
picked up by ovary / testis, which is stimulated to release a gonadal hormone
gonadal hormone detected by pituitary & hypothalamus- which are inhibited from releasing more
hormones

Oxytocin
important sex hormone secreted by pituitary gland
"hormone of love,"
released during sexual intercourse when orgasm is achieved
released in females when give birth or breast feeding;
involved in maintaining close relationships
prolactin & oxytocin stimulate milk production in

Hormones & Sexual Behaviour

Males,
Testosterone - major contributing factor to sexual motivation
Vasopressin - arousal phase
Female – role of hormones in sexual motivation is not well understood
Estrogen increasing motivation to engage in sexual behaviour
Progesterone decreasing it (rise & fall throughout menstrual cycle)
testosterone, oxytocin & vasopressin implicated in female sexual motivation in similar ways as they
are in

Sexual behaviour & environment

Sexual behaviour, arousal, & motivation occur only in special environmental situations (provide
particular types of sensory stimulation)
No stimulation will arouse sexual motivation & behaviour unless organism is physically ready to
mate
physiological readiness to respond selectively to sexual stimuli provided by hormonal changes (affect
neural & non-neural mechanisms)

Sexual behaviour & type of hormone

It was assumed that
male sexual behaviour is rooted in testosterone
female sexual behaviour rooted in estrogen
hormonal injections do not change nature of sexual behaviour
homosexual humans who have been given hormonal injections (estrogen to females and
testosterone to males) have showed increased homosexual behaviour

Sexual behaviour & type of hormone

both males and females possess the neural circuits for both types of sexual behaviour,
one circuit is more sensitive than the other, and
hormones will simply activate the tendency related to that circuit no matter what hormone is used.
So, hormones just activate sexual behaviour, but do not determine the type of behaviour

Neural circuits for sex

Theory: male & female sexual behaviour is determined by the sensitivity of neural circuits in the two
sexes. There are both “male” and “female” circuits in every individual, but one circuit- the “male”
circuit in the male and “female” circuit in the female- is more sensitive to stimulation
supported by structural difference (number of synaptic connections) in the brains of male & female
rats.
Autoradiography shows: estrogen sensitive neurons are present in the ventromedial hypothalamus,
preoptic area, septal area, hippocampus, & midbrain of females as well as males (in rats, fish, birds,
amphibians &

Neural circuits for sex

estrogen produced in males from testosterone by aromatization – stimulate estrogen sensitive
neurons in the male brain
Support: estrogen implants in brain more effective than testosterone implants in restoring male
sexual behaviour to castrated rats
effect of estrogen is incomplete - rats were deficient in intromission & ejaculatory behaviour.
returns to normal behaviour when dihydrotestosterone is administered along with estrogen

Molecular biology of hormone action

Hormones alter neural activity by altering synaptic activity, which they appear to do in one of the 3
ways
by increasing receptor sites on the post synaptic membrane
by decreasing the production of inhibitory neurotransmitter and
by increasing the production of proteins involved in neurotransmission by temporarily activating
DNA

Molecular biology of hormone action

estrogen & testosterone regulate sexual behaviour
In females, release of estrogen is cyclical,
level of estrogen  variations in female sexual receptivity of lower animals
In males, testosterone level is stable
provides a steady stream of stimulation & a constant state of “sexual readiness”

Pheromone
secreted or excreted chemical factor that triggers a social response in members of the same species
act like hormones outside the body of the secreting individual, impact the behavior of the receiving
individuals
alarm pheromones, food trail pheromones, sex pheromones, and many others that affect behavior
or physiology
from basic unicellular prokaryotes (ciliates) to complex multicellular eukaryotes (vertebrates &
plants)

Sex pheromones
chemical signals (pheromones), released by an organism to attract an individual of the opposite sex,
encourage them to mate with them, or perform some other function closely related with sexual
reproduction
indicating females ready for breeding, attracting the opposite sex, & conveying information on
species, age, sex and genotype
in social insects : Non-volatile pheromones, or cuticular contact pheromones, detected by direct
contact with chemoreceptors on the antennae or feet

Sex pheromones in pest monitoring and pest control

Monitoring: pheromone traps used to attract & catch a sample to determine whether control
measures are needed
Control,
by releasing enough pheromone to prevent males from finding females effectively drowning out
their signals,
by mass trapping, attracting & removing pests directly

Human sex pheromones

No chemical proved as true human sex pheromone
humans are highly dependent upon visual cues
in proximity, smells also play a role in sociosexual behaviors
three classes of putative human pheromones
axillary steroids,
vaginal aliphatic acids,
stimulators of vomeronasal organ

Human sex pheromones

Axillary steroids
produced by testes, ovaries, apocrine glands & adrenal glands
not biologically active until puberty when sex steroids influence their activity
activity change during puberty suggest role in sexual behaviour
possible human pheromones: androstadienol, androstadienone, androstenone, androstenol, &
androsterone.
Androstenol is the putative female pheromone
Androstenone, secreted only by men as an attractant for women - perceived as more pleasant at
time of ovulation

Human sex pheromones

Synchronization of Menstrual Cycles (Mcclintock Effect)
group of women were exposed to a whiff of
perspiration from other women
sweat was collected (before, during, or after ovulation)
-association with the recipient woman's menstrual cycle to speed up or slow down
pheromone produced prior to ovulation, shortens the ovarian cycle
produced just at ovulation, lengthens the cycle

Chemical interventions & sexual behaviour- chemicals that target dopamine, serotonin
Neurotransmitters: chemical messengers that carry electrical signals between neurons in the brain.
Dopamine & serotonin are two important neurotransmitters -affect mood, memory, sleep, libido,
appetite, etc.
Imbalances can contribute to addictions, mood conditions, memory issues, and attention difficulties.
In general, dopamine enhances, whereas serotonin inhibits, sexual motivation & performance and
thus may contribute to initiation and satiety, respectively.

Dopamine & sexual behaviour

has enabling effects on
sexual motivation,
copulatory competence
genital reflexes.
in nigrostriatal pathway influences motor activity
In mesolimbic pathway activates various motivational behaviours, including sexual activity
In medial preoptic area (MPOA) - controls genital reflexes, sexual configurations, & specifically libido
In PVN, activation of oxytocinergic neurons

Serotonin & Sexual Behaviour

generally inhibits sexual activity
Sexual behavior - impaired by many serotonin agonists & agents that increase serotonin
released in anterior lateral hypothalamus at the time of ejaculation
exerts inhibitory control over sexual activity, in part, by inhibiting dopamine release after an
ejaculation
Certain antidepressants, major side effects - impairment of ejaculatory & orgasmic ability & decreased
libido

Sexual orientation
person's sexual identity in relation to gender to which they are attracted; the fact of being
heterosexual, homosexual, or bisexual
Homosexuality: sexual attraction between members of the same sex or gender
Heterosexuality: sexual attraction or sexual behavior between persons of the opposite sex or gender
Bisexuality / pansexuality: sexual behavior toward both males and females or to more than one sex
or gender

Palatability
Positive hedonic evaluation of food's sensory characteristics.
Taste, odor, appearance, texture, sound, and trigeminal senses
which together constitute flavour - sensory characteristics of a food which people use to assess
palatability .
The palatability of a food or fluid varies with the state of an individual: it is lower after consumption
and higher when
deprived.

Create a hedonic hunger that is independent of homeostatic needs.

The palatability of a food, especially its taste pleasantness, is the most important factor that
determines food selection or preference
Macronutrient composition influences palatability, generally foods higher in fat and sugar content
have higher palatability. Foods higher in palatability are consumed in higher amounts in controlled
studies, independent of macronutrient composition.

Appetite is controlled by a direct loop and an indirect one- two feedback mechanisms-

First a positive feedback involving its stimulation by palatability food cues, and second, a negative
feedback due to satiation and satiety cues following ingestation.

More palatable foods reduce the effects of such cues upon satiation causing a larger food intake.

Microinjection of opioid agonists-morphine, into the nucleus accumbens shell produces increases in
eating behavior
Activation of accumbens opioid receptors in rats also augments food 'liking', or the hedonic impact of
taste.
Naloxone-is a medication used to block the effects of opioids. Naloxone infusions nucleus accumbens
shell or ventral pallidum –rat inhibit eating Identified a neural site that definitely contains receptors
capable of increasing food intake.
Opioid receptors also participate in the regulation of feeding.
Agonist stimulation of opioid receptors increases feeding in rodents, while opioid antagonists inhibit
food intake and weight gain in mice.

lateral hypothalamus (LH) nucleus accumbens (NAc) the ventral pallidum (VP) -
important roles in eating and reward, palatable food rewards
The ventral striatum -the limbic system
ventral tegmental area (VTA)
.
NAc- shell and core- basal forebrain, in each hemisphere, part
of the basal ganglia, main component of the ventral striatum- role in the "reward circuit“
opioid receptors - rostromedial shell part of the nucleus accumbens - spiny neurons. This area has
been called the "opioid eating site".

Opioid circuitry in both the nucleus accumbens and ventral pallidum has been reported to mediate
taste-reactivity responses to palatable events.
Taste-reactivity measures of palatability in rodents, several groups have reported evidence of an
opioid receptor-mediated network within the circuitry of the nucleus accumbens shell and ventral
pallidum mediating hedonic processing or reward “liking”

Endogenous opioids - naturally produces its own opiate-like substances- produced in the brain-
as neurotransmitters- bind to and activate opioid receptors on the surface of nerve cells-
endorphins, enkephalins, and dynorphin
All mammalian opioid peptides are derived from three precursors, i.e., pro-opiomelanocortin (POMC),
pro-enkephalin (PENK) and pro-dynorphin (PDYN)

The opioid system controls pain, reward and addictive

behaviors.
Opioids exert their pharmacological actions through three opioid receptors, mu, delta and kappa -
several pharmacological subtypes
Brain stem, limbic system, spinal cord-opioid receptors are widely involved in various physiological
and pathophysiological activities, including the emotional response, epileptic seizures, immune
function, feeding, obesity, respiratory and cardiovascular control as well as some neurodegenerative
disorders
mu receptors are responsible for opioids’ pleasurable effects and their ability to relieve pain-pleasure,
relaxation

Research suggested that syndyphalin-33 (SD33) - a μ-opioid receptor ligand, increases food intake in
sheep after intravenous injection, and its effects are mediated via opioid receptors.
Studies showed that stimulation of μ-opioid receptors preferentially increases the intake of a high fat
diet.
The increased levels of hypothalamic μ-opioid receptors in Osborne-Mendel rats could contribute to
their preference for a high fat diet and increased susceptibility to obesity .
The μ-opioid receptor signaling in the nucleus accumbens core and shell is necessary for palatable
diet-induced hyperphagia and obesity to fully develop in rats

The euphoric effect also appears to involve another mechanism in which the GABA-inhibitory
interneurons of the ventral
tegmental area (VTA) (in mid brain) come into play.
By attaching to their mu receptors, exogenous opioids reduce the
amount of GABA released.
Normally, GABA reduces the amount of dopamine released in the nucleus accumbens.
By inhibiting this inhibitor, the opiates ultimately increase the amount of dopamine produced and the
amount of pleasure felt.

Over 300 substances have been identified in chocolate.

Some of these, including caffeine and theobromine could actually cause dependency effects. But the
amounts of these substances in chocolate are too small to really have any effect.
Anandamide, a neurotransmitter produced naturally by
the brain, has also been isolated in chocolate. The active chemical in marijuana is called
tetrahydrocannabinol (THC)- "being high."

Physiological changes during sleep

►Sleep can be defined as “an active state of unconsciousness produced by the body where the brain
is in a relative state of rest and is reactive primarily to internal stimulus." Sleep is characterised by:
►low physical activity levels
►reduced sensory awareness
►Sleep is also regulated by the circadian rhythm and homeostatic mechanisms. Furthermore, certain
brain activity patterns, as well as the different phases of sleep can be visualised using
electroencephalography(EEG).

►NREM Sleep Stage 1 (N1)

►Transitional phase between wakefulness and sleep (the period during which we drift off to sleep)
►Shallow stage of sleep
►Reduced respiration rate
►Reduced heartbeat
►Brain wave activity (EEG)
►Associated with alpha and theta waves
►Earlier in N1 – alpha waves, low frequency (8-13 Hz), high amplitude patterns of electrical activity
(waves) that become synchronised
►This brain wave activity pattern is like someone who is very relaxed, but awake
►Further on in stage N1 – increase theta wave activity
►Theta waves – lower frequency (4 -7 Hz), higher amplitude brain waves
►Easy to wake someone from stage 1
►Lasts around 5 -10 minutes

►NREM Sleep Stage 2 (N2)

►the body goes into a deep relaxation state
►the onset of sleep
►drop in body temperature
►heart rate slows down
►the brain produces sleep spindles
►people are less aware of their surroundings
►lasts around 20 minutes
►Brain wave activity
►Theta waves still dominant, but interrupted by sleep spindles (rapid burst of higher frequency brain
waves – these may be important for learning and memory)

►NREM Sleep Stage 3 (N3)

►Also known as slow-wave sleep (SWS)
►Muscles relax
►Blood pressure drops
►Breathing rate drops
►Deepest sleep occurs
►People are less responsive
►Noises and activity in the surrounding environment may fail to generate a response
►Transitional period between light sleep and very deep sleep
►Lasts about 20 to 40 minutes.
►Brainwaves - low frequency (up to 4Hz), high amplitude delta waves

►REM Sleep
►Eyes move rapidly under closed eyelids
►Brain becomes more active
►Low amplitude, mixed frequency EEG (similar to an awake pattern)
►Desynchronized EEG activity
►Body becomes relaxed and immobilised
►Muscle atonia or paralysis
►Dreams occur
►Also referred to as paradoxical sleep because while the brain and other body systems become more
active, muscles become more relaxed

►A variety of physiological changes take place during the different stages of sleep.
►Periods of non-REM sleep are characterized by decreases in muscle tone, heart rate, breathing,
blood pressure, and metabolic rate. All these parameters reach their lowest values during slow-wave
sleep.
►In non-REM sleep, body movements are reduced compared to wakefulness, although it is common
to change sleeping position (tossing and turning).
►Periods of REM sleep, in contrast, are characterized by increases in blood pressure, heart rate, and
metabolism to levels almost as high as those found in the awake state. In addition, REM sleep, as the
name implies, is characterized by rapid, rolling eye movements, paralysis of large muscles, and the
twitching of fingers and toes. Penile erection also occurs during REM sleep, a fact that is clinically
important in determining whether a complaint of impotence has a physiological or psychological
basis. Interestingly, REM sleep is found only in mammals (and juvenile birds)

Biological perspectives on dreaming

►What Is a Dream?
►A dream includes the images, thoughts, and emotions that are experienced during sleep. Dreams
can range from extraordinarily intense or emotional to very vague, fleeting, confusing, or even boring.
Some dreams are joyful, while others are frightening or sad. Sometimes dreams seem to have a clear
narrative, while many others appear to make no sense at all.
►There are many unknowns about dreaming and sleep, but what scientists do know is that just
about everyone dreams every time they sleep, for a total of around two hours per night, whether
they remember it upon waking or not.
►How Do Scientists Study Dreams?
►Traditionally, dream content is measured by the subjective recollections of the dreamer upon
waking. However, observation is also accomplished through objective evaluation in a lab.
►In one study, researchers even created a rudimentary dream content map that was able to track
what people dreamed about in real time using magnetic resonance imaging (MRI) patterns. The map
was then backed up by the dreamers' reports upon waking.

►The Role of Dreams

►Some of the more prominent dream theories contend that the function of dreaming is to:
►Consolidate memories
►Process emotions
►Express our deepest desires
►Gain practice confronting potential dangers
►Many experts believe that we dream due to a combination of these reasons rather than any one
particular theory. Additionally, while many researchers believe that dreaming is essential to mental,
emotional, and physical well-being, some scientists suggest that dreams serve no real purpose at all.

►Dreaming during different phases of sleep may also serve unique purposes. The most vivid dreams
happen during rapid eye movement (REM) sleep, and these are the dreams that we're most likely to
recall. We also dream during non-rapid eye movement (non-REM) sleep, but those dreams are known
to be remembered less often.
►Dreams may Reflect the Unconscious
►Sigmund Freud’s theory of dreams suggests that dreams represent unconscious desires, thoughts,
wish fulfillment, and motivations. According to Freud, people are driven by repressed and
unconscious longings, such as aggressive and sexual instincts.
►While many of Freud's assertions have been debunked, research suggests there is a dream rebound
effect, also known as dream rebound theory, in which suppression of a thought tends to result in
dreaming about it.

►What Causes Dreams to Happen?

►In "The Interpretation of Dreams," Freud wrote that dreams are "disguised fulfillments of repressed
wishes." He also described two different components of dreams: manifest content (actual images)
and latent content (hidden meaning).
►Freud’s theory contributed to the rise and popularity of dream interpretation. While research has
failed to demonstrate that the manifest content disguises the psychological significance of a dream,
some experts believe that dreams play an important role in processing emotions and stressful
experiences.

►According to the activation-synthesis model of dreaming, which was first proposed by J. Allan
Hobson and Robert McCarley, circuits in the brain become activated during REM sleep, which triggers
the amygdala and hippocampus to create an array of electrical impulses. This results in a compilation
of random thoughts, images, and memories that appear while dreaming.
►When we wake, our active minds pull together the various images and memory fragments of the
dream to create a cohesive narrative.
►In the activation-synthesis hypothesis, dreams are a compilation of randomness that appear to the
sleeping mind and are brought together in a meaningful way when we wake. In this sense, dreams
may provoke the dreamer to make new connections, inspire useful ideas, or have creative epiphanies
in their waking lives.

►Dreams Aid In Memory

►According to the information-processing theory, sleep allows us to consolidate and process all of
the information and memories that we have collected during the previous day. Some dream experts
suggest that dreaming is a byproduct, or even an active part, of this experience processing.
►This model, known as the self-organization theory of dreaming, explains that dreaming is a side
effect of brain neural activity as memories are consolidated during sleep.
► During this process of unconscious information redistribution, it is suggested that memories
are either strengthened or weakened. According to the self-organization theory of dreaming, while
we dream, helpful memories are made stronger, while less useful ones fade away.

Sleep factors
►A variety of internal and external factors can dramatically influence the balance of this sleep-wake
system.
►Light
►Light is one of the most important external factors that can affect sleep. It does so both directly, by
making it difficult for people to fall asleep, and indirectly, by influencing the timing of our internal
clock and thereby affecting our preferred time to sleep
►Light influences our internal clock through specialized "light sensitive" cells in the retina of our
eyes. These cells, which occupy the same space as the rods and cones that make vision possible, tell
the brain whether it is daytime or nighttime, and our sleep patterns are set accordingly.
►Jet Lag and Shift Work
►Normally, light serves to set our internal clock to the appropriate time. However, problems can
occur when our exposure to light changes due to a shift in work schedule or travel across time zones.
Under normal conditions, our internal clock strongly influences our ability to sleep at various times
over the course of a 24-hour period, as well as which sleep stages we experience when we do sleep.
►Individuals who travel across time zones or work the night shift typically have two symptoms. One
is insomnia when they are trying to sleep outside of their internal phase, and the other is excessive
sleepiness during the time when their internal clock says that they should be asleep. Half of all night
shift workers regularly report nodding off and falling asleep when they are at work.

►Pain, Anxiety, and Other Medical Conditions

►A wide range of medical and psychological conditions can have an impact on the structure and
distribution of sleep. These conditions include chronic pain from arthritis and other medical
conditions, discomfort caused by gastroesophageal reflux disease, pre-menstrual syndrome, and
many others. Like many other sleep disruptions, pain and
discomfort tend to limit the depth of sleep and allow only brief episodes of sleep between
awakenings.

Individuals of all ages who experience stress, anxiety, and depression tend to find it more difficult to
fall asleep, and when they do, sleep tends to be light and includes more REM sleep and less deep
sleep. This is likely because our bodies are programmed to respond to stressful and potentially
dangerous situations by waking up. Stress, even that caused by daily concerns, can stimulate this
arousal response and make restful sleep more difficult to achieve.

►Medications and Other Substances

►Many common chemicals affect both quantity and quality of sleep. These include caffeine, alcohol,
nicotine, and antihistamines, as well as prescription medications including beta blockers, alpha
blockers, and antidepressants.
►The pressure to sleep builds with every hour that you are awake. During daylight hours, your
internal clock generally counteracts this sleep drive by producing an alerting signal that keeps you
awake. The longer you are awake, the stronger the sleep drive becomes. Eventually the alerting signal
decreases and the drive to sleep wins out. When it does, you fall asleep.
►A chemical called adenosine, which builds up in the brain during wakefulness, may be at least partly
responsible for sleep drive. As adenosine levels increase, scientists think that the chemical begins to
inhibit the brain cells that promote alertness. This gives rise to the sleepiness we experience when we
have been awake for many hours. Interestingly, caffeine, the world’s most widely used stimulant,
works by temporarily blocking the adenosine receptors in these specific parts of the brain. Because
these nerve cells cannot sense adenosine in the presence of caffeine, they maintain their activity and
we stay alert.

►Alcohol is commonly used as a sleep aid. However, although alcohol can help a person fall asleep
more quickly, the quality of that individual's sleep under the influence of alcohol will be
compromised.
►Beta blockers, which are used to treat high blood pressure, congestive heart failure, glaucoma, and
migraines, often cause decreases in the amount of REM and slow-wave sleep, and are also associated
with increased daytime sleepiness.
► Alpha blockers, which are also used to treat high blood pressure and prostate conditions, are
linked to decreased REM and increased daytime sleepiness. Finally, antidepressants, which can
decrease the duration of periods of REM sleep, have unknown long-term effects on sleep as a whole.
►Some antidepressants, from the class of drugs known as SSRIs, have been found to promote
insomnia in some individuals.
►Sleep environment
►The bedroom environment can have a significant influence on sleep quality and quantity. Several
variables combine to make up the sleep environment, including light, noise, and temperature. By
being attuned to factors in your sleep environment that put you at ease, and eliminating those that
may cause stress or distraction, you can set yourself up for the best possible sleep.

Taste aversion learning

Different species- different eating strategies Crocodile- huge meal, eat nothing for months Birds- what
they need
Polar bear- as much they can
Man- eat more than we need today
Which food to eat and how much- important decision Newborn mammals-survive first on mothers
milk Age of weaning- lose intestinal lactase-lactose-
Man with partial exception-can not tolerate large amount of milk products

Carnivores- selection of satisfactory diet is simple

Herbivores, omnivores- distinguish between edible and inedible-minerals, vitamins
Strategies to select food-
1.select sweet food, avoid bitter ones, eat salty food,
2.prefer any thing that tasted familiar-safe 3 learn the consequences of eating each food

Humans,- omnivores - there is a wide range of substances that potentially can serve as food. Some of
these substances provide nutrients and calories necessary for survival, but others are harmful and
potentially lethal.
In humans, a number of sensory systems are engaged when processing foods, including visual,
gustatory, and olfactory systems. For most mammals, however, taste is the primary cue that identifies
the post-ingestion consequences of the food.

When one becomes ill after consuming a meal, even hours later, there is a tendency to target a
particular taste as the cause of the illness. Our brain blames the illness on the food. It wont taste good
to us for the next time. This association between a particular taste and illness is a form of learning
that is termed conditioned taste aversion (CTA).
/Taste aversion learning .

A consequence of the learned association is that the taste will become aversive. When experiencing
the taste again, individuals will show aversive reactions such as expressions of loathing, will
experience mimicked illness sensations such as nausea, and subsequently, will avoid further exposure
to the taste. The ability to acquire CTA occurs across species and across ages within a species.

Learned taste-illness association serves the critical function of informing individuals of the toxic
nature of certain foods, thus preventing further illness and potentially death.

In the rodent laboratory, CTA typically is induced by intraperitoneal injections of a lithium chloride
(LiCl) solution after consumption of a highly palatable novel solution such as sucrose or saccharin
flavored water.
LiCl evokes nausea and vomiting in humans and a gaping response in nonemetic rats that appears to
be an incipient vomiting response.
The consequences of acquisition of a CTA are threefold.
When experiencing that sweet solution again, individuals will:
(1)exhibit rejection reactions to this solution
(2)experience and show mimicked illness reactions, that is, reactions that mimic some of the
behavioral and physiological reactions that occur during true illness and
(3)reduce or cease consumption of this solution
During acquisition, an association is made between the taste of a food that has been consumed and
subsequent illness. This association is stored and any encounter with this taste after acquisition will
evoke rejection, such as spitting out the food, mimicked illness responses and sensations such as
nausea, and subsequently, avoidance, by ceasing further exposure to the taste.

Ingestiun
Responses

Avoidance Responses

Taste

Rejection Responses
Taste

Illness
Responses
0

Mimicked Illness Responses

Rejection reactions are species specific- in rat -In rats, LiCl elicits hypothermia, decreased heart rate,
and the behavior lying-on-belly.
Humans report that the avoided food is distasteful and simply thinking of learned food aversions
elicits facial expressions of loathing. Premature and full-term neonatal humans and neonatal rats
show ingestion orofacial responses to sweet tastes and rejection orofacial responses to bitter tastes
One sensation that commonly is reported during illness in humans is nausea. Simply hearing or
thinking about a conditioned taste elicits nausea
Anorexia nervosa is an eating disorder characterized primarily by persistent behaviors or attitudes
that interfere with expected weight gain and maintenance. The essential features are persistent
energy intake restriction, fear of gaining weight, and disturbance of self- perceived weight and shape.

Although the positive or negative value of these predispositions generally are stable, they can change.
Some changes are tied to the internal state of the individual such that preferred tastes can become
temporarily less positive and aversive tastes can become temporarily less negative
The change in internal state can be either a shift away from homeostasis or a shift back to a
homeostatic state. For example, rats deprived of sodium increase their preferences for solutions that
contain this substance, even when the solution contains concentrations that are normally aversive.
When homeostatic levels of sodium are restored, their aversion to the hypertonic solutions returns.
On the other hand, reactions to calorie-rich sweet solutions change from positive to negative as
humans and rats go from food depletion to food repletion.When a depleted state returns, reactions
to calorie-rich sweet solutions become positive again. These temporary shifts in hedonic value are
referred to as allesthesia.
.

PHYSIOLOGICAL BASIS OF DRINKING

Dr. PRADEEP KUMAR R.

Assistant Professor Dept. of Zoology
Govt. College for Women
Thiruvananthapuram

Thirst is the physiological urge to drink water and the sensation created by the hypothalamus that
drives organisms to ingest water. It is sometimes associated with feelings of dry mouth, headache, or
irritability but these symptoms are not specific to thirst
Water gain
As preformed water ingested food and drink
to a lesser extent, as metabolic water that is produced as a by-product of aerobic respiration and
dehydration synthesis.
In the normal resting state, the input of water through ingested fluids is approximately 2500 ml/day.
Water loss
lost through normal physiological activities, such as urination, defecation, respiration and sweating.
The majority of fluid output occurs from urination, at approximately 1500 ml/day (approximately 1.59
qt/day) in a
normal adult at resting state.
Some fluid is lost through perspiration (part of the body’s temperature control mechanism) and as
water vapor in expired air; however these fluid losses are considered to be very minor.
An osmoreceptor is a sensory receptor that detects changes in osmotic pressure and is primarily
found in the hypothalamus. Osmoreceptors detect changes in plasma osmolarity (that is, the
concentration of solutes dissolved in the blood).
When the osmolarity of blood changes (it is more or less dilute), water diffusion into and out of the
osmoreceptor cells changes. That is, the cells expand when the blood plasma is more dilute and
contract with a higher concentration.

Body fluids-intracellular ans extracellulr

Normal concentration of salt in bodyfluid -0.9%

Two types of thirst

Water Loss: respiration, sweating, urination, defecation, bleeding.

Salt loss.
(a) Hypovolemic thirst

Water Intake: drinking, feeding,

Salt content.

1.Hypovolemic thirst
•Thirst that arise due to a decreases in extracellular fluid volume and arterial pressure
•Blood volume loss by hemorrhage stimulates thirst even though there might be no change in plasma
osmolarity.
•Water deprivation, vomiting
•This stimulation probably occurs because of neural input from cardiopulmonary and systemic arterial
baroreceptors in the circulation
•10-15% drop in blood volume also stimulates thirst centre- weak stimulus
2.Osmotic thirst / intracellular thirst
•Thirst arising from depletion of fluid within cells due to the increase in interstitial fluid solute
concentration after ingestion of salt.
•This increase draws water out of the cells, and they shrink in volume. This increase draws water out
of the cells, and
they shrink in volume and causing cellular dehydration
•An increase of 2-3% in plasma osmolarity triggers thirst centre of the hypothalamus

Many stimuli that trigger thirst cause both intracellular and extracellular dehydration simultaneously.
For example, sweating causes extracellular dehydration, because it reduces the volume of water
available to the blood and interstitial fluids. Sweating also causes intracellular dehydration, because
sweat is less salty than the blood and therefore leaves behind excess salt that increases blood
osmolality. Thus these two mechanisms often go hand in hand in normal circumstances.

All water in the body is present either inside or outside of cells, and the loss of water from these two
compartments triggers different behavioral responses
Intracellular dehydration refers to the loss of water from inside cells and is typically caused by an
increase in blood osmolality, which draws water out of cells by osmosis and causes them to shrink.
By contrast, extracellular dehydration refers to a decrease in the total blood volume, such as occurs
during bleeding.
Intracellular dehydration can be corrected by drinking water alone, extracellular dehydration requires
consumption of both water and salt in order to regenerate the blood at its correct osmolality. For this
reason extracellular dehydration triggers not only thirst but also salt appetite.

Thirst Receptors
Increased blood osmolality is the most important homeostatic signal for drinking in everyday life.
Changes in blood osmolality are detected by two small structures in the forebrain known as the
subfornical organ (SFO) and organum vasculosum of the lamina terminalis (OVLT)
Specialized neurons in these two brain regions are activated by increases in blood osmolality, and
their
activation is necessary and sufficient for generation of thirst.
It is thought that these SFO and OVLT neurons monitor the blood osmolality directly, possibly via
stretch-sensitive ion channels embedded in their plasma membranes that detect changes in cell
volume following intracellular dehydration. projections from the lamina terminalis to the
paraventricular nucleus of the hypothalamus (PVH) and the supraoptic nucleus (SON).The SFO is the
principal site in the brain where ANGII acts to promote drinking behavior
Median preoptic nucleus (MnPO)- integrate this information and communicate with other brain
regions.
Specialized cells carotid arteries (carotid sinus) respond to pressure and thus detect volume changes.
Parasympathetic neurons carry the signals to the brain, where they eventually reach the vasomotor
center of the medulla and the paraventricular nuclei of hypothalamus.

When blood pressure in the catotid sinus bulb decreases, stimulation of the sinus baroreceptors slows
and secretion of an antidiuretic hormone (ADH) / vasopressin from the paraventricular nuclei into
circulation diminishes.
Low blood volume is likely to generate a distinct and probably weaker thirst-inducing signal.
The thirst signal in response to low blood volume is elicited by angiotensin II acting on angiotensin II
receptors in the subfornical organ, a brain region near the ventricles with high vascularization, and
lack of separation of the brain tissue from blood circulation by a blood–brain barrier
The body’s homeostatic control mechanisms maintain a balance between fluid gain and fluid loss.
The hormones ADH (anti-diuretic hormone, also known as vasopressin) and aldosterone, a hormone
created by the renin–angiotensin system, play a major role in this balance.
If the body is becoming fluid deficient, there will be an increase in the secretion of these hormones
that causes water to be retained by the kidneys through increased tubular reabsorption and urine
output to be reduced. Conversely, if fluid levels are excessive, the secretion of these hormones is
suppressed and results in less retention of fluid by the kidneys and a subsequent increase in the
volume of urine produced, due to
reduced fluid retention.

Subcommíssural organ

Pineal

Angiotensin I Angiotensin II

Angiotensinogen Renin

Angiotensin converting Enzyme (ACE)

Sodium & Water Retention

Increased BP

Adrends

Aldosterone —L
When the osmoreceptors detect high plasma osmolarity (often a sign of a low blood volume), they
send signals
to the hypothalamus, which creates the biological sensation of thirst. Osmoreceptors also stimulate
vasopressin (ADH) secretion, which starts the events that will reduce plasma osmolarity to normal
levels.
Hypovolumic thirst-Renin–Angiotensin-aldosterone System (RAAS)-Mediated Thirst
The renin–angiotensin system is a complex homeostatic pathway that deals with blood volume as a
whole, as well as plasma osmolarity and blood pressure. low blood volume activates the
juxtaglomerular apparatus(JGA) in a variety of ways to make it secrete renin into the bloodstream.
Renin cleaves angiotensinogen into angiotensin I. Angiotensin converting enzyme (ACE) in the lungs
converts angiotensin I into angiotensin II.
Angiotensin II acts on the hypothalamus to cause the sensation of thirst. It also causes
vasoconstriction, and the release of aldosterone to cause increased water reabsorption in a
mechanism that is very similar to that of ADH. Renin cleaves angiotensin I from the liver -produced
angiotensinogen.
Angiotensin II has a variety of effects (such as increasing thirst) but it also causes release of
aldosterone from
the adrenal cortex.
Aldosterone has a number of effects that are involved in the regulation of water output. It causes
greatly increased reabsorption of sodium and water, while causing the secretion of potassium into
urine.

•RENIN ANGIOTENSIN ALDOSTERONE SYSTEM

VOLUMIC THIRST

JG cells in kidney
Hypothalamic taste centre

Sensation of taste

Person drinks water

*Water moistens mouth,throat

*Stretch receptors of GI,intestine

Water absorbed from GI tract

Plasma volume back to normal

Osmotic thirst-ADH Feedback

When blood volume becomes too low, plasma osmolarity will increase due to a higher concentration
of solutes per volume of water. Osmoreceptors in the hypothalamus detect the increased plasma
osmolarity and stimulate the posterior pituitary gland to secrete ADH.

ADH causes the walls of the distal convoluted tubule and collecting duct to become permeable to
water—this drastically increases the amount of water that is reabsorbed during tubular reabsorption.
ADH also has a vasoconstrictive effect in the cardiovascular system, which makes it one of the most
important compensatory mechanisms during hypovolemic shock (shock from excessive fluid loss or
bleeding.
Activation of these regions is sufficient to trigger multiple homeostatic responses, including the
generation of thirst, activation of the sympathetic nervous system to increase blood pressure, and
release of the hormones vasopressin (AVP) and oxytocin (OXT). Excitatory lamina terminalis neurons
also synapse directly on neurons in the PVH and supraoptic nucleus (SON) that release AVP and OXT
into the bloodstream via their axon terminals in the posterior pituitary gland

Blood pressure is also monitored by stretch-sensitive mechanoreceptor neurons called baroreceptors

that innervate blood vessels and the heart. Baroreceptors respond to decreases or increases in blood
pressure by inducing or inhibiting thirst, respectively, through their projections via cranial nerves IX
and X to a brainstem region called the nucleus of the solitary tract.

OSMOTIC THIRST

Hypothalamic taste centre activated

Sensation of taste

Negative feedback

Person drinks water

*Water moistens mouth,throat

*Stretch receptors of GI,intestine

Water absorbed from GI tract

Plasma osmolality back to normal

THRESHOLD FOR OSMOLAR STIMULUS OF DRINKING

•The kidneys must continually excrete an obligatory amount of water even in a dehydrated person to
rid the
body of excess solutes that are ingested or produced by metabolism.
•Water is also lost by evaporation from the lungs and the gastrointestinal tract and by evaporation
and
sweating from the skin.
•Therefore, there is always a tendency for dehydration, with resultant increased extracellular fluid
sodium concentration and osmolarity.
• When the sodium concentration increases only about 2 mEq/L above normal, the thirst
mechanism is activated, causing a desire to drink water. This is called the threshold for drinking.
•even small increases in plasma osmolarity are normally followed by water intake, which restores
extracellular fluid osmolarity and volume toward normal.
Stimulates thirst center in the hy thal amus

Increases 1hirst

HCO take n in '

Decreases bl ood osmolal ity

PHYSIOLOGICAL BASIS OF DRINKING-2

Dr. PRADEEP KUMAR R.

Assistant Professor Dept. of Zoology
Govt. College for Women
Thiruvananthapuram

NEUROSCIENCE OF DRINKING

•Drinking water in response to thirst following fluid loss is a pleasant experience, whereas drinking
water after thirst has been satiated is unpleasant. over the course of drinking, pleasure and incentive
motivation for drinking decreases rapidly, resulting in the termination of drinking. Mouth sensation,
swallowing, and gastro-intestinal sensation provides the basis for terminating drinking well before
fluid balance is restored.
•The pleasantness of drinking when thirsty is associated with activation in the anterior cingulate
cortex and orbitofrontal region. Subset of individual neurons in the median preoptic nucleus (MnPO)
appeared to respond to and integrate drinking signals from the mouth and throat, satiation signals
from the gut, and information about an animal’s overall hydration level from the bloodstream. These
regions may contribute to the termination of drinking (Drinking satiety).
•Overdrinking with hyponatraemia and cerebral edema can occur in schizophrenia, reflecting that this
brain disorder can derange physiological mechanisms regulating water balance.

Thirst can also be regulated by anticipatory signals

Normal drinking behavior is not regulated by changes in the blood directly, and instead appears to
anticipate those changes before they occur. There is a delay of tens of minutes between the ingestion
of water and its full absorption into the bloodstream. However drinking can quench (satisfy) thirst
within seconds, long before the ingested water alter the blood volume or osmolality. Brain terminates
thirst by using sensory cues from the oropharynx to track ongoing water consumption and then
estimate how this water intake will alter fluid balance in the future, after the water has been
absorbed. These anticipatory signals are transmitted from the oral cavity to the SFO, where they
inhibit the same thirst neurons that respond to change in the blood volume and osmolality. This
circuit organization allows SFO thirst neurons make a comparison between the physiologic need for
water, which they measure directly by monitoring the blood, and the amount of water that has
recently been consumed, which they measure by tracking oropharyngeal signals of fluid intake. SFO
thirst neurons then compare these two values to decide when drinking should be terminated. It is
likely that a similar integration occurs within other structures of the lamina terminalis that control
drinking behavior and hormone release.

Thirst can also be regulated by anticipatory signals

One signal appears to be temperature, since cold liquids inhibit SFO thirst neurons more efficiently
than warm liquids, and oral cooling alone can reduce both thirst and the activity of these SFO cells.
One explanation for this temperature-dependence is that water ingestion tends to cool the
oropharynx, and as a result animals may learn to associate changes in oral temperature with the post-
ingestive effects of water consumption.
In addition to temperature, other somatosensory signals that report on the sensation of water in the
oral cavity are likely to be important. There is also evidence that signals from further down the
gastrointestinal tract, such as stretch receptors and osmosensors in the stomach, may play a role in
thirst satiation. However in all cases the identity of the relevant sensory neurons and the neural
pathway by which they transmit information to the lamina terminalis remains nebulous.

Eating generates thirst in anticipation of food absorption

•Eating is an important stimulus for thirst in many animals. It increases the need for water for two
reasons:
(1)in order to replace the fluid utilized for swallowing (e.g. saliva) and digestion (e.g. water diverted
from the circulation into the gastrointestinal tract),
(2)in order to counteract the increase in blood osmolality caused by the absorption of salts and
other osmolytes from food.
Meal-associated (prandial) thirst could be secondary to changes in the blood that result from these
water demands imposed by food digestion and absorption. Prandial thirst develops before any
change in blood osmolality or volume can occur. The act of eating itself triggers thirst, in a way that
anticipates the impending homeostatic burden imposed by ongoing food consumption. As a result,
animals drink at the same time that they eat, and changes in blood osmolality and volume are
mitigated.

•Eating activates the same thirst neurons in the lamina terminalis that monitor blood osmolality and
volume, and activation of these neurons is necessary and sufficient for prandial thirst.
•Possible mechanisms include somatosensory signals from the oral cavity that report on food
swallowing or its effects on the saliva; osmosensory signals from the gastrointestinal tract, portal vein,
or other organs that report on the early effects of food ingestion on the osmolality of internal fluids;
and learned associations between food consumption and its eventual effects on the blood that enable
animals use arbitrary sensory cues to anticipate their water needs.
•In addition to these neural mechanisms, several hormones associated with eating and satiety have
been proposed to modulate thirst neurons, including amylin, cholecystokinin (CCK), ghrelin, glucagon-
like peptide-1 (GLP-1), histamines, insulin, and leptin. It is possible that one or more of these
circulating nutritional signals is also critical for the regulation of prandial thirst.
•If prandial thirst is not quenched by drinking, then further food consumption is reduced, a
phenomenon known as dehydration-induced anorexia
Cellular dehydration
•Fluid/Electrolyte Dynamics
•The balance between mineral salts and water in the body is controlled largely by the
Fluid/Electrolyte Balance.
•There are 2 basic Electrolyte imbalances -Electrolyte Stress Overload and Electrolyte Insufficiency.
•Electrolyte Stress Overload
•excess of certain mineral salts and a deficient amount of fluids in the cells results in high blood
pressure
and edema (tissue fluid retention), high blood volume
•This means that people with edema and high blood pressure are very often dehydrated
•Abnormal variations of cell membranes can also inhibit the flow of electrolytes
•Major causes of electrolyte stress also include aluminum toxicity, drinking chemically treated tap
water that contains fluoride, chlorine, and not drinking enough water.

•Electrolyte Insufficiency
•caused by either an insufficient amount of certain mineral salts such as sodium, or by the kidney’s
inability to retain
mineral salts
•hormone aldosterone is largely responsible for the retention of sodium.
•Low levels of aldosterone and other mineralcorticoids can cause electrolytes to be excreted instead
of retained.
•The result of electrolyte insufficiency is low blood volume, weak endocrine and cardiovascular
function, chronic fatigue and poor circulation.
•Drinking reverse osmosis water, distilled water and chemically treated water can cause abnormal
variations in electrolyte balance. RO and distilled water function like diuretics, causing minerals to be
excreted.
•Restoring normal fluid and electrolyte balance begins with hydrating your body with high quality
water, and electrolytes contained therein.
•a person’s demand for water may increase if they: consume caffeine, alcohol, take diuretic
medications, sweat excessively, have chronic diarrhea or vomiting.

Intracellular and extracellular dehydration

•Two kinds of dehydration trigger thirst

•All water in the body is present either inside or outside of cells, and the loss of water from these two
compartments triggers different behavioral responses .
•Intracellular dehydration - loss of water from inside cells and is typically caused by an increase in
blood osmolality, which draws water out of cells by osmosis and causes them to shrink.
•Extracellular dehydration - decrease in the total blood volume, such as occurs during bleeding.
•intracellular dehydration can be corrected by drinking water alone, extracellular dehydration
requires consumption of both water and salt in order to regenerate the blood at its correct
osmolality. For this reason extracellular dehydration triggers not only thirst but also salt appetite.

Polydipsia is excessive thirst. Polydipsia is a nonspecific symptom in various medical disorders. This
symptom is characteristically found in diabetics, often as one of the initial symptoms, and in those
who fail to take their anti-diabetic medications or whose condition is poorly controlled. It can also be
caused by a change in the osmolality of the extracellular fluids of the body, decreased blood volume
(as occurs during major hemorrhage), and other conditions that create a water deficit. This is usually a
result of osmotic diuresis. Diabetes insipidus can also cause polydipsia. Zinc is also known to reduce
symptoms of polydipsia by causing the body to absorb fluids more efficiently and it causes the body to
retain more sodium; thus a zinc deficiency can be a possible cause.

Adipsia is a condition that can affect both humans and other animals and involves an absence of
thirst. Its underlying causes vary but have included anomalies involving the hypothalamus, pituitary
and corpus collosum. It may also be seen medically in association with hypothalmus/pituitary
involvement in Diabetes Insipidus (Adipsic Diabetes Insipidus) and/or hypernatremia or following
pituitary/hypothalmus surgery.

Diabetes insipidus is defined as the passage of large volumes (>3 L/24 hr) of dilute urine (< 300
mOsm/kg). Causes a significant risk of dangerous dehydration as well as a range of other illnesses and
conditions. The disease takes two main forms: Nephrogenic diabetes insipidus and central or
neurogenic diabetes insipidus. Central diabetes insipidus occurs when the pituitary gland fails to
secrete the hormone vasopressin, which regulates bodily fluids. In nephrogenic diabetes insipidus,
vasopressin secretion is normal, but the kidneys do not correctly respond to the hormone.