feeding: motivated behavior in a social context graham redgrave, md johns hopkins university school...
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Feeding: Motivated Behavior in a Feeding: Motivated Behavior in a Social ContextSocial Context
Graham Redgrave, MD
Johns Hopkins University School of Medicine
Department of Psychiatry and Behavioral Sciences
ObjectivesObjectives
• Recognize what it means for eating to be a “motivated” behavior
• Identify embodied elements governing feeding behavior in brain and gut
• Identify external factors influencing eating behavior
Motivated BehaviorsMotivated Behaviors
• Drive toward some goal
• Stereotyped behaviors satiate the drive
• Satiation is always temporary, giving rise to a behavioral cycle
• Cycle may be modulated by internal and external factors (e.g., illness, food availability)
• Learning takes place over time, with repeated iteration through the cycle
What is Drive?What is Drive?
• A construct, the element of the behavioral model that provides the “motive force,” hence “motivated behaviors”
• Embodied in multiple physiological control mechanisms
• The drive to eat serves the organism’s energy homeostasis
• In order to ensure repetitive feeding, the act is rewarding (hedonic)
HomeostasisHomeostasis
• Maintenance of a stable internal state despite changing environment (e.g., body temperature in mammals)
Cycle of Feeding BehaviorsCycle of Feeding Behaviors
time
hunger
foodacquisition
food consumption
satiety
meal patterns- frequency/timing- size- content- social context
satiety signals
meal initiation signals
learning
GI physiology
long-term homeostatic signals
pathways & transmitterssatiety signals
long-term homeostatic signals
pathways & transmitters
meal initiation signals
ObjectivesObjectives
• Recognize what it means for eating to be a “motivated” behavior
• Identify embodied elements governing feeding behavior in brain and gut
• Identify external factors influencing eating behavior
Smith, 2000
Control of Feeding is OverdeterminedControl of Feeding is Overdetermined
CorticotrophinReleasing Hormone
Bombesin
Peptide YY(3-36)
Insulin
Growth HormoneReleasing Hormone
Endorphin
Neuropeptide Y
Decrease IntakeIncrease IntakeLeptinGhrelin
Glucagon-likePeptide-1
Orexins
Serotonin
Norepinephrine
MelanocyteStimulating Hormone
Norepinephrine
MelanocyteStimulating Hormone
DopamineDopamine
CholecystokininGalanin
PancreaticPolypeptide
Agouti-RelatedProtein
CCK is a Prototypic Peripheral CCK is a Prototypic Peripheral Satiety SignalSatiety Signal
• Peptide released from gastric and duodenal mucosa into blood and surrounding tissue when stimulated by food in the enteric lumen
• Plasma level peaks 10-30 min after meal initiation and gradually subsides over 3-5 h
• CCK receptors in the vagus nerve allow communication with central satiety centers via the brainstem
• CCK also functions as a central neurotransmitter in multiple brain regions
Moran & Kinzig, 2004
CCK-A CCK-A Receptor Receptor Antagonism Antagonism Increases Increases Food IntakeFood Intake
CCK is a satiety signal, so blockade of its receptor should, and does, increase food intake.
Hunger Signals: GhrelinHunger Signals: Ghrelin
• Neuropeptide synthesized in the stomach
• Levels increase in food deprivation, peak prior to meals
• Receptors in the arcuate and ventromedial hypothalamus
Cummings et al., 2002
Ghrelin Peaks Ghrelin Peaks Before Meals, Before Meals, Levels Levels Increase After Increase After Weight LossWeight Loss
Saper, Chou, & Elmquist, 2002
Embodiment of Feeding Drives in Embodiment of Feeding Drives in the CNS: Big Picturethe CNS: Big Picture
PeripheryPeriphery
PeripheryPeriphery
HypothalamusHypothalamus
BrainstemBrainstemRewardRewardCentersCenters
de Castro, 2000
Hedonic Hedonic Control: Control: Meal Size as Meal Size as A Function of A Function of Ratings of Ratings of Food Food Palatability Palatability And And Macronutrient Macronutrient ContentContent
Mechanisms of Hedonic Control Mechanisms of Hedonic Control of Feedingof Feeding
• The nucleus accumbens (NAc) is an important reward locus and contains multiple types of opioid receptors
• NAc receives input from feeding centers, such as the lateral hypothalamic area
• Opioid antagonists block food intake, particularly intake of sweet food
Levine et al., 1995
Opioid Antagonist Naloxone Blocks Opioid Antagonist Naloxone Blocks Intake of Sweet FoodIntake of Sweet Food
ObjectivesObjectives
• Recognize what it means for eating to be a “motivated” behavior
• Identify embodied elements governing feeding behavior in brain and gut
• Identify external factors influencing eating behavior
Homeostasis?Homeostasis?
• What can cause a population’s energy balance to shift?
hunger
acquisition
consumption
satiety
learning
Definition of ObesityDefinition of Obesity
• Body Mass Index (BMI)
–Weight (kg)/ Height (m2)
• Overweight: BMI > 25
• Obese: BMI >30
Obesity Trends* Among U.S. AdultsBRFSS, 1985
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14%
Source: Behavioral Risk Factor Surveillance System, CDC.
Obesity Trends* Among U.S. AdultsBRFSS, 1986
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14%
Obesity Trends* Among U.S. AdultsBRFSS, 1987
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14%
Obesity Trends* Among U.S. AdultsBRFSS, 1988
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14%
Obesity Trends* Among U.S. AdultsBRFSS, 1989
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14%
Obesity Trends* Among U.S. AdultsBRFSS, 1990
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14%
Obesity Trends* Among U.S. AdultsBRFSS, 1991
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19%
Obesity Trends* Among U.S. AdultsBRFSS, 1992
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19%
Obesity Trends* Among U.S. AdultsBRFSS, 1993
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19%
Obesity Trends* Among U.S. AdultsBRFSS, 1994
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19%
Obesity Trends* Among U.S. AdultsBRFSS, 1995
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19%
Obesity Trends* Among U.S. AdultsBRFSS, 1996
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19%
Obesity Trends* Among U.S. AdultsBRFSS, 1997
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19% ≥20%
Obesity Trends* Among U.S. AdultsBRFSS, 1998
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19% ≥20%
Obesity Trends* Among U.S. AdultsBRFSS, 1999
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19% ≥20%
Obesity Trends* Among U.S. AdultsBRFSS, 2000
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19% ≥20%
Obesity Trends* Among U.S. AdultsBRFSS, 2001
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19% 20%–24% ≥25%
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
Obesity Trends* Among U.S. AdultsBRFSS, 2002
No Data <10% 10%–14% 15%–19% 20%–24% ≥25%
Obesity Trends* Among U.S. AdultsBRFSS, 2003
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19% 20%–24% ≥25%
Obesity Trends* Among U.S. AdultsBRFSS, 2004
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19% 20%–24% ≥25%
Obesity Trends* Among U.S. AdultsBRFSS, 2005
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person)
No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%
Contributions to Increased Obesity Contributions to Increased Obesity PrevalencePrevalence
• Increased energy intake
• Decreased energy expenditure
Increased Energy IntakeIncreased Energy Intake
• Portion size – “Supersizing”
• Availability of cheap, high calorie prepared foods, particularly those using high-fructose corn syrup
In Defense of HomeostasisIn Defense of Homeostasis
• Homeostasis is said to be “defended” against perturbation
• Observation or manipulation of the environment can demonstrate what is being defended
Spiegel et al., 1993
Meal Size is Meal Size is Defended in Defended in HumansHumans
Top panel: ingestion of small pieces of sandwich results in slower ingestion of calories.
Middle panel: subjects eating smaller pieces of sandwich ate for longer.
Bottom panel: there are no differences between consumers of small or large pieces of sandwich in terms of total calories consumed.
B Rolls et al, 2006
Energy Intake is Energy Intake is NotNot Defended in the Defended in the Presence of Increased Portion SizePresence of Increased Portion Size
Elliott et al, 2002
Annual Per Capita Use of Annual Per Capita Use of SweetenersSweeteners
Teff et al., 2004
Fructose Less Effective At Fructose Less Effective At Reducing Subsequent IntakeReducing Subsequent Intake
Barbie: www.flickr.com/photos/thomashawk/214495265/in/set-72157594491975505/; Report Card: NYT 12/0/07
Highly Energy Dense Food is Highly Energy Dense Food is Everywhere in the Culture!Everywhere in the Culture!
Bjursell et al., 2008
Decreased Locomotor Activity in Decreased Locomotor Activity in Response to a Western DietResponse to a Western Diet
ReviewReview• Homer eats to maintain energy homeostasis• When he eats, a complex, overdetermined
system of physiological elements drive Homer’s behavior
• Homer eats donuts because they taste good, are high in high-fructose corn syrup and do not satiate his appetite, and are cheap and available everywhere…
• …finally, when Homer eats his donuts, he may be less likely to go run around the track at Springfield High….
AcknowledgmentsAcknowledgments
• Paul McHugh, MD• MBU Rounds
• Contact: [email protected]• Website: http://jhedjournalclub.pbwiki.com
Eating Disorders Research Group
• Tim Moran, PhD
• Angela Guarda, MD
• Janelle Coughlin, PhD
• Ellen Ladenheim, PhD
• Shauna Reinblatt, MD
• Nick Bello, PhD
