Feeding: Motivated Behavior in a Social Context

Feeding: Motivated Behavior in a Social Context
Graham Redgrave, MD Johns Hopkins University School of Medicine Department of Psychiatry and Behavioral Sciences My clinical interest is eating disorders, and my research interest is in the neuroimaging of anorexia nervosa, but in order to understand eating disorders, it is helpful to understand all of ingestive behavior, and to understand it as a *motivated behavior*. I use the term ‘feeding’ rather than ‘eating’ because we are going to be talking about both animal and human behavior.

As a psychiatrist, I am interested in behavior and practice making observations about behavior; for example, why does Homer eat the donut? What happens when he does? When does he get hungry? How does he know when to stop? Will Homer eat more donuts than brussels sprouts, and if so, why? Will he eat more when he’s alone or with his family or at work? I note that his eyes are locked on target, that his mouth is wide open, and so forth… The point is we are going to need a model to structure our investigation, and, eventually, our clinical work, and this model comes first from the Perspectives of Psychiatry, which in turn for its account of behavior, draws on the description of “motivated behaviors”

Objectives 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 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 More about Drive later.

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) Embodied by multiple control mechanisms - in the case of eating, embodiments are in the brain and gut The drive to eat serves the organism’s energy homeostasis - Homer always looks the same In order to ensure repetitive feeding, the act is rewarding - Homer always eats the donuts Both homeostatic and hedonic aspects of feeding must be understood

Homeostasis Maintenance of a stable internal state despite changing environment (e.g., body temperature in mammals)

Cycle of Feeding Behaviors
learning food consumption meal patterns frequency/timing size content social context GI physiology satiety signals long-term homeostatic signals pathways & transmitters meal initiation signals long-term homeostatic signals food acquisition satiety pathways & transmitters The cycle of feeding begins with hunger, followed by the acquisition and consumption of food, and finally satiation. Learning’s arc goes in the opposite direction of time’s arrow because we learn from the consequences of our behavior - chocolate donuts may taste better than jelly donuts, for example, in which case Homer will stick to the chocolate donuts. There are many ways to approach the study of behaviors, because they are complex. At the macroscopic level, we can study meal patterns, and different aspects of meal patterns, such as frequency and timing of meals, meal size, macronutrient content, and social context. GI physiology helps us understand the relationship between food that’s been consumed and is being metabolized and the way the contents of the stomach lumen, for example, affect the rate of food consumption, or why we only eat a little of rich food and more of lower-calorie food. On the neural and even molecular biological level, elements of the homeostatic and hedonic aspects of drive and their interrelationships can be determined by studying the pathways and transmitters, second messengers, etc. of the system. We will now talk a little more about the embodiment of the feeding drive before moving on to description… satiety signals meal initiation signals hunger time

Control of Feeding is Overdetermined
Increase Intake Decrease Intake Ghrelin Neuropeptide Y Leptin Insulin Orexins Endorphin Glucagon- l ike Peptide YY(3-36) P eptide-1 Agouti-Related Melanocyte Pancreatic Melanocyte Protein Stimulating Hormone P olypeptide Stimulating Hormone Galanin Growth Hormone Cholecy stokinin Bombesin These are 19 of the dozens of compounds that affect nutrient intake. There are a couple of point to make: Control of feeding behavior is overdetermined, which means that there are multiple physiological elements controlling a single set of behaviors Some elements, depending on when or where or in what concentrations they appear, act to increase AND decrease behaviors We will only talk about 2 - ghrelin and CCK, as exemplars of how these elements work… Releasing Hormone Dopamine Norepinephrine Dopamine Norepinephrine Serotonin Cor ticotrophin Releasing Hormone Smith, 2000

CCK is a Prototypic Peripheral Satiety Signal
Peptide released from gastric and duodenal mucosa into blood and surrounding tissue when stimulated by food in the enteric lumen Plasma level peaks 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 Brainstem locus is the Nucleus of the Solitary Tract

CCK-A Receptor Antagonism Increases Food Intake
CCK is a satiety signal, so blockade of its receptor should, and does, increase food intake. Further evidence from Dr. Moran’s lab showing that blockade of the satiety signal CCK increases intake. From the article: Fig. 1. Effects of the specific CCKA receptor antagonist devazepide on daily food intake in Rhesus monkeys. Doses are expressed as micrograms per kilogram. Devazepide increased intake in a dose-related manner. The effect was maximum at a dose of 100 g/kg. Moran and McHugh were not able to explain why the highest dose (320 g/kg) showed less effect than 32 g/kg, except that devazepide might lose some of its non-specific effects at that dose, that they were not the only ones to find this in rhesus monkeys, and finally that this shows up in rats, too. Moran & Kinzig, 2004

Hunger Signals: Ghrelin
Neuropeptide synthesized in the stomach Levels increase in food deprivation, peak prior to meals Receptors in the arcuate and ventromedial hypothalamus

Ghrelin Peaks Before Meals, Levels Increase After Weight Loss
This slide illustrates two main points. First, ghrelin peaks just before meals, and second, ghrelin levels are consistently higher in subjects after behavioral weight loss (though it’s not clear if they are more hungry, from a subjective point of view). This study confirms similar meal-pattern changes in ghrelin in obese as in former studies of lean subjects. Findings in rodents: continuous administration of ghrelin durably increases body weight. exogenous ghrelin decreases the metabolic rate and the catabolism of fat, thereby affecting all aspects of the system of energy regulation in such a way as to increase body weight. Blockade of ghrelin in the brain leads to a reduction in food intake, suggesting that endogenous ghrelin signaling is required to maintain normal appetite. Post-gastric bypass patients have very low ghrelin levels (they have little functioning stomach so do not make ghrelin) and what they have does not fluctuate around meal times. Cummings et al., 2002

Embodiment of Feeding Drives in the CNS: Big Picture
Reward Centers Brainstem Hypothalamus Note the inputs from peripheral sites such as the stomach via the vagus nerve and the retina via the suprachiasmatic nucleus and the locus of action of these factors in the hypothalamus. Also note the presence of the nucleus accumbens, which we will discuss later. NTS - nucleus tractus solitarius CGRP - calcitonin gene related peptide PB - parabrachial nucleus ARC - arcuate nucleus VPpc - ventroposterior parvicellular thalamic nucl. LHA - lateral hypothalamic area DMH - dorsomedial hypothalamus NPY/AgRP - Neuropeptide Y/Agouti-Related Protein POMC/CART - Proopiomelanocortin/Cocaine Amphetamine Regulated Transcript AIC/GIC - agranular and granular insular cortices ILC - infralimbic cortex Periphery Saper, Chou, & Elmquist, 2002

Hedonic Control: Meal Size as A Function of Ratings of Food Palatability And Macronutrient Content
Let’s talk a little about the hedonic control of eating. Homer has to choose between brussels sprouts and donuts - which does he choose? This slide shows meal size as a function of palatability - the better something tastes, the more is consumed. The relative proportion of both fat and protein increase, while the relative proportion of carbohydrate decreases minimally. Therefore, Homer eats more donuts than brussels sprouts because they taste better, largely due to their fat content and the amount of carbohydrate. de Castro, 2000

Mechanisms of Hedonic Control of 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 Nac contains delta-1, delta-2, mu and kappa receptors at least

Opioid Antagonist Naloxone Blocks Intake of Sweet Food
Naloxone, which blocks mu, delta, and kappa opioid receptors, reduces intake of food in 24- and 48-hr chow-deprived rats, as shown in the black bars above, but of particular note is the fact that naloxone exerts a greater influence in all the groups of these animals when they were fed sweet chow, which is more palatable, and therefore presumably more rewarding. Levine et al., 1995

Homeostasis? What can cause a population’s energy balance to shift?
hunger acquisition consumption satiety learning

Definition of Obesity Body Mass Index (BMI) Weight (kg)/ Height (m2)
Overweight: BMI > 25 Obese: BMI >30 The problem is, we are a nation of Homers…..

Obesity Trends* Among U.S. Adults BRFSS, 1985
(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person) No Data <10% %–14% Source: Behavioral Risk Factor Surveillance System, CDC.

(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person) No Data <10% %–14%

(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person) No Data <10% %–14% %–19%

(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person) No Data <10% %–14% %–19% ≥20%

(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person) No Data <10% %–14% %–19% %–24% ≥25%

(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person) We have never had an epidemic like this that we have been able to track so thoroughly and see. As I told you, this is conservative. About 60 million adults, or 30 percent of the adult population, are now obese, which represents a doubling of the rate since 1980. No Data <10% %–14% %–19% %–24% ≥25%

(*BMI ≥30, or ~ 30 lbs overweight for 5’ 4” person) We have never had an epidemic like this that we have been able to track so thoroughly and see. As I told you, this is conservative. About 60 million adults, or 30 percent of the adult population, are now obese, which represents a doubling of the rate since 1980. No Data <10% %–14% %–19% %–24% %–29% ≥30%

Contributions to Increased Obesity Prevalence
Increased energy intake Decreased energy expenditure There is evidence for both these mechanisms, and evidence they interrelate

Increased Energy Intake
Portion size – “Supersizing” Availability of cheap, high calorie prepared foods, particularly those using high-fructose corn syrup

In Defense of Homeostasis
Homeostasis is said to be “defended” against perturbation Observation or manipulation of the environment can demonstrate what is being defended

Meal Size is Defended in Humans
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. This is parallel data for humans. Subjects were given tuna or chicken salad wraps cut into 5g, 10g, or 15g pieces. The top panel shows that the rate of consumption of food was higher in the 15g compared with the 5g groups. The middle panel shows that those eating 5g pieces took statistically significantly longer than those eating the 10g and the 15g pieces, and the bottom panel shows that meal there were no significant differences in the total meal size, because the subjects eating the small pieces ate longer. Spiegel et al., 1993

Energy Intake is Not Defended in the Presence of Increased Portion Size
23 subjects fed (10 women) ad lib amounts of meals on each of 2 consecutive days per week over three weeks, but the portion sizes were varied. Persons fed larger portion sizes ate significantly more. Participants took in a mean excess of 4636 calories (1.3 lbs) over this time, with no significant diminution over time. Weight status (normal or overweight) did not affect amount ingested. Large portions were 150% of baseline portions. Abstract ROLLS, BARBARA J., LIANE S. ROE, AND JENNIFER S. MEENGS. The effect of large portion sizes on energy intake is sustained for 11 days. Obesity. 2007;15:1535–1543. Objective: A previous study showed that increasing the portion sizes of all foods led to an increase in energy intake that was sustained over 2 days. The objective of the present study was to determine whether participants would compensate for excess energy intake or continue to overeat when portion sizes were increased for 11 days. Research Methods and Procedures: Participants in the study were 23 normal-weight and overweight participants (10 women and 13 men). All of their foods and caloric beverages were provided during two different periods of 11 consecutive days, which were separated by a 2-week interval. During one period, standard portions of all items were served; during the other, all portion sizes were increased by 50%. Results: The 50% increase in portion sizes resulted in a mean increase in daily energy intake of kcal (p ), which did not differ significantly between women and men. This increase was sustained for 11 days and did not decline significantly over time, leading to a mean cumulative increase in intake of kcal. A significant effect of portion size on intake was seen at all meals and in all categories of foods except fruit (as a snack) and vegetables. The effect of portion size on intake was not influenced by the body weight status of participants. Discussion: These results strengthen the evidence suggesting that increased portions contribute to the overconsumption of energy and to excess body weight. B Rolls et al, 2006

Annual Per Capita Use of Sweeteners
In 1977, according to Michael Pollan in the NYT (1/28/07), George McGovern’s Senate Select Committee on Nutrition in 1977 recommended we eat less red meat and dairy. There was a huge backlash, which caused the rewording of the Committee’s recommendations, and eventually led to the “nutrition industry”, and, among other things Elliott et al, 2002

Fructose Less Effective At Reducing Subsequent Intake
Normal weight women in this study. FIG. 9. Left, Hunger ratings (AUC over a 15-h period) on d 1 during the HGl and HFr dietary manipulations. Significant treatment by time by behavioral trait (restraint) interactions were found on d 1 when food consumption was controlled. Restrained (n = 5), but not unrestrained (n=7), subjects reported greater hunger on the HFr day compared with the HGl day [(F(1,8)=8.0; P 0.03)]. Right, Total fat intake (kilocalories) on the day after dietary HGl diets and HFr diets during which subjects were permitted ad libitum and eating. Unrestrained subjects selected significantly more total fat than restrained subjects on the day after HGl (P <0.05). No significant differences in total fat intake between the HGl and HFr days were observed in unrestrained eaters. Significantly greater fat intake was observed on the day after HFr compared with after HGl in the restrained eaters [F(1,10) = 6.62; P<0.03]. Teff et al., 2004

Highly Energy Dense Food is Everywhere in the Culture!
Kelly Brownell, who researches what he calls the “Toxic Food Environment” has said that it is McDonald’s corporate policy to have one of its restaurants no more than 4 minutes from the average American. Barbie: Report Card: NYT 12/0/07

Decreased Locomotor Activity in Response to a Western Diet
The authors show that mice fed a western, high-fat diet (40% fat, 43% carbs) vs. chow (10% fat, 67% carbs): A: locomotor activity was significantly lower for mice given WD compared with chow diet measured over 72 h following food switch. B: locomotor activity was acutely lower after food switch in mice given WD than in mice given chow diet, measured during the 3–5 h after the switch. The authors also found that half the weight gain attributed to use of the WD was because of decreased locomotor activity Mice had access to normal chow (R36; Lactamin, Stockholm, Sweden) and water ad libitum. The R36 diet contains 3.5% cellulose (weight percent) and 22.9% protein, 67.1% carbohydrate, and 9.6% fat (energy percent). The WD used was RD Western diet (no. D ; Research Diets, New Brunswick, NJ) containing 5% cellulose (weight percent) and 16.9% protein, 42.8% carbohydrate, and 40.3% fat (energy percent). Bjursell et al., 2008

Review 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….

Eating Disorders Research Group
Acknowledgments Eating Disorders Research Group Tim Moran, PhD Angela Guarda, MD Janelle Coughlin, PhD Ellen Ladenheim, PhD Shauna Reinblatt, MD Nick Bello, PhD Paul McHugh, MD MBU Rounds Contact: Website:

As a psychiatrist, I am interested in behavior and practice making observations about behavior; for example, why does Homer eat the donut? What happens when he does? When does he get hungry? How does he know when to stop? Will Homer eat more donuts than brussels sprouts, and if so, why? Will he eat more when he’s alone or with his family or at work? I note that his eyes are locked on target, that his mouth is wide open, and so forth… The point is we are going to need a model to structure our investigation, and, eventually, our clinical work, and this model comes first from the Perspectives of Psychiatry, which in turn for its account of behavior, draws on the description of “motivated behaviors”

Feeding: Motivated Behavior in a Social Context

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