Obesity: Addiction and

Reward
By: Nick Sasser
Undergraduate Seminar
10/20/2010
 Background
 Obesity is defined as a Body
Mass Index (BMI) of 30 or
greater
 Major risk factors are type 2
diabetes, cardiovascular
disease, and certain cancers.
 In 2008, annual health care
cost was an estimated 147
billion per year.
 Global Epidemic
Fig.1 Percent of Obese (BMI
≥30) in U.S. Adults
Causes of Obesity
 Inactive lifestyle
 Genes and family
history
 Addiction and food is
rewarding
 Emotional factors and
pregnancy
 Age

Jared Fogle—Subway
 Animal Studies
 Researchers found 20 years
ago that leptin plays a huge
role in obesity.
 Society of Neuroscience fed
mice a high-fat, high-calorie Researchers’ studies of these animals led
diet, the brain pleasure to the discovery of the hormone leptin,
which helps control appetite.
centers become less
responsive over time.
 When the mice were offered
healthy food after weeks of
junk food, they were less
likely to eat it than mice fed
on healthy food only.
 Human Studies
 As in mice, leptin and
several hormones in the
hypothalamus affect
hunger or fullness.
 Neuroscientists learned
fatty food taps the pleasure
centers in the brain.
Fat cells produce a hormone called leptin,
which travels through the body’s blood stream
and acts on a brain region called the
hypothalamus. Leptin helps to regulate
appetite and metabolism. A lack of leptin, or its
receptor in the brain, can lead to uncontrolled
food intake and obesity.
 Human Studies
 Research shows that
Dopamine modulates
rewarding properties of food
 Dopamine receptors (D2)
availability were significantly
lower in obese patients.
 Individuals with the lowest D2
levels had the highest BMI. Brain scans show that when people view
images of appetizing foods (right), there is
 Cohen’s paper proposed 10 more activity in the striatum — a brain
neurophysiological pathways. region associated with reward — than when
the foods are distasteful (left). This image
shows brain activity in a teenager with
deficiencies in the hormone leptin, which
helps control appetite. After taking leptin
supplements, his brain responses show this
normal pattern of activation.
Characteristic Mechanism How it is exploited
Physiological response to food Dopamine secreted when food is perceived; Ubiquitous availability of food and
and to images of food dopamine creates motivations for food food images in multiple settings

Inborn preferences for sugar Under stress, people choose items that Excessive availability and production
and fat provide immediate calories to respond to of high-fat and high-sugar content
increased energy demands foods

Hardwired survival strategies Automatically respond to abundance and Increase shelf space and abundance of
variety by greater consumption high-calorie foodstuffs; increased
introduction of product variety
without nutritional variety

Inability to judge calorie Visual system cannot judge volume or Excessively large portion sizes
content content; signals of satiety are imprecise,
based more on volume than energy density

Natural tendency to conserve People prefer labor-saving innovations to Marketing convenient, ready-to-eat
energy reduce calorie expenditure foods, drive-ins

Mirror neurons People unconsciously mimic others’ eating Modeling eating behaviors
behaviors

Conditioned responses to Hunger (dopamine secretion) stimulated by Pairing food advertising with images
stimuli associating food products with other human promising fun, pleasure, love, power,
wants and needs and sex; use of inaccurate labeling

Priming Automatically respond to items made music, lighting, images, symbols, to

salient through indirect methods enhance purchase of foods

Automatic stereotype Automatic responses to items that are Use of racial/ethnic groups and
activation associated with the self and with social celebrities to model eating behaviors
groups and expectations
Future Studies & Treatments
 Strategies aimed at improving dopamine
function may be beneficial in the treatment of
obese individuals.
 Stem Research
 Exercise
 Diet
References
Center for Disease Control (CDC)
Cohen, D. (2008). Neurophysiological pathways
to obesity: below. Diabetes, 57.
Obesity and the brain. (n.d.). Retrieved from
http://www.sfn.org/index.aspx?pagename
=publications_rd_obesity
Paul C. Fletcher and Sadaf Farooqi, University
of Cambridge. ©2007.
Wang, G, Volkow, D, Logan, J, Pappas, N, &
Zhu, W. (2001). Brain dopamine and
obesity. The Lancet, 357, 354-357.